Heart Failure- Dr. Chintan

- AP (Physiology)

- Dt. 21/11/14

Outline• Physiological Anatomy of circulatory system

• Heart as a pump - Cardiac Cycle

• Cardiac Output

• Intro. To heart failure

• Pathophysiology

• Compensated Heart Failure (Acute/Chronic)

• Decompensated Heart Failure

• Types of Heart Failure

• Edema – peripheral, pulmonary

Inside_Healthy_Heart.mp4

Heart as a pumpRight pump, left pump

Electrical events,mechanical events

The cardiac events that occur from the beginning of oneheartbeat to the beginning of the next are called the cardiaccycle - Each cycle is initiated by spontaneous generation of anaction potential in the sinus node.

AP→ Atria→ A – V bundles→ Ventricles.

AV Delay - .1 sec

Diastole: Period of relaxation – heart fillswith blood.

Systole: Period of contraction – heart pumps the blood.

Cardiac cycleNormal average HR 75 bpm. Duration of each cardiac cycle is 60/75=0.8 sec

Atrial cycle:1. Atrial systole – 0.1 sec2. Atrial diastole – 0.7 sec

Ventricular cycle:Ventricular systole (0.3 sec)1. Isovolumic contraction – 0.05 sec2. Ventricular ejection: rapid ejection – 0.1 sec, slow ejection – 0.15 sec

Ventricular diastole (0.5 sec)1. Protodiastole - 0.04 sec2. Isovolumic relaxation – 0.06 sec3. Rapid passive filling – 0.11 sec4. Reduced filling (diastasis) – 0.19 sec5. Last rapid filling – 0.1 sec

Terminology• EDV – amount of blood remain at the end of diastole

– 130 ml

• ESV - amount of blood remain at the end of systole – 50 ml

• SV – amount of blood ejected by each ventricle per beat(EDV – ESV) – 80 ml

• CO - amount of blood ejected by each ventricle per minute –SV x HR – 5 lit.

• EF - the % proportion of blood in the heart pumped out ofthe heart during a single contraction – SV/EDV X 100= 60 %

Cardiac Output• Cardiac output (CO) = Stroke volume (SV) x Heart Rate

(HR)

• Control of HR

• Autonomic nervous system

• Hormonal (humoral) control

• Control of SV

• Preload (VR, EDV)

• Contractility

• Afterload (PR)

Adaptive mechanisms of the heart to increased load

• Frank - Starling mechanism

• Ventricular hypertrophy

• increased mass of contractile elements → ↑strength of contraction

• Increased sympathetic adrenergic activity

• increased HR, increased contractility

Intro.• Essential functions of the heart

• to cover metabolic needs of body tissue (oxygen,substrates) by adequate blood supply

• to receive all blood coming back from the tissueto the heart

• Essential conditions for fulfilling these functions

• normal structure of the heart

• adequate filling of the heart by blood

Intro.

• Definition - failure of the heart to pump enough blood tosatisfy the needs of the body

• chronic heart failure (CHF), congestive heart failure (CHF),congestive cardiac failure (CCF)

• The cause usually is decreased contractility of themyocardium resulting from diminished coronary blood flow(MI)

• damaged heart valves,• external pressure around the heart,• vitamin B deficiency,• primary cardiac muscle disease (cardiomyopathy)

Heart FailureEtiology

• Primary risk factors– Coronary artery disease (CAD)– Advancing age

• Contributing risk factors – Hypertension– Diabetes– Tobacco use– Obesity– High serum cholesterol– Valvular heart disease– Hypervolemia

Intro.

• Acute – Chronic

• compensated – decompensated

• Forward - backward

• Systolic - diastolic

• Left – right

• Low – high output

• HeartFailureExplained.mp4

Pathophysiology• Reduced force of contraction (↑ preload)

• due to overloading of the ventricle (normal – frank starling low)

• A reduced stroke volume

• Increased ESV is usually caused by reduced contractility.

• Decreased EDV results from impaired ventricular filling – whenthe walls stiffen

• Increased heart rate

• Increased sympathetic activity - increasing coronary perfusionrequirements

• Hypertrophy (↑ afterload)

• increased stiffness and decreased ability to relax during diastole.

Dynamics of the Circulation• Acute Cardiac Failure

• MI

• (1) reduced cardiac output and

• (2) impeding of blood in the veins, resulting inincreased venous pressure

• acute stage usually lasts for only a few seconds,

• because sympathetic nerve reflexes occur immediatelyand compensate for the damaged heart

Compensation for Acute Failure

• circulatory reflexes

• Baroreceptor reflex,

• chemoreceptor reflex,

• CNS ischemic response

• Sympathetic system becomes strongly stimulatedwithin a few seconds – parasympathetic systembecomes reciprocally inhibited

• two major effects on the circulation:

• first on the heart itself,

• second on the peripheral vasculature

Sympathetic stimulation• Normal muscle is strongly stimulated by sympathetic

stimulation - compensating for the nonfunctional muscle

• Sympathetic stimulation also increases venous returnbecause it increases the tone of most of the blood vessels ofthe circulation, especially the veins

• increased filling pressure greatly increases the tendency forblood to flow from the veins back into the heart.

