Chapter 22 Cardiac Failure: Causes and Dynamics

Cardiac Failure (Heart Failure)

• A heart condition reduces the ability of the heart to pump enough blood and meet the body's needs
• Decreased myocardial contractility from diminished coronary blood flow is the main cause
• Other causes: damaged heart valves, external heart pressure, vitamin B deficiency, primary cardiac muscle disease, or any abnormality

Circulatory Dynamics in Cardiac Failure

Acute Effects of Moderate Cardiac Failure:

• Sudden heart damage, such as from myocardial infarction, immediately depresses the heart's pumping ability

• Results in:

  • Reduced cardiac output
  • Blood pooling in the veins, increasing venous pressure

• Progressive changes in heart pumping effectiveness occur, seen after acute myocardial infarction

• Normal cardiac output curve illustrates a normal operating point with 5 L/min output and 0 mm Hg right atrial pressure

• After heart damage, cardiac output drops significantly

• Cardiac output falls to 2 L/min and right atrial pressure rises to +4 mm Hg

• A new circulatory state establishes a few seconds after damage.

• This acute stage potentially causes fainting

Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes

• Sympathetic nervous reflexes quickly compensate for the damaged heart
• The reflexes activated include:
  • Baroreceptor reflex from diminished arterial pressure
  • Chemoreceptor reflex
  • Central nervous system ischemic response
• Sympathetic stimulation impacts the heart and peripheral vasculature
• With diffused damage, sympathetic stimulation strengthens musculature
• For non-functional muscles, sympathetic stimulation strengthens normal muscle
• Increases venous return by increasing blood vessel tone
• Significantly raises the mean systemic filling pressure
• Damaged heart becomes primed with inflowing blood
• Right atrial pressure rises and the heart pumps larger quantities

Chronic Stage of Failure: Fluid Retention and Compensated Cardiac Output

• A prolonged semichronic state follows initial minutes of an acute heart attack
• Involves kidney fluid retention and varying degrees of heart recovery over weeks to months
• Renal retention of fluid helps compensate for decreased pumping ability
• Increased blood volume increases venous return:
  • Increasing the mean systemic filling pressure
  • Distending the veins, reducing venous resistance
• With increased venous return, normal cardiac output is possible, even with reduced heart pumping ability
• When the heart's pumping is reduced, the kidneys can't excrete enough salt and water
• Fluid retention increases the workload on the damaged heart, causing severe edema and death

Detrimental Effects of Excess Fluid Retention in Severe Cardiac Failure

• Excessive results in increased workload on the heart
• Overstretching of the heart muscle further weakens the heart
• Filtration of fluid into the lungs, causing pulmonary edema and hypoxia
• Widespread edema development

Recovery of the Heart After Myocardial Infarction

• The body begins natural reparative processes

• A new collateral blood supply penetrates the infarcted area

• Undamaged heart musculature hypertrophies

• The degree of recovery varies from no recovery to near-complete recovery

• Rapid recovery in first days and weeks

Cardiac Output Curve After Partial Recovery

• Shows heart function after an acute myocardial infarction

• Considerable fluid retention in the body and venous return

• The right atrial pressure rises

• The circulation changes to show normal output with elevated right atrial pressure.

• Renal fluid output returns to normal

• Heart recovers, sympathetic stimulation decreases

• Fast pulse rate, cold skin, and pallor gradually disappears

Summary of Changes After Acute Cardiac Failure: Compensated Heart Failure

• Stages of dynamics after acute heart attack:
  • Initial damage
  • Sympathetic nervous system compensation
  • Chronic, partial heart recovery with fluid retention
• Compensated heart failure as the final state

Compensated Heart Failure

• Indicates max pumping ability of recovered heart is less than half-normal
• Increased right atrial pressure maintains cardiac output despite weakness
• Older adults have normal resting cardiac outputs with elevated right atrial pressures
• Cardiac damage is often gradual
• Performing can result in return of acute heart failure symptoms
• Reduced cardiac reserve is caused

Dynamics of Severe Cardiac Failure: Decompensated Heart Failure

• No compensation helps weakened heart pump a normal output, resulting in:
  • Fluid retention
  • Edema
  • Death
• Decompensated is failure to make kidneys remove fluids

Graphic Analysis of Decompensated Heart Failure

• Progressively increasing venous return leads to progressively worsening edema

• Occurs from failure of the cardiac output to maintain renal function

• Failure of cardiac output results in; progressive fluid retention, and elevation of venous pressure, and heart failure

