Heart Failure

Outline

• Definition of Heart Failure

• Pathophysiology of Heart Failure
• Right Sided vs Left sided Heart Failure
• Low Output vs High Output Cardiac Failure
• Systolic vs Diastolic Heart Failure
• Chronic vs Acute Cardiac Failure
1. Definition: Heart failure is the inability of the Heart to maintain an output adequate to meet the
metabolic demands of the body.

It is an increasingly common condition associated with extremely high Morbidity and Mortality.

2. Pathophysiology of heart failure: The clinical syndrome of Heart failure manifests as organ
hypoperfusion and inadequate tissue oxygen delivery due to low cardiac output and decreased
cardiac reserve, as well as pulmonary and systemic venous congestion.

Cardiac Reserve is the work that the heart can perform beyond that required of it under the
ordinary circumstances of daily life, depending upon the state of the myocardium and the degree to
which, within physiologic limits, the cardiac muscle fibers can be stretched by the volume of blood
reaching the heart during diastole.

Reminder:

Cardiac Output (CO)= HR X SV: The quantity of blood pumped by the heart each minute. Normal
output in an adult is 3.5-5.5 L/min.

Stroke Volume (SV): EDV-ESV

Cardiac Index (CI): Cardiac output divided by the patient’s body surface area.
It is used to compensate for body size. The normal cardiac index is 2.8-4.2 L/min/m2.
A cardiac index of less than 2.5 requires immediate assessment and treatment.

Cardiac output is determined by heart rate and stroke volume. Stroke volume depends on:
– Preload
– Afterload
– Contractility

Starling’s Law: When the myocardial muscle cell is stretched, the developed tension increases to a
maximum and then declines as the stretch become more extreme.

Heart failure with reduced ejection fraction (HFrEF)

Formerly called "systolic heart failure," is defined as a left ventricular Ejection fraction < 40%.
Symptoms of dyspnea and fatigue result from reduced cardiac output.

The body responds with sodium and water retention, vasoconstriction, and ventricular remodeling.
These responses initially improve symptoms but eventually contribute to worsening heart function.

Treatment goals include

• Reducing symptoms
• Improving functional status
• Improving quality of life
• Reducing hospitalizations and mortality

HFrEF results primarily from several endogenous Neurohormonal mechanisms:

• The renin-angiotensin-aldosterone system (RAAS)

• The sympathetic nervous system
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 • The natriuretic peptide system

Evolution of pharmacologic approaches in Heart

Failure: Neprilysin inhibition as a new therapeutic
strategy1

3. Forms of heart failure

a. Right ventricular failure : It is associated with Blood damming up in the systemic venous
circuit includes symptoms and signs of:
• Edema.
• Congestive Hepatomegaly.
• Ascites.

Most common cause of Right Heart Failure is left sided

• Heart Failure.
• Also Diseases that affect the right ventricle primarily.
• Like (primary pulmonary hypertension)

b. Left sided heart failure: dyspnea, orthopnea and pulmonary congestion

c. Left ventricular failure: Symptoms and signs are due to Blood damming up behind the left
ventricle and due to pulmonary congestion. Long standing left ventricular failure may
eventually result in signs of right ventricular failure with generalized accumulation of fluid.

4. Low output VS high output failure

Heart failure causing low cardiac output is the most common form of Heart failure
Low output failure is characterized by:
a) Reduced stroke volume.
b) Peripheral vasoconstriction.
c) Cold and pale extremities.
d) Reduced or narrow pulse pressure.
If the pulse pressure (Systolic pressure – Diastolic pressure) is extremely low, i.e. 25 mmHg or less,
the cause may be low stroke volume, as in Congestive Heart Failure and/or shock.

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 A narrow pulse pressure is also caused by aortic valve stenosis and cardiac tamponade.

Causes of low output failure:

• ischemic heart disease
• Low output: Hypertension (end stage)
• ( SVR) Dilated cardiomyopathy
• Valvular and pericardial disease

Causes of high output failure:

• Hyperthyroidism: Thyrotoxicosis
• Anemia
• High output: Pregnancy
• ( SVR) Arterio venous fistula ( Plasma volume SVR).
• Beriberi: (severe thiamine deficiency -  C.O 2º to reduced SVR,  venous return).
• Paget’s disease (extremely rapid bone formation and resorption associated with increase in
Blood flow and significant augmentation of cardiac output).

High output failure is characterized by:

o Peripheral vasodilatation.
o Warm and flushed extremities.
o Widened or normal pulse pressure.
o The resting pulse pressure in healthy adults, sitting position, is about 30-40 mmHg

5. Systolic VS Diastolic failure

Impaired contraction: systolic failure Impaired relaxation: diastolic failure.

