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Cardiovascular Disorders Disease Models Part 2

cadiovascular disorders:d isease models part ii

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Page 1: cadiovascular disorders:d isease models part ii

Cardiovascular DisordersDisease Models

Part 2

Page 2: cadiovascular disorders:d isease models part ii

Objectives

See Part 1

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Angina Pectoris

"Angina" meaning to choke.

• When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart, myocardial ischemia occurs.o The clinical manifestation of this is:  Angina pectoriso Can be caused by:

An increase in demand for oxygen A decrease in oxygen transport in the blood

o Almost 90% of cases involve some level of atherosclerosis

o symptoms don't develop until the lumen of the coronary artery narrows 75%.

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Why do we care about Angina and Coronary syndromes?

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Causes of Angina Pectoris

Lack of Supply to the myocardium:• Blood flow factors or low blood pressure (hemodynamic

factors).• Vasospasms• Cardiac Factors• Hematologic Factors

o low hgb/hct Most often (>90%) of cases, lack of blood supply to the myocardium is caused by atherosclerosis of a main coronary artery

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Causes of Angina Pectoris

Myocardium demands an increase in blood supply (increased need for O2)• High Systolic BP• Increased Ventricular Volume• Increased Heart Rate and Contractility

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Risk Factors for Angina pectoris

 

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Patterns of Angina

1. Stable Angina (Chronic Stable Angina)

2. Variant or Prinzmental's angina

3. Unstable Angina

4. Silent Ischemia

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Stable Angina

This is caused by a fixed coronary obstruction that causes intermittent decreases in blood flow and a lack of vessel flexbility (the vessel can't dilate to allow more blood flow).• symptomatic chest pain or pressure that is associated with

transient myocardial ischemia• usually precipitated by some sort of activity or stress that

causes an increased need for oxygen in the myocardium• usually resolves with rest or by alleviating the stressor, use

of nitrates to increase coronary blood flow also can reduce the pain

• pain usually resolves within 3-5 minutes.

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Page 11: cadiovascular disorders:d isease models part ii

Variant or Prinzmental's Angina

This is an angina pain that occurs mainly at rest, and results from vasospasm of the coronary arteries (strong contraction of the smooth muscle in the coronary artery).• Vasospasm can occur in individual who have no underlying

coronary disease, but can also confound the problem of CAD in individuals.

• Seen in patients with a history of migraine headaches and Raynaud's disease.

• Thought to occur due to increased myocardial demand and increased levels of certain substances.

• Treated with nitrates and primarily calcium channel blockers• Often see anginal pain and ST segment elevation

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Unstable Angina

This form of angina, also called crescendo angina, is new onset angina, angina that occurs at rest (but is not due to vasospasm), or angina that is worsening in pattern (increased frequency of events, increased intensity of events).• s/s include:  fatigue, SOB, anxiety, indigestion (and can also

include the chest pressure and pain associated with stable angina), ST segment depression.

• A result of an unstable plaque (post rupture, where there is platelet aggregation and thrombus formation).

• This is considered an emergency, and often is seen pre-myocardial infarction

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Silent Ischemia

This is ischemia that occurs in the absence of anginal pain.  • Diagnosed often with an EKG showing ischemic changes in

the heart.• Thought to be the same pathophysiology as stable angina

(r/t atherosclerotic disease).• Why don't they feel pain (different theories):

o these episodes may be shorter and involve less tissueo the patient may have a defect in their pain threshold or

pain tolerance patients with diabetes mellitus have a higher incidence

of silent ischemia (have some cardiac autonomic nerve dysfunction)

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Comparison of the types of angina

 

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Page 16: cadiovascular disorders:d isease models part ii

Clinical manifestations of angina pectorisThink about what disease process may be causing these s/s? • Substernal chest discomfort, described as squeezing,

constricting, or suffocating.o usually steady, increasing in intensity at the beginning

and the end of the attack• Can radiate to the left shoulder, jaw, arm, between the

shoulder blades, or other areas of the chest.• May complain of indigestion or a burning sensation in the

epigastic region• Can be associated with a feeling of apprehension,

impending doom

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Page 18: cadiovascular disorders:d isease models part ii
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Potential Medical Complications

1. Myocardial Infarction2. Arrhythmias

 

These are both worse case scenarios, as both have a high mortality rate, especially when left untreated.

