Congestive Heart Failure

Epidemiology/Pathophysiology

Definitions of Congestive Heart Failure (CHF):

-The presence of heart failure symptoms, reversibility on treatment and objective evidence of cardiac dysfunction (European Society of Cardiology, 1995)

-Can be viewed as a consequence of disordered circulatory dynamics and pathologic cardiac remodelling.

Overview: 

Congestive Heart Failure occurs when the heart is unable to pump enough blood to meet the needs of the body.

-This reduces Cardiac Output, leading to hypoperfusion to tissues and Edema (explained below).

Cardiac Output=SV X HR                          Blood Pressure=TPR X Cardiac Output

-This stimulates various physiological responses (e.g. Increased sympathetic Nervous System-Baroreceptor Reflex, Increase in Renin-Angiotensin Aldosterone System and inflammation due to ischemia)

Why is the heart unable to pump sufficient blood in the first place?

-Due to decreased myocardial contractility (possibly due to myocardial infarction) (Results in Systolic Dysfunction)

-Cardiomyopathies (Deterioration of Myocardium which leads to inadequate pumping)-Could be due to hypertrophy which results in Systolic Dysfunction

-Long-standing hypertension (Results in Diastolic Failure)

-Severe mitral valvular regurgitation (Results in Systolic Failure)

-Arteriovenous fistulae (Abnormal passageway between an artery and vein)

Definition of fistulae: Abnormal connection or passageway between two epithelium lined organs or vessels that do not normally connect.

-Thiamine deficiency (Vitamin B1) –>Disease: Beriberi

-Severe anemia

-Alcohol (cardiotoxic in large quantities), Drugs (e.g. Beta-Blockers, Calcium channel blockers may depress myocardial contractility) (Chemotherapeutic agents such as doxorubicin may cause  myocardial damage).

-Persistent arrhythmias (Reduce cardiac efficiciency)

***Diastolic myocardial dysfunction-Impaired myocardial relaxation (due to increased ventricular wall stiffness and reduced compliance, results in impaired diastolic ventricular filling, decreasing preload). Could be due to:

(a) Ischemic myocardial fibrosis (Coronary artery disease)

(b) Left Ventricular Hypertension

(c) Hypertrophic cardiomyopathy

-Diastolic dysfunction often co-exists with systolic failure but may occur in isolation in 20-40% of patients presenting with heart failure.

-Diagnosis of diastolic dysfunction is via Doppler mitral diastolic flow velocity profile.

How does the heart deal with the lack of cardiac output and drop in BP?

Ans: Compensatory responses to maintain perfusion to vital organs

*Heart has to adapt to maintain sufficient cardiac output and blood pressure.

1. [Drop in Cardiac Output] Myocardial hypertrophy occurs  

-Attempts to increase myocardial contractility

-This increases the mass of contractile elements and improves systolic contraction

-Increase in Angiotensin II levels also induces myocardial hypertrophy.

-However it also increases ventricular wall stiffness which means it is less elastic and pumps less blood eventually.

2. [Drop in Blood Pressure and CO due to Reduced Renal perfusion] Renin Angiotensin Aldosterone system activated (Activation of neurohumoral system)

-Attempts to increase arterial tone.

-Stimulates the Renin-Angiotensin-Aldosterone System (RAAS) which increase levels of renin, levels of plasma angiotensin II and aldosterone.

-The drop in blood pressure also stimulates the baro-receptor reflex (sympathetic tone) which increases the release of catecholamines (NAdr) which stimulates more renin release.

-Aldosterone, Angiotensin II promotes Na+ and water retention and decreased excretion of K+.

3. [Drop in Blood Pressure and CO] Sympathetic nervous system is activated (Activation of neurohumoral systems)

-Baroreceptors are activated in CHF, resulting initially in enhanced myocardial contractility.

-Later on, it furthur activates the RAAS and the humoral system.

-Overall effect of this is an increased venous return (Increases cardiac preload)arterial tone (cardiac afterload–>Pressure to overcome arteriolar resistance), increased plasma concentration of NAdr, progressive retention of water and salt and edema.

-Chronic sympathetic stimulation results in down-regulation of cardiac B-receptors (Bark* enzyme decreases). Thus, it reduces responsiveness of heart to sympathetic stimulation.

4. [Drop in Blood Pressure] Regulatory Substances released 

(a) Atrial Natriuretic Peptide (ANP) is released from the cardiac atria in response to stretch, leading to natriuresis and vasodilation.

-ANP are physiological antagonists to the effects of AngT II on vascular tone, aldosterone secretion and renal sodium absorption.

(b) Endothelin is a potent vasoconstrictor peptide secreted by vascular endothelial cells which promotes the renal reabsorption of sodium.

-Constriction of systemic veins. Promoting sodium and water reabsorption increases atrial pressure (cardiac preload), sarcomeres lengthen and myofibril contraction is enhanced (Frank-Starling Mechanism).

-Beyond a certain stretch point, myocytes loses contractility, thus any increase in end-diastolic volume will not have an increase in stroke volume anymore,  stroke volume decreases (see heart failure region)

-Stroke Volume=End Diastolic Volume – End Systolic Volume

5. [Decrease in SV] Increasing left ventricular preload

Overall effect: Sustained cardiac output allows heart to operate at higher end-diastolic volume, leading to increased SV. Peripheral vasoconstriction attempts to allow for regional redistribution of cardiac output to vital organs. However, each of these compensatory responses promote disease progression.

