Images have been removed from the PowerPoint slides in ... · Torsades de Pointes. Practice Alert - Dysrhythmia 37 Monitoring Acute Coronary Syndromes ... Images have been removed

Images have been removed from the PowerPoint slides in this handout due to copyright restrictions.

CCRN®/PCCN® Review Course - Day 1 ©TCHP Education Consortium, September 2003, Rev. June 20171

CCRN Review – Cardiovascular

Cleo Bonham, MSN, RN, CCRN

CCRN Review – Cardiovascular

• Cardiovascular (18% CCRN) (33% PCCN)

• General KnowledgeLooks at concepts related to disease and injury. Looks at nursing actions and judgements.

Coronary Arteries

• Right Coronary Artery

Supplies: Left Ventricle

Inferior Wall

Posterior Wall

Right Ventricle

SA Node (55%)

AV Node (90%)

Coronary Arteries

• Left Main Coronary ArteryLeft Anterior Descending

Left VentricleAnterior WallVentricular Septum

CircumflexLeft Ventricle

Lateral Wall

The Cardiac Anatomy in Relation to Coronary Arteries – Anterior View

The Cardiac Anatomy in Relation to Coronary Arteries – Posterior View



Electrode Placement AACN Procedure Manual

• Limb leads (I,II,III)• Place to decrease muscle artifact during limb movement

• Placement• Right Arm (RA) infra-clavicular fossa close to right

shoulder• Left Arm (LA) infra-clavicular fossa close to left shoulder• Left Leg (LL) below rib cage on left side of abdomen• Ground (RL)

• Precordial Leads - depends on patient’s needs

Practice Alert - ST Segment Monitoring7

5 Lead Electrode Placement

5 lead systems allow for the recording of any of the six limb leads plus one precordial (V) lead.

Shown lead placement for recording V1 or V6.

5 Lead monitoring systems are recommended over 3 lead systems for monitoring QRS morphology

Practice Alert - Dysrhythmia Monitoring8

Lead Selection

• Monitoring ST segment changes in 12 leads provides the most accurate data for identification of ischemic events.

• If only two leads are available for ST segment monitoring, use leads III and V3 (unless otherwise indicated)


ST Segment Fingerprint

• If 12 lead monitoring is not available, use the patient’s “ST Fingerprint”.

• Defined as the pattern of ST segment elevation and/or depression unique to a particular patient based on the anatomic site of coronary occlusion

• Can be obtained during STEMI or PCI

Practice Alert - ST Segment Monitoring

10

Other Considerations

• If the ST fingerprint is not known, use leads III and V3.

• For patients without definitive ACS, with suspected of having or being ruled out for ACS, use leads III and V5.

• For non-cardiac surgical patients lead V5 is valuable for identifying demand-related ischemia.


11

12 Lead Review



Cause for Concern

• ST depression or elevation of 1-2 mm that lasts for at least one minute can be clinically significant and warrants further patient assessment.


13

Flanders SA. Continuous ST-segment monitoring: Raising the bar. Crit Care Nurs Clin N Am 2006;18(3):172

Alarm Parameters

• Patients at high risk for ischemia• Set ST segment alarm parameters 1

above and below baseline ST segment

• Stable Patients• Set ST segment alarm parameters 2

mm above and below baseline ST segment


Patient Positioning

• Evaluate ST segment with the patient in the supine position.

• Change in body position can alter ST segment, mimic ischemia.

• If ST alarm sounds with patient in side-lying position, return patient to supine. If deviation persists in supine may indicate ischemia.


