CHF & cardiac remodelling Flashcards
Furosemide MOA
inhibit sodium and chloride reabsorption by competing with Cl for the Na/K/Cl symporter in the ascending limb of the loop of Henle (decrease in intracellular Na, K, Cl)
- also inhibits absorption of sodium and chloride in the proximal & distal tubules)
- increases excretion of calcium, Mg, bicarb, ammonium, phosphate
Frank-Starling curve
SV vs LVEDV/P
curve depends on contractility
increase in LVEDP = increase in SV, to some extent
HF: increase LVEDP in order to increase SV
Ejection fraction
EF = SV/end-diastolic volume
usually 50-75%
Pressure-volume loops for cardiac cycle
a = mitral valve opens (atrial P > ventricular P)
a-b =diastolic filling (slope dependent on compliance)
b = mitral closes
b-c = isovolumetric contraction
c = aortic valve opens
c-d: systolic ejection (vol decreases, but P rises until ventricular relaxation occurs) - pressure at this point = afterload
d = aortic valve closes
d-a = isovolumetric relaxation
b-a = SV
Effect of preload on P-V curve
Increase in preload = increase in SV (longer a-b, but also higher slope as pressure increases)
Effect of afterload on P-V curve
Increase in afterload = longer isovolumetic contraction (need to reach higher P before ejection)
- lower SV, higher ESV
Relationship between afterload and ESV mostly linear (ESPVR)
Effect of contractility on P-V curve
Slope of ESPVR line
Increased contractility - increased slope
Increase in contractility –> higher SV, lower ESV
Compensatory response to low CO
Raise HR (reflex tachycardia) Neurohormonal activation via RAAS and SNS Ventricular remodelling (concentric for higher pressure, eccentric for higher volume)
Cardiac hypertrophy incidence
15% of popn
50% popn with moderate HTN
90% popn with CV disease
Concentric hypertrophy
more relative wall thickness results from P overload increased LV mass increased contractility increased LVEDV (only when dilated) Length increases by 5% X-sectional area increases by 150%
Eccentric hypertrophy
Less relative wall thickness Results from V overload Increased LV mass Decreased contractility Increased LVEDV (when dilated) Length increased by 30% X-sectional area increased by 50%
Qualitative compensation due to increased myocardial workload
Decrease amount of work by SR Ca ATPase Increase contractile proteins Increase glycolysis, decrease FA oxidation Increase cardiac epi/nepi receptors increasing ANP/BNP expression
Pathological hypertrophy
No long term benefit Interstitial fibrosis Fetal gene expression increase Decreased cardiac function over time Associated with heart failure Not reversible, unless HTN treated cardiac work drops significantly after ischemia
Heart failure definition
Inability of the heart to pump blood at sufficient rate (low CO) to meet metabolic demands of the body, or to do so at abnormally high filling pressures, or both.
Mechanisms of heart failure
Low preload
High afterload
Reduced contractility
Neurohormonal
Neural response to low CO
Decreased baroreceptor firing –> increased SNS and decreased PNS
o Increased HR via beta-1 receptors
o Increased ventricular contractility
o Arterial/venous vasoconstriction via alpha receptors (NB, this increases VR too)
o Increase renin release via stimulation of JG beta-1 receptors
Hormonal response to low CO
•RAA Axis: Decreased renal artery perfusion pressure due to reduced CO, decreased salt delivery to macula densa, and stimulation of JG beta-1 receptors by SNS Increased renin secretion from granular cells in JG apparatus Renin converts angiotensinogen to angiotensin I Angiotensin I (via ACE) Angiotensin II
o Vasoconstriction
o Increased intravascular volume by stimulating thirst via hypothalamus, increased aldosterone from adrenal cortex (increased sodium/water resorption at distal convoluted tubule)
o Increased ADH secretion from posterior pituitary – more water resorption by increased water retention in the distal nephron, and systemic vasoconstriction.