–>Neurohumoral activation leads to arterial and venous constriction (Arterial constriction increases afterload, whereas venous constriction decreases preload)

Thus this decreases stroke volume

–>Secreted substances (NAdr and Angiotensin II) may act directly on myocardium to promote unfavourable remodelling.

∴ Thus, this increases wall stress and decrease myocardial contractility.

Pharamological aims:

1. Drugs reduce ventricular wall stress by inhibiting renin-angiotensin system (e.g. selected vasodilators, ACE-inbibitors, aldosterone antagonists)

-Preload Reduction, Afterload reduction.

2. Drugs may inhibit sympathetic nervous system. This decreases pathological ventricular remodelling, slows disease progression and decrease mortality  in patients with due systolic dysfunction (e.g. B-adrenergic antagonists)

– Afterload Reduction, Preload reduction

3. Enhancement of inotropic state

-These drugs are therefore vital in the long-term treatment of heart failure.

-Some drugs that slow progression provide immediate benefit on hemodynamic function and symptoms  (e.g. vasodilators and ACE inhibitors)

-Other drugs that slow disease progression can adversely affect hemodynamic function and worsen symptoms in the short term. Thus, they must be used with caution (e.g. B-blockers)

A vasodilator’s more prominent effect may be to reduce either preload or afterload. However most agents affect both.

Diagnosis of Congestive Heart Failure:

1. Echocardiogram which measures the Ejection fraction (Ef)

-Ef represents the volumetric fraction of blood pumped out of the ventricle (heart) with each heart beat

E_f = \frac{SV}{EDV} = \frac{EDV - ESV}{EDV}

2. Chest radiography 

-Will show Cardiomegaly (Cardiothoracic Ratio/CTR >50% abnormal)

Definition of Cardiothoracic ratio (CTR) which measures heart size= Cardiac Width : Thoracic Width

3. Electrocardiography (Abnormality in most patients). Abnormalities in Q waves, ST/T wave changes, Left Ventricle hypertrophy, conduction disturbance and arrhythmias.

4. Ambulatory ECG (detects arrhythmias)

5. Blood tests (For detection of anemia and renal function assessment)

-Thyroid dysfunction (hyperthyroidism)  may also cause heart failure so thyroid function tests are conducted as well.

6. Radionuclide imaging

-A method of assessing ventricular function and is useful when adequate Echocardiograms are hard to obtain.

7. Cardiac catheterisation 

-For rare cases of cardiomyopathy or myocarditis when myocardial biopsy is required

8. Exercise/Stress testing

-Assess the presence of myocardial ischemia and to measure maximum oxygen consumption (VO2)

Definition of VO2: Level beyond which oxygen consumption does not rise any further despite increasing levels of exertion (i.e. the limits of aerobic exercise tolerance and is considerably reduced in CHF)

Clinical Presentation/Symptoms of CHF

Depends on various factors:

1. Extent of cardiac damage

2. Extent of Hemodynamic overload

3. Secondary compensating mechanisms that arise as heart failure develops.

4. Rate of progression of the disease and whether secondary compensating mechanisms had time to develop (e.g. acute mitral valve regurgitation may be tolerated poorly compared to slow gradual development)

-Atrial filbrilation occurs in 10-50% of patients with established heart failure and the onset of AF may result in an acute deterioration.

-Ventricular arrhythmias (Ectopics, ventricular tachycardia) are also common.

-Symptoms (non-specific) presented during the early stages: Malaise, lethargy, fatigue, dyspnea, exercise intolerance

***Note: Heart failure may principally affect the left heart, right heart or both sides (biventricular). In practice, left heart is most commonly affected because it has to pump blood to the rest of the body.

  • Isolated Right Heart Failure may be due to major pulmonary embolism, pulmonary hypertension or pulmonary stenosis.
  • However, the ventricles share the interventricular spetum so dysfunction of either ventricle can potentially influence the function of the other

*Left Heart Failure

-Increase in left atrial pressure raises pulmonary venous pressure

-This results in pulmonary congestion and eventually alveolar edema, causing breathlessness, coughing, dyspnea and sometimes hemoptysis (expectoration of blood or of blood-stained sputum from the bronchi)

-Refer to drawing

-As Left Ventricular failure progresses (may occur at rest), orthopnea (breathlessness when lying down) and paroxysmal noctural dyspnea (Sudden acute breathlessness at night) precipitates.

-Symptoms include:

  • Cool and pale skin (indicating peripheral vasoconstriction)
  • Blood pressure may be high, low or normal as cardiac dysfunction worsens
  • Pulse may be low volume and rhythm may be normal or irregular due to ectpics or AF (pulsus alternans-alternative strong and weak beats may occur)
  • Resting sinus tachycardia may occur during severe heart failure or may be partially reflex due to drug-induced vasodilation.
  • Venous pressure is normal in isolated LHF

*Right Heart Failure

  • Symptoms: Minimal especially if diuretics already given.
  • Ankle swelling
  • Dyspnea
  • Reduced exercise capacity and angina pectoris occurs

The reduction in cardiac output in both LHF and RHF will result in low blood perfusion to the brain, kidneys and skeletal muscle. Thus, the general symptoms are mental confusion, tiredness and reduced exercise tolerance.

-The annual overall incidence of stroke or thromboembolism in CHF is 2%.

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