Acute Coronary Syndromes

• Unstable angina

• Chest pain without increase in cardiac enzymes

Pain in Acute Coronary Syndrome

ChestNeck and/or jaw

Arms (left more common than right)

Epigastric and abdominal

Back

Pathways to Thrombosis

Placque rupture vessel

injury

Thrombosis

Red Clot Pathway

White Clot Pathway

Platelet activation and fibrinogen binding

Fibrinogen

Von Willebrand factor & Collagen

Platelet adhesion

Tissue factor/VIIa complex

Xa

FibrinPlatelet aggregation




• Ischemia• Injury

• Infarction

12‐Lead ECG Variations in AMI and Angina

Baseline

Ischemia—tall or inverted T wave ST segment may be depressed

Injury—elevated ST segment, T wave may invert

Infarction (Acute)—abnormal Q wave,ST segment may be elevated and T wavemay be inverted

Infarction (Age Unknown)—abnormal Q wave,ST segment and T wave returned to normal

T wave inversionAcute Coronary Syndromes

Non ST elevated Myocardial Infarction (NSTEMI)


ST Elevated Myocardial Infarction - STEMI


• 12 lead analysis



Normal EKG Anterior‐Lateral MI

Lateral MI Inferior MI

Inferior Posterior MI Right Ventricular MI



RV Infarct

• 50% of inferior MI patients, 10 – 15% will have hemodynamic compromise. mortality. Associated with SA and AV conduction issues

• Hemodynamics: preload, RV and RA compliance. BP and atrial kick

• Treatment Options: colloids and crystalloids to PAW to 15-20. Add Dobutamine. Maintain AV synchrony. NO NTG!

Practice Question

12 lead ECG that shows Q waves and ST elevation in leads V2 through V4 indicates:

A. Occlusion of the left anterior

descending B. Occlusion of the circumflexC. Occlusion of the right coronaryD. Prinzmetal’s angina (coronary spasm)

Practice Question

Which of the following 12 lead ECG changes would be expected in a patient having an acute inferior MI?

A. Q waves, ST elevation & inverted T waves in V4-V6, I and aVL

B. Q waves in aVL, I, and all precordial leads and ST elevation in II and III

C. Deep Q waves, ST elevation and inverted T waves in II, III and aVF

D. Deep Q waves, ST depression and T wave elevation in II, III and aVL

Practice Question

A patient is admitted to the ICU c/o chest pain and nausea. The ECG monitor reveals second degree AV block, Type II. These findings are probably the results of occlusion of which of the following coronary arteries?A. Left Anterior DescendingB. Left circumflex

C. Left mainD. Right

QT Interval

• Approximate measure of the duration of ventricular repolarization.

• Measured from the beginning of the Q wave to the end of the T wave

• Varies with heart rate• Lengthens with bradycardia• Shortens with tachycardia

Practice Alert -Dysrhythmia 35

QT Interval

Practice Alert -Dysrhythmia Monitoring36

Measure from beginning of the QRS complex to the end of the T wave



QTc Interval

• QT interval corrected for heart rate (QTc)• Formula for calculating QTc (Bazett’s formula)

• QTc > 0.50 seconds considered dangerously prolonged and is associated with a higher risk of Torsades de Pointes.

Practice Alert -Dysrhythmia

Monitoring37


• Interventions• Cath lab procedures – Diagnostic vs Interventional

• Diagnostic – Right sided heart cath • Insertion of a Pulmonary Artery catheter• Measures pressure on right side


Interventional

• PCI – Balloon angioplasty, Stents

Cardiac Surgery

CABG

Cardiac Surgery

Valve SurgeryMitral

Aortic

Types of valves – MechanicalCadaver

Animal

Minimally Invasive Cardiac Surgery• Trans-aortic Valve Replacement (TAVR)

• Balloon Valvuloplasty




• Complications• Hypotension• Bradycardia• Papillary muscle rupture

Complications: With or Without Trauma

Cardiac rupture, ventricular septal defect,and papillary muscle rupture

Signs and symptoms include:• New murmur• Acute decompensation• Cardiogenic shock• Death

Treatment: Emergency Surgery

Cardiogenic Shock

• High mortality• Occurs in 10 – 15% of all MI’s

• Also, post CABG, papillary muscle rupture, acute VSD, end stage valve disease, coarctation of the aorta, pericardial tamponade

Cardiogenic Shock Signs & Symptoms• CI < 2.0, MAP 60, SBP 80, thready pulses, cap

refill > 2 seconds, SVR > 1200 dynes, UO (< 30cc/hr)

• LOC, restless, confused, agitated, • bowel function • Cold, clammy, mottled skin• Hypoxia, with respiratory symptoms

