Heart Failure

Heart Failure Overview

Definition

• Heart Failure (HF): Inability of the heart to provide enough blood to meet the oxygen needs of tissues and organs.

  • Impedes on cardiac output (CO)

  • Decreased tissue perfusion

  • Impaired gas exchange

  • Fluid volume imbalances

  • Decreased functional ability

Significance in the U.S.

• Prevalence: Impacts 6.2 million Americans, expected to rise to 8.5 million by 2030.

• Lifetime Risk: 25%, or 1 in 4 adults will develop heart failure (moderate to severe).

• Hospital Admissions: Most common reason for admission to hospital in adults over 65 years.

• Readmissions: Approximately 25% of those hospitalized & discharged are readmitted within 30 days.

  • Insurance wont pay for a second visit within 30 days.

• Mortality Rate: Up to 50% mortality within 5 years after diagnosis.

• Overall: Decreased fitness levels, engage in fewer social actives, more physical complaints.

Learning Objectives

• Understand the significance of heart failure in the United States.

• Identify risk factors for heart failure.

• Define principles of cardiac physiology.

• Describe types of heart failure: right versus left sided, systolic versus diastolic.

• Recognize signs and symptoms of heart failure.

• Anticipate diagnostic studies for evaluation.

• Understand compensatory and counterregulatory mechanisms.

• Distinguish between pharmacologic strategies in heart failure treatment.

• Implement nursing interventions for patients with heart failure.

Etiology and Risk Factors

Primary Causes (Going to lead to HF if not taken care of)

• Uncontrolled Hypertension: Long-term aggressive treatment reduces HF by 50%.

• Coronary Artery Disease (CAD).

• Cardiomyopathy (any condition affecting heart muscle): Genetic components, alcohol and drug abuse (especially methamphetamines).

• Valvular Disorders (stenosis, regurgitation)

Precipitating Causes (HF based off another disease process)

• Anemia: Lack of RBCs, lack of perfusion to tissues & heart will take on more blood and pump faster. See a baseline tachycardia to make up for oxygenation.

• Thyrotoxicosis/hypothyroidism.

• Sleep Apnea: Deoxygenation, develop polycythemia (more RBC production that heart pumps out → HF)

• Pulmonary Embolism (PE): Affect conduction system & changes heart structure

• Endocarditis (inflammation of inner layer of heart muscle): Affect conduction system & changes heart structure

• Dysrhythmias: Affect conduction system & changes heart structure

• Noncompliance with medication

Contributing Causes (Enhance likelihood of developing)

• Diabetes/Metabolic Syndrome.

• Age.

• Diet.

• Smoking → increases HTN.

• Vascular Disease: Reynaud’s, CAD

Cardiac Physiology Principles

Starlings Law of the Heart

• Frank: Strength of ventricular contraction increases when the ventricle is stretched prior to contraction.

  • More stretch = Holds more volume and harder contraction.

• Starling: Increased venous return raises filling pressure of ventricle, leading to increased stroke volume and contraction.

  • More volume = bigger the stroke

• Systole Phase: Blood pumped out of heart (ventricular).

  • Depolarization of electrical conduction.

• Diastole Phase: Heart fills with blood (relaxation).

  • Repolarization of electrical conduction.

Stroke Volume and Cardiac Output

• Stroke Volume (SV): Amount of blood ejected from the ventricle with each contraction/beat.

• Cardiac Output (CO): SV x HR, normal range 4 - 8 L/min.

  • Amount of blood pumped by ventricle in one minute.

  • Normal ventricle holds 150 mL of fluid

• Pumps out 55-65% (usually refers to left ventricle)

Factors Contributing to Cardiac Output

• Preload: Venous blood return to atria.

  • Filling pressure of left and right side of heart

  • Volume affects preload

• Afterload: Force of resistance to open pulmonary/aortic valves.

  • Force of resistance that ventricle generates to open aortic valves.

  • Factors affecting afterload: Strength of the ventricular contraction, blood pressure, and systemic vascular resistance.

• Contractility (Inotropy): Force of ventricular ejection.

• Ejection Fraction: Blood pumped out of the ventricle divided by the amount present prior to systole.

  • Normal range is 55-65%. When given, refers normally to left ventricle.

  • Numbers don’t always correlate with being good depending on the HF type (diastolic HF has a normal range >50%).

    • Looks at left ventricle since left ventricle is bigger than the right ventricle.

