Heart failure Flashcards
Define Heart Failure
the clinical syndrome that results when the heart cannot adequately pump enough blood to serve the body’s needs while at the same time maintaining normal pressures in the heart chambers and lung vessels
Describe the two major major pathophysiologic types of HF
Systolic heart failure: contractile function of the heart is impaired
• Rarely completely reversible
• If untreated: poor prognosis, progressive disease
• Death due to progressive pump failure or sudden arrhythmic death
• If treated: improved or stabilized for long time
Heart failure with preserved ejection fraction: multifactorial disease, relaxation of the heart is often impaired
Causes and prevention of HF
o Commonly ischemic heart disease and HT o Any heart abnormality can result in heart failure: • Idiopathic dilated cardiomyopathy • Inflammatory heart disease • Restrictive cardiomyopathy • Extramyocardial cardiomyopathy • Secondary cardiomyopathy • Hypertrophic cardiomyopathy
Prevention:
o Aggressive HT and atherosclerotic treatment
Pathophysiology of HF
Myocardial injury → muscle gets weak
• Hemodynamic abnormalities = Symptoms & Disease progression
• Neurohormonal activation and remodeling = Direct myocardial effects, Disease progression, Death
• Genetic abnormalities (Sarcomere proteins, Cytoskeletal proteins, Calcium handling)
o Most often asymptomatic patients due to compensatory mechanisms:
o Goals: maintain stroke volume and Systolic BP
• Uses mechanisms designed for acute decreases in CO or peripheral resistance
• Over time (with chronic HF) = detrimental
o Results: vasoconstriction and fluid retention
o Three compensatory mechanisms:
1) Frank-Starling mechanism
2) Myocardial remodeling
3) Neurohumoral activation
o Over time → decompensation
• Unable to maintain both volume and perfusion → symptoms
Result: progressive cardiac dysfunction
• Fluid overload
• Symptoms due to salt and fluid retention
• Pressures in heart and lungs elevated
• Vasoconstriction → impaired tissue perfusion
o Late stages = fatigue
Frank-Starling mechanism in HF
Increased preload → increased cardiac contractility/ strok volume (normal heart)
• With LV dysfunction → flattening of curve, lower EF
o Decreased SV with increased preload
Result: altered state of contractility
Normal heart with exercise:
o Increased sympathetic NS activation: (B1 binding)
• Increased depolarization of autonomic SA node cells → increased HR
• Increased preload
• Increased Ca2+ influx
• Increased force of contraction
o Result: increased CO (hops to new Frank-Starling curve)
HF with exercise:
o With contractile dysfunction → decreased CO
• Rightward and downward shift of curve
o At rest, sympathetic NS activated
o Under stress, little ability to increase further
o Also, decreased adrenergic responsiveness:
• Downregulation of B1 receptors
• Uncoupling of receptors from intracellular messenger systems
o Decreased ability to increase stroke volume against higher afterload
o Result: inability to increase contractility normally
Myocardial remodeling in HF
- Increase mass of cardiac tissue
* Raises arterial resistance
Neurohumoral activation in HF
- Improve cardiac contractility
- Retain fluid
- Vasoconstriction to maintain perfusion
Factors leading to decompensation of chronic HF
- Discontinuation of therapy
- Start meds that worsen HF or renal function (NSAIDs, steroids, thiazolidnediones)
- Dietary indiscretion (fluid or salt)
- Alcohol
- Arrhythmias
- Fever or infection
- Myocardial ischemia or infarction
- Worsening HT
- Anemia
Treating HF
Vasodilation to move fluid forward out of venous system into arteries
Drugs: to prevent worsening of LV function, arrhythmias and sudden cardiac death, make people feel better, live longer
• ACE inhibitors and ARBs
• Beta blockers
• Aldosterone blockers
• (a combination of diuretics, vasodilators, and neurohormonal blocking agents best)
Devices
• Monitor and treat ventricular arrhythmias = implantable cardiac defibrillator (ICD)
• Restore electrical and mechanical synchrony to a dyssynchronous heart = resynchronization (biventricular) pacemaker
• Augment LV function = LV assist device (LVAD), an implanted pump that provides added CO
Future: cell and gene therapy
HF disease management in multi-disciplinary team!
Discuss the clinical presentation of heart failure and the underlying cardiac, vascular and renal mechanisms responsible for the symptoms.