Heart failure is usually associated with an abnormality of systolic function (reduced ability to
expel blood from the ventricular cavities).

It may occur with an abnormality of diastolic function (reduced ability of the left ventricle to
accept or fill with blood) despite normal systolic function.

When the ventricles fail to relax adequately to accept blood, ventricular diastolic pressures
increase, causing atrial pressures to increase and leading to systemic or pulmonary congestion.

Impaired ventricular relaxation can be due to:

o Acute myocardial ischemia.
o Myocardial fibrosis.
o Infiltrative disease.

Diastolic Heart Failure occurs more frequently in women than man, especially elderly women with
hypertension.

Diastolic HF can be caused by:

Increased resistance to ventricular inflow and reduced ventricular diastolic capacity:
• Constrictive pericarditis.
• Restrictive disease
• Hypertensive disease
• Hypertrophic cardiomyopathy

HF: Abnormality both of contraction and relaxation coexist in most patients.

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 6. Acute VS chronic HF
a. Acute: Sudden rupture of cardiac valve leaflet (Trauma, infective endocarditis, massive MI)
b. Chronic: Dilated Cardiomyopathy and multivalvular Heart Disease

Outline

• Functional Classification of Heart Failure

• Physical Examination in Heart Failure
• Clinical Manifestation in Heart Failure
• Epidemiology of Heart Failure
• Causes of Systolic and Diastolic Heart Failure
• Cor Pulmonale
1. Functional classification of heart failure

The New York Heart Association (NYHA) devised a functional classification of Heart disease that
grades the severity of Heart failure according to the amount of exertion required to cause
symptoms.

The classification is useful in following the course of patients during their disease, assessing
results of therapy, and comparing groups of patients.

Class I: No limitation of physical activity. No dyspnea, fatigue or palpitations with ordinary

physical activity.
Class II: Slight limitation of physical activity. These patients have fatigue, palpitations, and
dyspnea with ordinary physical activity, but

are comfortable at rest.

Class III: Marked limitation of activity. Less than ordinary physical activity results in symptoms but
patients are comfortable at rest.
Class IV: Symptoms are present at rest and any physical exertion exacerbates the symptoms.
2. Symptoms of RHF: those of systemic venous congestion:
• Dependent edema.
• Right upper quadrant abdominal pain due to stretching of hepatic capsule From liver
engorgement.
• Anorexia. Nausea
• Bloating is due to congestion of the mesentery and liver. Jaundice (late finding in HF).
• Fatigue as forward output diminishes.

3. Symptoms of LHF:
• With severe failure, patients at mild exertion or at rest, may have:
• Tachypnea, Orthopnea, Paroxysmal Nocturnal Dyspnea (Cardiac Asthma), Nocturia and
• Cerebral Symptoms Due to Low Cardiac Output

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 • Patient appears to be in: Severe distress
• May Look Pale, May be cyanotic, may have cool Extremities.

4. Lung examination in HF:

• It can vary according to the severity of Heart failure from
Moist rales at the bases to rales over the entire lung fields
• Rales may be associated with blood-tinged sputum.
• Dullness on percussion at the lung bases may reflect a
pleural effusion.

5. Cardiac exam: hard sound

• A protodiastolic, or S3 gallop, heard 0.13 to 0.16 second after the S2, is a common sign of
congestive heart failure. The S3 sound occurs in association with increased ventricular
volumes and is caused by a rapid deceleration of ventricular inflow from the left atrium
occurring just after the early filling phase of the ventricle. Reduced ventricular distensibility
or stretching may contribute to the gallop sound.
Synonymous terms include ventricular gallop, early diastolic gallop, ventricular filling
sound, and protodiastolic gallop.

• Fourth heart sounds (presystolic gallop) may be heard when congestive heart failure is
associated with conditions in which the atrium contracts forcibly into a noncompliant
ventricle and occur with ventricular hypertrophy.
• Murmurs due to mitral regurgitation or tricuspid regurgitation secondary to ventricular
dilatation are not uncommon in heart failure.

6. Other findings on physical examination

• Tachycardia is another common manifestation of heart failure and is a compensatory
mechanism whereby the heart attempts to maintain cardiac output in the setting of reduced
stroke volume.
• Pulsus alternans is characterized by a regular rhythm in which there is an alternation of
strong and weak contractions as detected by palpation of the pulse or by
sphygmomanometry. This phenomenon occurs secondary to an alternating stroke volume
due to incomplete recovery of contractile cells on every other beat.
• Cheyne-Stokes respiration occurs in patients with advanced cardiac failure and is
characterized by alternating periods of Apnea and Hyperpnea. This condition is due to
prolonged circulation time from lung to brain associated with left ventricular failure. When
congestive failure is severe and long-standing, cardiac cachexia may occur with anorexia
and weight loss.
7. Further cardiac tests
• Abdomino-jugular reflux: Gently
press over the abdomen for 10
Seconds. This is increase venous
return to the right side of the heart
temporarily and JVP normally rises.
This rise may take 15 seconds to
decrease in congestive heart failure.
• + testicular edema