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Myocardial Infarctions

This occurs as a result of sustained ischemia.  Heart muscle can tolerate 20 minutes of sustained hypoxia.  Then cellular death begins to occur.  After 4-6 hours, if the ischemia persists, there entire thickness of the myocardium can become necrosed.• This is a worst case scenario

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Clinical manifestations of an MI

• Pain:  Severe, immobilizing chest pain that is not relieved by rest, position change, or nitrate administrationo commonly in the early morning hourso pain is from the buildup of toxic metabolites in the heart

cells• Sympathetic Nervous System activation:  epinephrine and

norepinephrine are released in large amounts from the damaged myocardial cells.  Activates the sympathetic nervous system and causes peripheral vasoconstriction and diaphoresis.  Patient will appear pale and feel cool, and clammy to the touch.

• Nausea and Vomiting: there is reflex stimulation of the vomiting center in the medulla by the severe pain

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Clinical Manifestations of an MI

• Cardiovascular Manifestations:  the release of the epi/norepi can initially increase the BP and HR.  but the BP eventually drops due to decreased cardiac output.  May decrease renal perfusion and ARF and decreased renal output.  Left ventricular dysfunction may cause blood to back up in the lungs causing crackles.

• Fever:  Temperature increase up to a week post MI due to the systemic manifestation of inflammation from myocardial cell death.

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Page 24: cadiovascular disorders:d isease models part ii
Page 25: cadiovascular disorders:d isease models part ii

Potential complications of an MI

• Dysrhythmias:  Occur in 80% of patients post acute MI.  Life threatening dysrhythmias often occur with anterior wall infarctions.  Ventricular fibrillation is a common cause of sudden cardiac death and often occurs within 4 hours of an acute MI

• Heart Failure:  the pumping power of the heart is diminished.• Cardiogenic shock:  occurs when the heart is not perfusing

the tissues because of severe Left ventricular failure.o very emergent if it occurs

• Ventricular Aneurysms:  the infarcted myocardial wall thins and develops an outpouching that doesn't function with normal contractile properties.

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http://www.hrt.org/ecghome.html

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Page 28: cadiovascular disorders:d isease models part ii

Medical Management of Angina/MI

1. Diagnostics

2. Pharmacologic

3. Surgical

4. Pre-hospital emergency management of suspected MI.

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Diagnostic Studies

1. EKG/ECG

2. Serum enzyme level test

3. Serum lipid level test

4. Exercise stress test

5. Nuclear imaging

6. Coronary Angiography

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EKG/ECG

There are classic ECG changes that can occur with Angina and MI.• T-wave inversion• ST-segment elevation• Development of an abnormal Q-wave

 These findings can vary based on the duration of the ischemic event (acute vs. evolving), extent of ischemia (subendocardial vs. transmural), and the location.

Findings may "disappear" when the angina isn't occuring, need to check ECG with the anginal pain.

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Page 32: cadiovascular disorders:d isease models part ii

Serum Enzyme Level Tests

The damaged heart muscle will often release proteins into the bloodstream that are indicative of cardiac damage.  • These levels can be checked with a blood test• There are varying levels of specificity for cardiac vs. general

muscle damage.o CK-MBo Troponin I, Troponin To Myoglobino Beta type Natiuretic peptide (BNP)

• Albumin Cobalt Binding Test

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Serum Enzyme Level Tests

CK-MB:• Creatinine Kinase MB is

an intracellular enzyme found in the muscle cells

• increases outside the normal range within 4-8 hours post myocardial injury

• there are 3 bands of CK enzymes

• CK-MB is very specific for cardiac muscle damage

Troponin:•  This protein regulates the

Ca++ mediated Actin-Myosin contractile process

• Troponin I/T begin to rise within 3 hours after the onset of MI and may remain elevated for 3-4 days post MI

• More sensitive then CK-MB

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Serum Enzyme Level Tests

Myoglobin:• oxygen carrying protein, which is normally present in cardiac

and skeletal muscle.• It is a small molecule, so it is released into the system

quickly• Starts rising 1 hour post cardiac damage, peaks 4-8 hours

post MI• myoglobin is rapidly excreted in the urine, so blood levels

return to normal within 24 hours post MI• Not Cardiac Specific

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Page 36: cadiovascular disorders:d isease models part ii

Serum Enzyme Level Tests

Cobalt Albumin binding test:• in an MI, albumin

molecules in the blood are altered, and unable to bind cobalt properly

• Helpful to determine if the patient didn't have a heart attack if their ECG and troponins are negative.

• negative predictive value

Beta-type Natriuretic peptide:• this is used for diagnosis,

assessment of severity and prognosis of congestive heart failure.