• Metabolic acidosis (poor prognosis with lactic acidosis > 4 mmol/l)

Cardiogenic Shock

• Treatment: contractility afterloadImprove oxygenationMaintain preload tissue O2 demands

IABP Therapy



IABP Therapy

• Circulation is augmented or increased

• Ventricular workload is reduced

IABP Therapy

• Balloon inflation upon closure of the aortic valve or diastole

• Balloon deflation before systole or ventricular ejection

IABP Therapy

• Inflation: Increased aortic diastolic

pressureIncreased coronary perfusionIncreased systemic perfusion

IABP Therapy

• Deflation:Decreased aortic pressureDecreased afterloadDecreased myocardial oxygen

consumptionIncreased stroke volume

IABP Therapy ‐ Complications

Dissection of femoral arteryEmbolization to LE – the 6 P’s

Pain (Isometric), paresthesia, pallor, polar, paralysis, pulseless

Hemorrhage at insertion siteInfectionPerforation of the aortaArterial obstruction (femoral, mesenteric, renal subclavian)CoagulopathyThrombosis

PRACTICE QUESTION

The primary purpose of the IABP is to decrease:A. Stroke volume index

B. AfterloadC. Coronary perfusion pressureD. Ejection fraction



PRACTICE QUESTION

Which of the following is a contraindication to IAB counterpulsation?A. Aortic valve insufficiency

B. Mitral valve regurgitationC. Ventricular aneurysmD. Ventricular septal defect

PRACTICE QUESTION

A patient with unstable angina has an IABP inserted. Hemodynamics are: HR = 148 (Sinus tachycardia); MAP = 40 mm Hg; PCWP = 25 mm Hg; CI = 1.4 L/min.Which of the following should be included in this patient’s plan of care?

A. Check the timing of the IABP, decreasing balloon inflation frequency to 1:2

B. Stat echo, lasix, check balloon timingC. Dobutamine, 12 lead EKGD. Adenosine, stat Hgb & Hct, dobutamine

Heart Failure ‐ AHA 2015 Statistics

• About 6 million Americans

• 870,000 new cases each year

• 1 in 9 deaths related to HF

• Almost 1 million hospitalizations each year (cost of approx. $15.6 Billion)

• 50% die within 5 years of HF diagnosis

• Current mortality rate >57,000 / year

• Prevalence: men>women (all ages); Almost 20% of population >75

• Most common DRG for patient > age 65

Etiology and Diagnosis

• Heart failure is a set of clinical signs and symptoms that follow injury to or dysfunction of the myocardium

• Cardiac Output is insufficient to meet the metabolic needs of the body tissues

• Due to failure of the heart as a pump (MI, structural defects, cardiomyopathy, valve disease, arrhythmias)

• Or to excessive metabolic demands, eg thyroid crisis

• Failure of compensatory mechanisms to preserve CO

Symptoms:

• Shortness of breath

• Crackles • Edema • Fatigue or poor exercise tolerance

New York Heart Assn Classification

Functional Capacity Objective Assessment

Class I: No symptoms with normal activity

No objective evidence of cardiovascular disease

Class II: Symptoms with ordinary activity

Evidence of minimal cardiovascular disease

Class III: Symptoms with less than ordinary activity

Objective evidence of moderately severe cardiovascular disease

Class IV: Symptoms at rest Evidence of severe cardiovascular disease.



Two common ways of describing heart failure:

1.Left sided heart failure versus right sided heart failure

2.Systolic versus diastolic

Left sided heart failure vs right‐sided heart failure

• Left-sided heart failure• Cardiac output decreases • Pressure in the LV, left atrium and pulmonary rises • Leads to pulmonary congestion,• Demonstrated as dyspnea and fatigue.

