Ch.17 - Heart Failure

Basic concepts of heart failure

Heart cannot meet circulatory needs due to ventricle’s inability to pump blood forward

• normal ejection fraction: 50-70%

• HF ejection fraction: less than 40%

NOT cardiac arrest because heart has not stopped

PROGRESSIVE disease with HTN as the #1 risk factor

• other risk factors: MI, CAD, metabolic syndrome, DM

Heart failure with REDUCED ejection fraction (HFrEF)

Ventricles are unable to contract and ability to move blood forward is reduced

• EF: 40% or less

• systolic failure - poor contraction - decreased CO and SV

  • LV backs up into LA, pulmonary veins, pulmonary capillaries, results in pulmonary edema

  • activation of RAAS, SNS, vasoconstriction as compensation, which actually worsens it

• half of HF cases; older men more predisposed to it

• EX: CAD, ischemia heart disease, acute MI

Heart failure with PRESERVED ejection fraction (HFpEF)

Ventricle cannot relax and fill properly because it cannot expand easily

• EF: 50% or more - amount of blood pumped out is actually normal because the squeezing is not a problem, it’s the filling that’s the problem

• diastolic failure - decreased elasticity, stiff ventricles

• half of HF cases, women more predisposed

• long standing HTN, atrial dysrhythmias, anemia, COPD

Factors of heart function

Cardiac output: amount of blood pumped by LV/min (HR x SV = approx. 5 L/min at rest)

Cardiac index: cardiac output/body surface area (larger person needs more blood flow than smaller person)

Preload: amount of blood filled in both ventricles per beat (THINK STRETCH)

• EDV: end diastolic volume - amount of blood in ventricle when filling is complete

• more blood returns to heart → more ventricular filling → increased EDV, SV

Afterload: resistance the ventricles must overcome to eject blood; increased afterload reduces cardiac output (THINK SQUEEZE)

• L side: PVR comes from systemic circulation (HTN)

• R side: PVR comes from pulmonary circulation (pulmonary HTN)

Contractility: force of contraction independent of preload

• SNS activation increases contractility

• high afterload decreases contractility - heart gives up, reduced EF

Pathophysiology of HF

1. Weakened heart cannot adequately pump excess fluid d/t increased fluid volume/overload)

2. increased preload fills heart (volume overload is hallmark sign of HF, AEB weight gain, decreased urine output)

3. ventricular filling becomes impaired

4. excess filling overtaxes ventricular fibers

5. leads to decreased contractility, SV, CO

• AKA heart cannot move blood forward and the amount of blood being pushed into circulation decreases

HF and capillary hydrostatic pressure

Fluid retention and “back up” in HF can increase hydrostatic pressure at capillaries, increasing risk of edema

• Hydrostatic pressure: forces fluid from ECF to ICF

Causes of HF

• Ischemia heart disease: heart muscle doesn’t receive enough oxygen and heart tissue is weak and unable to generate adequate pressure

  • repeated ischemia creates greater zone of ischemia, cells are less preserved

• HTN leading to LVH: coronary circulation unable to meet demands of hypertrophied tissue

  • hypertrophic cardiomyopathy: heart muscle becomes thick (enlarged LV), so less filling space

    • this can be genetic - think young soccer player that just dies on field

Causes of HF - Cor pulmonale

Right sided HF due to pulmonary issues

• EX: COPD → hypoxia → pulmonary artery vasoconstriction → increased workload on RV

  • afterload is increased for RV as it has to work harder to pump blood into pulm. circuit

Causes of HF - Cardiomyopathies

• Ischemic: myocardial muscle stiffening and scarring of heart

• Dilated: enlargement of ventricles (think stretched hair band)

• Restrictive: rigid muscles that do not pump blood forward (no stretch)

• Hypertrophic: usually LV enlarged, interferes with ejection of blood (afterload)

  • primary: genetic (HCM)

  • secondary: due to HTN

Causes of HF - Dysrhythmias, Cardiac infection, Pulmonary embolism

• Dysrhythmias: irregular heart rhythms may precipitate failure

• Cardiac infection: endocarditis, myocarditis

• Pulmonary embolism: acute RV failure due to increased pulmonary artery pressure

Causes of HF - heart valve abnormalities

• Mitral regurgitation (insufficiency) - leaky

  • valve does not close properly

  • backward flow into LA

  • decreased blood ejected from LV

• Aortic stenosis - stiff

  • LV must generate more pressure to eject blood (increased afterload)

  • LVH develops

  • LV failute

Acute vs. Chronic HF

• Acute: rapid, sudden development of HF

  • from substantial ventricular muscle injury (MI)

  • sudden, severe shock (cardiogenic shock: heart cannot pump enough blood to supply the body’s organs)

• Chronic: gradual weakening of heart

  • from HTN, more common

Systolic vs. Diastolic Dysfunction HF

• Normal: ventricles fill normally with blood

• Systolic: weak, distended LV cannot pump blood forward

• Diastolic: stiff, nonelastic LV with less filling of blood

High output vs. Low output HF

• High output: heart cannot meet high circulatory needs d/t high metabolic demand