• peptide that is produced by the ventricular myocardium

• studies are showing that it can predict the risk for cardiac death in patients post MI

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Serum Lipid Panels

Elevated serum lipids are one of the most firmly established risk factors for coronary artery disease.

• Trigylcerides• Total Cholesterol• Cholesterol Fractionation:  This usually includes HDL/LDL

and total cholesterol. • C-reactive protein- inflammatory marker that is associated

with recurrent cardiovascular events• N-High Sensitivity C-Reacitve Protein-tested with

Cholesterol to help manage atherosclerosis

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Exercise Stress Test

• Treadmill exercise testing is an important diagnostic test done for the patient with chronic stable angina.

• Patient is on a treadmill (or is injected with adenosine if they can't tolerate exercise) with a ECG/EKG hooked up and a BP cuff on.  The patient then walks for however long they can tolerate it, and they are to stop and report chest pain or pressure if it occurs.

• ST segment and T-wave abnormalities are used as an INDIRECT MEASURE of CORONARY PERFUSION

•  Can differentiate anginal chest pain from other chest pain.

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Nuclear Cardiology Imaging

A small amount of blood is removed and a radionucleotide dye is mixed and the "tagged" blood is returned to the body.  The radiologic machine can then scan the body and assess:• Blood flow• Ventricular structures/Motion of the ventricles• Areas darkness where infarctions have occured ("cold

spots")• Perfusion of the myocardium

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Coronary Calcium Scan

This is a specialized CT scan that is able to assess the amount of calcium that has built up in the arteries of the heart:• A score is attached to the amount of calcifications seen• Can help determine amount of atherosclerosis in the

coronary vessels• INDIRECT MEASURE OF CORONARY BLOOD FLOW

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Coronary Angiography

A catheter is inserted into one of the larger arteries of the heart and is advanced to the coronary arteries, where dye is injected.• DIRECT EVALUATION OF CORONARY BLOOD FLOW• helps to evaluate collateral circulation• can assess the extent of the coronary vascular disease• only way to evaluate if the angina is variant type or due to

obstruction• Need to assess platelets, PT, INR, PTT, and kidney function

prior...why?• Also, can engage in therapeutic management during PCI

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Page 43: cadiovascular disorders:d isease models part ii

Pharmacologic Therapy

Acute Attacks:• Nitroglycerine SL

Chronic Anginal Prophylaxis• Nitroglycerin ointment• Transdermal Nitrates• Long-acting Nitrates• SL nitroglycerine prior to activity• Beta-Adrenergic Blockers• Calcium Channel Blockers• Antithrombotic Therapy...Aspirin (ASA), Clopidogrel (Plavix)

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Page 45: cadiovascular disorders:d isease models part ii

Acute Attacks

Short acting nitrates are the first line therapy for anginal attacks, the drug works by:1. dilating peripheral blood vessels (decreases SVR, increased

blood return to the heart)2. dilating coronary arteries and collateral vessels (increases

coronary artery circulation, increases O2 to the heart) Sublingual Nitroglycerin:for an acute attack:  give 0.4-0.6mg sublingual x1, may repeat 2 more times every 5 minutes if no pain relief.

o 1 pill sublingual, or 1 metered spray sublingual 

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Chronic Anginal Prophylaxis

Nitroglycerin Ointment:• Nitropaste is a 2% nitroglycerin topical ointment.• Dosed by inch• place on the skin, in an area free of hair and scars.• lasts 3-6 hours, especially good for nocturnal and unstable

angina Transdermal Nitrates:• Small, thin adhesive patch• Apply to a intact, hairless skin q24hours• Allows for a steady state of drug

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Chronic Anginal Prophylaxis

Long-Acting Nitrates:•  Extended release

tablets/capsules• Taken every 8 to 12 hours• work to reduce the

incidence of anginal attacks

• Imdur and Isordil (both isosorbide base)

Sublingual Nitroglycerin:• take a pill or a nitrospray

5-10 minutes before engaging in a activity that could precipitate anginal attack

• Better to use before the pain develops

• increases exercise tolerance and stress tolerance

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Chronic Anginal Prophylaxis

Beta-Adrenergic Blockers:•  These are the preferred

drugs to help manage chronic stable angina

• decrease myocardial contractility

• decrease HR, SVR, and BP (dec. renin secretion)

