cardiac failure - wordpress.comby the end of lecture student should be able to : define cardiac...
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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.
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