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8. Epidemiology and Etiology of Heart Failure

Mortality following
admission for acute
heart failure exceeds
that of most cancers

HF etiology
CHD
Valve disease
Cardiomyopathies
Other*

• Most patients with HF experience symptoms due to impaired LV myocardial function 1

• The most common causes of HF are coronary heart disease (CHD), valve disease and
cardiomyopathies2

• CHD is the underlying cause of 60–70% of acute HF cases3

• Many patients with chronic HF have a range of co-morbidities that contribute to the cause of the
disease and play a key role in its progression and in the response to therapy

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 • hypertension*
• ischemic heart disease*
• diabetes mellitus
• cardiac arrhythmias
• ventricular arrhythmias
• atrial fibrillation
• respiratory disorders
• cognitive dysfunction
• hyperlipidemia
• chronic anemia
• renal failure
• arthritis

This can result in patients burdened with multiple pills per day, each with different dosage
schedules, with an increased potential for drug–drug interactions

9. Cor Pulmonale

Definition: enlargement of the Right ventricle secondary to increase in RV afterload. It sometimes

lead to RV failure.

Causes: Pulmonary diseases

o Pulmonary vascular diseases.
o Pulmonary parenchymal diseases.
o Pulmonary emboli (chronic and acute).
o Pulmonary vasculitis.
o Pulmonary vasoconstriction secondary to high altitude.
o Congenital heart disease with left to right shunting.
o Pulmonary veno-occlusive disease.

If no clear cause cannot be defined, the condition is referred to

as primary pulmonary hypertension.

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Outline

• Chest X ray and EKG in Heart Failure

• Echocardiography and Angiography
• Laboratory Examination
• Non-Pharmacologic Treatment
• Medical Treatment
• Surgical Treatment
1. Chest X-Ray examination in Congestive Heart Failure

Chest-X-Ray findings include:

• Cardiomegaly.
• Interstitial pulmonary edema.
• Kerley B lines (interlobular edema).
• Alveolar edema and pleural effusions may be seen.

EKG:

• May help define Etiology of Heart failure (especially Figure 1- pulmonary edema
ischemia).
• Presence of ventricular hypertrophy.

2. Echocardiography and angiography

It is useful in assessing the severity and etiology of Heart Failure.

• Surgically correctable valvular disease must be Excluded.
• Global or diffuse left ventricular dysfunction suggests a
cardiomyopathic process.
• Regional wall motion abnormalities are suggestive of coronary
artery disease.

Coronary Angiography: May be undertaken to diagnose significant

coronary artery disease.

3. Blood tests Figure 2 - Kerley B line

a. Several blood chemistry tests may be abnormal (SGOT, SGPT,
Bilirubin secondary to hepatic congestion).
b. BUN becomes elevated with reduced renal flow.
c. Hyponatremia is secondary to:
• *Diuretic therapy.
• * Salt restriction.
• * Reduced ability of kidneys to excrete Water
d. Polycythemia may occur with chronic cor pulmonale (Hypoxia)
e. Hypokalemia may result from:
• Thiazide Diuretics (distal tubule).
• Loop Diuretics (Loop of Henle).
f. Hyperkalemia results from:
• Spironolactone administration (distaltubule)
• * Non steroidals anti-inflammatory drugs.
• * Ace Inhibitor.
• * Markedly reduced renal flow.
• * Diabetic nephropathy.
g. BNP: They are formed in the ventricles (Myocyte stretch).
• These hormones are highly accurate for identifying and excluding Heart Failure with
high sensitivity and specificity.
• Independent predictive power.
• BNP is particularly valuable in differentiating cardiac from pulmonary causes of
dyspnea.
• BNP is also useful in prognosis and in monitoring therapy.

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4. Heart Failure treatment:
• Restriction of physical activity and Bed Rest are useful acutely to reduce myocardial
workload and oxygen consumption in patients with symptomatic Heart failure. After
stabilization, carefully guided cardiac rehabilitation and exercise may improve functional
capacity in some patients with Heart Failure.
• Weight loss in obese patients reduces SVR as well as myocardial O2 demand; however,
maintenance of adequate caloric intake in patients with severe Heart failure is necessary to
prevent or correct cardiac cachexia.
• Dietary Sodium Restriction: Will facilitate control of signs and symptoms of Heart failure
and minimize diuretic requirements

Adjuvant Nonpharmacologic Measures in treatment of Heart failure

Dialysis or ultra-filtration may be necessary in patients with severe Heart failure and renal
dysfunction who cannot respond adequately to fluid and Sodium limitation or diuretics.
Other mechanical methods of fluid removal such as therapeutic:
▪ Thoracentesis.
▪ Paracentesis.
▪ Phlebotomy.