• can decrease morbidity and mortality in patients who are s/p MI

• Counsel patients not to stop beta-blockers abruptly

Calcium Channel Blockers:• Drug of choice for

prinzmental's angina• Inhibits the transport of

calcium into the myocardial and smooth muscle vasculature inhibiting muscle contraction

• cause systemic vasodilation, decreased myocardial contractility, and coronary vasodilation

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Chronic Anginal Prophylaxis/ManagementAspirin (ASA):• Inhibits cyclooxygenase,

which decreases the productions of thromboxane A2, a potent platelet activator

• 81mg po qd

Clopidogrel (Plavix):• Inhibits platelet

aggregation (ADP Blocker)• Alternative for patients

who can't tolerate ASA• indicated in combination

with aspirin in patients who've had a heart attack or ACS

• 75mg po qd

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Fibrinolytic Therapy

This is a rapid and available method to break up a blockage in a coronary artery.• Aimed at dissolving the thrombus in the coronary artery and

reperfusing the heart.• IV infusion of a thrombolytic agent• Will break down any clot...not just in the heart, need to

watch for bleeding.• Nursing Management:

o Assess V/S, pulse Ox, ECGo heart and lung assessments

• Should see an improvement in the ST segment changes• Watch for reperfusion arrhythmias• Likely start heparin drip in the immediate post fibrinolytic

period to prevent reocclusion.

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Page 52: cadiovascular disorders:d isease models part ii

Invasive and Surgical Treatment

1. Percutaneous Transluminal Coronary Angioplasty (PTCA)

2. Intracoronary Stents

3. Laser Angioplasty

4. Atherectomy

5. Coronary Artery bypass grafting (CABG)

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Percutaneous Transluminal Coronary Angioplasty (PTCA)• Catheter is inserted through a large peripheral vessel and

advanced to the coronary vessels where a dye is injected (see previous slides)

• Allows for a direct assessment of coronary blood flow• The atherosclerotic plaques can be shaved off and

circulation to the coronary myocardium improved.• Need to assess:

o PT/INR, PTT, Platelets, Kidney functiono V/S and continuous monitoring of pulse ox and ECG

before, during and post procedure.

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Page 55: cadiovascular disorders:d isease models part ii

Intracoronary Stents

• PTCA with intravascular stent over a balloon• The catheter that is advanced to the coronary arteries had a

balloon that can push aside the plaque and a stent is placed holding open the vessel.

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Page 57: cadiovascular disorders:d isease models part ii

Invasive Management of Angina/ACS

Laser Angioplasty:• A laser tipped angio

catheter is introduced via a large peripheral vessel

• the laser vaporizes the plaque and creates channels between the left ventricle and microcirculation

• used in patients who are not a CABG Candidate and who have failed maximal medical treatment for their angina

Atherectomy:• Plaque is shaved off using

a rotational blade• removes atheromas• Can embolize the

atheroma

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Coronary Artery Bypass GraftThis is the construction of new passages for block around a blocked coronary vessel• Traditional CABG involves a stenotomy and the use of

cardiopulmonary bypass• A vessel is harvested from the saphenous vein area or

internal mammary artery and are grafted from the aorta or left subclavian to an area beyond the occlusion (bypassing it)

• Significant morbidity and recovery period (6-8 weeks off work)

 MIDCABG:  (minimally invasive) thorascopic approach to the heart and beta-blockers or adenosine are used to slow the heart and allow for suturing of the bypass

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Page 60: cadiovascular disorders:d isease models part ii

Prehospital Emergency Care of Chest PainFor person with Unknown CHD:• Recognize symptoms-

Chest pain, SOB, nausea, weakness

• Stop activity and sit or lie down

• If pain persists for 5 minutes or more, activite the EMS

For Person with Known CHD:• Recognize symptoms-

Chest pain, SOB, Nausea, weakness

• Stop Activity, sit or lie down

• place 1 nitro-tab under your tongue or dispense one spray SL, repeat at 5 minute intervals x3 doses

• If symptoms persist, activate EMS

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Congestive Heart Failure

Impaired cardiac function rendering the heart unable to maintain proper

output (PUMP FAILURE)

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Cardiac Failure:

High Output Failure:  (not common)  caused by an excessive need for cardiac output.  The function of the heart may be normal to even excessive, but the body needs are higher.• severe anemia, thyroxicosis, conditions that cause

arteriovenous shunting, and Paget's disease• Treatment involves treating the underlying disease

