integrate evidence based competencies into their ... · “Professional nursing practice can only advance as ... efficient, patient centered, equitable care.” ... epigastric pain

2016

CNEA / Key Choice 1

1

Presented by:

Karen Marzlin DNP, RN, ACNPC-AG, CCNS, CCRN-CMC, CHFN

Cynthia Webner DNP, RN, ACNPC-AG, CCNS, CCRN-CMC, CHFN

www.cardionursing.com 2016

“Professional nursing practice can only advance as

much as individual nurses are aware that a

knowledge gap exists in their practice, feel

empowered to access further learning, and

integrate evidence based competencies into their

professional practice to provide safe, effective,

efficient, patient centered, equitable care.”

www.tigersummit.com

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2016

CNEA / Key Choice 2

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8

Acute Coronary Syndrome (ACS)

No ST Elevation

Non STEMI

Unstable Angina

ST Elevation

STEMI

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2016

CNEA / Key Choice 3

9

1, 190,000 Hospital Discharges with primary or

secondary diagnosis of ACS

UA/NSTEMI STEMI

NRMI-4*: 71%

AHA Get with the Guidelines: 69%

GRACE** Study: 62%

NRMI-4*: 29%

AHA Get with the Guidelines: 31%

GRACE** Study: 38%

Heart Disease and Stroke Statistics – 2012 Update. Circulation 2012; 125:e2-e220.

*NRMI-4: National Registry of Myocardial Infarction; **GRACE Study: Global Registry of Acute Coronary Events.

2016

Acute Coronary Syndrome refers to any rupture of plaque or thrombotic event that leads to symptomatic ischemia or infarction.

STEMI NonSTEMI /

Unstable Angina 10 2016

2016

CNEA / Key Choice 4

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Deposit of lipids, calcium, fibrin, and other cellular substances within the lining of the arteries.

Initiates a progressive inflammatory response in an effort to heal the endothelium.

End result of inflammatory process: the production of a fibrous atherosclerotic plaque.

Plaque can progress to cause coronary stenosis

Plaque can also rupture prior to causing significant stenosis

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CNEA / Key Choice 5

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Non-Modifiable Risk Factors Previous history Family history

1st degree relative (parents, siblings)

Men < 55; Women < 65

Age

Gender

Socioeconomic Factors and Ethnicity

9 easily measured and potentially modifiable risk factors account for over 90% of the risk of an initial acute MI

Smoking

Hypertension

Dyslipidemia

Diabetes

Obesity

Metabolic Syndrome

Inactivity

Alcohol

Mortality Rate Age > 40 years:

1 year: F- 23%, M- 18%

5 year: F- 43%, M – 33% 14 2016

2016

CNEA / Key Choice 6

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Classic Symptoms

Stable angina

Unstable angina

MI

Symptom Variations

Women Elderly Diabetics

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CNEA / Key Choice 7

Stable Angina

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Typical angina is defined as angina that meets all three of the following characteristics:

Substernal chest discomfort with a characteristic quality and duration

Provoked by exertion or emotional stress

Relieved by rest or nitroglycerin.

Atypical angina is

defined as angina meeting two of the characteristics of typical angina

Non cardiac chest pain is defined as chest pain with none or only one of the characteristics of typical angina.

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Caused by unstable or ruptured plaque that causes abrupt closure of a coronary artery which may spontaneously reperfuse.

Occurs with minimal exertion or at rest

Angina that increases in severity or is very severe on first presentation

OR increased dose of nitroglycerin is required to achieve relief (Progressive angina)

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2016

CNEA / Key Choice 8

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• Usually no described as a sharp or stabbing pain (? women)

• Should not worsen with changes in position or respiration.

• Not usually located in the middle to lower abdomen and does usually not radiate to the lower extremities.

• Not typically defined in seconds or hours.

CAUTION WHEN ASKING THE PATIENT ABOUT “PAIN”! 2016

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Quality:

Use the word “discomfort” or “symptoms” when assessing

Many patients with dyspnea or chest pressure deny the presence of

pain.

Location:

Assessment of location includes radiation of symptoms.

Time:

Both the time of onset and duration of symptoms

Aggravating and alleviating factors:

Key in differentiating stable from unstable angina.

Reproducibility:

Reproducibility of chest pain by applying pressure to the chest wall

suggests a musculoskeletal etiology.

Does not completely rule out the presence of angina.

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2016

CNEA / Key Choice 9

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Autonomic dysfunction can affect symptoms experienced with angina

Less likely to experience pain

Approximately 20 - 25% of all patients presenting with ACS have diabetes

More severe multi-vessel disease

Greater proportion of ulcerated plaques resulting in intracoronary thrombi

Higher rates of complications from ACS, higher mortality, and high rates of sudden death

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Angina in Women

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Delay presenting with symptoms

Attribute symptoms to other non-cardiac causes

Presentation

More epigastric discomfort

Less specific complaints: dyspnea or fatigue

More atypical (sharp) chest pain WISE Study: 65% of women presented with atypical symptoms

Symptoms of discomfort from nose to navel should be evaluated for presence of CAD

Less documented stenotic disease of major epicardial coronary arteries Altered microvascular and endothelial function

Downstream microembolization

WISE study- Women’s Ischemic Syndrome Evaluation

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2016

CNEA / Key Choice 10

23

Stable angina is often initial presentation

Women with Non-STEMI and unstable angina are older than men and have more co-morbid conditions (diabetes and HTN)

The average age for first MI is 64.7 years for men and 72.2 years for women (Go et al., 2013)

Female sex is a risk factor for mortality in STEMI

Women receive less evidence based therapies including

reperfusion

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Generalized symptoms Dyspnea, diaphoresis, N&V, and syncope

Confusion, weakness

Symptoms often attributed to the aging process Importance of assessment with activity tolerance

Don’t complain about chest pain 37% of patients > 65

42% of patients > 75 years

75% of those > 85 years

Silent MIs account for 60% of MIs in those > 85 years of age STEMI

< 65 years = 90% pain

> 85 years = 57% pain

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LBBB complicates the recognition of STEMI

LBBB is present 33.8% of STEMI patients > 85 years.

STEMI recognized only 70% of time in patients > 85 years

Often co-existing heart failure with the ACS diagnosis

NSTEMI

44% not diagnosed on admission

HF with STEMI

< 65 years = 12%

> 85 years = 45%

Diagnosis of “Other”

< 65 years = 5%

> 85 years = 24%

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Decreased arterial compliance

Increased cardiac afterload

Diastolic dysfunction of the left ventricle

Inflammatory dysregulation

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Mobility and function Activities of daily living

Strength

Frailty: state of declining reserves in physical strength and functional status

Poor Nutrition Status Albumin

Weight loss

More co-morbid conditions

Altered renal and hepatic function

More co-morbid conditions

Altered renal and hepatic function

Poly pharmacy

Cognitive Impairment

Hearing Alterations

Vision Alterations

Isolation

Resources / Education

Socioeconomic

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> 75 years of age:

high risk for short

term death or non-

fatal MI.

In hospital death:

< 65 years: 1 in 100

> 85 years: 1 in 10

Morbidity and mortality

after STEMI also increased

due to electrical and

mechanical complications.

Heart failure and

pulmonary edema occur in

more than half of patients

> 75 years

Shock occurs in > 10% of

patients > 75 years.

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29-38% of ACS patients

Complete occlusion of a vessel by a thrombus

Fibrin stable clot (red clot)

Classified more specifically by the portion of the left ventricle suffering injury.

Mortality is greatest within the first 24 to 48 hours of symptom onset

TREATMENT FOCUS = REPERFUSION 30 2016

2016


Nationally under treated according to evidence based practice guidelines (Crusade Registry)

Pathophysiology often involves a platelet plug or white clot

Less stable clot

Opportunity for spontaneous reperfusion

Differentiated from unstable angina by troponin levels

TREATMENT FOCUS = ANTIPLATELET THERAPY 31 2016

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Increase myocardial oxygen demand: Hyperthermia

Hypertension

Tachycardia

Conditions producing over stimulation of the sympathetic nervous system (cocaine use, hyperthyroidism)

Decrease myocardial oxygen delivery: Anemia

Pulmonary disease.

Increase myocardial oxygen demand and decrease myocardial oxygen supply: Aortic stenosis

Hypertrophic cardiomyopathy

Type 2 MI

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I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Inferior Wall:

II, III, aVF

Lateral Wall:

I, aVL, V5, V6

Anterior Wall: V1-V4

Septum: V1, V2

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Chest pain or severe epigastric pain, non traumatic in origin, with components typical of myocardial ischemia or MI: Central/substernal compression or crushing chest pain

Pressure, tightness, heaviness, cramping, burning, aching sensation

Unexplained indigestion, belching, epigastric pain

Radiating pain in neck, jaw, shoulders, back, or 1 or both arms

Associated dyspnea

Associated nausea/vomiting

Associated diaphoresis

If non diagnostic:

Repeat q 15 to 30 minutes

Use ST segment monitoring

Perform V7-V9

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I LAD

II RCA

III RCA

aVR

aVL LAD

aVF RCA

V1 LAD

V2 LAD

V3 LAD

V4 LAD

V5 Circ

V6 Circ

Inferior Wall:

II, III, aVF

Lateral Wall:

I, aVL, V5, V6

Anterior Wall: V1-V4

Septum: V1, V2

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Found only in cardiac muscle

Most sensitive indicator of myocardial damage Capable of diagnosing small amounts of myocardial necrosis not

measured by rises in CK-MB levels

Approximately 30% of patients with non-ST elevation and normal CKMB levels will test positive for Non-STEMI

Of equal sensitivity and specificity

Troponin remains elevated for a long period Beneficial for late presentation Challenging for re-infarction

Positive troponin + ECG changes of injury / ischemia or

ACS symptoms = INFARCT 41 2016

Non infarct cardiac causes of elevated troponin: heart failure, left ventricular hypertrophy, tachyarrhythmias, pericarditis, cardiac trauma

Non CAD causes of troponin elevation (sepsis, pulmonary emboli, chronic kidney disease, chemotherapy, respiratory failure, burns, neurological disease )

Troponin I more specific in renal dysfunction Patients with ESRD commonly have elevated troponin T

Not a false positive - relates to overall dysfunction of the cardiorenal system

< 10% of patients with ESRD have elevated troponin I in absence of ACS

Elevated troponin levels are marker of risk and associated with an increased mortality – even when diagnosis is not myocardial infarction

Degree of troponin elevation correlates with risk of death

New high sensitivity troponin T

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Cardiac Biomarker Summary

Cardiac

Biomarker

Specificity /

Sensitivity

Rise Peak Duration

CK-MB Highly specific 4 to 6 hours 18 to 24 hours 2 to 3 days

Troponin I or T Highly specific

and sensitive

4 to 6 hours 18 to 24 hours 10 or more days

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Timing of Release of Various Biomarkers After

Acute Myocardial Infarction

44

Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester,

MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80.

Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5. 2016

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ASA: 325 mg (non enteric coated) If fibrinolytic therapy – 162-325 mg

P2Y12 inhibitor (loading dose before or at time of PCI) If fibrinolytic therapy - clopidogrel only

Anticoagulants (related to reperfusion strategy) If fibrinolytic – weight based heparin x 48 hours

Oral beta blockers ASAP IV if hypertensive or tachycardic

NTG – Sublingual vs IV Morphine Sulfate (Class I) Oxygen if hypoxemic (arterial oxygen saturation < 90%) High intensity statin therapy D/C NSAIDS ACE Inhibitors (within 24 hours)

Greatest benefit in anterior wall MI, LVEF < 40%, HTN, diabetes or chronic kidney disease

Aldosterone Antagonists Initiate within 7 days in those with LVEF <40% , HF , or diabetes

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It is reasonable to use an insulin-based regimen to achieve and maintain glucose levels less than 180 mg/dL while avoiding hypoglycemia* for patients with STEMI with either a complicated or uncomplicated course.

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Reperfusion is number one treatment strategy

Primary Coronary Intervention (PCI) preferred treatment strategy if within 90 minutes Goal: 90 minutes from 1st medical contact

Fibrinolytics within 30 minutes of hospital presentation (or 30 minutes from EMS to

fibrinolytics)

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The Winner!

2016

2016


Interventional Revascularization: PCI (Primary Coronary Intervention (in STEMI) or

Percutaneous Coronary Intervention)

PTCA: Percutaneous transluminal coronary

angioplasty

Coronary Stent

BMS: Bare metal

DES: Drug eluting

Coronary Extraction Atherectomy

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Interventional Revascularization

Indications Reperfusion in STEMI

Strategy of choice if 90 minute reperfusion time

Unstable angina / NSTEMI High risk features

Stable angina Courage Trial -2007

Contraindications When antiplatelet

therapy is contraindicated

Complications Abrupt closure Dissection In stent thrombosis (acute or

late) Down stream embolization Emergency CABG Bleeding or hematoma Pseudoaneurysm* Retroperitoneal Bleed Arterial Embolus Contrast nephropathy Restenosis (late) Coronary artery aneurysm (late) MI Stroke Death

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Missed diagnosis of unequivocal ECG due to

atypical symptoms

Unrecognized unequivocal ECGs

Delay in diagnosis of subtle ECGs or failure to

perform serial ECGs

Delay in administration of therapy or inappropriate

abortion of treatment.

Resolution of pain alone is not an indication for aborting

therapy. Look for 50-100% resolution of ST-segment

elevation before considering suspending reperfusion

therapy based on further assessment

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Each community should develop a STEMI system of care consistent with minimum standards of AHA’s Mission Lifeline

Door to device time alone is not sufficient to further reduce mortality

The average time of presentation after symptom onset is 1.5 to 2.0 hours.

Patient populations with the longest delays are women, African Americans, and the elderly.

Nurses can make an impact through patient and community education and awareness campaigns.

60 minutes is the golden hour: Survival rates improve significantly.

2016

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Dual antiplatelet Anticoagulation Oxygen if SpO2< 90% NTG

IV in first 48 hours for persistent ischemia, HTN, HF Should not interfere with mortality reducing beta blockers or ace

inhibitors

MS (if NTG unsuccessful and other anti ischemic drugs on board )

Beta Blockers (within 24 hours) Start PO when hemodynamically stable May use IV if hypertensive

ACE Inhibitors (within 24 hours) In select patients – pulmonary congestion or LVEF < 40%) – may also

be used in other patients

High intensity statin

DC – NSAIDS

Medical Supportive Therapy:

Similar to STEMI

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Attacking Platelet is number one treatment strategy

Two antiplatelets agents are indicated

There are 3 types of antiplatelet agents

Aspirin

P2Y12 Receptor Antagonists

Intravenous GP IIb/IIIa Inhibitors

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Dual antiplatelet therapy for invasive strategies in medium to high risk patients ASA (and one of following) P2Y12 / ADP Receptor

blockers Clopidogrel Prasugral Ticagrelor * preferred over

clopidogrel

GP II b / III a Inhibitors

(*eptifibatide, * tirofiban, abciximab) * preferred agents Used only in special

circumstances

Antiplatelet therapy also in conservative treatment Prasugrel not unless

PCI is planned Abciximab not unless

PCI is planned

Dual antiplatelet

therapy is also

used after STEMI

and after any

coronary

intervention. 2016

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Stent

Restenosis

Compared to

Stent Thrombosis

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What is it? Not waiting for failed medical treatment Not waiting for + noninvasive test Angiography with intent of revascularization Done within 12 to 24 hours

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Algorithm for Management of Patients With Definite or Likely NSTE-ACS

NSTE-ACS: Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy1. ASA (Class I; LOE: A)

2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) :· Clopidogrel or

· Ticagrelor

3. Anticoagulant:· UFH (Class I; LOE: B) or

· Enoxaparin (Class I; LOE: A) or

· Fondaparinux† (Class I; LOE: B)


2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):· Clopidogrel or

· Ticagrelor

3. Anticoagulant:· UFH (Class I; LOE: B) or


· Fondaparinux† (Class I; LOE: B) or

· Bivalirudin (Class I; LOE: B)

Medical therapy chosen based on cath

findings

PCI With StentingInitiate/continue antiplatelet and anticoagulant

therapy1. ASA (Class I; LOE: B)

2. P2Y12 Inhibitor (in addition to ASA) :· Clopidogrel (Class I; LOE: B) or

· Prasugrel (Class I; LOE: B) or

· Ticagrelor (Class I; LOE: B)

3. GPI (if not treated with bivalirudin at time of PCI)· High-risk features, not adequately pretreated

with clopidogrel (Class I; LOE: A)· High-risk features adequately pretreated with

clopidogrel (Class IIa; LOE: B)

4. Anticoagulant:· Enoxaparin (Class I; LOE: A) or

· Bivalirudin (Class I; LOE: B) or

· Fondaparinux† as the sole anticoagulant (Class III: Harm; LOE: B) or

· UFH (Class I; LOE: B)

CABGInitiate/continue ASA therapy and

discontinue P2Y12 and/or GPI therapy1. ASA (Class I; LOE: B)

2. Discontinue clopidogrel/ticagrelor 5 d before, and prasugrel at least 7 d before elective CABG

3. Discontinue clopidogrel/ticagrelor up to 24 h before urgent CABG (Class I; LOE: B). May perform urgent CABG <5 d after clopidogrel/ticagrelor and <7 d after prasugrel discontinued

4. Discontinue eptifibatide/tirofiban at least 2-4 h before, and abciximab ≥12 h before CABG (Class I; LOE: B)

Late Hospital/Posthospital Care1. ASA indefinitely (Class I; LOE: A)

2. P2Y12 inhibitor (clopidogrel or ticagrelor), in addition to ASA, up to 12 mo if medically treated (Class I; LOE: B)

3. P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), in addition to ASA, at least 12 mo if treated with coronary stenting (Class I; LOE: B)

Can consider GPI in addition to ASA and P2Y12 inhibitor in high-risk (e.g., troponin positive) pts (Class IIb; LOE: B)

· Eptifibatide

· Tirofiban

TherapyIneffective

TherapyEffective

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NSTE-ACS: Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy


2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) :

· Clopidogrel or

· Ticagrelor

3. Anticoagulant:

· UFH (Class I; LOE: B) or


· Fondaparinux (Class I; LOE: B)


2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):

· Clopidogrel or

· Ticagrelor

3. Anticoagulant:

· UFH (Class I; LOE: B) or


· Fondaparinux† (Class I; LOE: B) or

· Bivalirudin (Class I; LOE: B)

Medical therapy chosen based on cath

findings

PCI With StentingInitiate/continue antiplatelet and anticoagulant

therapy1. ASA (Class I; LOE: B)

2. P2Y12 Inhibitor (in addition to ASA) :

· Clopidogrel (Class I; LOE: B) or

· Prasugrel (Class I; LOE: B) or

· Ticagrelor (Class I; LOE: B)

3. GPI (if not treated with bivalirudin at time of PCI)

· High-risk features, not adequately pretreated with clopidogrel (Class I; LOE: A)

· High-risk features adequately pretreated with clopidogrel (Class IIa; LOE: B)

4. Anticoagulant:


· Bivalirudin (Class I; LOE: B) or

· Fondaparinux† as the sole anticoagulant (Class III: Harm; LOE: B) or

· UFH (Class I; LOE: B)

CABGInitiate/continue ASA therapy and

discontinue P2Y12 and/or GPI therapy1. ASA (Class I; LOE: B)

2. Discontinue clopidogrel/ticagrelor 5 d before, and prasugrel at least 7 d before elective CABG

3. Discontinue clopidogrel/ticagrelor up to 24 h before urgent CABG (Class I; LOE: B). May perform urgent CABG <5 d after clopidogrel/ticagrelor and <7 d after prasugrel discontinued

4. Discontinue eptifibatide/tirofiban at least 2-4 h before, and abciximab ≥12 h before CABG (Class I; LOE: B)

Late Hospital/Posthospital Care1. ASA indefinitely (Class I; LOE: A)

2. P2Y12 inhibitor (clopidogrel or ticagrelor), in addition to ASA, up to 12 mo if medically treated (Class I; LOE: B)

3. P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), in addition to ASA, at least 12 mo if treated with coronary stenting (Class I; LOE: B)

Can consider GPI in addition to ASA and P2Y12 inhibitor in high-risk (e.g., troponin positive) pts (Class IIb; LOE: B)

· Eptifibatide

· Tirofiban

TherapyIneffective

TherapyEffective

†In patients who have been treated with fondaparinux (as upfront therapy) who are

undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at

the time of PCI because of the risk of catheter thrombosis. 63 2016

64

When to do it? Refractory angina Hemodynamic

instability Electrical instability Initially stable

patients with a high risk for clinical events

Excluded: very frail elderly, severe hepatic, renal or pulmonary disease / active or inoperable cancer

Early invasive therapy is not recommended in patients with acute chest pain with a low likelihood of ACS

Early invasive therapy

is not recommended in patients who do not want to consent to revascularization.