• the damaged heart becomes primed with more inflowingblood than usual - helps the heart to pump larger quantitiesof blood (Frank Starling Law)

Chronic Stage of Failure• A low cardiac output has a profound effect on renal function

causing anuria - Renal Retention of Fluid

• a moderate increase in body fluid and blood volume is animportant factor in helping to compensate by increasing thevenous return

• Severe fluid retention - severe edema – detrimental - canlead to death

• (1) overstretching of the heart, thus weakening the heartstill more;

• (2) filtration of fluid into the lungs, causing pulmonaryedema

Myocardial recovery

Decompensated Heart Failure

• the main cause of decompensated heart failure is failureof the heart to pump sufficient blood to make thekidneys excrete daily the necessary amounts of fluid.

Forward / backward Heart Failure

• Forward failure – poor ventricular contractility –inadequate perfusion

• Fatigue, Weakness, oliguria, hypotension – CNSischemia, ↑ EDV – cardiomegaly

• Backward failure – poor ventricular filling – venouscongestion – ↑ venous pressure – CCF/CHF

• LVF

• RVF

Systolic / Diastolic heart failure• systolic heart failure

• reduced ejection fraction

• left ventricular systolic dysfunction

• poor myocardial contractility

• diastolic heart failure

• preserved ejection fraction

• defective relaxation

• poor ventricular filling

Left Heart Failure• When the left side of the heart fails→ blood continues to be

pumped into the lungs

• it is not pumped adequately out of the lungs by the left heartinto the systemic circulation

• the mean pulmonary filling pressure rises because of shift oflarge volumes of blood from the systemic circulation intothe pulmonary circulation

• pulmonary vascular congestion and pulmonary edema

• Dyspnea, PND, Sputum• LeftSideFailure.mp4

Right Heart Failure• When the right side of the heart fails - ↑ systemic

venous pressure

• Dependent edema – feet, sacral region

• Distended neck veins (↑ JVP)

• Hepato-splenomegaly

• Ascites

• RightSideFailure.mp4

Low Output Cardiac Failure• circulatory shock syndrome caused by inadequate

cardiac pumping is called cardiogenic shock or simplycardiac shock

• the low arterial pressure that occurs during shockreduces the coronary blood supply

• – heart becomes weak

• - arterial pressure fall still more

• - makes the shock still worse

• - eventually becoming a vicious circle

• IHD, HT, valvular-pericardial diseases

High Output Cardiac Failure• Arteriovenous fistula that overloads the heart because

of excessive venous return - pumping capability of theheart is depressed.

• Beriberi, in which the venous return is greatly increasedbecause of diminished systemic vascular resistance -pumping capability of the heart is depressed

• weakening of the heart because of the avitaminosis(mainly lack of thiamine) – peripheral vasodilatation

• Anemia, fever, thyrotoxicosis, A-V malformations

Edema• Acute left heart failure can cause rapid congestion of the

lungs, with development of pulmonary edema and evendeath within minutes to hours.

• Either left or right heart failure is very slow to causeperipheral edema because of fluid retention by the kidneys.

• The retention of fluid increases the mean systemic fillingpressure, resulting in increased tendency for blood to returnto the heart → elevates the right atrial pressure to a stillhigher value and returns the arterial pressure back towardnormal.

• The capillary pressure now also rises markedly, thus causingloss of fluid into the tissues and development of severeedema.

Fluid retention by kidneys• 1. Decreased glomerular filtration.• A decrease in cardiac output has a tendency to reduce the

glomerular pressure in the kidneys because of• (1) reduced arterial pressure• (2) intense sympathetic constriction of the afferent arterioles of

the kidney

• 2. Activation of the renin-angiotensin system• The reduced blood flow to the kidneys causes marked increase in

renin secretion by the kidneys• increased reabsorption of water and salt by the renal tubules

• 3. Increased aldosterone secretion• potassium concentration rises in response to reduced renal

function• ADH secretion – Role of ANP

Acute Pulmonary Edema in Late-Stage

• Pulmonary edema occurs in a person without newcardiac damage - temporary overload of the heart

• heavy exercise, some emotional experience, or severecold

• temporarily increased load on the already weak leftventricle

• → blood begins to dam up in the lungs

• → elevates the pulmonary capillary pressure

• → fluid begins to transude into the lung tissues andalveoli.

Acute Pulmonary Edema in Late-Stage

• increased fluid in the lungs diminishes the degree ofoxygenation of the blood

• → The decreased oxygen in the blood further weakens theheart and also weakens the arterioles everywhere in thebody, thus causing peripheral vasodilation.

• peripheral vasodilation increases venous return of bloodfrom the peripheral circulation still more

• → The increased venous return further increases thedamming of the blood in the lungs,

• → still more transudation of fluid,

• → more arterial oxygen desaturation,

• → more venous return and so forth.