Left sided heart failure vs right‐sided heart failure• Right-sided heart failure

• leads to similar problems in the systemic venous circulation

• neck distension • peripheral edema (and consequent weight gain)• engorgement of the hepatic and gastric vessels

Systolic versus diastolic* Systolic• Systolic – most common type – occurs in about 2/3

of patients with HF• Chronic volume overload

• Distended left ventricle • Elevated LV end diastolic volume• Decreased cardiac output• Decreased ejection fraction; EFs less than 40%,

sometimes as low as 15-20%

Systolic versus diastolic* Diastolic• Stiff left ventricle that cannot fill adequately with

normal filling pressures • Decreased LV end diastolic volume

• Normal to elevated ejection fraction

Systolic versus Diastolic

Systolic Diastolic

S3 gallop S4 Gallop

Solid Tx guidelines Tx guidelines lacking

Poor prognosis Better prognosis

Large dilated heart Small or normal size heart, thicken left ventricle

BP low to normal BP Elevated

EF < 40% EF Normal or > 40%

Less common in women More common in women



Pathophysiology

• Three neurohormonal responses occur to help body try to compensate.

1. Sympathetic nervous system stimulation

2. Renin-angiotensin-aldosterone activation

3. Ventricular remodeling

Sympathetic nervous system stimulation• Baroreceptors stimulate the medulla • Catecholamines are released causing

vasoconstriction and increased heart rate

• Sympathetic nervous system stimulation can trigger arrhythmias and sudden death

• Sinus tachycardia is a compensatory mechanism, used to increase cardiac output

Renin‐angiotensin‐aldosterone activation• Promotes fluid retention.• Angiotensin II is a potent vasoconstrictor which

increases BP and afterload.

• Aldosterone causes sodium and water retention.

Ventricular Hypertrophy

Ventricular remodeling

• Cardiac cells (myocytes) change configuration• Hypertrophy yields large abnormal cells that do not

contract as efficiently

• Shape of the ventricle changes, increases muscle mass and impairs contractility

• Myocardial oxygen demand increases with increased size

Apoptosis

• Preprogrammed cell death without inflammation or scarring

• Certain neurohormones such as angiotensin II and catecholamines promote apoptosis



Neurohormones

• Atrial natriuretic peptide (ANP)

• Brain natriuretic peptide (BNP)

Neurohormones

• Both ANP and BNP promote vasodilatation, reduce sodium and water retention, and inhibit sympathetic tones

• Limit cardiac hypertrophy and remodeling

Neurohormones

• Nesiritide is a commercially prepared form of BNP

• Given IV for severe decompensated HF

Neurohormones

• BNP Test is used for patients that present to Emergency Room with shortness of breath

• Test helps differentiate between HF and respiratory problems such as COPD or pneumonia

• Results in 15 minutes

BNP Results

• BNP< 100 pg/ml, not heart failure• BNP 100 – 250 pg/ml. probably heart failure,

compensated

• BNP > 500 decompensated heart failure• BNP > 1000, only due to heart failure

N‐Terminal proBNP (NT‐proBNP)

• Age related

• Age < 50 450 pg/ml• Age 50-75 900 pg/ml• Age > 75 1800 pg/ml

On average a 5-10 fold increase over previous measures.



BNP Questions

The main stimulus for BNP production is :

A.aldosterone production.B.fluid overload.C.kidney failureD.increased myocardial wall stretch.

BNP Questions

Which of the following factors can affect the sensitivity and specificity of BNP for the diagnosis of HF?

A. Patient’s age

B. Severity of HFC. Cut-off value usedD. Type of ventricular dysfunction

E. All of the above.

BNP Questions

Higher BNP levels are associated with increased mortality independent of age, NYHA class, prior MI, or LVEF.A. True

B. False

Treatments: Pharmacological

• Diuretics • Angiotensin Converting Enzyme (ACE) Inhibitors – often

given in conjunction with the diuretics.

captopril, enalapril, lisinopril


• Beta-Adrenergic Blockers – use in combination with diuretics and ACE-Inhibitors

• For NYHA class I through III heart failure

• Do not use with class IV heart failure, asthma or other pulmonary disease, or severe bradycardia or conduction problem

• Carvedilol, metoprolol - only two FDA approved for HF


• Angiotensin II Blockers – usually used if patient cannot take ACE – Inhibitors

• Losartan, valsartan




• Vasodilators

• isosorbide


• Positive inotropic agents

• Dobutamine, usually used for short term therapy• Milrinone (a phosphodiesterase inhibitor• Nesiritide – acute only, not long term


Calcium Channel Blockers

• Amlodipine, felodipine

Treatments: Ultrafiltration

• Therapy to remove excess salt and water from patients with fluid overload.