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Recurrent angina / ischemia Rest or low level activity with medical treatment

Troponin +

New or presumed new ST depression

S&S HF or worsening mitral regurgitation

High risk findings on noninvasive testing EF < 35%, large anterior perfusion defect, multiple perfusion defects)

Hemodynamic instability

Sustained VT

PCI within 6 months

Prior CABG

Reduced LV Function

High risk TIMI or GRACE Score

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TIMI Risk Score Age > 65

3 or > risk factors for CAD

Prior 50% or > stenosis

ST deviation on ECG

2 or > anginal events in previous 24 hours

Use of ASA in prior 7 days

Elevated cardiac biomarkers

GRACE

Older age

Killip class

Systolic BP

Cardiac arrest during presentation

Serum creatinine

Positive initial cardiac markers

HR

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TIMI Risk Score* for NSTE-ACS

TIMI Risk

Score

All-Cause Mortality, New or Recurrent MI, or

Severe Recurrent Ischemia Requiring Urgent

Revascularization Through 14 d After

Randomization, %

0–1 4.7

2 8.3

3 13.2

4 19.9

5 26.2

6–7 40.9

*The TIMI risk score is determined by the sum of the presence of 7

variables at admission; 1 point is given for each of the following variables:

≥65 y of age; ≥3 risk factors for CAD; prior coronary stenosis ≥50%; ST

deviation on ECG; ≥2 anginal events in prior 24 h; use of aspirin in prior 7

d; and elevated cardiac biomarkers.

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Feature High Risk

≥ 1 of the

features below

must be

present:

Intermediate Risk

No high-risk features, but must have 1 of

the following:

Low Risk

No high- or intermediate- risk

features but may have any

features below:

History Accelerating

tempo of

ischemic sx in

preceding 48 h

Prior MI, peripheral or cerebrovascular

disease, or CABG; prior ASA use

Character

of pain

Prolonged

ongoing (> 20

min) rest pain

• Prolonged (> 20 min) rest angina,

now resolved, w/ moderate/high

likelihood of CAD

• Rest angina (> 20 min) or relieved with

rest or sublingual NTG

• Nocturnal angina

• New-onset or progressive CCS class

III/IV angina in past 2 wks w/o

prolonged (> 20 min) rest pain but with

intermediate/high likelihood of CAD

• ↑ Angina frequency,

severity or duration

• Angina provoked at lower

threshold

• New onset angina with

onset 2 wks to 2 mos prior

to presentation

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Feature High risk Intermediate risk Low risk

Clinical

findings

• Pulmonary edema, most

likely due to ischemia

• New/worsening MR murmur

• S3 or new/worsening rales

• Hypotension, bradycardia,

tachycardia

• Age > 75 y

Age > 70 y

ECG •Angina @ rest with transient

ST-segment changes > 0.5

mm

•BBB, new/presumed new

•Sustained VT

• T-wave changes

• Pathological Q-waves/resting ST-

depression < 1 mm in multiple lead

groups (anterior, inferior, lateral)

Normal or

unchanged

ECG

Cardiac

markers

↑ Cardiac TnT, TnI, or CK-MB

(e.g., TnT/TnI > 0.1 ng/mL)

Slightly ↑ cardiac TnT, TnI, or CK-MB

(e.g., TnT > 0.01, but < 0.1 ng/mL)

Normal

Estimation of the short-term risk of death and nonfatal cardiac ischemic events in UA/NSTEMI is a complex multivariable problem that cannot be

fully specified in a table such as this; this table is mean to offer general guidance & illustration rather than rigid algorithms. Braunwald E, et al.

AHCPR Publication No. 94-0602:1–154. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Table 7.

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Medications to improve prognosis Aspirin

ASA benefits > in those > 65 years Long term benefit with 81 mg

Clopidogrel / Prasugrel / Ticagrelor Dual antiplatelet therapy in conservative management

for 12 months Higher risk of bleeding with dual antiplatelet therapy

No elderly sub group data for clopidogrel

Statins Have greater benefit in elderly for reduction of future MI

and death than in younger patient populations

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Medications to improve prognosis Beta-blockers ACE inhibitors Definite in select patients / reasonable in

all ARBs if ACE-I intolerant

Aldosterone antagonists EF < 40 with HF or diabetes

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SL NTG Instruction

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No more than 1 dose of SL NTG If chest discomfort is unimproved or is

worsening 5 min after 1 NTG call 9-1-1

immediately before taking additional NTG.

May take additional NTG while waiting EMS.

Chew ASA while waiting EMS.

In chronic stable angina if symptoms are significantly

improved by 1 dose of NTG may repeat NTG every 5

min for a maximum of 3 doses and call 9-1-1 if

symptoms have not resolved completely.

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• Acetaminophen, ASA, tramadol,

narcotic analgesics (short term)

• COX-2 Selective

NSAIDs

• Nonacetylated salicylates

• Non COX-2 selective NSAIDs

• NSAIDs with some

COX-2 activity

Select patients at low risk

of thrombotic events

Prescribe lowest dose

required to control symptoms

* Addition of ASA may not be sufficient protection

Antman EM, et al. J Am Coll Cardiol 2008. Published ahead of print on December 10, 2007. Available at

http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001.

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Smoking cessation Reduction of hyperlipidemia

LDL < 100 mg/dL or < 70 mg/dL (optimal)

Hypertension control <130/80 for kidney disease or diabetes

Diabetes control Hb AIc < 7 Physical activity minimum of 5 days / per

week 7 days recommended

BMI 18.5 – 24.9 kg/mm2

Phase II Cardiac Rehab Influenza Vaccine / PneumoniaVaccine

2016

http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001

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75

Use oxygen for hypoxemia

Assess response to beta-blocker therapy. HR / BP

Arrhythmia control

Assess for complications related to specific type of MI Assess heart sounds for new holosystolic murmurs

Risk for myocardial rupture

Observe for signs of left ventricular dysfunction, including hypotension or clinical signs of heart failure.

Monitor ECG for conduction disturbances and arrhythmias

Assess for presence of RV infarct 2016

76

Management of arterial access site

Assessment for contrast nephropathy

Restrict activity for the first 12 hours, and then begin Phase I Cardiac Rehabilitation (progressive mobility)

Referral to Phase II Cardiac Rehabilitation

Utilize cardiac monitoring ST-segment monitoring

Uninterrupted monitoring for first 24-48 hours

Address addiction to nicotine Consideration for nicotine withdrawal

Focus on holistic approach to anxiety reduction Include the family. Family visits do not have a negative

impact on vital signs or cardiac rhythm 2016

2016


77 2016

Proximal LAD

Proximal to first diagonal

Anterolateral

Proximal to first septal

perforator

Anteroseptal

Mid LAD

Anterior MI

78

2016

2016


Myocardium at risk

Mortality and morbidity

Post Infarction ejection fraction

79 2016

Tachycardia Sinus tachycardia

Atrial tachycardia

Ventricular tachycardia

Right BBB and left anterior hemiblock

Complete heart block

Ventricular septal defect New loud systolic

murmur

Cardiogenic shock

Long term ventricular modeling and heart failure

80 2016

2016


RCA occlusion 80% to 85% of time

Marginal branch: Right ventricle

Posterior descending artery = Posterior wall of

LV

Concept of right versus left dominant

81 2016

82 2016

2016


83

Cellular edema produces an inflammatory response.

Recruitment of some stem cells leads to some tissue

regeneration.

Damaged tissue is bruised and cyanotic.

Catecholamines are released from myocardial cells, thus

increasing the risk of arrhythmias.

Cardiac biomarkers are released.

White blood cells invade the necrotic tissue within 2 to 3 days.

Scavenger cells release enzymes to break down necrotic tissue.

The necrotic wall can become very thin during this phase, and

the patient is at risk for cardiac rupture.

2016

84

A weak collagen matrix forms by second week, myocardium is still vulnerable to

re-injury.

Scar formation has started by third week.

Necrotic area is completely replaced with scar tissue by week 6. Scar tissue does

not contribute to the contractile function of the myocardium.

Myocardial necrosis (transmural and non transmural) and stunned or hibernating

viable myocardium adversely affect the synergy of left ventricular contraction.

Surviving myocytes hypertrophy in an attempt to compensate for damaged

tissue.

Excessive non-contractile collagen is present in the newly hypertrophied

myocardium, leading to a ventricle that is stiff and noncompliant.

Regional wall motion dysfunction may improve due to recovery of post-ischemic

viable myocardium. Does not necessarily correlate with an improvement in

overall left ventricular ejection fraction.

Non-uniform left ventricular dilatation occurs. Occurs even in patients with

recovery of regional wall motion abnormalities. 2016

2016


85 2016

86 2016

2016


87

Cold extremities

Cyanosis

Oligurua

Decreased mentation

Large LV infarction (>

40% myocardium)

Right ventricular infarct

Mechanical

complication

Heart Failure:

• Cause: Ischemic, stunned, hibernating, or injured

myocardium.

• HF after a STEMI is a predictor of mortality.

• Functional mitral valve regurgitation can co-exist.

2016

88

V-fib preventable cause of

death

90% of sustained

arrhythmias occur in first

48 hours

Higher mortality than

arrhythmias early in course

ICD consultation if no

reversible cause

2016

2016


89 2016

90 2016

2016


91 2016

92

Transmural infarct extending to the epicardium and causing an inflammatory response

Decreased incidence with reperfusion

Persistent pain > one week: Dressler’s syndrome

Accompanied by fever and malaise

High dose (650 mg) enteric coated aspirin every 4-6 hours can be used

If pain is not controlled with aspirin, then colchicine, acetaminophen, or narcotic agents can be used

Non-steroidal anti-inflammatory medication and glucocorticoids should not be used due the increased risk of myocardial scar thinning

2016

2016


93

Occurs in approximately 5% of STEMI patients

If no reperfusion, the incidence of ventricular aneurysm is as high as 10% to 30%

More common with transmural anterior wall MI patients

Localized myocardial wall thinning and bulging of the left ventricle at the site of infarction

Stretched portion of the myocardium contains three layers and is connected to a ventricle by a wide neck

Expands during systole during the acute phase and thus contributes to mechanical dysfunction of the left ventricle Can contain thrombus

Site of junction can be source of ventricular arrhythmias

2016

94

Persistent ST elevation after AMI (anterior) often indicates true aneurysm

Often accompanied by deep QS waves and T wave inversion

Persistent ST elevation may be associated with systolic dyskinesis, akinesis, or a large area of necrosis, even in the absence of anatomic aneurysm

Considered chronic if

persist for > 6 weeks

ACE inhibitors can reduce

true aneurysm

development

NSAIDs can increase

development of aneurysms

Left-ventricular

aneurysmectomy

Heart failure

Ventricular arrhythmias

Thrombus on

anticoagulation 2016

2016


95 2016

96 2016

http://www.google.com/url?sa=i&rct=j&q=&esrc=s&frm=1&source=images&cd=&cad=rja&docid=OOH29NOF_2Xj9M&tbnid=eQzeIudvcqQz5M:&ved=0CAUQjRw&url=http://archive.ispub.com/journal/the-internet-journal-of-thoracic-and-cardiovascular-surgery/volume-13-number-2/giant-left-ventricular-saccular-true-aneurysm-at-posterobasal-localization.html&ei=sB82UrDiK9as4AOtpIDgDw&psig=AFQjCNErIckgQdy2Hl30qqbh2_EffkLJ3g&ust=1379365146683012

2016


97

Cardiac tamponade from

free wall rupture

Formation of left

ventricular diverticulum or

pseudoaneurysm from

free wall rupture

Left to right shunt from

septal rupture

Acute mitral regurgitation

from papillary muscle

rupture.

10% of MIs

15% of in hospital deaths

after MI

Without surgical

intervention, the mortality

rate for rupture is > 80%

at two weeks.

Two high risk periods

1st 24 hours

Within 1st week ( 3 to 5 days)

Associated with delayed

fibrinolytics and late

presentation Examples in next class! 2016

Post DISCHARGE AFTER MI

98 2016

2016


After the patient achieves a rehabilitation level equivalent with

activities of daily living, he/she can begin a walking program

3 to 4 METS

Should be by time of discharge

Begin walking 5 to 10 minutes at a time

Patients should rate activity as moderate

Shortness of breath means overexertion. Other signs of

activity intolerance include: angina, dizziness, diaphoresis,

prolonged fatigue, and nausea.

The use of force to open windows or tight jar lids should be

avoided in patients with lifting restrictions.

99 2016

100 2016

2016


Typical MET Levels of Common Activities

Activity MET Level Activity MET Level Washing, dressing,

grooming 2.1 Grocery shopping 2.1

Light housework 2.51 Heavy equipment operation 6.0 Interior cleaning 3.01 Vehicle repair 2.93 Laundry 2.07 Walking (moderate to

brisk)

3.0 to 5.0

Food preparation

and clean up 2.54 Jogging / Running 6.3 to 8.0

Light shoveling

(<10 pounds) 6.0 Golfing

(Pulling Clubs)

3.75

(4.3) Lawn and garden 3.45 to 3.66 Strength training 3.0

Physical care for

children 2.67 to 2.72 Dancing 4.5

Physical care for

adults 2.89 Biking 8.0

Source: National Cancer Institute; Sanderson, 2010)

101 2016

Driving requires only 1.5 to 3.0 METS.

Most patients with an uncomplicated hospital course can

drive 1 week after discharge. Driving instructions should

be compliant with any existing state regulations.

Patients should be accompanied when they resume driving

and should avoid stressful driving situations such as night

driving, rush hour, high speeds, and driving during heavy

rain or snow.

Driving should be delayed for 2 to 3 weeks in patients with

a complicated myocardial infarction. This includes patients

who had a cardiac arrest, hypotension, arrhythmias, or heart

failure during hospitalization.

102 2016

2016


Travel Patients can usually travel by air within 2 weeks if accompanied

by a travel companion, and if the patient has sublingual

nitroglycerin

If free of all angina symptoms and complications of their myocardial

infarction

Patients should also have airport transportation assistance to avoid

excessive stress and rushing in the airport

Patients should also take precautions when traveling to avoid the

development of deep vein thrombosis

103 2016

Sex After an acute coronary syndrome, stable patients can resume sexual

activity with their usual partner in one week to 10 days (Anderson et al., 2011).

Patients are uncomfortable asking about resuming sexual relationships, so instructions regarding sexual activity should be included as a routine part of all discharge instructions.

Patients with a history of angina during sexual relationships may be instructed to take nitroglycerin prior to engaging in sexual activities.

The average intimate session ranges from 2.5-4 METS for most people.

Walking at 2 mph on level ground is 2.5 METS. Mowing the lawn with a power mower or walking at 3.5 mph is 4 METS. Climbing up a flight of stairs is 8 METS.

The biggest risk with sex in the cardiac patient is the possibility of arrhythmias, which is associated with sympathetic activity increased during arousal. Patients with uncontrolled or untreated hypertension need to discuss specific guidelines with their physician (Sotile & Cantor-Cooke, 2003).

104 2016

2016


Return to Work Low risk myocardial infarction (LVEF > 45%, successful

revascularization with PCI, age < 70 years) can generally return to work after 2 weeks.

Most myocardial infarction adverse events reach a low steady state at 10 weeks. This may guide decision making in some types of employment.

Patients who need to return to physically demanding activities can have an exercise stress test that compares their performance on the stress test to the METs required for the activity. This will provide information about the ability and safety of engaging in activities based on the MET level achieved during exercise stress test.

(Anderson et al., 2011).

105 2016

Cardiac Rehabilitation Goals:

Increase functional capacity

Reduce disability

Improve quality of life

Modify cardiac risk factors

Reduce morbidity and mortality.

Pooled data from a meta-analysis of studies involving the

exercise portion of cardiac rehabilitation show a benefit of

reduced all-cause mortality of approximately 25% when

compared to usual care.

In one study of over 600,000 Medicare patients, mortality

rates were 21% to 34% lower in patients who participated in

cardiac rehabilitation (Suaya, Stason, Ades, Normand, & Shepard, 2009).

106 2016

2016


Cardiac Rehabilitation

Low-risk patients can implement an exercise prescription at

home or in a community setting. Low-risk patients include

those with absence of ischemia or arrhythmias on a stress test.

