Cardiac FailureDr. Sumaira Iqbal

Learning Objectives

By the end of lecture student should be able to :

Define cardiac failure.

Enlist its types.

Explain compensated heart failure and effect of

sympathetic stimulation.

Explain decompensated heart failure and its

complication.

Summarize mechanism of development of peripheral

and pulmonary edema.

Outline the management plan.

Introduction

Definition

A state in which the heart cannot provide

sufficient cardiac output to satisfy the metabolic

needs of the body

Classification

On the basis of sides

1. Left sided cardiac failure

2.Right sided cardiac failure

On the basis of duration

1.Acute cardiac failure

2.Chronic cardiac failure

On the basis of compensation

1.Compensated cardiac failure

2.Uncompensated cardiac failure

Classification

Acute cardiac failure--sudden in onset (sec or

minutes) e.g. MI

Chronic Cardiac Failure--Gradual in onset (days

months) e.g. I.H.D, valvular heart disease

Left sided/or L.V Failure: ↓L.V output, ↓L. Atrial

Pressure or ↓pulmonary Pressure

Rt. Sided/or R.V Failure: ↓R.V output e.g. pul

valve disease, cor pulmonale etc.

Causes of Cardiac Failure

Reduced ventricular

contractility

MI, Myocarditis etc

Ventricular overflow

obstruction: (pressure

overload):

Hypertension, Aortic

stenosis

Pul. Hypertension,

Pul. Valve Disease.

Ventricular Inflow obstruction:

Mitral Stenosis, Tricuspid stenosis

Constrictive pericarditis

Ventricular volume overload:

Mitral Regurgitation

Aortic Regurgitation

AV Septal Defect

Increase Metabolic Demand (high C.O)

Severity of Cardiac Failure

Normal Cardiac Output = 5 L/min

End Diastolic Volume = 110-120 ml

End systolic Volume = 40-50 ml

Stroke volume = 70 ml

Normal Ejection Fraction (EF) = 60% or 0.6

Mild Cardiac Failure = EF < 45-55%

Moderate Cardiac Failure = EF < 45-30%

Severe Cardiac Failure = EF < 30%

Acute Stage of cardiac failure

Pumping ability of heart is compromised

1.Reduced cardiac output

2.Damming of blood in the veins

Cardiac failure leads to fainting and chest pain

Sympathetic stimulation--Occurs within 30

seconds

Returns cardiac output almost back to normal

Sympathetic Stimulation

Cardiac output low– circulatory reflexes are

activated

Baroreceptor Reflex and other responses

originate

Initiates sympathetic stimulation

On heart– increased myocardial contractility

Functional part is stimulated more to

compensate

Sympathetic Stimulation

On Vasculature—Increase mean systemic filling

pressure 12-14mmHg

Increase VR—increase blood flow into atria—

increase pressure in atria– more pumping

Inhibits parasympathetic response

Chronic Stage of cardiac failure

Semi chronic state

1.Renal retention of salt and water

2.Varying degree of heart itself

Renal retention of salt and water

↓ cardiac output → ↓Arterial Pressure → ↓Urine volume

Urine volume returns to Normal → as cardiac output

and arterial pressure becomes normal

Fluid retention is detrimental to cardiac failure

More blood volume → more venous return

Mild fluid retention increase systemic filling

pressure/pressure gradient thus increases venous

return

Renal Na+ and H2O retention-- ↓Blood volume and

↑venous resistance

1. Sympathetic constriction of afferent arterioles ↓ GFR

and ↓ Urinary Output

2. Ag-II release ↑↑Na+ retention

3. Aldosterone release (by Ag-II and K+)--↑↑Na+ retention

4. ↑ ADH release leads to H2O balance → H2O retention

5. ↑ MAP initially then → returns to normal

Cardiac recovery (repair of muscle)

ANP causes extra Na+ excretion

Damaging effects of salt and water

retention

1. Increasing the workload on the damaged heart

2.Overstretching of the heart, which further

weakens the heart

3.Filtration of fluid into the lungs, causing

pulmonary edema and consequent

deoxygenation of the blood

4.Development of extensive edema in other parts

of the body.

Recovery of heart

Repair of heart tissue starts

New collateral blood supply to heart

Undamaged portion hypertrophies to meet the

demands

Heart recover from days to few weeks

Recovery depends on damage

DECOMPENSATED HEART FAILURE

When sympathetic stimulation and fluid

retention mechanisms fails to compensate the

damage and restore the function—

DECOMPENSATED HEART FAILURE

Cardiac output does not become normal

Edema develops

Eventually leads to death

Mechanisms

Fluid retention causes overstretched sarcomeres

Increase edema of heart muscle

Decrease longitudinal tubules of sarcoplasmic

reticulum fail to accumulate enough Ca++.