Respiratory distress (from increased pulmonary capillary pressures) o Exertional dyspnea o Wheezing o Orthopnea (increased venous return increases pulmonary pressures enough to cause symptoms) o Paroxysmal nocturnal dyspnea o Dyspnea at rest Reduced exercise capacity Symptoms of fluid overload (“right heart failure” = commonly due to LV dysfunction) o Edema o Abdominal bloating o Early satiety o Abdominal discomfort o Solid weight loss (but may be masked by fluid weight) Late stage = symptoms of impaired perfusion o Fatigue o Weakness o Anorexia o Confusion Physical exam findings o Elevated neck veins o Hepatojugular reflex o Edema o Rales (crackles) in lungs o S3
Diagnosis of HF
Diagnose based on accumulation of signs
o Framingham Criteria (2 major or 1 major and 1 minor)
• Imperfect (70% accuracy)
Major criteria • Paroxysmal nocturnal dyspnea • Neck vein distention • Rales • Cardiomegaly • Acute pulmonary edema • S3 gallop • Increased venous pressure (>16 cmH2O) • Positive hepatojugular reflux
Minor criteria • Extremity edema • Night cough • Dyspnea on exertion • Hepatomegaly • Pleural effusion • Vital capacity reduced by 1/3 from normal • Tachycardia (>120 bpm) Major or minor = weight loss > 4.5 kg over 5 days treatment
Effects of RAAS in HF patients
o Highly active in HF o Degree of activation related to disease severity Effects: • Vasoconstriction • Increase Na+ resorption in proximal tubule • Increase sympathetic NS activation • Increase aldosterone • Stimulate thirst centers in brain Acute compensation: • Maintain arterial pressures Long-term detrimental effects: • Cardiac fibrosis and hypertrophy • Subsequent ventricular remodeling • Possible mismatch of ventricular muscle mass and capillary density • Vasoconstriction → increased afterload → ventricular remodeling • Salt and sodium retention Therapy • ACE inhibitors benefit HF patients • Reduces HF mortality by 30% • Leads to reverse remodeling of heart o Smaller size o More ellipsoid shape o Contractility improves • Ex. Captopril, enalapril, lisinopril, ramipril, quinapril
Differentiate the beneficial short-term effects of neurohormonal compensatory mechanisms from the detrimental long-term effects in HF.
Sympathetic Nervous system (norepinephrine)
o Highly activated in HF
o Degree of activation related to disease severity
Effects:
• Increased HR
• Increased contractile force (positive inotropy)
• Activation of renin-angiotensin system → vasoconstriction
• Net effect = arterial vasoconstriction
• Renal sodium and water retention
• Increased renin release
o Acute compensation
• Increases CO via increased HR and increased contractility
Long-term detrimental effects:
• Increased ventricular remodeling
• Vasoconstriction → increased afterload → ventricular remodeling
• Myocyte damage and death
• Salt and water retention
Therapy:
• Beta blockers = reduce mortality by 35-40%
• Improve remodeling and contractile functioning
• Effective: carvedilol, metroprolol succinate, bisoprolol
Aldosterone system in HF patients
o Increased levels in HF
o Degree of activation related to disease severity
Effects:
• CV: cardiac fibrosis
• Vascular: vascular fibrosis
• Renal: sodium reabsorption in distal tubule
Acute compensation
• Increases plasma volume to maintain BP
Long-term detrimental effects:
• Increased cardiac stiffness
• Worsened diastolic and systolic function
• Adverse remodeling
• Increased vascular stiffness → increased afterload
• “Aldosterone escape” contributes to volume retention, increasing heart/vascular stiffness
• Normal decreases in aldosterone with increase body water are blunted in HF
• Neurohormonal activation in HF → proximal tubular NA+ reabsorption → decreased Na+ delivery to distal tubule
Therapy
• Aldosterone receptor blockers → reduced mortality in patients with moderate to severe HF and those with systolic dysfunction after MI
• Side effect: hyperkalemia
• Ex. Spironolactone, eplerenone
Natriuretic peptides in HF
o Small peptide secreted by heart in response to increased chamber pressure and wall stress
o Subtypes = ANP, BNP
• Elevated levels in HF
• Degree of elevation correlates with severity HF
• DO measure BNP routinely
Effects:
• No known cardiac effects
• Vasodilation
• Decreased vascular fibrosis and hypertrophy
• Decreased vascular stiffness
• Decreased Na+ reabsorption in proximal tubule = “natriuresis”
• Water follows Na+ → mild diuresis
Therapy
• IV BNP can be given to increase vasodilation and relieve symptoms in decompensated HF patients
• Naturally elevated amounts in HF not enough to counteract vasoconstriction
• Monitor blood levels of BNP to help determine if dyspnea due to HF
• Levels of BNP fall with effective therapy
• Lowest achievable level gives prognostic info
• Imperfect test (false positives and false negatives)