High-risk patients should be in medically supervised exercise

programs. They are defined as patients with ischemia or

serious arrhythmias on a stress test.

Under utilization of cardiac rehabilitation.

107 2016

Treating the Whole Patient

Depression

Approximately 1 in 5 patients hospitalized with MI have major depression. There is also evidence that depression continues for several months after discharge (Fihn et al., 2012; Bush et al., 2005).

There is strong evidence that patients who are depressed post MI have a higher rate of mortality from both cardiac and non-cardiac causes (Bush et al., 2005).

Anxiety and Stress

In post MI patients, interventions to reduce stress can reduce recurrent cardiac events by as much as 35-75% (Gibbons et al., 2002).

Social Support

Role Identity 108 2016

2016


109

Cardiovascular

Assessment in

Emergency Situations

2016

110 2016

2016


Key Assessment Tools

Integration with Obstructive Shock and Mechanical Emergencies

Pulling it All Together

111 2016

Heart Sounds An essential

assessment tool!

112 2016

2016


Auscultatory Areas

113 2016

Cardiac Diastole (Atrial & Ventricular): Early Passive Ventricular Filling

114

RIGHT

ATRIUM

LEFT

ATRIUM

AORTA

Pulmonary

Artery

2016

2016


Atrial Systole & Ventricular Diastole: Late Active Ventricular Filling

115

Atrial Kick

RIGHT

ATRIUM

LEFT

ATRIUM

AORTA

Pulmonary

Artery

2016

Beginning Ventricular Systole: Isovolumic Contraction

116

RIGHT

ATRIUM

LEFT

ATRIUM

AORTA

Pulmonary

Artery

2016

2016


Ventricular Systole: Ejection

117

RIGHT

ATRIUM

LEFT

ATRIUM

AORTA

Pulmonary

Artery

2016

Murmurs

• High blood flow through a normal or abnormal valve

• Forward flow through a narrowed or irregular orifice into a dilated chamber or vessel

• Backward or regurgitant flow through an incompetent valve

118 2016

2016


Murmur Fundamentals

• Stenotic Murmurs – Valve does not open appropriately

– Heard during the part of the cardiac cycle when the valve is open

• Regurgitant Murmurs – Valve does not close appropriately

– Heard during the part of the cardiac cycle when the valve is to be closed

119 2016

Systolic Murmurs: What is Happening During Systole

• Tricuspid and Mitral Valve Closed

– Tricuspid Regurgitation

– Mitral Regurgitation

• Pulmonic and Aortic Valve Open

– Pulmonic Stenosis

– Aortic Stenosis

120 2016

2016


AORTIC Stenosis Systolic Ejection Murmur

• May be present before any significant hemodynamic changes occur

• More severe AS longer murmur

• Timing: Midsystolic

• Location: Best heard over aortic area

• Radiation: Toward neck and shoulders – May radiate to apex

• Configuration: Crescendo-decrescendo

• Pitch: Medium to high

• Quality: Harsh

121 2016

Mitral Regurgitation

• Timing: Holosystolic

• Location: Mitral area

• Radiation: To the left axilla

• Configuration: Plateau

• Pitch: High

• Quality: Blowing, harsh or musical

122 2016

2016


BETWEEN AORTIC STENOSIS AND MITRAL REGURGITATION:

Which of these valvular disorders can develop acutely?

123 2016

Diastolic Murmurs: What is Happening During Diastole

• Tricuspid and Mitral Valves Open

– Tricuspid Stenosis

– Mitral Stenosis

• Pulmonic and Aortic Valves Closed

– Pulmonic Regurgitation

– Aortic Regurgitation

124 2016

2016


Diastolic Murmurs Mitral Stenosis

• Timing:

– Holodiastolic if severe MS

– Mid to Late diastole if moderate MS

• Location: Apex

• Configuration: Crescendo

• Pitch: Low

• Quality: Rumbling

• Best heard with patient in left lateral position

• Increases with isometric exercise, and expiration

125

2016

Aortic Regurgitation

• Diastolic Murmur of AR – Length of murmur correlates severity of AR – Timing: Early diastole – Location: left sternal boarder

• 3rd,4th ICS

– Radiation: Towards apex – Configuration: Decrescendo – Pitch: High – Quality: Blowing – Patient Position: Sitting and learning forward at end

expiration – Intensity: Increases with increased peripheral vascular

resistance: Squatting, exercising, hand gripping

126 2016

2016


BETWEEN MITRAL STENOSIS AND AORTIC REGURGITATION:

Which of these valvular disorders can develop acutely?

127 2016

When you have Tachycardia Ask

Yourself:

128

Why is my patient

compensating?

2016

CO = SV x HR

2016


Blood Pressure Monitoring

• Systolic: Maximum pressure when blood is expelled from the left ventricle – Represents stroke volume

• Diastolic: Measures rate of flow of ejected blood and vessel

elasticity – Represents state of arterioles

• Pulse Pressure: Difference between systolic and diastolic

pressure

• Mean pressure (MAP): calculated; pressure that determines end organ perfusion

129 2016

Blood Pressure Assessment

• Variation of up to 15mm Hg between arms is normal

• BP in legs - 10 mm Hg higher than arms

130 2016

2016


Etiology of Hypotension

Cardiac Output

SVR Blood

Pressure

2016 131

BP = CO x SVR • Low BP could be due to:

–Low CO • HR too slow or too fast

• Preload too low or too high

• Contractility low

–Low SVR • Vasodilation due to sepsis, anaphylaxis,

altered neurological function, drugs

2016 132

2016


Use of Pulse Pressure

• PP < 35 with tachycardia (C.O. problem)

– Early sign of inadequate

blood volume

– Will also be seen with cardiogenic shock

– Vasoconstriction is compensatory

• PP > 35 with tachycardia (SVR problem)

– Early sign sepsis

– Vasodilation is primary pathology

2016 133

Comparison of 2 Hypotensive Patients

History of CABG with LVEF 25%

Presents with SOB

Pulmonary edema on CXR

Cause: Decreased C.O.

Treatment may actually involve afterload reduction to increase cardiac output

88/70 1 week history of upper respiratory symptoms

Presents with confusion

CXR infiltrate LLL

WBC 15,000, Fever

Cause: Decreased SVR

Treatment is focused on filling tank and restoring vascular tone.

82/30

2016 134

No vasopressor! Fluid and

Vasopressors

2016


Pulsus Paradoxus • Patient is placed in a semirecumbent position • Respirations should be normal • BP cuff inflated to at least 20 mm Hg above the systolic pressure • Slowly deflated until the first Korotkoff sounds are heard only during

expiration. – Pulsus paradoxus is present at this pressure reading, if the cuff is

not further deflated and the first Korotkoff sound is not audible during inspiration.

• As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded.

• If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present.

(Yarlagadda, Chakri, 2005 Cardiac Tamponade. Retrieved 3-22-06 from

www.emedicine.com) 135

May be present in cardiac tamponade.

2016

JVD (Jugular Venous Distension)

2016 136

May be present in cardiac tamponade, tension pneumothorax, and large PE.

2016


Assessment Integration by Disease Process

Obstructive Shock and Mechanical Emergencies

137 2016

Cardiac Tamponade Who is at risk?

138

Trauma

Post CABG

Post MI

Pericarditis /

Effusion

2016

2016


139 139

Pericardial Effusion

• Abnormal amount and/or type of fluid in the pericardial space

• Acute or chronic

• Increase capillary permeability due to inflammation may cause fluid leak into pericardial space – >120cc can cause tamponade if rapid

– 2 Liters may not cause tamponade if slow

2016

140 140

Pericardial Effusion – Signs /Symptoms

• Friction Rub • Tachycardia • Decreased breath sounds – if subsequent pleural

effusions • Pulsus Alternans • Chest Pain

– Want to sit up and lean forward if pericarditis

2016

2016


141 2016

Cardiac Tamponade

• Clinical syndrome caused by accumulation of fluid in the pericardial space

• Results in reduction in ventricular filling and ultimately hemodynamic compromise

• Differentiation between pericardial

effusion and tamponade is hemodynamic status.

142 2016

2016


Cardiac Tamponade: Signs and Symptoms

• Same as with pericarditis and pericardial effusion

• Feeling of impending doom • Beck’s Triad

• Hypotension, Distended neck veins, Muffled heart sounds

• Equalization of filling pressures (RAP, PAD, PAOP within 5mm of each other)

• Pulses paradoxus – Also observed in constrictive pericarditis, tension

pneumothorax, severe obstructive pulmonary disease, restrictive cardiomyopathy, PE, and RV infarct with shock.

143 Echocardiogram

2016

144 2016

2016


Cardiac Tamponade: Treatment

• Supportive

– Oxygen

– Volume expansion

– Bedrest with leg elevation

– Dobutamine (increase pump without increasing SVR)

– Avoid positive pressure mechanical ventilation (decreases venous return)

145

Pericardiocentisis Percutaneous

Surgical window *

2016

Tension Pneumothorax

Who is at risk?

146

Trauma

Mechanical Ventilation

Chest Tubes

2016

2016


147


• Accumulation of air into the pleural space without a means of escape causes complete lung collapse and potential mediastinal shift

• Etiology • Blunt trauma

• Positive pressure mechanical ventilation

• Clamped or clotted water seal drainage system

• Airtight dressing on open pneumothorax

2016

148


• Pathophysiology • Air rushes in-cannot escape pleural space

• Creates positive pressure in pleural space

• Ipsalateral lung collapse

• Mediastinal shift

• Contralateral lung compression

• Potential tearing of thoracic aorta

•Can also compress heart decrease RV filling

•Shock

2016

2016


Tension Pneumothorax: Signs and Symptoms

• Anxiety / agitation

• Diminished / absent breath sounds

• Dyspnea

• Tachypnea

• If mediastinal shift:

• Tracheal shift away from affected side

• LATE SIGN

• JVD

• Hypotension

149 2016

150

0Hypotension with Mechanical Ventilation

0 Sedation

0 Conversion to positive pressure ventilation. 0 Assure adequate circulating fluid

volume

0 Development of auto PEEP 0 Increase expiration time

0 Tension Pneumothorax 0 Chest tube required

2016

2016


151


• Oxygen (100%)

• Emergency decompression

• Perpendicular insertion of large bore needle

• Second anterior space at mid clavicular line

• Flutter valve to prevent atmospheric air from entering into the space

• Chest Tube

Treatment

2016

Aortic Dissection

Who is at risk?

152 2016

2016


153

Risk Factors for Development of Thoracic Aortic Dissection

Conditions Associated With Increased Aortic Wall Stress

• Hypertension, particularly if uncontrolled • Pheochromocytoma

• Cocaine or other stimulant use

• Weight lifting or other Valsalva maneuver

• Trauma

• Deceleration or torsional injury (eg, motor vehicle crash,

fall)

• Coarctation of the aorta

Note: Information on this slide is adapted from Table 9 in full-text version of TAD Guidelines

2016

ISSUE:

Patient’s are usually asymptomatic until a catastrophic event occurs. Therefore: Identifying disease in high risk patients while still stable is a priority.

154 2016

2016


Pathophysiology

• Intimal tear

• False channel

155 2016

156 2016

2016


Classification of Dissections

• Acute or chronic

• Type A Dissections: Dissections involving the ascending aorta.

• Type B Dissections: Dissections involving the descending thoracic aorta. These dissections begin distal to the left subclavian artery.

157 2016

Complications of Dissection

• Aortic regurgitation from retrograde dissection involving aortic valve or from aortic dilatation.

• MI from retrograde coronary artery dissection. • Cardiac tamponade from ascending aorta or aortic arch

rupture. • Intraplerual rupture from descending aortic dissection

ruptures into intrapleural space – most commonly left sided. • Retroperitoneal bleed from rupture of abdominal aorta

dissection. • Stroke from brachial artery compromise. • Paraplegia, reduced blood flow to kidneys, bowels, and lower

extremities from compromise of arterial branches.

158 2016

2016


Clinical Presentation

Chest or back pain with variation in upper extremity blood pressure is key assessment finding in aortic dissection. Recurrent chest or back pain can indicate extension or rupture. The presence of aortic regurgitation in the setting of chest pain is also suspicious for aortic dissection.

159 2016

Estimation of Pretest Risk of Thoracic Aortic Dissection

* Loeys-Dietz syndrome, vascular Ehlers-Danlos syndrome, Turner syndrome, or other connective tissue disease.

†Patients with mutations in genes known to predispose to thoracic aortic aneurysms and dissection, such as FBN1, TGFBR1, TGFBR2, ACTA2, and MYH11.

160

High Risk Conditions

• Marfan Syndrome

• Connective tissue disease*

• Family history of aortic disease

• Known aortic valve disease

• Recent aortic manipulation (surgical or

catheter-based)

• Known thoracic aortic aneurysm

• Genetic conditions that predispose to AoD†

1

2016

2016


161

Genetic Disorders

• Marfan Syndrome

• Ehlers-Danlos Syndrome, Vascular Form

2016

162

Genetic Disorders

• Bicuspid Aortic Valve • Turner Syndrome

2016

2016



163

High Risk Pain Features

Chest, back, or abdominal pain features

described as pain that:

• is abrupt or instantaneous in onset.

• is severe in intensity.

• has a ripping, tearing, stabbing, or sharp

quality.

2

2016


164

High Risk Examination Features

• Pulse deficit

• Systolic BP limb differential > 20mm Hg

• Focal neurologic deficit

• Murmur of aortic regurgitation (new or not

known to be old and in conjunction with pain)

3

2016

2016


Risk-based Diagnostic Evaluation: Patients with High Risk of TAD

165

Patients at high-risk for TAD are those that present with at

least 2 high-risk features

The recommended course of action for high-risk TAD patients

is to seek immediate surgical consultation and arrange for

expedited aortic imaging.

• TEE (preferred if clinically unstable)

• CT scan (image entire aorta: chest to pelvis)

• MR (image entire aorta: chest to pelvis)

Expedited aortic imaging

2016

166 2016

2016


167

Recommendations for Initial Management

a. In the absence of contraindications,

intravenous beta blockade should be

initiated and titrated to a target heart rate

of 60 beats per minute or less.

b. In patients with clear contraindications to

beta blockade, nondihydropyridine calcium

channel–blocking agents should be used as

an alternative for rate control.

I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III


Initial management of thoracic aortic dissection should be

directed at decreasing aortic wall stress by controlling

heart rate and blood pressure as follows:

2016

168


c. If systolic blood pressures remain greater

than 120mm Hg after adequate heart rate

control has been obtained, then angiotensin-

converting enzyme inhibitors and/or other

vasodilators should be administered

intravenously to further reduce blood pressure

that maintains adequate end-organ perfusion.

d. Beta blockers should be used cautiously in the

setting of acute aortic regurgitation because

they will block the compensatory tachycardia.



2016

2016


169


Vasodilator therapy should not be initiated

prior to rate control so as to avoid

associated reflex tachycardia that may

increase aortic wall stress, leading to

propagation or expansion of a thoracic aortic

dissection.


Base treatment goals on highest

blood pressure reading.

2016

Rate/Pressure Control

Intravenous beta blockade

or Labetalol

(If contraindication to beta blockade

substitute diltiazem or verapamil)

Titrate to heart rate <60

1

Pain Control

Intravenous opiates

Titrate to pain control

Intravenous rate and pressure control

2

+

Hypotension

or shock state?

No

Yes

Systolic BP >120mm HG?

BP Control Intravenous vasodilator

Titrate to BP <120mm HG (Goal is lowest possible

BP that maintains adequate end organ perfusion)

Secondary pressure control

3

Anatomic based management

Acute Aortic Dissection Management Pathway

Initial management of aortic wall stress

170 2016

2016


Acute Aortic Dissection Management Pathway

171

Anatomic based management

Urgent surgical consultation

+

Arrange for expedited

operative management

Intravenous fluid bolus •Titrate to MAP of 70mm HG

or Euvolemia

(If still hypotensive begin

intravenous vasopressor agents)

Review imaging study for: • Pericardial tamponade

• Contained rupture

• Severe aortic insufficiency

1

2

3

Type A dissection

Intravenous fluid bolus

•Titrate to MAP of 70mm HG

or Euvolemia

(If still hypotensive begin

intravenous vasopressor agents)

Evaluate etiology of

hypotension

• Review imaging study for

evidence of contained rupture

• Consider TTE to evaluate

cardiac function

Urgent surgical consultation

2

3

Type B dissection

1

2016

172 2016

2016


173 2016

174 2016

2016


Pulmonary Embolus

Who is at risk?

175 2016

176

Pulmonary Embolism

• Obstruction of blood flow to one or more arteries of the lung by a thrombus (other emboli – fat, air, amniotic fluid) lodged in a pulmonary vessel

• 2nd most common cause of sudden death

• 3rd most common cause of death in hospitalized patient

– 80% of unexpected hospital deaths

• Often recurrent

2016


Risk Factors for DVT

177

PROLONGED IMMOBILIZATION

RECENT TRAUMA PLASTER CASTS BURNS ORTHOPEDIC / SPINE

SURGERY CENTRAL VENOUS

CATHETERS

PREGNANCY ORAL CONTRACEPTIVES

VARICOSE VEINS PHLEBITIS OBESITY DEHYDRATION /

HYPOVOLEMIA

POLYCYTHEMIA VERA SICKLE CELL DISEASE BEHCET’S DISEASE DEFICIENCY IN PROTEIN

C, PROTEIN S, OR ANTITHROMBIN III

FACTOR V LEIDEN MUTATION

HEART FAILURE MYOCARDIAL

INFARCTION

COPD STROKE HIV / AIDS MALIGNANCY SHOCK

SOURCE: OUELLETTE, HARRINGTON, & KAMANGAR, 2013

* Obesity is most common preventable cause of DVT.

2016

Risk Factors for PE in Hospitalized Patient

• Admitted to the medical intensive care unit

• Admitted with pulmonary disease,

• Post myocardial infarction

• Post cardiopulmonary bypass surgery

(Ouellette, Harrington, & Kamangar, 2013)

178

2016


Pulmonary Embolism

Acute

• Located centrally within the vessel lumen or causes vessel occlusion

• Results in distention of vessel wall

Chronic

Adjoins to vessel wall & reduces vessel diameter by > 50%

Recannulization through thrombus

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Pulmonary Embolism

Central

• Main pulmonary artery, the left and right main pulmonary arteries, the anterior trunk, the right and left interlobar arteries, the left upper lobe trunk, the right middle lobe artery, and the right and left lower lobe arteries

• Can cause massive PE

Peripheral

• Segmental and subsegmental arteries of the three lobes of the right lung, the two lobes of the left lung, and the lingula (a projection of the upper lobe of left lung)

• Pain by initiating inflammation close to the parietal pleura.