    • Don’t look at ejection fraction through atria; filling of atria to ventricles is a passive process as pressure builds up and opens valves, blood fills into ventricle → atrial kick occurs (last contraction of atria pushing out last of blood for vales to close, based off of pressure)

Types of Heart Failure (HF = Heart Failure = Heavy Fluid Buildup)

Classification Systems

1. Side of the Heart Affected?: Left, Right, or Biventricular (related to cardiomyopathy or a long-standing failure of one side that affects the other)?

2. Type of Ventricular Failure:

   • Systolic Heart Failure (HFrEF): Reduced left ventricular EF < 45% (lower number).

     • Affects outward pumping ability → ventricle thins, develops enlarged cavity & it can’t pump with enough force → “Eccentric hypertrophy“

     • Generally what we see with EJ that is reduced.

     • AKA dilated/eccentric CMP

     • Fluid backup into left atrium → fluid leaks into alveoli → pulmonary edema.

       • Smaller and weaker muscles that can’t squeeze hard enough to remove all blood.

     • Hallmark of systolic HF diagnosis: Reduced EF <50%, as low as 5-10% (severe)

   • Diastolic Heart Failure (HFpEF): Preserved left ventricular EF > 50% (normal number).

     • Affects relaxing ability → Ventricle thickens & fills with less blood than normal (<150 mL). Concentric hypertrophy (stiff and noncompliant ventricle).

     • Can’t get enough blood inside & less blood gets to body → blood pushes into noncompliant ventricle.

     • AKA hypertrophic CMP.

       • Stiff ventricle and noncompliant

     • Increased pressure leads to fluid leakage into alveoli → pulmonary edema

       • Causes: HTN, old age, female, diabetes, obesity.

   • Can have a mix of systolic and diastolic heart failure.

Left Sided Heart Failure (Most Common & Oxygenated Side) “Left = Lungs”

• Can be systolic, diastolic, or both (combined).

• Left side pumps out oxygenated blood to the body, while oxygenated blood enters it from lungs.

• Not efficient pumping = fluid buildup in the lungs.

• A condition leading to pulmonary edema (biggest complication for left-sided HF).

  • Increase of vasculature volume inside lungs (changes osmotic pressure from high-low pressure)

    • Increases osmotic pressure and moves through capillaries and into alveoli → leads to cough, sputum, potential crackles in lung, SOB. Risk for respiratory acidosis because CO2 cant move out through fluid → CNS depression → Decreased LOC.

      • Lethargic

    • X-Ray may show a “white out”.

  • Clinical Manifestations: BREATHING PROBLEMS!

  • Left = Lungs.

    • Pulmonary Edema:

      • Cough (frothy/blood-tinged sputum), bilateral crackles or rhonchi, tachypnea, tachycardia, wheezes.

    • Orthopnea (LATE SIGN):

      • SOB when lying flat (add pillows for comfort).

    • Paroxysmal Nocturnal Dyspnea (PND): Episodes of sudden SOB that occurs at night that awakens patient.

    • Nocturia

    • Fatigue and weakness from lack of oxygen.

    • Restlessness/confusion from lack of oxygen.

    • Cyanosis (presents first in lips and nailbed)

    • Fluid Retention: Leads to peripheral edema due to lowered glomerular filtration/impaired kidney function and increased kidney retention of sodium and water (Weight gain > 2 lbs daily = BAD SIGN)

    • Extra Heart Sounds: Gallops (adventitious/abnormal heart sound)

      • S3 = Systolic failure (heard between S1 and S2)

      • S4 = diastolic failure (heard prior to S1 and S2)

  • Causes:

    • HTN

    • MI

    • CAD

    • Old age (especially females)

    • Diabetes

    • Obesity

  • Left sided HF normally leads to right sided HF.

Right Sided Heart Failure (Deoxygenated blood) “Rest of the body”

• Blood backs up into the right atrium and then into the venous system AKA fluid buildup in the body.

  • Can be systolic or diastolic (EJ numbers wont be shown).

• Causes:

  • Mainly left-sided heart failure

  • Valve failure (tricuspid or pulmonic)

  • Right-sided MI

  • Pulmonary embolism

  • Secondary to respiratory problems (cor pulmonale) like COPD, pulmonary hypertension (idiopathic)

Clinical Manifestations

• Dependent Edema: Symmetric pitting edema (EARLY SIGN)

  • Sacral edema (bed bound patients)

  • Weeping edema: Fluid built up in tissues leaks out of skin.

  • Symmetric pitting edema

• Ascites: Abdominal fluid accumulation. (LATE SIGN)

• Anasarca (generalized body edema): Severe edema. (LATE SIGN)

• Anorexia, nausea, and GI Distress.

• Cyanosis of nail beds.