• Adjunct to diuretics or when diuretics fail to work effectively. (Hold diuretics during the procedure.)

• Removes isotonic fluid therefore removes more sodium than diuretics.

Treatments: Ultrafiltration

• Left sided failure• Typically pull 250 cc/hr for 24 hours• (6 Liters)

• Right side failure• Typically pull 100 cc/hr

Treatments: Mechanical

• Pacers –Dual chamber, biventricular

• VADs – Ventricular assist device• Bridge to transplant or destination therapy



Biventricular Pacemaker Acute Pulmonary Edema

• Cardiogenic vs Noncardiogenic• BNPs can assist in diagnosis

• Cardiogenic – Left ventricular failure• Noncardiogenic – Pulmonary issue such as ARDS

Cardiomyopathy

• Definition• Any heart muscle disease of unknown origin

• Structural or functional abnormality

• Primary or secondary

Primary Cardiomyopathy

• Unknown cause

• Only myocardium is affected

Secondary

• Caused by another condition

• Examples: Ischemia, ETOH, AIDS, pregnancy

Types of Cardiomyopathies

• Dilated

• Hypertrophic

• Restrictive



Dilated Cardiomyopathies

• Most common type

• Problem with contraction

• Progressive deterioration

Dilated – 4 Dominant Features

• Ventricular dilation• Impaired systolic function

• Atrial enlargement• Stasis of blood in the left ventricle

Dilated Cardiomyopathy –Physical Findings• S3, S4

• Narrow pulse pressure (difference between systolic and diastolic pressures)

If all else fails…..

• Possible candidate for transplant

Hypertrophic Cardiomyopathy

• 4 Dominant features• Ventricular hypertrophy• Rapid contraction of left ventricle• Impaired relaxation• Intracavity systolic pressure gradient

Dilated vs. Hypertrophy

• Dilated cardiomyopathy• Problem with contraction

• Hypertrophic cardiomyopathy• Problem with relaxation



Hypertrophic Cardiomyopathy

•Clinical presentation• Dyspnea, fatigue, angina, syncope• Some people are asymptomatic• Sudden death – teens and young adults

Hypertrophic Cardiomyopathy‐Physical Findings• Systolic murmur• Abrupt arterial pulses

• Split S2• S3, S4

Surgical Treatments

• Septal Myotomy

Restrictive Cardiomyopathy

• Least common type

• Abnormality of relaxation

Clinical Presentation

Dyspnea, fatigue, angina, syncope

Exercise intolerance

Physical Findings

• Peripheral Edema• Elevated CVP

• Ascites• S3, S4



Pericarditis

• ECG Changes• ST segment normal in V1 and aVR but all other leads

show ST elevation• PR Interval depression in limb leads and V5, V6

• Decrease in if pericardial effusion is present

Pericarditis

Valvular Heart Disease

• Structural or functional abnormalities• Stenosis - narrowed valve

• Regurgitation - backflow of blood through valve

• Mitral• Aortic

• Tricuspid (rarely isolated)

Myocardial Conduction System Defects• AV Blocks

• 1st degree

- 2nd degree type I• 2nd degree type II• 3rd degree (complete)

Review of AV Blocks – 1st Degree• Prolonged PR Interval

• Greater than 0.20 sec• Every P wave is followed by a QRS

Review of AV Blocks 2nd degree type 1 (Wenckebach)

Progressively longer PR intervals until one P wave does not produce a QRS.

Irregular rhythmP waves are regular QRS waves are irregular



Review of AV Blocks 2nd degree type 2 (Mobitz)

Intermittent conduction of P waves to the AV node.

Some P waves produce a QRS, some don’t.

PR intervals are all the same when the impulse does get through the AV node.