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Massive PE

• Present in less than 5% of patients presenting with PE (Kucher, Rossi, De Rosa, & Goldhaber, 2006).

• Involves both the right and left pulmonary arteries or causes hemodynamic collapse

• Presenting systolic BP of < 90 mmHg

• Mortality rates ange from 30% to 60% and most deaths occur within the first 1 to 2 hours (Ouellette et al., 2013; Wood, 2002).

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Pathophysiology

• Deep vein thrombosis (DVT) occurs at valves of vein due to physiological abnormality

• Clot can embolize or grow to occlude the vein

• Embolized clot returns to right heart and into pulmonary vasculature

• Lower lobes frequently affected due to increased perfusion

• Additional humoral response

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Pathophysiology

• Increased PVR – Proximal clots

– Substances (thromboxane A and serotonin) released in humoral response also cause vasoconstriction

• PA pressures double to compensate

• Increased work load of RV – Right heart failure

– Leftward shift of septum

– Right coronary branches can be compressed

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Pathophysiology • Increased V/Q ratio (alveolar dead space)

• Decreased V/Q ratio to other areas due to redistribution of blood flow

• Hypoxemia due to V/Q mismatching

• Increased minute ventilation to compensate for increased dead space – respiratory alkalosis – however, hypercapnea in massive

• Alveolar shrinkage (↓ CO2) – damage Type 2 alveolar cells – loss of surfactant – atelectasis – non cardiac pulmonary edema

• Pulmonary infarction rare due to dual blood supply

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Clinical Presentation

• Pleuritic chest pain, shortness of breath, and hypoxemia is not present in the majority of patients

• May have no respiratory complaint

• Atypical presentation: flank pain, abdominal pain, delirium, syncope, and seizures

• Potential diagnosis in any patient with respiratory symptoms in whom there is not another clear etiology

• Suspect when there is respiratory alkalosis

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Physical Exam Findings

• The most common physical sign, present in almost everyone with PE, is tachypnea (defined as respiratory rate > 16 per minute)

• Other:

– Dyspnea, rales, cough, hemoptysis

– Accentuated 2nd heart sound, presence of right sided S3 or S4, new systolic murmur of tricuspid regurgitation

– Tachycardia, low grade fever, diaphoresis

– Signs of thrombophlebitis, lower extremity peripheral edema

– Hypoxemia, cyanosis

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More on Assessment

Massive PE

• Shock presentation

Multiple Emboli

• More signs of pulmonary hypertension and cor pulmonale

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Diagnosis

• Cardiac troponins will be elevated in half of patients

with moderate to large PE (Konstantinides, 2008)

• Use of ultrasound to rule out DVT

• Computed tomography angiography (CTA) has become the standard test for the diagnosis of PE

• VQ scan is used as alternative

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ECG in PE

• Changes in only 20% of pts

• Non specific – ST

– Atrial fibrillation

• Small T wave inversion in limb and chest leads

• S1,Q3,T3

• Signs of right heart strain

– RV hypertrophy

– Right axis deviation – Large R waves in V1 and V2

– Deep S waves in leads V5 and V6

– Right atrial enlargement (tall P waves in lead II or dominant first ½ of P wave in V1)

– Incomplete right bundle branch block (RBBB)

– Delayed intrinsicoid deflection in leads V1 and V2

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ECG in PE

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ECG in PE

Treatment • Treatment with anticoagulation in non-massive PE reduces

mortality to less than 5%

• Full anticoagulation is the priority in any patient with suspected or confirmed PE. – Intravenous unfractionated heparin is the drug of choice in massive

PE, in patients with renal failure, and when there is concern about subcutaneous absorption.

• An initial bolus of 80 U/kg followed by an infusion of 18 U/kg/hour

– IV anticoagulation given before dabigatran and edoxaban; overlapped with warfarin

– IV anticoagulation does not need to be given before rivaroxaban or apixaban

– LMWH is preferred in cancer associated thrombus

– Low risk patients can have home treatment or early discharge

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Treatment

• Fibrinolytic therapy – Hemodynamic compromise as evidenced by

systolic BP < 90 mmHg and no high risk for bleeding

– Deterioration on anticoagulation and low bleeding risk

• Catheter assisted thrombosis removal if high bleeding risk / failed systemic therapy / shock – Surgical pulmonary embolectomy may also be considered

in select patients

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Treatment • Includes PE, DVT, and VTE (venous thromboembolic event) • 3 month long term anticoagulation if no cancer and if

provoked – Dabigatran, rivaroxaban, apixaban, edoxaban preferred over

warfarin

• If unprovoked – minimum of 3 months and then evaluation for risk benefit ratio – High bleeding risk – 3 months – Low to moderate bleeding risk – extended anticoagulation

• Active cancer – LMWH preferred agent – Extended anticoagulation even in high bleeding risk

• LMWH if recurrent VTE on oral anticoagulation

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Myocardial Rupture

Who is at Risk?

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Mechanical Rupture • Cardiac tamponade

from free wall rupture • Formation of left

ventricular diverticulum or pseudoaneurysm from free wall rupture

• Left to right shunt from septal rupture

• Acute mitral regurgitation from papillary muscle rupture.

– 10% of MIs

• 15% of in hospital deaths after MI

• Without surgical intervention, the mortality rate for rupture is > 80% at two weeks.

• Two high risk periods – 1st 24 hours – Within 1st week ( 3 to 5

days)

• Associated with delayed fibrinolytics and late presentation

2

0

0 2016

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IMPACTING RATES OF RUPTURE

Timely Reperfusion

• Beta blockers as soon as possible after MI unless contraindicated

• Blood pressure control in hypertensive patients

• Avoidance of non-steroidal anti-inflammatory agents.

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http://www.google.com/url?sa=i&rct=j&q=&esrc=s&frm=1&source=images&cd=&cad=rja&docid=gfSM-zGTTGtx9M&tbnid=0OQwuFrNzJd3BM:&ved=&url=http://www.readcube.com/articles/10.1186/1476-7120-4-7?locale%3Den&ei=gxc2UpitFtep4APymoC4Dg&psig=AFQjCNEjOJpEMJ_q2dfpi5wc-GxEQ6tjnw&ust=1379363075858277

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Free Wall Rupture

Incidence:

More common than ventricular septal rupture or papillary muscle rupture.

Warning Signs:

Recurrent chest pain and signs of regional pericarditis.

Consequences:

Hemipericardium, tamponade, electromechanical dissociation, and death.

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Risk Factors for Free Wall Rupture

• First MI, often relatively small • Anterior lateral wall MI • Advanced age • Female gender • Hypertension during acute phase • Absence of collateral blood flow • Q waves on ECG • Use of corticosteroids or non-steroidal anti-

inflammatory agents (NSAIDs) • Administration of fibrinolytics > 11 hours after

symptom onset. • Post infarction angina

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Myocardial Free Wall Rupture

• Post-infarction regional pericarditis most often precedes rupture

205

T Wave Patterns in Post-infarction

Regional Pericarditis

Persistently positive T

waves 48 hours after an MI

Premature reversal of T

wave inversion to

positive

ST segment

reelevation

2016

ECG Changes After STEMI

Non Reperfused

• T wave enlargement

• ST elevation

• Q wave formation or loss of R wave amplitude

• ST stabilization

• T wave inversion (within 48 - 72

hours) before ST resolution

• ST resolution

• T waves stays inverted for period of time (takes weeks to months)

• Possible disappearance of Q

waves

Reperfused

• Earlier ST normalization and stabilization

• T wave inversion may accelerate – Terminal T wave inversion

initially

– T waves deepen symmetrically over time

• Q wave development is less pronounced or even absent

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Types of Free Wall Rupture

Within 24 hours: Full thickness rupture.

1 to 3 days post MI: Erosion of myocardium.

Late: At border between MI and normal myocardium.

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• Sudden chest pain associated with coughing or straining.

• Transient bradycardia and other signs and symptoms of increased vagal tone prior to rupture.

• May have signs and symptoms of cardiac tamponade.

• Requires urgent surgical repair. – Resection of the infarcted

area – Closure of the ruptured

area with a patch or with the use of biological glues

• An emergency

pericardiocentesis may be required to stabilize the patient (not a definitive treatment)

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• Contained rupture by the parietal

pericardium.

• Outer wall of the

pseudoaneurysm is formed by

the parietal pericardium and

thrombus that lines the parietal

wall.

• Pseudoaneurysm communicates

with the left ventricle through a

narrow neck.

• To-and-fro murmur may be

heard.

• May result in persistent ST

elevation on the ECG.

• Represents the chronic phase of

a free wall rupture.

• May be clinically silent but at

high risk for rupture leading to

hypovolemic shock.

• Emergency surgery is

considered. 2016

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ST Segment Monitoring

A SUCCESS Story!!

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ECG 1 of 3 Day 1 5:30 am

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Ventricular Septal Rupture

• Without reperfusion average time frame is 5 days (2 to 8 days) post MI

• With fibrinolytic therapy post common time frame is within 24 hours

• Septum receives blood supply from branches of LAD and PDA arteries (apical septum)

• 60% ruptures with anterior MI and 40% with inferior posterior (posterior (inferior-basal)septum)

• Can be one large or a series of smaller defects

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Ventricular Septal Defect or Rupture

• Timing: Holosystolic

• Location: Left lower sternal border

• Radiation: Widely throughout the precordium

• Configuration: Plateau

• Pitch: High

• Quality: Harsh / Loud

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New loud

holosystolic

murmur

(+ thrill)

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2016


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Ventricular Septal Defect

Left to Right Shunt

• Poor systemic perfusion

• Right ventricular volume overload

• Heart failure

• Shock

• State of right and left ventricle affect hemodynamic status.

Medical Management

• IABP

• IV nitroprusside for MAP 60 to 75 mmHg.

• Do not reduce pulmonary vascular resistance more than systemic vascular resistance.

Surgical Considerations

• Direct closure or closure with patch

• Higher risk with posterior defects

• Higher mortality when done urgently

• If unstable – morality is higher when surgery delayed

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Papillary Muscle Rupture

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5% Acute MI Mortality

Complete transection=death.

Without reperfusion:

2 to 7 days.

Reperfusion era: Median time 13 hours.

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225

Vicious Cycle • Acute mitral valve regurgitation Backward flow

Pulmonary edema

• Decreased forward flow Acute decrease in cardiac output

• Increased SVR to compensate

• More blood flow to area of least resistance

• Further decrease in cardiac output further increase in SVR

• Increase in pulmonary edema

• Further decrease in cardiac output Further increase in SVR

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Systolic Murmurs Mitral Regurgitation

226

New holosystolic murmur: Often radiating to LSB.

OR

May be absent due to equalizing

pressures.

If acute pulmonary edema and shock – suspect papillary muscle rupture or ischemia in

absence of murmur.

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Medical Management

• Afterload reduction similar to septal rupture.

Surgical Intervention

• Mitral valve repair or replacement required.

• Operative mortality 20% - superior to medical management.

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ECG 1of 3

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ECG 2 of 3

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ECG 3 of 3

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Emergency Decision Making

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Cardiac Tamponade

Risk factors : (Trauma, Post OHS / procedure, MI - lateral wall, HTN during acute phase, late

presentation)

Checklist

√Beck’s triad (hypotension / JVD / muffled heart sounds

√ Pulses Paradoxus

√ Pulses / Electrical Alternans

233 2016

Risk Factors: (Trauma, Conversion to positive pressure ventilation, existing chest tube)

Checklist

√Diminished to absent lung sounds

√Hypotension

√JVD

√Mediastinal shift (very late sign)

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Pulmonary Embolus

Risk Factors: (Venous stasis, hypercoagulability, injury to vascular endothelium, any hospitalized patient without pharmacological prophylaxis)

Checklist

√Tachypnea (most common sign)

√Respiratory Alkalosis

√ECG signs: Right axis deviation, RBBB, Tall P waves inferior leads , T wave inversion (limb and precordial leads), Prominent S waves 1 and aVL, S1, Q3, T3

√ST / New atrial arrhythmia

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Aortic Dissection

Risk Factors: HTN, aortic cannulation, genetic abnormalities, known aortic valve disease, known thoracic aneurysm

Checklist

√Tearing or ripping description of chest or back pain

√Diastolic murmur of aortic regurgitation

√Bilateral arm BP variation

√ 4 extremity pulse variation

√ Neurological deficit or Co-existing Inferior MI

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Mechanical Complications of MI

• Septal Rupture • Papillary Muscle Rupture

High Risk

• Anteroseptal MI

Check List

• Loud holosystolic murmur

• RV volume overload

• Systemic hypoperfusion

High Risk

• Inferior posterior or posterior MI

Check List

• Holosystolic murmur (can be absent)

• Acute pulmonary edema

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BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE

COUNTING ON IT!

www.cardionursing.com

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UNDERSTANDING WHY WE DO WHAT WE DO

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Flow is determined by:

√Pressure

√ Resistance

√ Volume 242 2016

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Right Sided versus Left Sided System

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Cardiac Output

Heart Rate X Stroke Volume Preload Afterload Contractility Same four components also determine myocardial oxygen demand

245

Volume of blood ejected by the ventricle each

minute

Volume of blood ejected by the

ventricle each beat

Determinants of Myocardial Performance

•

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Heart Rate

Synergy

Synchrony

Stroke Volume Preload

Afterload

Contractility

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Preload • The ventricle is preloaded with

blood at the end of diastole: Creates stretch on myocardial muscles fibers

• Determined by: – Volume of blood filling the ventricle at

end of diastole – Greater the volume the greater the

stretch (muscle fiber length) – Greater the stretch the greater the

contraction – Greater the contraction the greater

cardiac output

TO A POINT

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Non-Invasive Preload Assessment

Right Ventricle

• JVD • Hepatojugular

reflux Less Specific • Peripheral edema • Weight

Left Ventricle

• Lungs sounds – Clear lungs do not rule out volume overload – Role of lymph system

• CXR – Vascular congestion – Interstitial edema – Pulmonary edema

• Orthopnea / Bendopnea / PND • S3

• Hypoxemia – Diffusion abnormality

Less Specific • Decrease in Blood Pressure and Urine

Output – Because stroke volume falls

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Factors Influencing Preload • Body Position

• Venous Tone

• Intrathoracic pressure

• Intrapericardial pressure

• Dysrhythmias

• Atrial Kick

• LV Function

• Circulating blood volume – Hypervolemia

– Hypovolemia

– Third spacing

• Size of Container – Sepsis

– Anaphylaxis

– Venous vasodilators

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Afterload

• After the ventricle is loaded: • Pressure ventricle needs to

overcome to eject blood volume

• Right ventricle: Pulmonary vascular resistance major component

• Left ventricle: Systemic vascular resistance major component – Other components

• Valve compliance • Viscosity of blood • Aortic and arterial wall compliance

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Afterload Assessment

• Left ventricle: – SVR – Pulse pressure and DBP – HTN = increased afterload – Hypotension does not =

decreased afterload • Vasoconstriction is

compensatory

• Right ventricle: – PVR – PA pressure from echo – Hypoxemia causes pulmonary

vasoconstriction – Positive pressure ventilation and

PEEP increase work load of left ventricle

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More on Pulse Pressure

• Vascular tone is affected by:

– Large vessel compliance

– Peripheral vascular resistance (smaller vessels)

• Vessel resistance changes more quickly than large vessel compliance

• Increased resistance = increased DBP and narrow pulse pressure

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– Arterial vasoconstrictors

– Hypertension

– Aortic valve stenosis

– Increased blood viscosity

– Hypothermia

– Compensatory vasoconstriction from hypotension in shock

– Arterial vasodilators

– Hyperthermia

– Vasogenic shock states (sepsis and anaphylactic) where the body cannot compensate with vasoconstriction

– Aortic Regurgitation – hyperdynamic cardiac output therefore lowering systemic vascular resistance

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Contractility

• By definition: Ability of myocardium to contract independent of preload or afterload

–Velocity and extent of myocardial fiber shortening

–Inotropic state

• Physiologically is related to degree of myocardial fiber stretch (preload) and wall tension (afterload).

• contractility myocardial workload myocardial oxygen

consumption

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Important Points about Contractility

• No accurate way to measure contractility

• Low cardiac output does not necessarily mean

diminished contractility (i.e. hypovolemia)

• Correct preload and afterload problems first in a patient with a low ejection fraction.

• Increasing contractility with medications will also increase myocardial oxygen demand.

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Noninvasive Assessment: Ejection Fraction

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Factors Altering Contractility

• Decreased contractility

– Excessive preload or afterload

– Drugs – negative inotropes

– Myocardial damage

– Ischemia

– Cardiomyopathy

– Hypothyroidism

– Changes in ionic environment: hypoxia, acidosis or electrolyte imbalance

256

• Increased contractility

– Drugs

• Positive inotropes

– Hyperthyroidism

– Adrenal Medulla Tumor

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Heart Rate

• Mathematically heart rate increases cardiac output

• Physiological limit where increased heart rate will decrease cardiac output due to decreased filling time (decreased preload)

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Backwards Failure:

Pulmonary Congestion

Forwards Failure:

Hypoperfusion

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Warm and Dry

Normal Perfusion

No Congestion

Warm and Wet

Normal Perfusion

Congestion

Cold and Dry

Low Perfusion

No Congestion

Cold and Wet

Low Perfusion

Congestion

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Treatment

Congestion with Adequate Perfusion

• Reduce Preload

Hypoperfusion with No Congestion

• Increase contractility – Must have adequate

preload

Hypoperfusion with Congestion

• Reduce Afterload

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Pharmacological Options for

INCREASING Preload

Volume expanders ▪ Isotonic crystalloids such as 0.9% saline or

lactated ringers

▪ Colloids such as albumin

▪ Blood and/or blood products

Decrease dose or stop diuretics or drugs that cause venous vasodilatation.

▪ Decrease or stop medications such as: loop

diuretics, intravenous nitroglycerin, neseritide, and

morphine sulfate (Venous vasodilatation pools blood away from the heart and

decreases preload – direct impact on right sided preload)

Exercise also increases venous return to the heart. 2016

262


DECREASING Preload

Stop or decrease fluid

Diuretics ▪ A loop diuretic such as furosemide eliminates circulating

volume

Venous Vasodilators ▪ Intravenous nitroglycerin, neseritide, or morphine sulfate (Venous vasodilatation pools blood away from the heart and

decreases preload)

ACE Inhibitors or

Angiotensin II

Receptor Blockers

▪ Interrupt renin- angiotensin- aldosterone system.