Endothelins
Natriuretic peptides - decrease in low CO
o Released in response to increased intracardiac pressure by atrial cells (Mechanoreceptors triggered by stretch, release ANP). Ventricular cells release BNP by the same means.
o Stimulate sodium and water excretion (decreased preload)
o Vasodilation – decreased SVR and increased forward CO (less afterload)
o Inhibition of renin secretion
o Antagonizes effects of angiotensin II (see above)
Sx of L-sided HF
exertional dyspnea - pulmonary congestion & decreased forward flow (compress airway, J receptor –> shallow, rapid breathing), accumulation of lactic acid
Dulled mental status
Decreased urine output and nocturia (renal perfusion at night)
Orthopnea
Paraoxysmal nocturnal dyspnea (severe breathlessness 2-3 hours into sleep)
Hemoptysis - rupture of engorged bronchial veins
Fatigue
Sx of R-sided HF
Right upper quadrant discomfort (liver engorgement, edema within GI tract –> anorexia and nausea)
peripheral edema
Physical signs of HF
Cachexia (frail, wasted appearance) Diaphoresis due to increased SNS Cool extremities Tachypnea Sinus tachycardia Pulsus alternans (alternating strong/weak contractions detected peripherally, sign of advanced ventricular dysfunction) Pulmonary rales: "popping open" of small airways that had been closed off by edema prior to inspiration Coarse rhonchi and wheezing Loud P2 S3 S4 may be heard Mitral regurgitation murmur (valve stretched open) Parasternal RV "heave" Tricuspid regurgitation murmur Elevated JVP Hepatomegaly Edema
Lab tests for HF
When mean LA pressure > 20 mmHg, Kerley B lines
> 25-30 mmHg, alveolar pulmonary edema
CXR: cardiomegaly, cardiothoracic ratio > 0.5, enlargement of azygous veins
Pleural effusions (more common with bilateral failure)
Ventricular function –> echo, radionuclide ventriculography
Sometimes cardiac cath is necessary –> valvular ischemic etiologies
Elevated BNP - LV dysfunction/prognostic marker
Elevated neurohormonal & cytokine stimulation - prognostic marker
Causes of R-sided HF
L failure Pulmonic valve stenosis R ventricular infarct parenchymal pulmonary disease pulmonary vascular disease
Causes of L-sided HF
Loss of contractility (MI, MR, AoR, pathological hypertrophy)
excessive afterload
impaired diastole
Systolic dysfunction
Volume buildup in ventricle - elevated pressure
increased back pressure, pulmonary congestion, low CO
Diastolic dysfunction
impaired relaxation (secondary to LVH, ischemia, cardiomyopathies)
filling at higher P
back pressure
impaired filling due to obstruction –> no filling –> low SV –> failure
Acute heart failure
- Reduced CO
- Decreased tissue perfusion
- Increased pulmonary congestion/peripheral congestion
- Orthopnea/PND
- Cough
- Increasing abdominal girth (ascites)
- Peripheral edema
- Fatigue associated with systolic or diastolic dysfunction, valve dysfunction, cardiac rhythm abnormalities
- Distressed
- Elevated JVP, audible S3, crackles in both fields, tachypnea and tachycardia
- MANAGEMENT DIFFERENT FROM CHRONIC
Chronic heart failure
- Dyspnea
- Orthopnea/PND
- Fatigue
- Weakness
- Exercise Intolerance
- Dependent edema
- Cough
- Weight gain
- Abdominal distension
- Normal HR/RR
- Not distressed
- Nocturia
- Cool extremities
Uncommonly: • Cognitive impairment • Altered mental state from normal • Nausea • Abdominal discomfort • Oliguria • Anorexia • Cyanosis
Complications of L-sided HF
Pulmonary edema
Renal perfusion drop
Brain - hypoxic encephalopathy, coma
Reduced CO - infarct/ischemia
Complications of R-sided HF
Hepatomegaly --> congestion Elevated P in portal vein & tributaries Congestive splenomegaly Chronic bowel edema (ascites) Kidney congestion Brain - hypoxic encephalopathy Pleural/pericardial effusion Sub-Q tissues: peripheral edema
Tx of acute HF
Monitor
o Vital signs
o Close observation of fluid balance
o CVP/Arterial line for Pt who may require pressors/inotropes
Investigations
o Bloodwork: CBC, electrolytes, BUN, Cr, Glucose, Troponin
o CXR
o ECG
Therapy
