Heart Failure (Almendral) - 11/11/16 Flashcards
What is heart failure?
Clinical syndrome of cardiac pump dysfunction → congestion and low perfusion
Heart Failure: signs & symptoms
Signs:
- Rales
- JVD
- Pitting edema
Symptoms:
- Dyspnea
- Orthopnea
- Fatigue
Heart Failure: w/ reduced EF
- Reduced EF
- Inc. EDV
- Due to ↓ contractility
- Myocyte loss
- ↑ fibrosis
- Abnormal systolic function
Heart Failure: w/ preserved EF
- Preserved EF
- Normal EDV
- Impaired diastolic filling:
- ↑ stiffness (passive)
- Impaired relaxation (active)
- Ventricle fills at higher than normal pressures
- ↑↑ diastolic pressures transmitted retrograde to pulmonary and systemic veins –> HF symptoms
Cor pulmonale
Isolated right HF due to primary pulmonary cause
Typically, right HF most often results from left HF
Treatment: HF
- ACE inhibitors
- ARBs
- Beta-blockers (except in acute decompensated HF)
- Spironolactone
- Hydralazine
- Thiazide diuretics
- Loop diuretics
Clinical Manifestations of Left HF (3)
-
Orthopnea
- Shortness of breathe when supine: inc. venous return from redistribution of blood (immediate gravity effect) → exacerbates pulmonary vascular congestion
-
Paroxysmal nocturnal dyspnea
- Breathless awakening from sleep: inc. venous return from redistribution of blood, reabsoprtion of peripheral edema, etc…
-
Pulmonary edema
- Inc. pulmonary venous pressure → pulmonary venous distention and transudation of fluid
- Presence of hemosiderin-laden macrophages (“HF” cells) in lungs
Clinical Manifestations of Right HF (3)
-
Hepatomegaly (nutmeg liver)
- Inc. central venous pressure → inc. resistance to portal flow
- Rarely, leads to cardiac cirrhosis
-
JVD
- Inc. venous pressure
-
Peripheral edema
- Inc. venous pressure → fluid transudation
Major determinants of cardiac output
What are the three major determinants of stroke volume?
CO = HR * SV
SV: Preload, Afterload, Contractility
Preload
Preload = ventricular wall tension at end of diastole
- Just before contraction
-
EDV (used as representation of preload)
- Influenced by chamber’s compliance
Contractility (inotropic state)
Changes in strength of contraction, independent of preload and afterload
Reflects chemical or hormonal influences (e.g., catecholamines) on force of contraction
- ESV (depends on afterload and contractility)
Stroke Volume
Volume of blood ejected from ventricle during systole
SV = EDV-ESV
Ejection Fraction
Fraction of EDV ejected from ventricle during each systolic contraction (normal range = 55%-75%)
EF = SV/EDV
Compliance
Describes pressure-volume relationship during filling
Reflects ease or difficulty with which the chamber can be filled
Change in vol / Change in pressure
Afterload
Afterload = ventricular wall tension during contraction
Force that must be overcome for ventricle to eject its contents (i.e. during aortic stenosis)
- ESV (depends on afterload and contractility)
Right Ventricular Heart Failure
Right Ventricle
- Thin-walled, more compliant
- Accepts wide range of volumes w/o significant changes in filling pressures
- Ejects to low resistance system (pulmonary)
- Not used to high afterload
- Most common cause of RV failure –> LV failure
- Other causes: Lung processes (COPD, PE, PAH, etc)
- Cor pulmonale – if RV failure due to lung process
- Leg edema, abdominal bloating, ascites
Compensatory Mechanisms in HF (4)
- Frank-Starling Mechanism
- Neuro-hormonal activation
- Natriuretic peptides
- Ventricular hypertrophy and remodeling
Frank-Starling Mechanism
Neuro-hormonal Activation
Sympathetic NS
- Fall in CO sensed by baroreceptors in carotid sinus and aortic arch
- ↑ Sympathetic and ↓ parasympathetic output to heart and periphery
- ↑ HR, ↑ contractility, ↑ vasoconstriction
- Regional α – receptor distribution – ↑ Peripheral vasoconstriction – Maintains central perfusion (heart/brain) at expense of skin, splanchnic viscera, kidneys
RAAS
- ↓ CO –> ↓ renal perfusion –> ↑ Renin –>
- Renin cleaves angiotensinogen to AI –> ACE cleaves AI –> AII
- Angiotensin II
- Potent vasoconstrictor ( ↑ SVR)
- Stimulates thirst
- ↑ aldosterone –> ↑ Na retention –> ↑ volume
ADH
- Secreted by posterior pituitary
- Mediated by arterial baroreceptor and AII
- ↑ water retention in distal nephron
Natriuretic Peptides
- ANP and BNP – beneficial hormones
- Response to stretch
- Increases Na and water excretion
- Promotes vasodilatation
- Inhibits renin secretion
- Good but usually not sufficient
Ventricular Remodeling and Hypertrophy
Increased mass of muscle serves as compensatory mec that helps maintain contractile force and counteracts elevated ventricular wall stress
However, b/c of increased stiffness of hypertrophied wall, these benefits come at expense of higher-than-normal diastolic ventricular pressures, which are transmitted to LA and pulmonary vasculature
Management of HF w/ reduced ejection fraction
Treatment of HF w/ reduced EF
- Diuretics
- Water and Na+ elimination
- Dec. diastolic volume –> dec. congestion
- Loop diuretics = MOST potent
- Thiazides - less potent; additive
- Vasodilators
- Venous vasodilators - Nitrates
- Inc. venous capacitance
- Dec. LV preload
- Arteriolar vasodilators - hydralazine, prazosin
- Dec. SVR/afterload
- BP = SVR * CO
- Dec. SVR –> Inc. CO = Inc. BP
- Dec. SVR/afterload
- ACEI
- ARBs
- Inotropes
- Beta-adrenergic agonists
- Dobutamine (beta 1)
- Dopamine
- Digoxin
- Blunts sympathetic drive
- Inhibits Na+/K+ ATPase –> Inc. intracellular Ca2+
- Beta-blockers (-olol)
- Aldosterone antagonists
- Spironolactone, epleronone
- Blunts cardiac fibrosis and remodeling
- Monitor K+ level, side effect
Classification of patients with Acute HF
- Volume overload (i.e. “wet” vs “dry”) –> reflection of elevated LV filling pressures
- “Wet” examples: pulmonary rales, JVD, edema of lower extremities
- Signs of decreased CO with reduced tissue perfusion (“cold” vs “warm” extremities)
Patient A: normal
Patient B & C: acute pulm edema but C is more serious (in addition to congestive findings, impaired forward CO –> marked systemic vasoconstriction… i.e. activation of SNS) and therefore “cold” extremities
Patient L: “cold” extremities due to low output but no signs of vascular congestion
- This profile may arise in patients who are actually volume deplete or those with limited cardiac reserve in absence of volume overload (e.g. a patient with a dilated LV and mitral regurgitation who becomes SOB w/ activity b/c of inability to generate adequate forward CO)