(RAAS). Aldosterone secretion is decreased and

there is less sodium and water retention.

Aldosterone

antagonists

▪ Spironolactone or epleranone

▪ Directly block aldosterone and there is decreased

sodium and water retention.

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INCREASING Afterload

Vasopressor is the term given to medications used to increase afterload.

Sympathomimetics stimulating the

alpha receptors of the sympathetic

nervous system

▪ Dopamine

▪ Norepinephrine

▪ Phenylephrine

▪ Epinephrine

Arginine Vasopressin ▪ Vasoconstrictive and antidiuretic effect

▪ Restores catecholamine sensitivity

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DECREASING Afterload

All therapies involve arterial vasodilatation

Smooth muscle relaxants ▪ Nipride

▪ Hydralazine

Calcium channel blockers ▪ Dihydropyridines (ending in “ine”) calcium channel

blockers such as amlodipine

Alpha1 receptor blockers

▪ Labetolol (combination alpha and beta blocker)

▪ Prazoxin, Terazosin

Central anti-adrenergics

Peripheral anti-adrenergics

Clonidine, Methyldopa

Resperine, Guanthidine

ACE Inhibitors

Angiotensin II Receptor

Blockers (ARBs)

▪ Interrupt the RAAS and limit production of

angiotensin II a potent arterial vasoconstrictor

▪ Medications ending in “pril”

▪ Directly block the effects angiotensin II

▪ Medications ending in “sartan”

Phosodiesterase Inhibitors

(PDE Inhibitors)

▪ Milrinone

▪ Is used as an intravenous inotrope but also has

arterial vasodilator properties 2016

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INCREASING Contractility

Inotrope is the termed used for medications used to increase contractility

Sympathomimetics stimulating the

β1 receptors of the sympathetic

nervous system

▪ Dobutamine: most commonly used because

it is predominant beta one stimulator

▪ Other sympathomimetics may have inotropic

properties even if not used primarily for an

inotropic purpose

Phosodiesterase Inhibitors

(PDE Inhibitors)

▪ Milrinone

▪ Is used as an intravenous inotrope but also

has arterial vasodilator properties

Cardiac Glycoside ▪ Digoxin

▪ Weak inotrope and is never used

intravenously to support left ventricular

dysfunction. Exerts weak inotropic properties

when given orally.

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DECREASING Contractility

Beta Blockers blocking

the β1 receptors of the

sympathetic nervous

system

▪ Metoprolol

▪ Carvedilol

▪ “lol” medications

Calcium Channel

Blockers

▪ Diltiazem

▪ Verapamil

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INCREASING Heart Rate

Parasympatholytic

(lyses the parasympathetic nervous

system)

▪ Atropine

Sympathomimetics stimulating the β1

receptors of the sympathetic

nervous system

▪ Epinephrine

▪ Dopamine

Note: The non-pharmacological intervention of pacing the heart with either

an external, temporary or permanent pacemaker is often the preferred

method of increasing the heart rate to a set and controlled rate.

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DECREASING Heart Rate 1. Beta Blockers blocking the β1

receptors of the sympathetic

nervous system

▪ “olol” medications

▪ Class II antiarrhythmics

2. Calcium Channel Blockers ▪ Diltiazem / Verapamil

▪ Class IV antiarrhythmic

3. Cardiac Glycoside ▪ Digoxin

4. Unclassified antiarrhythmic ▪ Adenosine: Slows conduction through

the AV node

5. Other antiarrhythmics ▪ Class I and Class III antiarrhythmics

▪ Used to establish and / or maintain a

normal rhythm and therefore control

heart rate

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Let’s Clear Up Some Terminology

• Vasopressors – Term given to any medication in any class that is

used to increase left ventricular afterload (systemic vascular resistance)

• Inotropes – Term given to any medication in any class that is

used to increase myocardial contractility • Increase mortality • Used in shock / decompensation when other

treatments fail • Used as bridge to transplant or palliation

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Autonomic Nervous System

Sympathetic

Beta 1

Beta 2

Alpha 1

Parasympathetic Vagal Response

270

Sympathomimetics

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Sympathetic Nervous System

• Fight or flight

Alpha1 Receptors Vasoconstriction of vessels

Beta1 Receptors (Heart)

Increased heart rate

Chronotropic Response

Increased conductivity

Dromotropic Response

Increased contractility

Inotropic Response

Increased automaticity

Beta2 Receptors (Vesseles, Lungs)

Bronchodilation

Peripheral Vasodilatation 271 2016

Epinephrine

What receptors are stimulated:

β1 and β 2

Alpha receptors

What are the resultant actions:

Increase contractility (+inotrope) β1

Increased heart rate (+chronotrope) β1

Bronchodilation β2

Selective vasoconstriction (alpha)

When and why do we use: ACLS first line drug for cardiac standstill; V-fib; pulseless electrical activity

Hypotension or profound bradycardia

Anaphylactic Shock

What are special nursing considerations:

Onset instant

Peak 20 minutes

1mg every 3-5 minutes during cardiac standstill

272

Endogenous catecholamine

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Dobutamine

273


Primarily β1

Some alpha1 receptor stimulation

Some β2 stimulation

Modest β2 (more β2 than alpha1)


Increase contractility (+ inotrope) (β1)

Increase AV node conduction

Modest vasodilation

When and why do we use: Used as an inotrope (resultant preload reduction) with modest afterload reduction

(ACC / AHA Guidelines for Heart Failure*)


Onset 1 to 2 minutes; Peak 10 minutes

Half-life 2 minutes

Note: Blood pressure response is variable; β2 causes vasodilatation; β1 increases cardiac output and may increase BP

Synthetic Compound

2016

274 2016

2016


2016 275

Continuous intravenous dobutamine is associated with an increased risk of death in patients with advanced heart failure: Insights from the Flolan International Randomized Survival Trial (FIRST)

Intermittent dobutamine treatment in patients with chronic refractory congestive heart failure: a randomized, double-blind, placebo-controlled study. (PMID:9663183) Intermittent dobutamine infusions in patients with refractory CHF have no effect on the need for hospitalization or on survival.

Dopamine


Dopaminergic at low doses (0.5-2.0 mcg/kg/min)

β1 also at moderate doses ( 2.0-10.0 mcg/kg/min)

Pure alpha stimulation at high doses > 10mcg/kg/min


Increase GFR at low doses

Increase contractility at moderate doses (greater effects on contractility than heart rate)

Vasoconstriction (alpha) at high doses

When and why do we use:

Refractory hypotension / shock

* Not indicated for routine treatment or prevention of acute renal failure


VT, atrial tachyarrhythmias

Onset 1-2 minutes; Peak 10 minutes

Maximal effects @20/mcg/kg/min

Large IV line or central line

Phentolamine for extravasation: 5 to 10 mg diluted in 10ml 0.9 NS, inject into area with fine needle

Leave cannula and needle in place, aspirate not flush line, dry warm compress 276

Mimics endogenous dopamine;

metabolic precursor

of norepinephrine and epinephrine

2016

http://europepmc.org/abstract/med/9663183/?whatizit_url_Chemicals=http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:4670

2016


Norepinephrine What receptors are stimulated:

Primarily alpha stimulation

Some β1

(In lower doses β1 can be more dominant)


Potent vasoconstrictor (increased afterload)

Some increased contractility (+inotrope)

When and why do we use: Refractory hypotension / shock

(used as a vasopressor but will have inotropic properties)


Onset: rapid; very short half-life

Duration 1-2 minutes (BP checks q2 minutes while titrating)

Large IV line or central line

Phentolamine for extravasation: 5 to 10 mg diluted in 10ml 0.9 NS, inject into area with fine needle

Leave cannula and needle in place, aspirate not flush line, dry warm compress

277

Endogenous precursor

of epinephrine

2016

Phenylephrine


Direct effect: Dominant alpha stimulation

No substantial β1 effect at therapeutic doses

Indirect effect: Releases norepinephrine


Vasoconstriction (increased afterload)

When and why do we use: As a vasopressor for Unresponsive hypotension


Pressor effect occurs almost immediately

Persists for 10 to 15 minutes

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Synthetic compound

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Pearls for Practice

• Titrate up based on onset of action & peak action

• Wean based on duration of action / half life

• Consider systolic, diastolic, pulse pressure and mean

• Vasoconstriction with a reduced ejection fraction increases work load of failing left ventricle!

279 2016

Comparison of Dopamine to Norepinephrine in Shock

280

• Backer et al. • Multi Center Randomized

Controlled Trial • New England Journal of

Medicine • March 4th 2010

• There were no significant differences between the groups in the rate of death at 28 days or in the rates of death in the ICU, in the hospital, at 6 months, or at 12 months

• More patients with arrhythmia in the dopamine group

• Rate of death was higher in predefined subgroup analysis for patients with cardiogenic shock treated with dopamine.

2016

2016


Arginine Vasopressin: Non Sympathomimetic Vasopressor

• Vasoconstrictive effects – Allowing for regional

vasodilation

• Antidiuretic effects • Restoration of

catecholamine sensitivity

• Low dose exogenous – 0.04 units / min

• Use in refractory shock – Also consider

methylene blue – Also consider adrenal

insufficiency • Hydrocortisone

281 2016

Milrinone: Phosphodiesterase Inhibitors

• Creates + inotropic effect by increasing availability of calcium • Inhibits the degradation of

cyclic AMP which is indirectly responsible for increasing the influx of calcium through the calcium channel

• Smooth muscle relaxant (venous and arterial vasodilator)

• Indications: – Refractory heart failure

(can be used in combination with dobutamine)

– Left ventricular failure in MI

– Patients waiting transplant

• Side Effects: – Ventricular arrhythmias – Atrial tachyarrhythmias

• Nursing Considerations: – Onset IV: Immediate – Peak: 10 minutes

282 2016

2016


Milrinone

283

Used as an

Inotrope

BUT…..

Also has……

Preload

Reduction

Afterload

Reduction

2016

OPTIME Trial

• Milrinone approved by FDA based on hemodynamic data • Future trials need to address outcome data • OPTIME

– Prospective trial, randomized, placebo controlled – 951 patients – Patients had indication for but not all required inotrope for end

organ perfusion. – Results: No difference in LOS, No difference in subjective

improvement – Treatment failures more common in milrinone group due to

hypotension, more atrial fibrillation in milrinone – Not powered for mortality differences

– Conclusion: Hemodynamic improvement does not translate into clinical improvement

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2016


A Closer Look at Venous Versus Arterial Vasodilators

285

Venous

Vasodilators

Arterial

Vasodilators

2016

A Closer Look at Venous Versus Arterial Vasodilators

• Some medications do both

• Some depend on dose • Nesiritide

• NTG

• Nitroprusside

• CA Channel blockers

• PDE Inhibitors

• ACE Inhibitors

• Other Vasodilators

286 2016

2016


Nesiritide (Natrecor) • Recombinant form of

human B type natriuretic peptide (BNP)

– BNP is a naturally occurring

cardiac neurohormone secreted by the heart in the body’s response to heart failure

– BNP allows the heart to

participate in the regulation of vascular tone and extracellular volume status

– The BNP system and the renin-angiotensin system counteract each other in heart failure

– BNP levels are elevated in

heart failure

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Onset: 15 minutes Peak: Within an hour

2016

Nesiritide (Natrecor)

• Balanced arterial and venous vasodilatation

– Causes rapid reduction in right and left sided ventricular filling pressures (preload reduction)

– Reduces afterload

• Indicated for acutely decompensated heart failure patients who have dyspnea at rest

288

• Patient must have systolic BP > 90 mmHg

• PAOP should be estimated to be > 20 mmHg

2016

2016


Nesiritide (Natrecor) • Given by IV bolus and

maintenance infusion

• Bolus 2mcg/kg

• Infusion 0.01mcg/kg/min - usually 24-48 hours

• Caution with higher doses

289

Monitor BP, hemodynamic assessment,

urine output, and renal function closely

during administration.

• Prime IV tubing with 5 ml of solution – prior to bolus or infusion

• Bolus to be taken from reconstituted IV bag and not from vial)

2016

Neseritide: Where do we stand?

• Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K: Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA 2005, 293:1900-1905.

– In the 3 trials, 485 patients were randomized to nesiritide

and 377 to control therapy. Death within 30 days tended to occur more often among patients randomized to nesiritide therapy (35 [7.2%] of 485 vs 15 [4.0%] of 377 patients; risk ratio from meta-analysis.

– P value did not achieve .05 or less.

290 2016

2016


Randomized Trial • Effect of Nesiritide in Patients with Acute Decompensated

Heart Failure • O'Connor et al. • July 7 2011

• 7141 patients

• Nesiritide was not associated with an increase or a decrease in the rate of death and rehospitalization.

• It was not associated with a worsening of renal function, but it was associated with an increase in rates of hypotension.

• Neseritide cannot be recommended for routine use.

291 2016

Nitroglycerin

• Minimal mortality benefit – Nitrates may be more helpful in patients > 70 years in reduction

of death and heart failure @ 6 month follow up

• Symptom benefit

• Mixed venous and arterial vasodilator – Dosage < 1mcg/kg/min = venous vasodilator

• Decrease preload

– Dosage > 1mcg/kg/min = arterial and venous vasodilator • Decrease preload and afterload

– Sublingual tablets provide high enough dosage to dilate arteries and veins

• Decrease preload and afterload 292

Mortality reducing agents should always take precedence over non mortality reducing agents: I.E. Beta blockers precede nitrate use

2016

2016


Nitrate Contraindications

• Systolic BP < 90 mm Hg or < 30 mm Hg below baseline

• Bradycardia < 50 BPM

• Tachycardia > 100 BPM (in absence of clinical HF)

• Right ventricular infarct

• Within 24 hours of sildenafil

• Within 48 hours of taldalafil

293

Question female patients: Pulmonary HTN

2016

Nitroglycerin • Onset IV: 1-2 minutes • Duration: 3-5 minutes

• Side Effects: H/A, Hypotension, flushing

Treat H/A with pain meds and decrease dose

• Pain activates the SNS

• Caution: Severe diastolic dysfunction

– Hypertrophic cardiomyopathy – Severe aortic stenosis

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2016


Caution with Vasodilators

2016 295

Nitroprusside

• Mixed venous and arterial dilator (primarily arterial)

• Decreases BP, SVR, PVR, PAOP, RAP

• Uses: – Hypertensive crisis

– CHF

– Acute Mitral Regurgitation

– Other Indications for Afterload Reduction

• Side Effects: – Hypotension – Thiocyanate toxicity:

tinnitus, blurred vision, delirium, seizures, muscle twitching, absent reflexes, dilated pupils [several days – high doses]

• Nursing Considerations: – Onset: 1-2 minutes – Duration: 1-10 minutes – Monitor BP carefully-

arterial line encouraged

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2016


Acute Coronary Syndrome

297 2016

Drugs Used to Alter Clotting in ACS

• Fibrinolytics – STEMI

– tPA • Alteplase

• Retaplase

• Tenecteplase

– Streptokinase (no longer used)

• Antiplatelets – STEMI / NonSTEMI / UA

– GP IIb/ IIIa Inhibitors • Eptifibitide (Integrelin)

• Tirofiban (Aggrastat)

• Abciximab (Repro)

– ADP Receptor Blockers • Clopidogrel

• Prasugrel

• Ticagrelor

– Thromboxane A2 Inhibitor • ASA

298

• Anticoagulants o STEMI / NonSTEMI / UA o Unfractionated Heparin o Low Molecular Weight Heparin o Direct Thrombin Inhibitors o Factor Xa Inhibitors

2016

2016


Clot Formation: Clotting Cascade

• Initiated by vascular injury

and direct exposure to

collagen

• Site of activated platelet

• Site of endothelial damage

• Subendothelial layer where

collogen is exposed

• From initiation to a clot is 2-6

minutes

• Measured by APTT

• Initiated by endothelial

release (secondary to tissue

injury) of thromboplastin

tissue factor

• From initiation to clot is 15

to 20 seconds

• Measured by Protime

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2016 300

The Clotting Cascade Intrinsic Pathway Extrinsic Pathway

XII XIIa

XI XIa

IX IXa

X Xa

Va

II Prothrombin IIa Thrombin

Fibrinogen Fibrin

VII Thromboplastin Tissue Factor III

VIIa

X

Activated platelets

Endo damage

Exposed collagen

Activated platelets

Endo /tissue damage

Phospholipid

Calcium

Factor VIIIa

Common Pathway

Fibrin Stable Clot

2016


2016 301

The Clotting Cascade Intrinsic Pathway Extrinsic Pathway

XII XIIa

XI XIa

IX IXa

X Xa

Va

II Prothrombin IIa Thrombin

Fibrinogen Fibrin

VII TF III

VIIa

X Common Pathway

Fibrin Stable Clot

Warfarin

UFH

LMWH

Bivalrudin

Dibigitran

Lirudin

Argatroban

Fondaparinox

Rivaroxaban

Apixaban

Edoxaban

Anticoagulants

• Unfractionated Heparin – Heparin by Weight – STEMI, NonSTEMI,UA – Mortality benefit

• Low Molecular Weight Heparin – STEMI, NonSTEMI, UA

• Direct Thrombin Inhibitors – If history of HIT, PCI

NonSTEMI • Factor Xa Inhibitors

– Not in PCI

• Warfarin (Vitamin K antagonist)

• Dabigatran (Direct thrombin inhibitor)

• Rivaroxaban (Factor Xa inhibitor)

• Apixaban (Factor Xa inhibitor)

• Edoxaban (Factor Xa inhibitor)

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Unfractionated Heparin • Works in the intrinsic and common pathway

• Antithrombin activator that inhibits factors Xa and IIa (thrombin) – Antithrombin III lyses factor Xa and thrombin and inhibits clotting

– When heparin binds with antithrombin III the inhibition is increased 1000 times

• Concern that unfractionated heparin results in platelet activation - although thrombin is a strong platelet activator and heparin is an antithrombin drug

• Anticoagulation is almost instant

• ½ life relatively short

• Antidote: Protamine 1 mg per 100 units

• In NSTEMI: continue for 48 hours or until PCI

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304 2016

2016


More About Heparin • Different dose and aPTT for ACS versus venous thrombotic event

• aPTT (activated partial thromboplastin time) is used to monitor effectiveness and safety • Goal is aPTT 1.5 -2Xs the control

• Weight based heparin dosing reaches goal 90% of time compared to 77% with standard therapy

• OR – Anti factor Xa levels • 0.3-0.7 IU/ml

• Baseline aPTT, PT/INR, platelets and CBC

• Increased bleeding can occur with renal failure • Heparin has dual clearance mechanism

2016 305

Complications of Heparin

• Bleeding • Mild thrombocytopenia – HIT 1

• Mild thrombocytopenia occurs in 10-20% of patients

• Severe thrombocytopenia – HIT 2 • occurs in 1-2% of patients • Heparin Induced Thrombocytopenia (HIT) • Platelet aggregation resulting in venous or arterial

thrombosis (HITT – Thrombocytopenia with thrombosis) • Determining patients at risk is unpredictable • Generally occurs 5 to 10 days after initiation of heparin

• Could be sooner if recent exposure to heparin • DC heparin if platelets fall below 100,000 (or > 50%

reduction from baseline) • Severe thrombocytopenia is due to an immune response

2016 306

2016


More on Heparin Induced

Thrombocytopenia • Immune system forms antibodies against heparin when bound to protein

platelet factor 4 [PF4] – antibodies bind to PF4-heparin complexes and induce platelet activation

• Immunoassay identify antibodies against PF4

• Detected in ELISA testing

• Function Assay

• Heparin-induced platelet aggregation assay (HIPA)

• Platelet activation test

• HIT antibodies are usually IgG class

• Take 5 days to form

• IgG antibodies associated with platelet activation and increased thrombin generation

• Antibodies not necessarily associated with thrombotic risk

• Can disappear 3 months after exposure

• Antibodies bind to platelets and trigger the development of thrombosis.