Review of AV Blocks 3rd degree (Complete Heart Block)

• No correlation between the P waves and the QRS waves

• Atria and ventricles are beating independently

• P waves are regular, QRS waves are regular

Myocardial Conduction System Defects

• Bundle Branch Blocks - Right or Left• Left anterior or left posterior hemiblocks



Left Anterior Hemiblock

Characteristic EKG changes

• Marked left axis deviation• Normal QRS width• rS complex in leads II, III, aVF• qR complex in leads I, aVL (not essential for

diagnosis)

Left Posterior Hemiblock

Characteristic EKG changes• leads I and aVL, you see rS pattern

• leads II, III, aVF, you see a qR pattern• Right axis deviation• Usually normal QRS duration

Posterior Hemi-block



Hypertensive Crisis ‐ Etiologies

• UNTREATED OR UNCONTROLLED HYPERTENSION.

• POOR COMPLIANCE WITH PRESCRIBED MEDICATION REGIMEN

• SUDDEN DISCONTINUATION OF

ANTI-HYPERTENSIVE MEDICATION

• DRUGS: COCAINE, AMPHETAMINES, MONO-AMINE OXIDASE INHIBITORS

(ADRENERGIC CRISIS)


• Head trauma, stroke, cerebral hemorrhage• Endocrine and Pituitary tumors

• Spinal cord injury• Guillain-Barre Syndrome• Post-operative hypertension• Pre-eclampsia and eclampsia


• Renovascular hypertension• Renal disease (acute glomerulonephritis, renal

tumors or occlusion)

• Collagen vascular diseases (Lupus, Scleroderma)

• Severe burns• Adrenocortical hyperfunction

Categories of HTN

• Normal – SBP <120 and DBP <80• Pre-HTN- SBP 120-139 or DBP 80-89

• Stage 1 – SBP 140-159 or DBP 90-99• Stage 2 SBP >160 or DBP >100

Quick review of the Basics:What is Hypertension?

• Hypertension, or high blood pressure, is the chronic state of elevated pressure in the arteries.

• Physiology:• Narrowing of vessels • Fluid retention• Both

• Under normal conditions: Autoregulation of blood pressure is done by release of:

• Endothelins (upward)• Prostacyclin (downward, short

term)• Nitric oxide (longer term)

131

Types of Hypertension

Primary• “Essential hypertension”

• No known cause

• Diagnosed by excluding secondary causes

• Progressive disease

• Incidence: 90-95% of hypertension diagnoses

Secondary• Hypertension caused by another

medical issue, including:• Kidney disease• Thyroid disease

• Appears quickly – controllable by treating underlying condition

• Incidence: 5-10% of hypertensive cases

132



Hypertensive Crisis has classifications of:1. Malignant Hypertension2. Hypertensive Emergency3. Hypertensive Urgency

Defined as a life-threatening elevation in BP.

Progressive or impending target organ damage.

BP >180/110

Target organs at risk:HeartBrainKidneysOptic nerve

Hypertensive Emergency vs. Urgency• Hypertensive Emergency

• Severe elevations in blood pressure (DBP usually >130)

• Evidence of target organ dysfunction

• Requires immediate controlled BP reduction

Hypertensive Emergency vs. Urgency

• Hypertensive Urgency

• Severe elevations of BP• Without evidence of target organ dysfunction• Requires BP reduction

Differentiating characteristic: Organ damage, not BP level.

Presentation and Treatment of Hypertensive Urgency• Severe elevation in blood pressure without end organ

damage

• Treat on an outpatient basis with oral antihypertensive

• Goal: reduce blood pressure mean by 25% in the first 24 hours

• Example: • BP = 170/105 (127)• 25% reduction: MAP = ?

Presentation and Treatment of Hypertensive Emergency• Severe elevation in blood pressure with end organ

damage• Treat emergently with titratable IV vasoactive

medications.

• Arterial line needed to monitor BP constantly.

Malignant Hypertension

Is a hypertensive emergency.

