Heart Failure - Pathophysiology

Introduction

Heart failure occurs when the heart is unable to maintain an adequate perfusion of the body's tissues at normal filling pressures (Nb, shock is an inability to maintain adequate circulation at low filling pressures).

The cardiovascular system has a large reserve capacity so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

Factors affecting cardiac output:

• Preload: Preload is the end-diastolic volume and when this increases so does the systolic function of the myocardium based on the Frank-Starling Law. Stretching of the myocytes engages more actin and myosin within the sarcomere and allows greater force generation. In a failing heart the Frank-Starling Law fails and stroke volume cannot increase with an increased preload.
• Afterload: Refers to the resistance the left ventricle encounters as it ejects blood into the peripheral circulation. Depends upon many variables; for example ventricular volume, arterial tone etc. In the failing heart, in order to maintain blood pressure with reduced cardiac output the peripheral resistnace and so the afterload has to increase.
• Contractility
• Heart rate
• Distensibility
• Synergy of contraction

Mechanisms of failure

Myocardial failure

E.g Dilated cardiomyopathy. Causes a failure in contractility.

Volume overload

E.g. Valve regurgitation and shunts (PDA).

Initial response based on the Frank-Starling Law and stroke volume increases as preload increases and enables the heart to expel the extra blood. Ultimately the heart decompensates and the chamber enlarges. Fluid will build up in the compartment preceding it. For example, failure of the left atrium in this manner due to mitral regurgitation leads to pulmonary oedema.

Pressure overload

E.g. aortic stenosis or systemic overload.

Increase afterload so heart muscle hypertrophies. The abnormally thick myocardium may predispose to:

• Diastolic failure.
• Arrhythmias.

Compliance failure

E.g. Cardian tamponade.

Prevent adequate relaxation of the ventricles and don't allow sufficient filling. Results in diastolic failure.

Abnormal rate/rhythm

E.g. sustained bradycardia leads to a low output failure.

Clinical Signs

Forward-Low output failure

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa.

• Low systemic blood pressure.
• Exercise intolerance.
• Pallor.
• Tachycardia.
• Weak femoral pulses.
• Pre-renal failre and azotaemia.

Backward-Congestive failure

Clinical signs are different for each side:

Left sided failure

• Dyspnoea and tachypnoea.
• Lung crackling on ausculatation due to pulmonary oedema.
• Cough due to left cardiomegaly comressing the left main stem bronchus.

Right sided failure

• Jugular distension.
• Hepatomegaly and splenomegaly.
• Ascites.
• Positive hepato-jugular reflux.
• Pleural effusion.

Compensatory Mechanisms

Renin-angiotensin-aldosterone system

• Sodium and water retention by the kidney.
• Vasoconstriction.

Sympathetic nervous system

Decreased blood pressure stimulates release of noradrenaline. Increase heart rate and contractility by the efect on beta-receptors. Peripheral vasoconstriction is activated by its action on alpha-receptors. Sinus arrhythmias are abolished.

Increased heart rate and rhythm imposed by the sympathetic nervous system increases the hearts oxygen consumption. As diastole is shortened the time available for blood to enter the coronary circulation is also shortened, decreasing blood flow to the myocardium. Resulting myocardial hypoxia may cause arrhythmias.

Classification

New York Heart Association Classification

Classification of congestive heart failure used in human medicine.

• Class 1: No clinical signs but evidence of heart disease.
• Class 2: Exercise intolerance or dyspnoea.
• Class 3: Marked exercise intolerance.
• Class 4: Cannot exercise, dyspnoea at rest.

Introduction

• The heart pumps unoxygenated blood from the venous circulation into the lungs where it is oxygenated. Newly oxygenated blood then travels to the left atria and ventricle where it is pumped into the arterial circulation to meet the oxygen demands of the body.

• Heart Failure is a condition that begins when the heart is unable to pump enough blood (cardiac output) at normal filling pressures to meet the body’s requirements. Heart Failure is the end result of heart disease (heart abnormality).

• Under normal circumstances the heart can adapt to moderate increases of pressure or volume using its functional reserve capacity. During acute episodes of increased volume or pressure load the dilated heart chambers respond by increasing their force of contraction. This is known as the Frank-Starling Phenomenon. However, in chronic conditions the cardiac chambers hypertrophy. Initially these adaptations are beneficial, but eventually the functional reserve mechanisms lead to heart failure.

• Heart failure can affect the right ventricle, the left ventricle, or both ventricles (biventricular). Clinical signs are characteristic and can help determine which ventricle is affected.

Etiology of Heart Failure

The five cardiac impairments that cause heart failure are the following:

1. Arrhythmias

Problem

• Irregularity of cardiac rhythm affects cardiac output

Cause

• Tachycardia: Increased heart rate does not allow for adequate cardiac filling during diastole and consequently cardiac output drops

• Bradycardia: Decreased heart rate lowers cardiac output by limiting the amount of blood pumped per minute

2. Diastolic Failure (Restricted Ventricular Filling)

Problem

• When the heart is unable to relax fully during diastole (to allow for complete ventricular filling) cardiac output drops

Cause

• Hypertrophic Cardiomyopathy (increased thickness of the ventricular myocardium reduces lumen size available for diastolic filling)

• Dilated Cardiomyopathy (dilation of the cardiac chambers lowers the contraction force and the cardiac output)

• Pericardial Effusion (increased pressure on the myocardium decreases space for diastolic filling)

3. Pressure Overload

Problem

• Increased pressure in the ventricle causes concentric hypertrophy in an effort to maintain adequate cardiac output. Eventually, high ventricular pressures can result in cardiac failure.

Cause

• Hypertension (Pulmonary and/or Systemic)

• Outflow tract narrowing (Aortic and/or Pulmonic Stenosis)

4. Systolic Failure (Myocardial Failure)

Problem

• Decreased myocardial contraction during systole causes reduced cardiac output

Cause

• Primary myocardial diseases (e.g. Dilated cardiomyopathy)

• Complication from another form of heart failure

5. Volume Overload

Problem

• The cardiac ventricles are required to work harder by pumping an increased volume of blood in order to maintain adequate cardiac output. Increased blood volume in the heart causes eccentric hypertrophy in an effort to accommodate the increased blood volume.

Cause

• Shunting Disorders (e.g. PDA)

• Valvular Regurgitation

• Anemia