• Hepatomegaly (enlarged liver)

• JVD (EARLY SIGN)

• Weight Gain: > 2 lbs daily = BAD SIGN

Diagnostic Studies

• Echocardiogram: Assesses EF (primarily systolic function), diastolic, size, and valve function.

  • Checks for stenotic valves, regurgitation, blood clots in heart.

  • Normal EJ range is 55-65%. When given, refers normally to left ventricle. Diastolic HF has a normal range >50%.

  • Transthoracic Echo (TTE): US on outside of heart; sees what EJ looks like, blood flow, and wall motion. (Used for ventricles)

  • TEE: Back-side of heart; used when someone had MI and unable to see or valve dysfunction. (Used for valves)

• Chest X-Ray: Looks for cardiac enlargement and vascular markings (edema).

• 12 Lead EKG: Evaluates for dysrhythmias. (Afib, PACs)

• Diagnostic R Heart Cath: Measures right heart pressures.

• Laboratory Tests:

  • BNP levels: Diagnostic if >100 pg/mL for dyspnea caused by HF.

    • More BNP released in response to ventricular stretch.

    • BNP is related to elevated blood volume.

      • May have dyspnea related to pneumonia or pulmonary emboli. In those instances, BNP will be drawn to determine if it’s cardiac etiology leading to dyspnea or pulmonary embolism.

  • Crt/BUN

    • Some medications and hypotension may cause renal impairment.

    • Crt is a direct indicator of kidney function.

    • BUN is an indirect indicator, affected by liver and kidneys.

  • Electrolytes (K, Mag, Na)

    • K and Mag are best friends → worry about both.

      • If potassium needs to be replaced on cardiac unit, give mag first.

    • Diuretics can cause potassium loss.

    • Dilutional hyponatremia: If we have increase in volume, electrolytes become diluted. Sodium primarily affects brain and cognition.

  • LFTs (AST/ALT/Alk Phos)

    • Liver congestion from fluid backup

    • May see more with right-sided HF.

• Trend BNP, potassium, and creatinine labs for HF patient.

Compensatory Mechanisms

*Neurohormonal Responses

1. Renin-Angiotensin-Aldosterone System (RAAS) → “Retains Fluid”:

   • Kidneys response to decreased cardiac output from decreased perfusion. Decreased GFR.

   • Activates SNS to increase BP (vasoconstriction) and HR (tachycardia from increased O2 demand).

   • Aldosterone released → increases sodium and water retention to increase cardiac output/workload. Reabsorbs sodium and water.

   • Aldosterone keeps sodium and water while releasing potassium.

   • Give ACEs and ARBs.

   • Negative Effects on Heart:

     • Increases blood volume.

     • Increases O2 demand of heart.

2. Sympathetic Nervous System Stimulation:

   • Triggered in response to decreased stroke volume, cardiac output, and BP → Increases heart rate, contractility (inotropy), and peripheral vasoconstriction, and cardiac output.

   • Give beta blockers,ACEs (-prils), and CCB)

   • Negative Effects on Heart:

     • Increased oxygen demand → ischemia and arrhythmias or dysrhythmias.

Physiologic Responses

• Hypertrophy: Heart muscle thickens over time, leading to decreased contractility and impaired pumping ability.

  • More muscle = more oxygen demand = decreased contractility (inotropy).

  • More likely to have arrhythmias.

• Dilation: Heart ventricles become thin and overstretched with enlarged cavities, leading to ineffective contraction. “Eccentric hypertrophy”

  • Decreased ejection fraction

    • Negative Effects on Heart:

      • Heart works harder and increases oxygen demand (shift to the right).

• Ventricular Remodeling: Large and stiff structural change that negatively impacts pumping effectiveness and increases risk of arrhythmias and SCD.

Beneficial Counterregulatory Mechanisms

• If counterregulatory mechanisms successful = “compensated heart failure”.

*Natriuretic Peptides (released if increased volume and stretch)

• Released in response to volume and stretch, counteracting RAAS and SNS.

  • Positive Effects:

    • Promotes cardiac vasodilation

    • increases GFR, naturesis, and diuresis.

    • Inhibits renin, aldosterone, and ADH (releases more fluid by inhibiting).

*Nitric Oxide & Prostaglandins (released first)

• Released from vascular endothelium in response to compensatory mechanisms (RAAS and SNS).

• Positive Effects:

  • Causes vasodilation

  • Decreases afterload

  • Relaxes arterial smooth muscle.