• Involves very rapidly rising blood pressure

• Results in papilledema (optic nerve swelling)

• Presenting symptoms:• Convulsions• Blurred vision• Headache

• Usually accompanied by other end organ damage:

•Heart failure•Kidney failure•Hypertensive encephalopathy



Presentation and Treatment of Hypertensive Emergency• Goal: Controlled lowering of blood pressure

• No more than 20% in first hour

• 160/110 (127) in next 2-6 hours

• Reduce MAP by 25% in 8 hours

• Example – CVA that needs thrombolytics

Nitroprusside (Nipride)

Drug Action• Arterial and venous dilator

• Decreases peripheral vascular resistance

• Preload and afterload reducer

• Improves LV function

• Rapid action with short half-life

Nursing Considerations • Arterial line for continuous BP monitoring

• Metabolizes into cyanide• Antidote: Sodium Thiosulfate• Increased risk of cyanide toxicity with renal failure

• Light sensitive: Shield from light

Nitroglycerin

Drug Action• Affects venous dilation

• Arterial dilation at high doses (1 mcg/kg/min)

• Decreases preload and/or afterload

• Response varies with patient’s baseline pressure

• Vasodilates the pulmonary vascular bed

Nursing Considerations • Headache

• Glass bottle requires vented tubing

• Absorbed by some IV tubing: May have increased response to drug when tubing is saturated

Labetalol

Drug Action• Alpha and Beta blocker

• Reduces systemic vascular resistance

• Use in pregnancy

Nursing Considerations • Onset 5-10 minutes

• Taper dose when discontinuing

• Caution with:• Bradycardia, Asthma, A-V Block, Renal impairment

Peripheral Vascular Disease

Vascular disease outside of the heart and brain

Narrowing of vessels carrying blood to:LegsArmsStomachKidneys


• Two Types• Functional -Example – Raynaud’s disease

• No structural defect in vasculature• Caused by spasm• Short term effects

• Organic - Example – peripheral artery disease

• Structural changes of vasculature• Inflammation• Tissue damage• Atherosclerosis




• Incidence• 10 million Americans

• 5 million are asymptomatic• 2.5 million undiagnosed• 2.5 million are treated (2.1 million medically

managed)• Increases with age (1/3 of adults over 70)


• Symptoms• Claudication• Numbness or tingling in feet• Burning or aching pain• Ischemic ulceration


• Symptoms• Change in color of skin• Loss of hair on legs• Gangrene


• Risk Factors• >50 years old• Smoker• Diabetic• High blood pressure• Overweight• High cholesterol, atherosclerosis• Family history

PVD ‐ Diagnostic Tests

• Doppler ultrasound

PVD ‐ Diagnostic Tests

• Angiography



Ankle‐Brachial Index

• Why is it ordered?• Indicator of arterial occlusion

• How is it calculated?• SBPA /SBPB = ABI• SBPA = 90; SBPB =120; • ABI = 90/120 = 0.75

Ankle‐Brachial Index

How is it interpreted?• ABI= 1-1.3 Normal: No PAD

• ABI = 0.8-0.99 Mild blockage: Beginning PAD• ABI = 0.5-0.79 Moderate blockage: Pain with

exercise• ABI < 0.5 Severe blockage: Pain at rest • ABI < 0.25 Potential for limb loss

PVD – Treatment

• Medical Management• Lifestyle Changes• Pharmacologic

• Aspirin• Clopidogrel or Ticlopidine• Cilostazol• Heparin• Lipid Lowering drugs

PVD – Treatment

• Invasive Procedures• Angioplasty / stents

• Surgery• Atherectomy• Bypass

Treatments:Thrombolytics

• Retavase (Retaplase) or Tenecteplase (TNK)

• Converts plasminogen to plasmin, a natural fibrinolytic

• Thrombolytic drips directly onto the clot

• Heparin infusion also given

• May need additional balloon angioplasty and/or stent

PVD – Treatment

• Surgery is named by artery(s) that are bypassed• Examples – Fem/Fem, Fem/Pop,



Post‐op Assessment

• Vital signs• Pulmonary

• Fluid Balance (Urine output)• Bedrest• Neurovascular checks

Post‐op Complications

• Graft thrombosis• Hemorrhage

• Edema• Lymphatic Edema• Infection

Graft Thrombosis

• Inadequate arterial flow• Clamp Injury

• Decreased cardiac output• Vasospasm• Thromboemboli

Complications after Reperfusion

• Reperfusion injury• ATN

• Rhabdomyolysis• Tissue breakdown releases myoglobin into plasma• Can overwhelm renal system and lead to kidney failure• Differential diagnosis: CPK > /= 5 times normal• Treatment: Fluid load to maintain urine output of 100 ml/hr.• Alkalinize urine with NaHCO3