 Low Output Failure:  (common) caused by failure of the heart as a pump• ischemic heart disease, cardiomyopathy, long standing

hypertension• Treatment is focused on symptom management and slowing

the natural disease state

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General clinical features of heart failure

The failure of the compensatory mechanisms of the heart results in heart failure:• heart rate fails to compensate for inadequate cardiac output• dilation of the heart fails to compensate for inadequate

cardiac output• hypertrophy of the heart fails to compensate for inadequate

cardiac output• kidneys, sensing decreased circulation, increase the

production of renin, causing increased angiotensin II/increased SVR and Aldosterone/increasing blood volume

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Systolic Dysfunction

Involves a decrease in cardiac contractility and ejection fraction• Caused by:  

o conditions that impair the contractile performance of the heart (ischemic heart disease and cardiomyopathy)

o produce a volume overload (valvular insufficiency and anemia)

o generate a pressure overload (hypertension and valvular stenosis) on the heart

 Symptoms result from reduction in ejection fraction and cardiac output

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Diastolic Dysfunction

This accounts for 40% of all cases of CHFCharacterized by:• smaller ventricular chamber• ventricular hypertrophy• poor ventricular compliance (ability to stretch)• Symptoms:

o because impaired filling, congestive symptoms predominate

o symptoms increase in situations where the heart rate increases

 CHF is often a combination of systolic and diastolic dysfunction

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Compensatory Mechanisms in Heart FailureVentricular Dilation:•  Chambers stretch and

dilate to allow more blood in the ventricle

• The ventricle can dilate to the point of overstretching where the actin and myosin fibers are unable to contract properly and allow for a proper ejection of blood

• Frank Starling Law...page 605 Porth

Ventricular Hypertrophy:• there is an increase in the

muscle mass and cardiac wall thickness in response to overwork and strain

• occurs slowly and over time

• allows for initial increases in CO, but demands more Oxygen, has poor contractility, is poorly vascularized, and is prone to dysrhythmias

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Compensatory Mechanisms in Heart FailureSympathetic Nervous System Activation:• decreased CO causes a

release of catecholamines (epinephrine and norepinephine)

• initially increases HR, myocardial contractility, and peripheral vasoconstriction

• Overtime, causes an overload on the failing heart (inc. O2 needs, inc. preload)

Neurohormonal Response:• Renin-Angiotensin-

aldosterone mechanism with low CO to kidney

• Low CO to the brain causes increase ADH secretion, which increases preload

• Vascular endothelium releases endothelin which causes vasoconstriction (inc. SVR)

• Inflammatory cytokines are released

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Page 69: cadiovascular disorders:d isease models part ii

Left Sided Heart Failure

The left side of the heart moves blood from a low pressure circuit (the lungs) to a high pressure circuit (the peripheral circulation).• S/S:

o Decrease in cardiac outputo Increase in Left Atrial and left ventricle end diastolic

pressureso Congestion in the pulmonary circulationo Pulmonary edema

• Most common cause is Acute Myocardial Infarction and Cardiomyopathy

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Page 71: cadiovascular disorders:d isease models part ii

Right Sided Heart Failure

This is the failure of the right of side of the heart.• S/S:

o Jugular Venous Distentiono Hepatomegalyo Splenomegalyo Vascular congestion of the GI tract

get N/V/Reflux/hematemesiso Peripheral Edema

• Caused by (most commonly) Left sided heart failure, 2nd primary pulmonary HTN , 3rd Right ventricle AMIo Lung disease can cause hypertrophy of the right ventricle

called Cor Pulmonale

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Page 73: cadiovascular disorders:d isease models part ii

Clinical Manifestations of Heart Failure

1. Fluid Retention and edema

2. Respiratory manifestations

3. Fatigue and limited exercise tolerance

4. Cachexia and malnutrition

5. Cyanosis

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Clinical Manifestations of Heart Failure:Fluid Retention and EdemaEdema:  • Common sign and usually

appears in the dependent areaso peripheral edemao livero abdominal cavityo lungs

• Can be pitting (can indent the skin with a finger tip)

• Acute development of edema or wt. gain of >3lbs in 2 days is a sign of decompensation

Nocturia:• During the day, the

decreased CO causes decreased urine production

• At night, with the patient lying back, the fluid from the interstitial space moves back into the circulation where the kidneys are able to process it and make urine

• Can be 6-7 times per night

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Clinical Manifestations of Heart Failure:Respiratory Manifestations Pulmonary Edema:• Sign of ADHF, caused by

increased pulmonary venous pressure caused by the decreased efficiency of the LV

• the lungs are less compliant and there is increased resistence in the small airways