2016 307

Treatment of HIT 1. Discontinue and avoid all heparin.

2. Give a non-heparin alternative anticoagulant: Direct thrombin inhibitors.

3. Postpone warfarin pending substantial platelet count recovery (give vitamin K if warfarin has already been started). Warfarin is associated with protein C deficiency and increased risk for microthrombosis

4. Avoid platelet transfusions – leads to platelet activation.

5. Test for HIT antibodies (ELISA and washed assay)

6. Investigate for lower-limb deep-vein thrombosis.

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2016


• Enoxaparin, dalteparin, tinzaparin, and nadroparin

• Smaller in size • Antithrombin by inhibiting factor Xa • Causes less inactivation of thrombin and less bleeding than standard heparin

• More predictable anticoagulant response • No need to monitor APTT

• Anti Xa levels can be drawn 4 hours after SQ dose

• Lower incidence of heparin induced thrombocytopenia • Less platelet activation concern than with UFH

2016 309

Low Molecular Weight Heparin

Low Molecular Weight Heparin

• Can be self administered with Sub – Q administration

• ½ life 4-6 hours

• Protamine reverses 60% of drug effect

• Renal failure results in increased risk of bleeding because

LMWH is renally cleared • Special dosing for chronic renal insufficiency with enoxaparin

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2016


Enoxaparin Dosing

• Prevention of DVT • 40 mg SC daily in most situations

• 30 mg SC daily for renal adjustment (CR Clearance < 30 ml/min)

• NSTE-ACS (or as adjunct in STEMI) • 1 mg/kg SC q12 hours

• 1mg/kg SC daily if CR Clearance < 30 ml/min

• IV loading dose of 30 mg – in select patients

• Continued for duration of stay or until PCI

• Embolism with Atrial Fib • 1 mg/kg SC q12 hours

• Venous thrombosis / DVT • 1mg/kg SC q12 or 1.5 mg/kg daily depending of specific

circumstances

2016 311

Enoxaparin Administration

• Full length of 27 gauge ½ needle (prepackaged) should be injected

• Skin fold held until needle withdrawn

• Use anterolateral or posterorlateral walls of abdomen

• Rotate sites frequently

• Do not massage site

2016


Direct Thrombin Inhibitor

• Ability to inactivate fibrin bound thrombin

• Less binding to plasma proteins, therefore more reliable anticoagulation effect

• Indications

• HIT /HITT

• Approved in NSTE-ACS (Use only in patients with early invasive strategy) / PCI • Non inferior to heparin with a

GPIIb/IIIa with less bleeding

• Monitor in the cath lab with ACT

• Lipirudin / desirudin (hirudin)

• Argatroban

• Bivalirudin* • 0.10 mg/kg loading

• 0.25 mg/kg per hour

• Until diagnostic angiography or PCI is performed

2016 313

• Neutralizes Factor Xa and interrupts the clotting cascade

• Does not inhibit thrombin

• No reported HIT / HITT

• Indications • Venous thromboembolism and PE

• DVT prophylaxis

• ACS

• Contraindicated in severe renal dysfunction • No laboratory monitoring is needed – PT/aPTT not sensitive

• No antidote (Recombinant factor VIIa can help reverse anticoagulation effect)

2016 314

Synthetic Factor Xa Inhibitor

Fondaparinux (Arixtra)

2016


Synthetic Factor Xa Inhibitor

• DVT Prophylaxis: 2.5mg SC once daily in adults > 50 kg

• ACS • 2.5 mg SC daily for duration of hospital stay up to 8 days or until

time of revascularization

• If STEMI an initial dose 2.5mg should be given IV before starting daily SC

• Cannot be used as sole anticoagulant during PCI – add DTI or UH

• Acute DVT or PE – weight based for between 5mg and 10mg SC daily • Can use as a bridge for 5-7 days if warfarin is long term

anticoagulation choice

• Start warfarin on day 1 or 2 but continue Fondaparinux for at least 24 hours after therapeutic INR is achieved

2016


2016 317

New Dual Antiplatelet Therapy Guidelines Update

STEMI

NSTE CABG

Stable Ischemic

CAD

Non Cardiac Surgery

PCI

318 2016

2016


Figure 1. Master Treatment Algorithm for Duration of P2Y12 Inhibitor Therapy in Patients With CAD Treated With DAPT

2016 ACC/AHA Guideline Focused Update on

Duration of Dual Antiplatelet Therapy in Patients

With Coronary Artery Disease.

Figure 2. Treatment Algorithm for Duration of P2Y12 Inhibitor Therapy in Patients Treated With PCI




2016


Figure 3. Treatment Algorithm for Management and Duration of P2Y12 Inhibitor Therapy in Patients Undergoing CABG




Figure 4. Treatment Algorithm for Duration of P2Y12 Inhibitor Therapy in Patients With SIHD (Without ACS Within the Past Several Years)




2016


Figure 5. Treatment Algorithm for Duration of P2Y12 Inhibitor Therapy in Patient With Recent ACS (NSTE-ACS or STEMI)




Figure 6. Treatment Algorithm for the Timing of Elective Noncardiac Surgery in Patients With Coronary Stents




2016


2016 325

Variable Points Age ≥75 years -2 Age 65 to <75 years -1 Age <65 years 0 Current cigarette smoker

1

Diabetes mellitus 1

MI at presentation 1

Prior PCI or prior MI 1

Stent diameter <3 mm 1

Paclitaxel-eluting stent 1

CHF or LVEF <30% 2

Saphenous vein graft PCI 2

A score of ≥2 is associated with a favorable benefit/risk ratio for prolonged DAPT while a score of <2 is associated with an unfavorable benefit/risk ratio.

Levine GN, Bittl JA, Brindis RG, et

al. 2016 ACC/AHA Guideline

Focused Update on Duration of

Dual Antiplatelet Therapy in

Patients With Coronary Artery

Disease. J Am Coll Cardiol 2016;

doi=10.1016/j.jacc.2016.03.513.

Aspirin • Diminishes platelet reactivity

• Produces rapid clinical antithrombotic effect caused by immediate and near-total inhibition of thromboxane A2 production (released with vascular injury). • Thromboxane A2 is a potent vasocontrictor

• Inhibits COX1 and COX2 • NSAIDS reversibly bind to COX1 preventing inhibition by ASA and may cause

prothromotic events

• Inhibits the endothelium’s production of prostaglandin I2 which decreases platelet aggregation and induces vasodilation. • Prostaglandin I2 is also involved in inflammation.

• Reduces mortality

• Increase myocardial oxygen supply

• Use in ACS • Administered as soon as possible after presentation

• Initial dose: 162 mg to 325 mg chewed (non-enteric coated)

• Long Term: 81 mg daily

• If ASA intolerant load with clopidogrel and then daily dose

2016 326

2016


P2Y12 Receptor Inhibitors /

ADP Receptor Blockers • Clopidogrel (Plavix)

• 600 mg initial dose

• 75 mg daily

• Prasugrel (Effient) • 60 mg initial dose

• 10mg daily

• Contraindicated: > 75, < 60 kg, previous TIA, CVA

• Ticagrelor (Brilinta) • 180mg initial dose

• 90mg twice daily

• Not to be given with ASA doses > 100mg

• Adenosine Diphosphate (ADP) - Stored in platelets and released upon platelet activation

• ADP interacts with P2Y12 chemoreceptors to enhance adhesiveness and aggregation of platelets through the activation of the GP IIb/IIIa pathway

2016 327

P2Y12 Receptor Inhibitors /

ADP Receptor Blockers • Thienopyridines

• Clopidogrel

• Prasugrel

• Non thienopyridine

• Ticagrelor

2016 328

2016


Thienopyridines

• Thienopyridines are a class of ADP / P2Y12 receptor

blockers • Clopidogrel (Plavix)

• Prasugrel (Effient)

• Irreversibly inhibits P2Y12 receptor

2016 329

Clopidogrel Indications

• Alternative to ASA therapy in those who cannot take ASA

• Option in NSTE-ACS for the second antiplatelet agent

• Ticagrelor and prasugrel have upgraded indications

• Recommended agent in elective PCI with bare metal stent

2016


Clopidogrel

Issue of Non Responders • ACCF/AHA Clopidogrel Clinical Alert

• FDA Boxed Warning March 2010

• Role of genotype testing or routine platelet function testing

• Class II b recommendation pending results of randomized controlled

clinical trials.

• Prodrug

• 2 step process

• Involves several CYP450 isoenzymes

• CYP2C19 isoenzyme responsible for almost half of the first step formation

• 3 major genetic polymorphisms are associated with loss of function

• Observational studies have shown an association between an increased

risk of adverse cardiovascular events and the presence of one

nonfunctioning allele

2016 331

Clopidogrel and PPIs

11/8/2010: Expert Consensus Document

• Using proton pump inhibitors (PPIs) and antiplatelet drugs

(thienopyridines) together is an appropriate way of

treating patients with cardiovascular (CV) disease who

are at high risk of upper gastrointestinal (GI) bleeds,

despite recent concerns about an adverse interaction

between these two types of drugs, according to an Expert

Consensus Document released jointly today by the

American College of Cardiology (ACC), the American

College of Gastroenterology (ACG), and the American

Heart Association (AHA).

2016 332

2016


Clopidogrel and PPIs

2012: World Journal of Gastroenterology • Because PPI induced risk reduction clearly overweighs

the possible adverse cardiovascular risk in patients with

high risk of gastrointestinal bleeding, combination of

clopidogrel with the less CYP2C19 inhibiting pantoprazole

should be recommended.

• Several pharmacodynamic studies found a significant decrease of the

clopidogrel platelet antiaggregation effect for omeprazole, but not for

pantoprazole.

• More recent RCT and retrospective co-hort studies have not resulted

in same concerns with PPIs as observational studies suggested.

2016 333

Prasugrel

• TRITON TIMI 38 Trail • 13,608 patients with moderate to high risk ACS – all referred for

PCI; 3,534 STEMI

• Randomized to clopidogrel 300mg load and 75mg daily or prasurgrel 60mg load and 10mg daily

• Median follow up 14 ½ months

• Prasugrel (compared to Clopidogrel) associated with • Significant 2.2% reduction in absolute risk and a 19% reduction in

relative risk in the composite endpoint of death due to CV disease, nonfatal MI, or nonfatal stroke during the follow up period

• Significant increase in TIMI major hemorrhage (1.8% vs 2.4%)

• Prasugrel approved 2009

2016 334

Wiviott et al., 2007. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J

Med 2007; 357:2001-2015

2016


Prasugrel • TRILOGY

• Prasugrel versus clopidogrel in patients with NSTEMI or unstable angina who were not treated with PCI

• 7,243 patients

• No statistically significant difference in primary outcome (composite of: death from cardiovascular causes, myocardial infarction, or stroke) among patients under the age of 75 years

• A weak trend toward a reduced risk in the prasugrel group after 12 months (P = 0.07)

• Rates of severe and intracranial bleeding were similar in the two groups in all age groups. This is different than TRITON TIMI 38. Dose was adjusted in Trilogy for weight < 60 kg and age > 75 years.

• Conclusion: More research needed

• Higher recommendation for prasugrel in NSTE over clopidogrel in early invasive option only

2016 335

Take Away Prasugrel Points

• Less concern with PPI administration

• Less concern regarding non responders • Prodrug but not as

dependent on CYP2C19 isoenzyme

• Only used in patients with planned PCI • No benefit to

administration before the time of angiography

• Increased bleeding risk

• > 75 years old

• <60 KG

• Cannot be used: • Previous CVA / TIA

2016 336

2016


Ticagrelor (Non-Thienopyridine)

• Reversibly binds to P2Y12 receptor

• Not a PRO drug: does not requiring metabolic activation

• FDA approved July 2011

• Prevention of thrombotic events in patients with acute

coronary syndromes.

• Loading dose 180 mg then 90 mg twice daily

• Contraindicated in history of intracranial bleeding, active

pathological bleeding, severe hepatic impairment

• Higher recommendation for ticagrelor in NSTE over

clopidogrel in either ischemia guided or early invasive

option

2016 337

Clopidogrel versus Ticagrelor • PLATO trial

• Better anti-ischemic effect compared to clopidogrel

• No significant increase in major bleeding

• Faster onset and shorter duration than clopidogrel (known as reversible mode of action)

• BID dosing is a potential concern for compliance

• North American effect – thought to be due to higher dose ASA • Must not be given with maintenance ASA doses >

100mg

• Although shorter ½ life – recommendation to be held 5 days before surgery.

2016 338

Wallentin, L. et al., 2009. Ticagrelor versus clopidogrel in patients with acute coronary

syndromes. N Engl J Med; 361:1045-1057

Take Aways

2016


Guideline Directed Medical Therapy for ACS / CAD

Dual Antiplatelet Therapy • ASA • Clopidogrel/Prasugrel/Ticagrelor

Beta Blocker ACE Inhibitor

– Based on additional criteria

Eplerenone – Based on additional criteria

Statin – Regardless of baseline LDL-C

SL Nitroglycerin

Medications to control ischemia for medical

management / angina

• Beta-blockers

• Calcium channel blockers

• Long acting nitrate

• Ranolazine (Ranexa)

339 2016

Beta Blockers in ACS • Immediate as well as long term mortality benefit

• Immediate beta-blocker therapy – Reduces the magnitude of infarction and incidence of associated

complications

• Decreases myocardial oxygen demand

– Reduces rate of reinfarction

– Reduces frequency of life-threatening ventricular tachyarrhythmias.

• Long term benefit post ACS – Decreases myocardial oxygen demand

• HR Benefit

– Enhances overall well being

– Slows disease progression

– Inhibits ventricular remodeling and apoptosis

– Inhibits adverse effects of SNS

– Reduces mortality and repeat hospitalizations

340 2016

2016


Polymorphic VT with normal QT:

• Seen frequently in ischemic conditions (role of beta blockers)

341 2016

Beta Blockers at Presentation

• DO NOT administer in acute presentation IF:

– STEMI precipitated by cocaine

• Risk of exacerbating coronary spasm

– Heart blocks

• 1st degree AV block with PR > 0.24 sec

• 2nd or 3rd degree AV block

– Heart rate < 60 BPM

– SBP < 100 mm Hg

– Moderate LV failure is present (signs of HF or shock)

– Active asthma or reactive airway disease

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2016


A Closer Look at Beta Blockers

Decreases Myocardial Oxygen Demand

343

Decrease HR Decrease

Contractility

β1 blockade β1 blockade

Blood pressure =

CO x SVR

2016

Beta Blockers

• Nonselective: Block both Beta 1 and

Beta 2

– Propranolol (Inderal)

– Timilol (Blocadren)

– Nandolol (Corgard)

– Sotolol (Betapace)

– Labetolol (Normodyne, Trandate) (also alpha blockade)

– Carvedilol (Coreg)

(also alpha blockade)

• Cardio selective: Block Beta 1 – Acebutolol (Sectral)

– Metoprolol tartrate (Lopressor)

– Metoprolol succinate (Toprol XL)

– Atenolol (Tenormin)

– Esmolol (Breviblock)

– Bisoprolol (Z Beta)

– Nebivolol (Bystol) (also nitric oxide vasodilatory

properties)

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2016


345

• Start beta blocker prior ACE-inhibitor – Beta blockers most important medication to

reduce mortality early – However, cannot be given in patients at high risk

for shock

• Do not start beta blocker and ACE-I at the same time

• Hold ACE inhibitors for BP < 100 mm Hg systolic

or < 30 mm Hg below baseline. – Ideally ACE-I should be initiated within 24 hours

2016

Beta Blockers Recommended by Disease State

Post MI

• Atenolol

• Carvedilol

• Metoprolol

• Propanolol

• Timololol

Heart Failure • Bisoprolol

• Carvedilol

• Metoprolol Succinate (XL)

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2016


• Altered responses and vulnerability to drugs with:

– Hypotensive action (nitrates, calcium blockers)

– Cerebral effects (beta blockers)

• Caution with renally cleared drugs

347 2016

• Indicated for treatment of chronic angina • Mechanism of action in treating angina is

unknown – Possible relaxation of myocardium

• Does not impact heart rate or blood pressure • Dose: 500-1000mg BID • May prolong QTc interval • May worsen renal failure – DC if marked increase

in serum creatinine • Contraindicated in hepatic cirrhosis

348 2016

2016


349 2016

• The 2013 ACC/AHA Expert Panel included all 16 members of the National Heart, Lung, and Blood Institute Adult Treatment Panel (ATP) IV.

• Commissioned by NHLBI in June 2013

• Guidelines replace ATP III

350 2016

2016


• Focus is no longer on targeting the LDL-C – Treat to level of risk not to target LDL-C

• New guidelines focus on 4 groups of patients who can benefit from statin therapy with a good safety margin

• Benefit includes reduction in atherosclerotic cardiovascular disease events (ASCVD) – Nonfatal MI, CHD Death, nonfatal stroke

351 2016

• Individuals with clinical ASCVD – acute coronary syndromes – History of MI – Stable or unstable angina – Coronary or other arterial revascularization – Stroke/TIA – Peripheral arterial disease presumed to be of

atherosclerotic origin

• Without New York Heart Association (NYHA) class II-IV heart failure or receiving hemodialysis.