To beDiscussed in Details in Pharmacology of Heart Failure Medications

▪ Diuretics (loop, distal tubules).
▪ Aldosterone antagonist.
▪ Angiotension converting enzymes inhibitors.
▪ Angiotension receptor blockers.
▪ Angiotension receptor neprilysin inhibitor
1. Beta-adrenoceptor blockers.
2. SGLT2 Inhibitors
3. Sinus Node Inhibition If Funny Current Inhibition
▪ Enhancement of myocardial contractility.
1. Digitalis.
2. Dopamine.
3. Dobutamine.
▪ Phosphodiesterase Inhibitors.
▪ Vasodilators
1. Nitropusside
2. Nitroglycerin
3. Hydralazine

Heart Failure Surgical Treatment: Review the pictures from the slides

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Cardiogenic shock
Outline:

(1) Introduction (2) Diagnosis (3) Causes (4) Pathophysiology (5) Role of Echocardiography.(6) Treatment (6)
Role of Aortic Counter pulsation.

1. Introduction: Cardiogenic Shock is:

• Most commonly secondary to acute myocardial infarction.
• Less frequently secondary to cardiomyopathy or Myocarditis.
• Leading cause of Death of patients hospitalized with MI.
• Early reperfusion therapy for acute MI decreases the incidence of cardiogenic shock.
• Shock is typically associated with ST elevation MI and is less commonly with non ST elevation
MI.

2. Diagnosis:
• Systemic Hypoperfusion
• Depression of cardiac index < 2.2 L/min/m2
• Blood Pressure < 90 systolic
• Elevated PCWP > 18mmHg

3. Causes
• LV failure accounts for  80% of the cases of cardiogenic shock complicating acute MI. In
hospital mortality > 50%
• Acute severe mitral regurgitation.
• Ventricular septal rupture
• Right ventricular failure.
• Free wall rupture or tamponade account for the remainder.
• Acute severe mitral regurgitation.
• Ventricular septal rupture.
• Right ventricular failure.
• Free wall rupture or tamponade account for the remainder.

Acute Fulminant myocarditis

o Myocarditis Causes cardiogenic shock in 15 to 20% of cases.
o Patients are typically younger.
o Echo shows typical global LV dysfunction.
o Medical management is similar to other causes of cardiogenic shock.

4. Pathophysiology
• Depression of myocardial contractility usually due to ischemia.
• Reduced cardiac output and arterial pressure which result in hypoperfusion of the
myocardium and further ischemia and depression of the cardiac output.
• Hypoxemia and lactic acidosis develop as a result of pump failure.

5. Role of Echocardiogram
• Left ventricular function is assessed.
• Left to right shunt in patients with ventricular septal rupture
• A severe MR can be present.
• Proximal Aortic dissection and Aortic regurgitation can be present.
• Tamponade may be present.
• Evidence of pulmonary embolism can be seen.

6. Treatment
• Maintaining systemic and coronary perfusion.
• Ensures optimum LV filling pressures.
• Hypoxemia and acidosis must be corrected
• Negative inotropic agents should be discontinued.

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• Adjustment of doses of renally cleared medications.
• Bradyarrhythmias may require transvenous pacing.
• Ventricular tachycardia or rapid atrial fibrillation may require immediate treatment.
• Vasopressors and Inotropes as needed to support the Heart and the Blood Pressure.

Reperfusion

• Rapid Establishment of blood flow in the infarct-related artery is essential in the management
of cardiogenic shock.
• Percutaneous Coronary Intervention (PCI) or Coronary Bypass Surgery (CABG) is superior to
medical therapy.

Aortic counterpulsation - Intraaortic Balloon Pump (IABP)

• Augmentation of arterial diastolic pressure and cardiac output.

• The Balloon inflated during early diastole augmenting coronary blood flow.
• Balloon collapses in early systole reducing the afterload against which the left ventricle ejects.
• Myocardial O2 consumption is reduced, leading to amelioration of ischemia.
• IABP is useful as a stabilizing measure in patients with cardiogenic shock prior to and during
cardiac catheterization and PCI.

Contraindications to intraaortic balloon pump

• Aortic regurgitation (Inflation in Diastole and Increase Blood Flow may Worsens the
Regurgitation)
• Aortic dissection (Increase Blood Flow in the Aorta may Increase the Dissection)
• Severe peripheral vascular disease: (IABP Could cause Ischemic Leg)
• Very low platelets count: (IABP May Destroy Platelets During Inflation)

Figure 1 - Intraaortic balloon hemodynamics

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