• A serious condition of decompensation principally involves edema

• Dyspnea and lack of therapy at this stage rapidly leads to death

Treatment of Decompensation:

• Stopped by strengthening the heart
• Using cardiotonic drugs,
• Giving diuretic drugs to increase kidney excretion while reducing water and salt intake
• Methods to stop decompensation establish fluid balance

Mechanism of Action of Cardiotonic Drugs

• Little impact on contractile strength in healthy hearts
• Significant strength increase in failing hearts
• Increase calcium ions in muscle fibers
• Act to depress the sodium-calcium exchange pump and raise calcium

Unilateral Left Heart Failure

• Failure of the left side of the heart causes blood to be pumped into the lungs
• Not being adequately pumped out by the left heart into the systemic circulation
• Pulmonary filling pressure rises
• Volume of blood in lungs increases
• Pulmonary capillary pressure increases
• Pulmonary edema results from fluid filtering into alveoli
• Major problems: pulmonary vascular congestion and pulmonary edema
• Death by suffocation

Low-Output Cardiac Failure: Cardiogenic Shock

• The heart is incapable of pumping blood to keep the body alive
• Circulatory shock occurs
• Cardiovascular system deteriorates
• Cardiogenic/cardiac shock is caused by inadequate cardiac pumping
• Survival rate is less than 30%

Vicious Cycle of Cardiac Deterioration in Cardiogenic Shock

• The heart becomes progressively damaged when coronary blood supply is reduced
• Reduced arterial pressure reduces coronary blood supply even more
• For myocardial infarction heart, deterioration begins with major coronary vessel block
• Preventing any periods of hypotension is crucial

Physiology of Cardiogenic Shock Treatment

• Administering digitalis to strengthen the heart
• Infusion of blood, sustaining pressure to prevent deterioration
• Success achieved by removing the clot surgically or infusing clot dissolving enzymes, only within the first hour

Edema in Patients With Cardiac Failure

• Peripheral in acute failure
• Over time, peripheral occurs due to retention that increases blood return
• Long-term fluid retention is caused fluid retention by kidneys and urine output

Long-Term Fluid Retention by the Kidneys Causes Peripheral Edema in Persisting Heart Failure

• Fluid retention increases the mean systemic filling pressure

• Increasing blood return to the heart

• Elevating atrial pressure and arterial pressure

• Capillary pressure and fluid loss occur and severe edema develops

• Reduced renal output of urine during cardiac failure includes decreased glomerular filtration rate caused by reduced arterial pressure with intense sympathetic reduction

• Renin causes kidneys to retain water and activate angiotensin II

• Angiotensin constricts blood vessels which reduces blood flow and also induces more kidney water uptake

• Aldosterone secreted by the adrenal cortex leads to more water uptake

• ADH promotes water reabsorption by kidneys

• Sympathetic also increases alpha receptors which reduce fluids

• Role of natriuretic peptides that increases urine to prevent congestive symptoms

• BNP is often used

Acute Pulmonary Edema in Late-Stage Heart Failure

• Death in those with heart failure:
  • Volume accumulates in lung
  • Lungs and low O2 weaken heart
  • Weak heart sends blood to lungs
  • Eventually patient suffocates
• Cycle reverses with therapy:
  • Tourniquets and lower O2
  • Diuretics to decrease fluid
  • Cardiotonic (digitalis)

Cardiac Reserve

• Cardiac reserve represents the max percentage a heart can pump
• 300% - 400% is health adult max
• 500% - 600% for trained adults
• Zero Cardiac for those with damage in heart
• Prevents heart from pumping blood by disorders (vitamin deficiency, damage, and heart valves_
• Diagnosed with low rates is checked after exercise

Diagnosis of Low Cardiac Reserve (Exercise Test)

• Test occurs on treadmill:
  • Dyspnea causes shortness of breath and limited O2
  • Fatigue increases from muscle O2
  • Heart overreacts to compensate

Quantitative Graphic Analysis of Cardiac Failure

• Qualitative approach with graphics

Graphic Analysis of Acute Heart Failure and Chronic Compensation

• Venous return with curves indicating when the heart is working

• Curves show when circulatory system can operate

• Heart issues drop graph, but O2 intake compensates

• Beriberi and venous drop both cause curves and fluids in the end

• Compensates and the issues of the heart are alleviated through curve drops

Heart Failure with Diastolic Dysfunction and Normal Ejection Fraction

• Focused on cardiac failure for muscle damage/coronary
• Heart can encounter problems pumping blood

High-output cardiac failure

• Curves allow excessive return heart with no depression
• Bribers overloads return with heart capacity