• Lactic acidemia

Complications

• Compartment syndrome• Venous thrombosis

• Pulmonary embolus• Graft infection

Graft Infection

• Signs and Symptoms• Incisional swelling• Local tenderness• Drainage• Pulsatile mass• Diminished pulses• Leukocytosis• Fever



Carotid Artery DiseaseCarotid Artery Disease

• Probable Causes• Atherosclerosis• HTN

Carotid Artery Disease

• Risk Factors• Age

• Hyperlipidemia

• Diabetes

• Hypertension

• Smoking

• Obesity

• Sedentary lifestyle

• Family history of atherosclerosis

Carotid Artery Disease

• Clinical Manifestations• TIA• RIND – Reversible Ischemic Neurological Deficit• Amaurosis fugax – Transient blindness caused by

microemboli to retina

CAD – Diagnostic tests

• Hx and Physical – look for stroke symptoms• Ultrasound

• Arteriography (MRA)

CAD – Treatment

• Lifestyle Modification• Medications

• ASA• Gradual lowering of BP



CAD Treatment Continued

• Procedures• Carotid Stenting

Combined with medical management:• Aspirin and/or Plavix• Blood Pressure control

CAD Treatments

Surgical

• Carotid Endarterectomy

Post‐op Care

• Watch for potential complications• Hemorrhage (hematoma)

• Causes• Anticoagulation

• Dangers• Obstruction of airway• Sign - Hoarseness

Post‐op Care

• Watch for potential complications• Cranial Nerve damage

FacialGlossopharyngealSuperior LaryngealHypoglossal

Post‐op Care

• Watch for potential complications• Perioperative Stroke• Wound Complications• Recurrent carotid stenosis• Pulmonary complications

Post‐op Care

• Labile Blood Pressure• May have arterial line

• Hypertension• Nipride



Abdominal Aortic Aneurysm Abdominal Aortic Aneurysm

• Aneurysm Development• Atherosclerosis• Trauma• Arteritis (Infection)• Congenital abnormalities (Marfan’s)

Abdominal Aortic Aneurysm

• Risk Factors• Age• Male• Caucasian• Smoking• Diabetes• Hypertension• Family History


• Clinical Manifestations• Asymptomatic

• Severe Abdominal Pain


• Diagnostic Tests• History and Physical

• Echocardiogram

• CT

AAA Treatments

• Monitor

• Surgery• Percutaneous (Closed)

Stent graft• Open



AAA Post‐op Care

• Systemic Heparinization

• Postoperative Hypertension

AAA Post‐op Care

Post-operative Hypotension• Causes –

• Rewarming• Third spacing of fluids• Blood loss• Cardiac dysfunction

AAA Post‐op Care

• Vasoactive Medications• Dopamine• Nipride• Dobutamine

AAA Post‐op complications

• Cross clamping injuries• Renal failure• Bowel Ischemia

• Small areas to transmural necrosis• Can lead to acute perforation

• Signs/symptoms• pain• diarrhea• abdominal distention• fever

AAA Post‐op complications

Hypo-perfusion of lower extremities

Paralysis

Graft occlusion

Other aortic aneurysms



References

• Burns, Suzanne AACN Essentials of Critical Care Nursing, 3rd Edition 2014

• Fowler, Leanne Cardiovascular Nursing, 2016

• Urden, Linda et at Priorities in Critical Care Nursing7th Edition 2016

Documents

Images have been removed from the PowerPoint slides in ... · Torsades de Pointes. Practice Alert - Dysrhythmia 37 Monitoring Acute Coronary Syndromes ... Images have been removed