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CHF & cardiac remodelling Flashcards

1
Q

Furosemide MOA

A

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
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2
Q

Frank-Starling curve

A

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

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3
Q

Ejection fraction

A

EF = SV/end-diastolic volume

usually 50-75%

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4
Q

Pressure-volume loops for cardiac cycle

A

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

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5
Q

Effect of preload on P-V curve

A

Increase in preload = increase in SV (longer a-b, but also higher slope as pressure increases)

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6
Q

Effect of afterload on P-V curve

A

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)

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7
Q

Effect of contractility on P-V curve

A

Slope of ESPVR line
Increased contractility - increased slope
Increase in contractility –> higher SV, lower ESV

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8
Q

Compensatory response to low CO

A 
Raise HR (reflex tachycardia)
Neurohormonal activation via RAAS and SNS
Ventricular remodelling (concentric for higher pressure, eccentric for higher volume)
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9
Q

Cardiac hypertrophy incidence

A

15% of popn
50% popn with moderate HTN
90% popn with CV disease

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10
Q

Concentric hypertrophy

A 
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%
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11
Q

Eccentric hypertrophy

A 
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%
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12
Q

Qualitative compensation due to increased myocardial workload

A 
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
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13
Q

Pathological hypertrophy

A 
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
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14
Q

Heart failure definition

A

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.

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15
Q

Mechanisms of heart failure

A

Low preload
High afterload
Reduced contractility
Neurohormonal

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16
Q

Neural response to low CO

A

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

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17
Q

Hormonal response to low CO

A

•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)

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18
Q

Sx of L-sided HF

A

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

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19
Q

Sx of R-sided HF

A

Right upper quadrant discomfort (liver engorgement, edema within GI tract –> anorexia and nausea)
peripheral edema

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20
Q

Physical signs of HF

A 
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
21
Q

Lab tests for HF

A

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

22
Q

Causes of R-sided HF

A 
L failure
Pulmonic valve stenosis
R ventricular infarct
parenchymal pulmonary disease
pulmonary vascular disease
23
Q

Causes of L-sided HF

A

Loss of contractility (MI, MR, AoR, pathological hypertrophy)
excessive afterload
impaired diastole

24
Q

Systolic dysfunction

A

Volume buildup in ventricle - elevated pressure

increased back pressure, pulmonary congestion, low CO

25
Q

Diastolic dysfunction

A

impaired relaxation (secondary to LVH, ischemia, cardiomyopathies)
filling at higher P
back pressure
impaired filling due to obstruction –> no filling –> low SV –> failure

26
Q

Acute heart failure

A
  • 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
27
Q

Chronic heart failure

A
  • 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
28
Q

Complications of L-sided HF

A

Pulmonary edema
Renal perfusion drop
Brain - hypoxic encephalopathy, coma
Reduced CO - infarct/ischemia

29
Q

Complications of R-sided HF

A 
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
30
Q

Tx of acute HF

A

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

31
Q

Tx of chronic HF

A

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
32
Q

Benefits of cardiac rehab (exercise)

A

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

33
Q

Risks of exercise

A

Reduce “rate pressure product” = HR x SBP
Acutely increase risk of a medical event
- vigorous exercise (increase SNS, decrease vagal, increase max VO2) –> ischemia

34
Q

VO2 max

A

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

35
Q

Lactic threshold

A

lactate production > metabolism (>40% max VO2 in normal individuals)

36
Q

Metabolic equivalents

A

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

37
Q

Inotrope and pressor types

A

Dopamine, dobutamine, epi, norepi

38
Q

Inotrope/pressor MOA and indication

A

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

39
Q

Morphine (CHF) MOA and indiactions

A

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

40
Q

Diuretic use in HF

A

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)
41
Q

Nitrate use in HF

A

acute and chronic HF
improve pulmonary congestion
same adverse effect as diuretics

42
Q

ACEi in HF

A

Chronic CHF only
reduce pulmonary congestion, remodelling, reduce HF symptoms
CI: pregnancy, renal dysfunction
adverse effect: dry cough, hyperkalemia, hypotension, renal dysfunction, angioedema

43
Q

ARB for HF

A

chronic HF
Indiations: 2nd line after ACEi
CI: pregnancy

44
Q

b-blocker for HF

A

Chronic CHF
Effect: paradoxically improve CO - reduce hemodynamic deterioration, improve survival
CI: ACUTE HF, asthma

45
Q

Medical management of acute HF

A

diuretic, morphine, NTG, inotropes

NOT b-blockers, ACEi

46
Q

Medical management of chronic HF

A

ACEi, b-blocker, diuretic, digoxin

47
Q

ACC/AHA classification of HF

A

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

48
Q

NYHA classification of HF

A

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

CV (16 decks)

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