• High intensity statin – adults < 75

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2016


• Individuals with primary elevations of low-density lipoprotein cholesterol (LDL-C) ≥190 mg/dl.

353 2016

• Individuals 40-75 years of age with diabetes, and LDL-C 70-189 mg/dl without clinical ASCVD.

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2016


• Individuals without clinical ASCVD or diabetes, who are 40-75 years of age with LDL-C 70-189 mg/dl, and have an estimated 10-year ASCVD risk of 7.5% or higher

• Pooled Cohort Equations for ASCVD risk prediction.

– Men and women; black and non-Hispanic white

• May use non Hispanic White calculator for other populations (may under estimate risk in certain populations)

– Ages 40 to 79

– Identifies cohorts most likely to benefit from statin therapy

355 2016

• Required information to estimate ASCVD risk: – Age – Sex – Race – Total cholesterol – HDL cholesterol – Systolic blood pressure – Blood pressure lowering medication use – Diabetes status – Smoking status.

Source: Based on the Pooled Cohort Equations2 and the work of Lloyd-Jones, et al., Circulation, 2006

356 2016

http://www.cardiosource.org/Science-And-Quality/Practice-Guidelines-and-Quality-Standards/2013-Prevention-Guideline-Tools.aspx

http://www.cardiosource.org/Science-And-Quality/Practice-Guidelines-and-Quality-Standards/2013-Prevention-Guideline-Tools.aspx#fn2

2016


• No recommendations for treatment outside the 4 groups.

• No recommendation to start or stop statins in NYHA Class II-IV systolic HF that is ischemic in etiology

• In patients with a 10-year risk < 7.5%, other factors can be considered: – Family history – LDL-C>160mg/dL – HS C-reactive protein >2mg/dL – Coronary calcium score >300 – ABI < 0.9 – Etc.

357 2016

• Atorvastatin (Lipitor)

• Provastatin (Pravachol)

• Fluvostatin (Lescol)

• Simvastatin (Zocor)

• Lovastatin (Mevacor)

• Rosuvastin (Crestor)

• Inhibition of HMG-CoA reductase

• HMG –CoA reductase catalyzes an early step in cholesterol biosynthesis

Decrease mortality Reduce risk of major coronary events by 30% Stimulate plaque regression

358 2016

2016


High Intensity Moderate Intensity All patients <75 years with ASCVD (Group 1)

All patients > 75 years with ASCVD - consider

Patients (age > 21) with LDL-C> 190 mg/dL (Group 2)

Diabetic patients (age 40-75) with a 10 year ASCVD >7.5% (Group 3)

Diabetic patients with with a 10 year ASCVD <7.5% (Group 3)

Persons 40-75 years with a ≥7.5% 10-year ASCVD risk should receive moderate- to high-intensity statin therapy. (Group 4)

All patients > 75 years?

Patients with indication for high intensity but who are not able to take high intensity

359 2016

• High intensity: daily dose that lowers LDL-C by > 50%

• Moderate intensity: daily dose that lowers LDL-C by 30% to 50%

360

Atorvastatin (80 mg daily) in the PROVE-IT TIMI 22 demonstrated reduced mortality and ischemic events in patients with acute coronary syndrome.

2016

2016


• Atorvastatin 80 mg: 55-60% reduction

40 mg: 50% reduction

20 mg: 43% reduction

10 mg: 35-39% reduction

• Rosuvastatin 40 mg: 55-63% reduction



5 mg: 45% reduction

361 2016

High-Intensity Statin Therapy

Moderate-Intensity Statin Therapy

Low-Intensity Statin Therapy

Daily dose lowers LDL–C on average, by approximately ≥50%

Daily dose lowers LDL–C on average, by approximately 30% to

<50%

Daily dose lowers LDL–C on

average, by <30%

Atorvastatin 40-80 mg Rosuvastatin 20-40 mg

Atorvastatin 10-20 mg Rosuvastatin 5-10 mg Simvastatin 20–40 mg‡ Pravastatin 40 -80 mg Lovastatin 40 mg Fluvastatin XL 80 mg Fluvastatin 40 mg bid Pitavastatin 2–4 mg

Simvastatin 10 mg Pravastatin 10–20 mg Lovastatin 20 mg Fluvastatin 20–40 mg Pitavastatin 1 mg

362 2016

2016


• Lifestyle: Important prior to and during statin therapy

• Non-statin therapies, whether alone or in addition to statins, do not provide acceptable ASCVD risk reduction benefits compared to their potential for adverse effects in the routine prevention of ASCVD. – Addition of these other agents can be considered

in patients with LDL-C > 190 mg/dL.

363 2016

• Short or unknown half life: administration in evening for maximum efficacy – Simvastatin, lovastatin, and immediate release fluvastatin

• Hydrophilic (fluvastatin, pravastatin, and rosuvastatin*) – Minimally metabolized by the cytochrome P450 (CYP450)

enzyme system

– Lowest rates of myopathy *

• The lipid soluble statins are associated with insulin resistance and an increased Hemoglobin A1C. – Use cautiously with medications with strong CYP3A4

inhibition

– Benefit of cardiovascular risk reduction is felt to outweigh the downside of elevated glucose levels.

364 2016

2016


• Total CPK levels prior to initiation if at increased risk for adverse events and repeated for suspected myopathy.

• No > 1 quart per day of grapefruit juice – particularly with simvastatin and atorvastatin.

• Combined with gemfibrozil (a fibrate), increase the risk of rhabdomyolysis.

Risk Factors • Advanced age (> 80 years)

• Frailty

• Small body size

• Renal insufficiency

• Under treated hypothyroidism

• Co-administration of other drugs such as colchicine

365 2016

• Liver enzymes should be assessed at baseline and as clinically indicated.

• Routine monitoring of liver enzymes is not necessary.

• Statin therapy can result in an elevation of liver enzymes not associated with liver toxicity. – Association with higher dose statins.

• Contraindicated in active liver disease or in persistently and unexplained elevated liver enzymes. – AST and ALT > 3x the upper limit of normal.

• Considered safe in patients with mild to moderately elevated liver enzymes attributable to chronic conditions such as nonalcoholic fatty liver and hepatitis C.

366 2016

2016


• The purpose of the AIM-HIGH trial was to test whether adding Niaspan to patients at LDL-C goal but with continued low HDL-C levels, would improve cardiovascular outcomes.

• Despite an improvement in lipid levels the study was stopped early due to lack of effectiveness in achieving the primary endpoint which was a composite of cardiovascular death, non-fatal myocardial infarction, acute coronary syndrome, ischemic stroke, or symptom driven cardiac or cerebral revascularization (Boden et al., 2011).

• TREDAPTIVE: Niacin ER plus laropiprant

– No US approval

– No longer marketed outside US

• Failure to improve cardiovascular outcomes

• Increased adverse events

– Diabetic complications

– New onset diabetes

– GI problems

– Musculoskeletal complaints

– Heart failure

– Bleeding

– Skin complaints

368

2016


• Indicated for hyperlipidemia with Hypertriglyceridemia. • Contraindicated in severe renal (renally excreted) and hepatic

disease, pre-existing gall bladder disease • ACCORD Study

– No reduction in cardiovascular mortality or non-fatal myocardial infarction or stroke when a fenofibrate was added to simvastatin in patients with type 2 diabetes mellitus(Ginsberg et al., 2010).

• The FIELD study – effects of long-term fenofibrate therapy on cardiovascular events in

people with type 2 diabetes) did not show a statistically significant reduction in major coronary events in persons treated with fenofibrate therapy compared to placebo (Keech et al., 2005).

369

• Intestinal absorption inhibitor

– Decreased delivery of cholesterol to the liver

– Reduction in hepatic cholesterol stores

– Increased clearance of cholesterol from the blood

• IMPROVE IT study

370 2016

2016


371 2016

• Drug is an antibody that targets a specific protein (PCSK9) – PCSK9 reduces the number of receptors on the liver

that remove LDL cholesterol from the blood. – By blocking PCSK9’s ability to work, more receptors

are available to get rid of LDL cholesterol from the blood

• Average reduction in LDL cholesterol ranging from 36 to 59 percent, compared to placebo

• Alirocumab (Praluent) • Evolocumab (Repatha)

372 2016

2016


• Approved by FDA Aug 2015 • Amgen • Every 2 week injection • Approved for patients who have

heterozygous or homozygous familial hypercholesterolemia, HeFh or HoFh, which is an inherited condition that causes high LDL cholesterol levels.

• Also approved for patients who have had a heart attack or stroke.

• Outcomes: – Reduction of LDL was significant >71%

compared to placebo. – The effect of Repatha® on cardiovascular

morbidity and mortality has not been determined.

• Approved FDA Jul 2015 • Sanofi and Regeneron • Every two week injection • Approved for patients who have

heterozygous or homozygous familial hypercholesterolemia, HeFh or HoFh, which is an inherited condition that causes high LDL cholesterol levels.

• Also approved for patients who have had a heart attack or stroke

• Outcomes: – Reduction of LDL was significant > 44% at

24 weeks – The effect of PRALUENT on heart problems

such as heart attacks, stroke, or death is not known.

373

Treatment in conjunction with highest tolerated statin dose and diet modification.

ACC publishes non-statin therapies

guidelines for cholesterol

April 04, 2016

April 1, 2016, American College of

Cardiology -- The American College of

Cardiology today released expert

consensus guidance regarding the use of

non-statin therapies to lower cholesterol in

high-risk patients.

Lifestyle Monitoring Order of Non Statin Therapies Algorithms Tables Drug Specifics More

https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=0ahUKEwibiYDwzsLMAhULaD4KHdXNBLAQjRwIBw&url=http://paylessforoil.com/news/&psig=AFQjCNFxl7-94g95d6CLhJMU6z9qvofqlA&ust=1462526731585568

2016


375 2016

Classification LVEF Description

Heart Failure with

Reduced Ejection

Fraction (HFrEF)

≤40% Systolic HF. Randomized clinical trials have mainly enrolled

patients with HFrEF and it is only in these patients that

efficacious therapies have been demonstrated to date.

Heart Failure with

Preserved Ejection

Fraction (HFpEF)

≥50% Diastolic HF. The diagnosis of HFpEF is challenging because it is

largely one of excluding other potential noncardiac causes of

symptoms suggestive of HF. To date, efficacious therapies have

not been identified.

HFpEF, Borderline 41% - 49% These patients fall into a borderline or intermediate group. Their

characteristics, treatment patterns, and outcomes appear similar

to those of patient with HFpEF.

HFpEF Improved >40% It has been recognized that a subset of patients with HFpEF

previously had HFrEF. These patients with improvement or

recovery in EF may be clinically distinct from those with

persistently preserved or reduced EF.

376 2016

2016


377

Classification of Heart Failure New York Heart Association

2016

378 2016

2016


STAGE AAt high risk for HF but

without structural heart

disease or symptoms of HF

STAGE BStructural heart disease

but without signs or

symptoms of HF

THERAPY

Goals

· Control symptoms

· Improve HRQOL

· Prevent hospitalization

· Prevent mortality

Strategies

· Identification of comorbidities

Treatment

· Diuresis to relieve symptoms

of congestion

· Follow guideline driven

indications for comorbidities,

e.g., HTN, AF, CAD, DM

· Revascularization or valvular

surgery as appropriate

STAGE CStructural heart disease

with prior or current

symptoms of HF

THERAPYGoals· Control symptoms· Patient education· Prevent hospitalization· Prevent mortality

Drugs for routine use· Diuretics for fluid retention· ACEI or ARB· Beta blockers· Aldosterone antagonists

Drugs for use in selected patients· Hydralazine/isosorbide dinitrate· ACEI and ARB· Digoxin

In selected patients· CRT· ICD· Revascularization or valvular

surgery as appropriate

STAGE DRefractory HF

THERAPY

Goals

· Prevent HF symptoms

· Prevent further cardiac

remodeling

Drugs

· ACEI or ARB as

appropriate

· Beta blockers as

appropriate

In selected patients

· ICD

· Revascularization or

valvular surgery as

appropriate

e.g., Patients with:

· Known structural heart disease and

· HF signs and symptoms

HFpEF HFrEF

THERAPY

Goals

· Heart healthy lifestyle

· Prevent vascular,

coronary disease

· Prevent LV structural

abnormalities

Drugs

· ACEI or ARB in

appropriate patients for

vascular disease or DM

· Statins as appropriate

THERAPYGoals· Control symptoms· Improve HRQOL· Reduce hospital

readmissions· Establish patient’s end-

of-life goals

Options· Advanced care

measures· Heart transplant· Chronic inotropes· Temporary or permanent

MCS· Experimental surgery or

drugs· Palliative care and

hospice· ICD deactivation

Refractory symptoms of HF at rest, despite GDMT

At Risk for Heart Failure Heart Failure


· Marked HF symptoms at

rest

· Recurrent hospitalizations

despite GDMT


· Previous MI

· LV remodeling including

LVH and low EF

· Asymptomatic valvular

disease


· HTN

· Atherosclerotic disease

· DM

· Obesity

· Metabolic syndrome

or

Patients

· Using cardiotoxins

· With family history of

cardiomyopathy

Development of

symptoms of HFStructural heart

disease

379 2016

380 2016

2016


• Angiotensin-converting enzyme inhibitors (“pril” medications)

– Captopril, Enalapril, Lisinopril, Quinapril, Ramipril, Benazepril, Fosinopril

• Angiotensin II Receptor Blockers (“sartan”

medications)

– Losartan, Irbesartan, Candesartan,Telmisartan,Valsartan, Eprosartan

381 2016

A Closer Look at ACE Inhibitors

• ACE Inhibitors impact afterload and preload because they block the vasoconstrictive effects of angiotensin II by preventing its formation – Very important in reducing workload of left ventricle in

systolic dysfunction

– Decrease systemic vascular resistance without reflex stimulation of heart rate and contractility

• ACE Inhibitors have additional benefit in preload reduction by blocking the effects of aldosterone release

382 2016

2016


A Closer Look at ACE Inhibitors

• Overall cardioprotective, vasculoprotective effect, and renal protective – Prevents ventricular remodeling

– Reduce mortality in patients with systolic heart failure

– Reduction of left ventricular mass in LV hypertrophy

– Slows progression of both renal disease in diabetes and hypertensive nephrosclerosis

383 2016

• Renal protective in chronic kidney disease • However, can cause acute kidney injury (AKI) in patient’s at risk

(i.e. low stroke volume) due to preventing the compensatory mechanism of efferent vasoconstriction – When there is decreased blood flow into the glomerulus via the afferent arterioles,

the efferent arterioles constrict to raise glomerular filtration pressure on the back end

– ACE-I prevent efferent vasoconstriction

• Creatinine can be allowed to be 35% above baseline without stopping the drug. – As forward flow to the glomerulus improves – there is less

need for efferent vasoconstriction to compensate and glomerular filtration will stabilize

• Will cause acute renal failure in patients with bilateral renal artery stenosis – Dilation of efferent glomerular arterioles with no ability to dilate afferent arterioles

which results in decreased glomerular filtration – In bilateral renal artery stenosis there is fixed flow into the glomerulus – an

improvement in stroke volume will not improve flow into the glomerulus •

384 2016

2016


ACE Inhibitors and GFR

385 2016

• Influences bradykinin and can produce cough

• Cough is side effect in 10-20% of patients

• Need to assure cough is not sign of worsening heart failure

• Patient may need changed to ARB

386 2016

2016


ACE Inhibitor Monitoring and Contraindications

• Assess renal function and potassium within 1 to 2 weeks of initiation if outpatient

• High risk features for AKI: diabetes, hyponatremia, hypotension, azotemia, potassium supplementation, combination with aldosterone antagonist.

• Note * difference between AKI (hold regardless of creatinine) and CKD may give until creatinine of > 3.0)

387

ESRD: ACE Inhibition ok . SBP most often limiting factor. Need reasonable SBP for

dialysis. Cautions/Contraindications

Bilateral renal artery stenosis Creatinine > 3 mg /dL Potassium > 5.0 mEq/L Systolic BP < 80 mmHg 2016

• ACE Inhibitors remain the first choice for inhibition of RAAS

• ARB’s are a reasonable alternative to ACE Inhibitor if intolerant to ACE Inhibitor due to cough or angioedema

• Reasonable alternative to ACE I as 1st line therapy for patients with mild / moderate HF & reduced LVEF, especially if already take ARB for other reason (HTN)

• Directly blocks angiotensin II

• Combination of ACE I and ARB – not recommended

388 2016

2016


• New class of medication: ARNI – Angiotensin Receptor Blocker with Neprilysin Inhibitor

• Combo drug: sacubitril (Neprilysin Inhibitor) with valsartan (ARB)

389

• PARADIGM-HF Trial

• Multinational, randomized, double-blind trial

• Comparing ENTRESTO with enalapril

• 8,442 adult patients with symptomatic chronic heart failure (NYHA

class II–IV) and systolic dysfunction (left ventricular ejection

fraction ≤40%).

• Results:

• 20% reduction in the rate of death or hospitalization for heart

failure

• 16% reduction in the rate of all-cause death compared to

enalapril at 3.5 years of follow-up.

390

Endogenous Vasoactive

Peptides • Naturetic peptides

• Adrenomedullin

• Bradykinin

• Substance P

• Calcitonin gene-related

peptide

↓ Neurohormonal activation ↓ Vascular tone

↓ Cardiac fibrosis, hypertrophy

↓ Sodium retention

N

E

P

R

I

L

Y

S

I

N

Neprilysin Inhibitor

2016


391

392

2016


393

Sacubitril /Valsartan (Paradigm HF listed doses) 24 mg/26 mg (50 mg)

49 mg/51 mg (100 mg) 97 mg/103mg (200 mg)

Valsartan in Entresto is more bioavailable in Entresto than valsartan alone.

Dosing equivalents: Valsartan In Entresto = Valsartan alone

24 mg in Entresto = 40 mg alone 49 mg in Entresto = 80 mg alone 97 mg in Entresto = 160mg alone

• Do not administer with ACE I – Increased risk of angioedema

– Stop ACE I for 36 hours before starting Entresto

– Do not administer in patients with history of angioedema

• Monitor kidney function, blood pressure and potassium levels

• BNP levels will not be accurate with Entresto but pro-BNP levels may be used

394

2016


COR LOE Recommendations

I ACE I: A Inhibition of the RAS with ACE I OR ARB OR ARNI in conjunction with evidence-based betablocker, and aldosterone antagonist in selected patients, is recommended for patients with chronic HFrEF to ↓ mortality and morbidity.