Drug Therapy in Heart Failure

• *Inotropes: Modify force of contraction (increase or decrease)

  • Digoxin → causes deep contractions → pushes fluid forward → breathing is easier (no fluid in lungs)

    • Monitor electrolytes (Ca+) and HR

    • Digoxin levels over 2.0 is BAD aka “over 2 is bad for you”

    • Check renal function prior (risk of nephrotoxicity) → over 3.0 means bad kidney

    • If potassium is <3.5 = increased digoxin toxicity

• Beta Blockers: Block SNS (fight response)

  • Monitor HR (hold if <60) and BP

  • Hide hypoglycemia in diabetics

• Vasodilators: Dilate blood vessels.

  • Hydralazine, isosorbide dinitrate (Isodur)

• *Diuretics: Decrease circulating volume and BP by draining fluid; watch for hypotension and hypokalemia.

  • Less fluid circulating = less pressure against the blood vessel walls.

    • Loop Diuretics #1 (most end in “-ide”) → wastes K+

      • Eat green leafy veggies, melons, and avocados, bananas, oranges, blueberries.

    • Thiazide Diuretics (hctz, metolazone) → wastes K+

      • Eat green leafy veggies, melons, and avocados, bananas, oranges, blueberries.

    • Potassium Sparing: Aldosterone antagonist (spironolactone/eplerenone) spare (hold onto) K+ while excreting Na and H2O.

      • Avoid K+ rich foods like green leafy veggies, melons, salt substitutes, and avocados

    • Diuretic Assessment: I&Os, edema, BP, BUN & Crt, HR, skin turgor. May need to be on potassium supplement (never push K+ IV). May need cardiac monitor. Low sodium diet (sodium swells).

• SGLT-2 Inhibitors: Causes osmotic diuresis by increasing urine glucose concentration (as we lose glucose from kidneys into the urine, water will also follow)

  • Watch for dehydration, UTI, and yeast infections (a lot of glucose in urine)

• ACE Inhibitors (not first line unless many symptoms): “-pril”

  • Block RAAS to stop conversion of angio I to II

  • Spares potassium

  • Generally used when EJ drops below 40% and lower BP.

• ARB (not first line unless many symptoms): “-sartan”

  • Block angio II at receptor site.

  • Spares potassium

  • Generally used when EJ drops below 40% and lower BP.

Classification Systems

• ACCF/AHA Stages vs NYHA Functional Classification (doctors use this):

  • Stage A: High risk without heart disease.

  • Stage B: Heart disease present without symptoms.

  • Stage C: Heart disease with prior/current symptoms.

    • Can’t carry out many activities and symptoms present at rest.

    • Classes I, II, III, IV.

  • Stage D: Advanced heart disease requiring specialized treatments.

Interprofessional Care & Patient Education

• Dietary Changes: Fluid and sodium restriction (<2L, <2g), daily weights (report to HCP if weight gain by 2 lbs in one day, 3lbs in two days, or 5lbs in one week) → RULE OF 2s

• Use compression stockings.

• Recognizing Worsening Symptoms: Weight gain by 3 lbs in two days, 2 lbs in one day, or 5 lbs in one week and increasing edema, SOB, or orthopnea (how many pillows do you sleep with?).

• Positioning slowly (orthostatic hypotension from meds).

• Alternate rest periods with activity.

• Oxygen Therapy (Bipap or Cpap) and Tobacco Cessation.

• Avoid NSAIDs due to water retention + any other OTC medication.

• Care Devices:

  • ICD: EJ <35% at risk for SCD. Both a pacemaker and defibrillator. Must sit down for the shock.

  • CRT w/ bi-v pacing

    • Used in severe HF symptomatic pts. Paces both ventricles and improves EF.

  • LVAD:

    • Heart pump supporting failing ventricle and used as a bridge for heart transplant.

Complications of Heart Failure

• Acute Pulmonary Edema: Requires O2 treatment (NC, BiPAP, mechanical ventilation), pt seated in semi to high-fowler’s, legs up if edema, listening to heart/lung (cap refill, MM, pulse ox, apical HR), strict I&Os.

  • Drug Treatment:

    • Furosemide #1 (Lasix)

      • Dries body → decreases K+ → watch for hypokalemia and hypotension → no sodium and needs fluid restriction.

      • Normal urine output is 30mL/hr.

    • NTG

    • Morphine: causes vasodilation

    • Dobutamine, digoxin (positive inotropic effects)

    • Natrecor (nesiritide) IV infusion (human BNP to stop volume from being produced and letting go of volume)

    • WORSENING S/S: persistent productive cough, dyspnea, restlessness, frothy and pink-tinged sputum.