o Oxygen until hypoxemia corrected – first by FiO2, then CPAP/BiPAP, then intubate
o If below meds don’t work – intraaortic balloon pump
o Medications
Lasix (Loop diuretic)*
Natriuretic Peptides
Nitroglycerin*
Inotropes
Pressors
* indicates contraindicated if hypotensive. NB that the goal of treatment is to reduce preload, pulmonary edema, wall stress, increase CO, and maintain BP
Tx of chronic HF
Investigations – Bloodwork, ECG, CXR, Echo
Management
o Exercise training
o Salt/fluid restriction
o Weight management
o Medications
ACEi (Reduce preload and afterload)
Beta-blockers (Reduce cardiac workload)
ARB (Reduce preload and afterload)
Digoxin (Inotrope, negative chronotrope, anti-arrhythmic)
Nitrates (Reduce preload and some afterload)
Spironolactone (Aldosterone blocker) (Reduce preload)
o Procedures Cardiac Resynchronization Therapy ICD Revascularization if indicated Cardiac transplant
Benefits of cardiac rehab (exercise)
Reduced HR and systolic BP to submaximal heart workload
Increase peak coronary flow
Improvement in CV and pulmonary function
Reduction in CAD risk factors
Changes in systemic circulation during exercise
- increase in systolic BP, decrease SVR, decrease diastolic BP
Risks of exercise
Reduce “rate pressure product” = HR x SBP
Acutely increase risk of a medical event
- vigorous exercise (increase SNS, decrease vagal, increase max VO2) –> ischemia
VO2 max
The maximum about of O2 taken in, transported and used while performing at peak intensity
Fick Equation: VO2= (HRmax × SVmax) × (CaO¬2max × CvO¬2max)
CaO2 = arterial oxygen content
CvO2 = venous oxygen content
Lactic threshold
lactate production > metabolism (>40% max VO2 in normal individuals)
Metabolic equivalents
standard unit to measure oxygen usage during exercise
1 MET = O2 used at rest (3.5 ml O2/kg/min)
3-6 METs - moderate intensity
>6 - vigorous
Inotrope and pressor types
Dopamine, dobutamine, epi, norepi
Inotrope/pressor MOA and indication
beta adrenergic –> increase Ca availability –> increase contractility –> increase SV/CO
alpha –> increase peripheral v/c
Norepi: more on alpha 1
Epi: more on beta 1 and 2
Indications: more useful for patient with systolic ventricular dysfunction
- iv, temporary hemodynamic support for acutely ill, hospitalized patients
Morphine (CHF) MOA and indiactions
release of vasoactive histamine –> peripheral v/d
Sympatholytic (central)
Reduce systemic catecholamines –> decrease HR, BP, contractility
Effect: decrease preload (improve pulmonary congestion), decrease O2 demand, agitation, sense of SOB
Indicated in: acute CHF + pulmonary congestion
Diuretic use in HF
Pulmonary congestion (rales) or edema
Adverse effects: vigorous diuresis --> decrease in CO electrolyte disturbances (hypokalemia) --> arrhythmia Patients with LV diastolic dysfunction, be careful with overdiuresis (need high preload to sustain function)
Nitrate use in HF
acute and chronic HF
improve pulmonary congestion
same adverse effect as diuretics
ACEi in HF
Chronic CHF only
reduce pulmonary congestion, remodelling, reduce HF symptoms
CI: pregnancy, renal dysfunction
adverse effect: dry cough, hyperkalemia, hypotension, renal dysfunction, angioedema
ARB for HF
chronic HF
Indiations: 2nd line after ACEi
CI: pregnancy
b-blocker for HF
Chronic CHF
Effect: paradoxically improve CO - reduce hemodynamic deterioration, improve survival
CI: ACUTE HF, asthma
Medical management of acute HF
diuretic, morphine, NTG, inotropes
NOT b-blockers, ACEi
Medical management of chronic HF
ACEi, b-blocker, diuretic, digoxin
ACC/AHA classification of HF
A. At risk for heart failure but without structural heart disease or symptoms
B. Structural heart disease but without heart failure
C. Structural heart disease with prior or current heart failure symptoms
D. Refractory heart failure requiring specialized interventions
NYHA classification of HF
I. Asymptomatic HF: no symptoms
II. Mild HF: symptomatic with moderate exertion
III. Moderate HF: symptomatic with minimal exertion
IV: Severe HF: symptomatic at rest