ARB: A

ARNI: B-R

395

COR= Class of Recommendation (strength); green is recommended (Strong)

LOE = Level of Evidence (Quality); A = high quality evidence; B = moderated quality

evidence; R = randomized Yancy C, Jessup M, et al. Circulation. 2016;134: e Pub (May 20).


I ACE I: A Use of ACE I is beneficial for patients with prior or current symptoms of chronic HFrEF to ↓ morbidity and mortality

ARB: A The use of ARB to ↓ morbidity and mortality is recommended in patients with prior or current symptoms of chronic HFrEF who are intolerant to ACE inhibitors because of cough or angioedema

ARNI: B-R In patients with chronic symptomatic HFrEF NYHA class II or III who tolerate an ACE I or ARB, replacement by ARNI is recommended to further ↓ morbidity and mortality

396

COR= Class of Recommendation (strength); green is recommended (Strong)

LOE = Level of Evidence (Quality); A = high quality evidence; B = moderated quality

evidence; R = randomized Yancy C, Jessup M, et al. Circulation. 2016;134: e Pub (May 20).

2016



III B-R ARNI should not be administered concomitantly with ACE I or within 36 hours of the last dose of ACE I

III C-EO ARNI should not be administered to patients with a history of angioedema

397

COR= Class of Recommendation (strength); red IS HARM

LOE = Level of Evidence (Quality); B = moderated quality; 1 or more randomized trail

C-EO = expert opinion, based on clinical experience Yancy C, Jessup M, et al. Circulation. 2016;134: e Pub (May 20).

• Point 1: Why do we use them when they decrease contractility? – Inhibits adverse effects of SNS

• Decrease myocardial oxygen consumption – Decreases HR – Decreases contractility (however, benefit outweighs)

– Inhibits ventricular remodeling and apoptosis – Slows disease progression – Can improve LVEF – Decrease mortality/hospitalization

• When to initiate? – Do not initiate in an acutely decompensated patient

• Remember you are giving a negative inotrope – Can be initiated in hospital for HF admission if inotropic therapy

not required • If decompensation occurs on a beta blocker it is generally

not stopped unless inotrope is needed. Dose may need to be decreased.

398 2016

2016


• Even better in combination with ACE Inhibitor – Started after initiation of ACE-I but before getting to target

dose of ACE-I

• Must be used with diuretic if any recent or current fluid retention

• Start very low doses with gradual up-titration • Titration to target dose essential

• Pearl: If hypotension – consider administration opposite of ACE-I or decrease in diuretic dose

• Pearl: Fatigue may be multifactorial – address over diuresis, sleep apnea and screen for depression

399 2016

• Cannot assume class effect • Bisoprolol – β1

– CIBIS III randomized trial – 2005 (enalapril)

• Metoprolol succinate - β1

– MERIT-HF randomized trial – 1999 (placebo)

• Carvedilol - β1, β2, α1

– CAPRICORN randomized trial – 2001 (placebo)

– COMET randomized trial – 2003 (metoprolol tartrate)

400 2016

2016


• Mineralocorticoid Receptor Antagonist (MRA)

• ACC/AHA Class IA Recommendation

• LVEF < 35% with NYHA Class II-IV Heart Failure to reduce mortality and morbidity

401

RALES Trial (1999) – 1663 pts

• NYHA Class III-IV

• LVEF < 35%

• Standard rx. vs standard rx.

with spironolactone

• 30% ↓ in mortality

• 35% ↓ in hospitalization

EMPHASIS-HF (2011) – 2737 pts

• NYHA Class II

• LVEF < 35%

• Standard rx. vs standard rx. with

epleranone

• 24% ↓ in all cause mortality

• 42% ↓ in HF hospitalization

• Promotes retention of sodium

• Promotes loss of potassium and magnesium

• Potentiates catecholamines

• Inhibits the parasympathetic nervous system

• Decreases arterial compliance

• Promotes direct remodeling

• Has prothrombotic properties

• Causes vascular inflammation and injury

402

2016


• Potassium sparing medications

• Any potassium supplements should be stopped after initiating - consider potassium based

salt substitutes

• Counsel patients about avoiding foods high in potassium

Lab Monitoring • Potassium, sodium

and renal function

checked 2-3 days after

initiation and again at

7 days then at the one

month mark. If stable

then every 3 months.

• Adding or increasing

ACE I or ARB should

increase potassium

and creatinine

surveillance. 403

• Non selective aldosterone blocker – Blocks aldosterone and

androgen; stimulates progesterone

• RALES Trial

• Selective aldosterone receptor antagonist

• EMPHASIS-HF

• EPHESUS (Post MI)

404

Major side effect:

gynecomastia (10%), sexual

dysfunction and menstrual

problems due to non

selectivity

Eliminates most

gynecomastia and sexual side

effects associated with

aldactone

2016


• The combination of hydralazine and isosorbide dinitrate (ISDN) is recommended to REDUCE MORBIDITY AND MORTALITY for : – Self-described African Americans with NYHA class III–IV HFrEF

receiving optimal therapy with ACE inhibitors and beta blockers, unless contraindicated (Class I, LOE: A)

– Anyone with current or prior symptomatic HFrEF who cannot be given an ACE inhibitor or ARB because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated (Class IIa, LOE: B)

405

Self-identified African Americans are thought to have a less

active renin-angiotensin system and a lower bioavailability

of nitric oxide than those self-identified as white.

• African American Heart Failure Trail (2004) - A-HeFT

• 1050 self-described African American patients

• NYHA Class III or IV

• LVEF < 35% or < 45 with a dilated left ventricle

• Currently on standard therapy with BB for at least 3 months prior to enrollment

• Randomized to standard therapy + placebo (1 tablet TID) or standard therapy + 37.5mg of hydralazine and 20mg of ISDN (combined in one tablet TID)

• Dose increased to 2 tablets TID if no side effects with 1 tablet TID

• Trial ended early due to significantly higher rate of mortality in placebo group

– 43% reduction in rate of death from any cause

– 33% reduction in the rate of first hospitalization for heart failure in treatment group

– Significant improvement in quality of life score in treatment group

406

2016


• Initiation: • Hydralazine 37.5 mg / ISDN

20mg 3 times daily

• Target dose: – Total DAILY dose of

Hydralazine 225 mg (75mg TID) and ISDN 120 mg (40mg TID)

• Bidil – combo drug: – Hydralazine 37.5mg / ISDN

20mg

– 1 up to 2 tablets TID

• Adherence difficult

• Adverse Reaction – Headache

– Dizziness

– GI complaints

407

Consider slower titration to enhance

tolerance

Digoxin • Stage C Recommendations

– Added in patients with persistent symptoms already on ACE Inhibitor, Beta-blocker and diuretic

• Positive inotropic effect – weak effect • Enzyme inhibition in noncardiac tissues – reduces

sympathetic flow • Improved symptoms, exercise tolerance and quality of life • No reduction in mortality • Beta-blocker better for rate control • Low dose: 0.125mg daily • No need for loading dose • Narrow therapeutic range in HF

– 0.5 to 0.9 ng/ml 408 2016

2016


Impact of HR on Heart Failure

• In patients with coronary artery disease and left-ventricular dysfunction, a heart rate of 70 beats per minute (bpm) or higher was associated with a 34% increased risk of cardiovascular death and a 53% increase in admission to hospital for heart failure compared with heart rate lower than 70 bpm1

• Heart rate is also directly related to risk of death, cardiovascular death, or admission to hospital in patients with heart failure2

• Heart-rate reduction is associated with improved outcomes3

409

1. Fox K et al. on behalf of the BEAUTIFUL investigators. Heart rate as a prognostic risk

factor in patients with coronary artery disease and leftventricular systolic dysfunction

(BEAUTIFUL): a subgroup analysis of a randomised controlled trial. Lancet 2008; 372:

817–21

2. Pocock SJ, et al. Predictors of mortality and morbidity in patients with chronic heart

failure. Eur Heart J 2006; 27: 65–75.

3. Flannery G et al. Analysis of randomized controlled trials on the effect of magnitude of

heart rate reduction on clinical outcomes in patients with systolic chronic heart failure

re

• Sinus node inhibition • Inhibition of the Hyperpolarization –activated

cyclic nucleotide-gated channels (If channel or f-channel or “Funny” channel)

• If current is an inward Na+/K+ current that activates pacemaker cells of the SA Node

• Ivabradine binds the “Funny” channel in a current dependent fashion

• Slows diastolic depolarization → slows the firing of the SA Node → slows heart rate

410

Ivabradine (Corlanor)

2016


411


• SHIFT Trial (2010) • Double-blinded, placebo-controlled, parallel-

group study • Symptomatic HF, LVEF < 35%, in NSR with HR

> 70 bmp, admitted for HF in previous year, on stable HF treatment

• 6558 patients randomized to ivabradine 7.5mg BID or matching placebo

• Primary endpoint: composite of CV death or hospital admission for worsening HF

412

2016



• Median follow up 22.9 months • Mean HR lowered to • Statistically significant outcomes:

– Composite endpoint (CV death or Hospitalization for HF): 18% reduction with Ivabradine

– Hospitalization for worsening HF: 26% reduction with Ivabradine – Deaths due to HF: 26% reduction in Ivabradine group (CV deaths

and all cause deaths not statistically significant) – The higher the baseline heart rate the better the outcome – Quality of Life scores better with ivabradine

• Side Effect: Phosphenes (visual disturbances) reported in 3% of ivabradine group (1% in placebo – p<0.0001)

413

ACC/AHA/HFSA Guideline Update Recommendations for Ivabradine (Stage C HFrEF)


IIa B-R Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III), stable chronic HFrEF (LVEF < 35%) who are receiving GDEM, including beta blocker at maximum tolerated dose, and who are in NSR with a heart rate of > 70 bmp at rest.

414

COR= Class of Recommendation (strength); yellow, is reasonable/useful (Moderate)

LOE = Level of Evidence (Quality); B = moderated quality; 1 or more randomized trials;

GDEM: Guideline-directed evaluation and management Yancy C, Jessup M, et al. Circulation. 2016;134: e Pub (May 20).

2016


415

Drug class Brand name

generic name Starting dose Target dose

ACE Inhibitor Prinivil or Zestril

lisinopril 5 mg once daily 20 mg once daily

maximum dose might be 40 mg once daily

ACE Inhibitor Monopril

fosinopril sodium 10 mg once daily

5 mg if weak kidneys 40 mg once daily

ACE Inhibitor Vasotec

enalapril maleate 2.5 mg BID 20 mg BID

maximum dose might be 40 mg BID

ACE Inhibitor Mavik

trandolapril one mg once daily 4 mg once daily

ACE Inhibitor Capoten captopril

25 mg 2 to 3 times a day 100mg TID (450 mg per day maximum)

ACE Inhibitor Lotensin

benazepril

5 mg once daily if on diuretic

10 mg once daily if not on diuretic

40 mg per day in one 40 mg dose or two 20 mg doses

ACE Inhibitor Accupril quinapril

5 mg BID 2.5 mg BID if weak

kidneys 20 mg BID

ACE Inhibitor Altace

ramipril 1.25 mg to 2.5 mg BID 10 mg BID

ACE Inhibitor Aceon

perindopril erbumine

1 mg BID if on diuretic 2 mg BID if not on

diuretic 4 mg BID (8 mg BID maximum)

2016

416

Drug class Brand name

generic name Starting dose Target dose

ARB Cozaar

losartan

25 mg BID or 50 mg once daily

12.5 mg BID or 25 mg once daily if weak

liver function

50 mg BID

ARB Atacand

candesartan cilexetil 4 to 8 mg once daily 32 mg once daily

ARB Diovan

valsartan 80 mg once daily 160 mg once daily

80 mg once daily if weak liver function

ARB Avapro

irbesartan 150 mg 300 mg once daily

Beta-blocker Coreg

carvedilol 3.125 mg BID

25 mg BID under 188 pounds

50 mg BID over 187 pounds

Beta-blocker Toprol XL

metoprolol extended release (succinate)

12.5 mg for class 3 to 4 patients

25 mg for class 1 to 2 patients

200 mg once daily

Beta-blocker Zebeta

bisoprolol 2.5 mg once daily 10 mg once daily

Aldosterone Antagonist

Aldactone spironolactone

25 mg once daily 25 mg once daily

Aldosterone Antagonist

Inspra eplerenone

25 mg once daily 50 mg once daily 2016

http://www.chfpatients.com/ace.htm

http://www.chfpatients.com/text/lisinopril.txt

http://www.chfpatients.com/text/enalapril.txt



http://www.chfpatients.com/glossary.htm




http://www.chfpatients.com/ace.htm

http://www.chfpatients.com/text/candesartan_cilexetil.txt

http://www.chfpatients.com/text/valsartan.txt

http://www.chfpatients.com/text/irbesartan.txt

http://www.chfpatients.com/beta_overview.htm



http://www.chfpatients.com/coreg.htm

http://www.chfpatients.com/CHFinfo.htm




http://www.chfpatients.com/meds_old.htm

http://www.chfpatients.com/meds.htm

2016


Medical Therapy for Stage C HFrEF:

Magnitude of Benefit Demonstrated in RCTs

GDMT RR Reduction

in Mortality

NNT for Mortality

Reduction

(Standardized to 36 mo)

RR Reduction

in HF

Hospitalizations

ACE inhibitor or

ARB 17% 26 31%

Beta blocker 34% 9 41%

Aldosterone

antagonist 30% 6 35%

Hydralazine/nitrate 43% 7 33%

417 2016

Incremental Benefit with HF Therapies (Cumulative % Reduction in Odds of Death at 24 Months Associated with Sequential Treatments)

+20% to -68%

P=0.1566

-43% to -91%

P<0.0001

-70% to -96%

P<0.0001

Fonarow GC,Yancy CW. J Am Heart Assoc 2012;1:16-26. 418 2016

2016


Diuretics • Decrease congestive

symptoms

– No mortality benefit

• First line: Loop diuretics – Thiazide diuretic my be added

• Potassium and magnesium monitoring

• Use with moderare NA restriction

• Fluid restriction criteria

• Monitor response to therapy

– Adequate diuresis

• BNPt goal

• JVP assessment

• Orthopnea

– Over diuresis

• Hypotension

• Dizziness

• Orthostatic BP

419 2016

Diuretic Therapy

Outpatient

• Weight loss goal of 0.5 to 1.0 kg per day

• Patients can be educated for adjustable diuretic dosing • Weight gain

• Weight loss

• Change in oral intake or during periods of illness

Diuretic Resistance

• Diuretic resistance – Reasons

• High sodium levels

• NSAIDs

• Severe renal impairment

• Renal hypoperfusion

– Strategies • IV instead of PO

• Continuous infusion versus intermittent dosing if BP is a concern

• Change the loop diuretic

• Addition of thiazide

420 2016

2016


Renal Anatomy: Nephron and Loop Diuretics

421

• Work in ascending loop of Henle • Loss of H2O, K+, Na+, Cl-, H+ • More loss of H2O and less K+ and Na+ than

thiazides • Promotes venous vasodilatation • Rapid onset and short duration • Can be effective in presence of renal failure • High ceiling diuretic / threshold medications 2016

Loop Diuretics

• Equivalents – Furosemide 40 mg – Torsemide 20 mg – Bumetanide 1 mg

• Dosing

– Recommended max dose

• 600 mg furosemide • 200 mg torsemide • 10 mg bumetanide

422

Bumetanide (Bumex)

Furosemide (Lasix)

Torsemide (Demadex)

2016

2016


Differences in Loop Diuretics

Bumetanide Furosemide Torsemide

Lack of randomized control data with comparison to furosemide. Better pharmacokinetic profile (oral bioavailability) than furosemide but turosemide has evidence of more efficacy and more safety. (Wargo &Banta, 2009)

BID Dosing when GFR is low 2 randomized trials comparing Torsemide and Furosemide N=471 Torsemide associated with reduction in HF and CV readmission in systolic HF with a trend towards reduction of all cause mortality. (DiNicolantonio, 2012)

423 2016

More on Loop Diuretics • DOSE Trial

– NEJM: Felker et al., 2011

– No significant difference in symptoms or renal function between continuous drip versus intermittent dosing

– Non significant trend toward improvement in symptoms with high dose (IV at 2.5 x PO dose) versus low dose; (IV at same as PO dose) no change in renal function

424 2016

2016


Thiazide Diuretics

– Inhibit reabsorption of Na+ and Cl-

• In the distal tubule

• More sodium loss than loop diuretics

– Delayed onset but longer duration of action than loop diuretics

• Give 30 minutes before a loop diuretic

– Low ceiling diuretics

– Less potent diuretic than loop diuretics

– Diminished effectiveness in presence of renal failure 425 2016

Thiazide Diuretics Bendrofluazide (Naturetin) Side effects:

Blood Chemistry changes:

Hyponatremia (↓ Na+)

Hypokalemia (↓ K+)

Hypomagnesemia (↓ Mg+)

Hyperglycemia (↑ blood sugar)

Hyperuricemia (↑ uric acid)

Hypercalcemia (↑ Ca++)

Decreased glomerular filtration in

kidneys (↑ BUN, creatinine)

↑ cholesterol

↑ triglycerides

↓ HDL cholesterol

Other side effects:

Impaired glucose tolerance

Gout

Impotence

Ventricular arrhythmias (↓ K+)

Nausea, dizziness, headache

Benthiazide (Aquatag, Exna)

Chlorothiazide (Diuril)

Chlorthalidone (Hygroton)

Cyclothiazide (Anhydron)

Hydrochlorothiazide (HCTZ) (HydroDiuril, Esidrix)

Hydroflumethazide (Saluron, Diucardin)

Indapamide (Lozol)

Metolazone (Zaroxolyn)

Polythiazide (Renese)

Trichlormethiazide (Metahydrin, Naqua)

426 2016

2016


Diuretics and Renal Function

• Role of venous congestion in worsening renal function

• Role of volume depletion / hypotension and worsening renal function

427 2016

Cardiorenal Syndrome

• Moderate to severe renal dysfunction with fluid overload

– Continue to treat with diuretics

• In severe fluid overload renal dysfunction my improve with continued treatment

• May need to hold ACE I secondary to AKI

• Venous congestion plays a role in worsening renal function (not just hypoperfusion)

428 2016

2016


Pharmacology for Atrial Fibrillation will be discussed during atrial

fibrillation class in the AM.

429 2016

BE THE BEST THAT YOU CAN BE

EVERY DAY. YOUR PATIENTS ARE

COUNTING ON IT!

www.cardionursing.com

430 2016

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