Norepinephrine in sympathetic nerves

decreases

Decompensated heart Failure

Mechanism

Point A—RAP: <4mmHg C.O 2.5L/min(No compensation)

Point B---RAP: 5mmHg C.O 4L/min (salt water retention, good

not for longer time)--Psf increases as volume increases

Point C---RAP: 7mmHgC.O 4.2L/min(increases salt water

retention)

Point D—RAP: 9mmHg C.O 4.2L/min(increases salt water

retention)

Point E & F fluid retention becomes detrimental instead of

being beneficial

Treatment of Decompensated

Heart Failure

Cardiotonic drugs—strengthens heart

Digitalis

Diuretics

Increase renal excretion

Reduce water and salt intake

Input=Output

Mechanism of

action of

Digitalis

Strengthens heart—

increase cardiac

activity 50-100%

Digitalis increase

cardiac strength by

increasing calcium in

muscle fiber

Unilateral Left Heart Failure

Failing left heart but right side is normal

Blood pumped by right side vigorously but left side

fails to pump into systemic circulation

Mean pulmonary filling pressure rises above the colloid pressure of

plasma i.e. 28mmHg

Fluid filters into lung interstitium and alveoli

Pulmonary congestion and edema develops

Low Cardiac Output Heart Failure—

Cardiogenic Shock

Myocardial infarction– reduced blood supply

Shock occurs—further reduces coronary supply

Weakens cardiac muscles– further reduces arterial pressure

Vicious cycle develops

Digitalis increases myocardial strength

Peripheral Edema– Long Term Heart

Failure Decreased Glomerular filtration rate

Reduced arterial pressure

afferent arteriolar constriction—sympathetic effect

Decreased urinary output

Activation of renin angiotensin system

Angiotension increases salt and water reabsorption

Decrease loss of water from the body

Water accumulates in blood and tissue spaces

Peripheral Edema– Long Term Heart Failure

Increased aldosterone secretion

Stimuli: increased angiotensin II, increased K+

in response to decreased renal function

Promotes Na+ reabsorption, reduces osmotic

pressure

Promotes water reabsorption

Increases ADH

Peripheral Edema– Long Term Heart Failure

Sympathetic Stimulation

1.Afferent arteriolar constriction

2.Salt and water reabsorption by alpha

adrenergic receptors

3.Stimulation of renin angiotensin system

4.Stimulation of aldosterone

Role of ANP

Released by atrial walls of the heart when

stretched

Heart failure increases both the right and left

atrial pressures that stretch the atrial walls

ANP in the blood increase 5- to 10-fold in severe

heart failure

Direct effect on kidneys– increase excretion of

salt and water

Prevent extreme congestive symptoms during

cardiac failure.

Acute Pulmonary Edema

Increased load on weak left ventricle

Limited pumping– blood dams up in the lungs

Increase pulmonary capillary pressure

Fluid filters into lung interstitium and alveoli

Diminishes oxygenation—peripheral vasodilation

Increases Venous Return—increase damming of blood

in lungs

Acute Pulmonary edema

Treatment

1.Apply tourniquet on limbs, sequester blood flow

in the veins– decrease workload on heart

2.Diuretics to cause rapid fluid loss

3.Pure oxygen

4.Digitalis

Cardiac Reserve

The maximum percentage that the cardiac output can

increase above normal is called the cardiac reserve.

The cardiac reserve in

Healthy young adult--300 to 400 percent

Athletically trained persons-- 500 to 600 percent or

more

Severe heart failure--no cardiac reserve

Example—during vigorous exercise the cardiac output of

a healthy young adult increases five times normal, a

cardiac reserve of 400 percent.

High Cardiac Output Heart Failure

AV fistula

Beri Beri

Manifestation of heart failure

Right heart failure

Raised JVP

Peripheral edema

hepatomegaly

Left heart failure

Pulmonary congestion

Pulmonary edema

Basal crepitations at lung bases

Dyspnea

Nocturnal dyspnea

Cough with red tinged sputum

General

Reduced exercise ability

Fatigue

Increase heart rate

Low blood pressure

Role of diuretics

Increased excretion of salt and water

Reduces workload on heart

Reduces edema

Improves pumping ability of heart

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