  • uncommon

  • presents in thyrotoxicosis (excess thyroid hormone) and severe anemia (not enough hemoglobin to carry oxygen so heart pumps more blood to compensate

• Low output: heart cannot pump enough blood to meet body’s need even when metabolic demand is normal

  • impaired venous return AKA heart is not getting filled up

  • EX: blood loss from severe leg trauma preventing blood return

Heart failure classifications: forward and backward effects

• Forward effects: heart cannot pump enough blood forward to meet body’s needs; decreased pressure and tissue perfusion

  • body needs oxygen

• Backward effects: backup of hydrostatic pressure due to heart’s failure to eject blood; fluid build up

Left ventricular failure (LVF) overview

• Diastolic: can’t fill as LV is stiff; LVH due to HTN

• Systolic: can’t eject; MI, heart damage

• Forward effects: decreased perfusion - weakened pulse, cool extremities, sluggish GI tract/hypoactive bowel sounds

  • SNS activated: HR increases, contractility goes up, vasoconstriction

  • RAAS activated: retaining fluid due to decreased perfusion (kidneys don’t know any better)

• Backward effects: hydrostatic backup to LA, pulmonary capillaries

  • pulmonary edema - crackles causing impaired O2 exchange

  • orthopnea - difficulty breathing lying down, need pillows

  • paroxysmal nocturnal dyspnea (PND) - fluid accumulates in lungs while supine, pt reports night terrors that suddenly wake them up

  • pink frothy sputum

  • reduced activity tolerance with RR high, O2 sat low

Pathophysiology of LVF

LV starts to fail, activation and cycling of RAAS due to poor renal perfusion

Results in:

• increased vasoconstriction (angiotensin II)

• increased blood volume (aldosterone)

• increases resistance against LV (increased afterload)

• ventricular remodeling - becomes thicker, enlarged

LV fails, further fueling these responses

Cerebral and Constitutional symptoms of LVF

• Cerebral: takes time to develop, confusion, memory loss, anxiety

• Constitutional: decreased blood flow to GI tract, muscle weakness, poor urinary output, cold and pale extremities

Why is it bad to increase BP with LVF?

Increasing BP makes the LV work harder

• high bp = higher afterload (heart has to push harder to overcome increased pressure)

• LV is already struggling, so with high BP, heart has to work harder

Right ventricular failure

RV cannot pump blood effectively into lungs, so it backs up into RA, SVC/IVC, body

• Backward effects are most significant

  • JVD (jugular vein distention)

  • increased central venous pressure = increased pressure going to head

  • hepatomegaly, splenomegaly, ascities

    • can potentially elicit JVD by placing firm pressure on liver

  • venous congestion of GI tract causing anorexia, nausea

• Hypoxia and cyanosis may develop because blood is not moving to pulmonary circuit for oxygenation

• Peripheral edema

Biventricular failure

• dysfunction in one heart chamber affects other chambers

• pts most often present with failure of both sides of heart, starting with one, then the other

• SXS of both right and left side failure are normally present - lungs and body

HF: lab and diagnostic studies

• elevated BNP because of ventricles stretching

• diluted electrolytes due to fluid retention - hyponatremia

• chest x-ray (quick) - determines if problem is cardiac or respiratory

  • cardiomegaly

  • vascular congestion in pulmonary fields

• ECG - nonspecific, can have enlarged QRS, ST elevation

• echocardiogram - GOLD standard, estimates LVEF, size of heart chambers, valve disorders

  • expected EF = 50-70%

  • less than 40% EF = LVF

HF Treatment

• low sodium diet

• diuretics - can lead to hypokalemia

• ACE inhibitors to block RAAS (angiotensin I converting to angiotensin II)

  • more vasodilation, less aldosterone

• Beta blockers - decrease HR, vasodilation

• positive ionotropic agents - increase strength of heart’s contraction (digoxin, dopamine, dobutamine)

• negative chronotropic agents - decrease HR (digoxin)

• positive chronotropic agents - increase HR (dopamine, dobutamine)

Ionotropic vs. Chronotropic agents

• Ionotropic: changes force of contraction

• Calcium and SNS activation - positive ionotropic agents

• Digitalis (digoxin) - positive ionotropic agent AND negative chronotropic agent

  • increase contractility, decrease HR

  • HOLD if apical pulse <60 bpm

  • evaluate potassium levels because it can cause digitalis toxicity as they both bind to the same receptors

Devices and cardiac transplants for HF treatment

• Left ventricular assist device (LVAD) - enhances LV ejection and helps pump blood into aorta

• Intra-aortic balloon pump - inserted into thoracic aorta, helps facilitate adequate coronary flow

• Heart transplant may be needed for end stage HF

Forward vs. Backward effect for LVF EXAMPLES

Forward (perfusion)

• reduced peripheral pulses

• hypotension

• decreased ejection fraction

Backward

• sleeping propped up on several pillows

• pulmonary edema

• crackles