• see dyspnea, anxiety, cool, pale, diaphoretic skin, cough with frothy sputum, orthopnea

• Hear crackles, wheezes, and rhonchi

Paroxysmal Nocturnal Dyspnea:• Occurs in the middle of the

night when the patient is recumbant

• Fluid from the dependent body areas are reabsorbed

• often wake up in a panic with a feeling of suffocation

Cough:•  often persistent, dry, hacking

cough• sputum +/-

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Clinical Manifestations of Heart Failure:Fatigue and Limited Exercise ToleranceFatigue:• caused by decreased CO• fatigue occurs in activities

that were not previously tiring

• Anemia is often associated with CHF and compounds the fatigue

Tachycardia:• Early clinical sign• SNS response to

decreased CO• Beta-blockers can mask

this

Anxiety and Restlessness:• Secondary to poor gas

exchange in the lungs and impairment in cerebral circulation

• Family may report anxiety, restlessness, confusion and decreased attention span

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Clinical Manifestations of Heart Failure:Weight Loss and MalnutritionWeight Loss:•  Cardiac Cachexia is a

condition hallmarked by tissue wastingo caused by fatigue and

depressiono also hepatomegaly and

congestion of GI vasculature contributes to feeling of fullness

o inflammatory mediators suppress hunger

Malnutrition:• closely linked to the

cardiac cachexia

Page 78: cadiovascular disorders:d isease models part ii

Clinical Manifestations of Heart Failure:CyanosisThis is the bluish discoloration of the skin and mucous membranes caused by excess desaturated hemoglobin in the blood.  Often a late sign of heart failure.

Central Cyanosis:  caused by conditions that impair oxygenation of the arterial blood like pulmonary edema• Lips and mucous membranes

 Peripheral Cyanosis:  caused by conditions that cause low-output failure that cause delivery of poorly oxygenated blood to the peripheral tissues.• finger tips and toes

Page 79: cadiovascular disorders:d isease models part ii

Complications of Heart Failure

1. Pleural Effusion

2. Arrhythmias

3. Left Ventricular Thrombus

4. Hepatomegaly

Page 80: cadiovascular disorders:d isease models part ii

Management of Heart Failure

1. Chest Xray

2. EKG

3. Echocardiogram

4. Radionuclide Angiography

5. Labs

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Page 82: cadiovascular disorders:d isease models part ii

Pharmacologic Therapy

ACE Inhibitor:• Angiotensin Converting

Enzyme Inhibitors• Prevents the conversion of

angiotensin I to angiotensin II and also inhibits the subsequent release of aldosterone

• Decreases both SV and PVR (preload and afterload)

• Decreases mortality due to heart failure

Inotropics:•  Digitalis Glycosides

o good at reducing symptoms but doesn't improve survival

o Increase the force of cardiac contraction while decreasing the rate of contraction

• Beta-Adrenergic Agonistso Dopamine/dobutamine

• Calcium Sensitizers:  in clinical trials here

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Page 84: cadiovascular disorders:d isease models part ii

Pharmacologic Therapy

Diuretics:• Utilized in CHF to mobilize

edematous fluid and decrease pulmonary venous pressure

• Reduces vascular volume/preload

• Different types of diuretic available, and they work in the different areas of the kidneyo Potassium sparing vs.

potassium wasting

Vasodilators:•  Class of drugs clearly

shown to improve survival in CHF

• Work to increase venous capacity, improve EF by improving contractility, slowing ventricular dysfunction, decreasing heart size, and avoiding the neurohormonal changes of CHF

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Beta-Adrenergic Blocking Agents

Marked improvement in patient survival is seen in patients on beta-blockers• Specifically Carvedilol (Coreg) and metorprolol (Toprol XL)• Blocks the negative effects of the SNS on the failing heart• Use in combination with other drugs and increase the dose

slowly (because there can be a decrease in myocardial contractility)

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Supportive Care of Heart Failure

Oxygen:• 2-6 lpm, increase amount

of available Oxygen to the heart and the tissues

 Rest:  • decrease cardiac demand

 Daily Weights:• Check for fluid retention• Call provider if there is a

weight gain of >3lbs in 2 days or 3-5lbs gain in 1 week

Sodium Restricted Diet:•  DASH diet

o <2.4gm sodium a dayo normal american diet is

7-10gms of sodium/day Fluid Restrictions:• In acute cases• want to be careful in

emergency situations

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