CHF and Cardiomyopathy Reduced Flashcards Preview

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What is heart failure?

The inability of the heart to properly fill or empty the ventricle


What usually causes heart failure?

  1. CAD (collaterals arent enough to feed the heart)
  2. Cardiomyopathy (infectious or ideopathic)
  3. Valve abnormalities (esp mitral and aortic)
  4. HTN (poorly managed or untreated) 
  5. Pericardial diseases
  6. Pulmonary HTN (smoking or lung disease)


Patho - Heart Failure

  1. Pressure overload (Aortic stenosis or HTN)

  2. Volume overload (Mitral or Aortic Regurge)

  3. Myocardial Ischemia/Infarction

  4. inflammatory disease (connective tissue diseases that restrict cardiac filling)

  5. Restricted diastolic filling (Constrictive periicardidits, restrictive myocardiditis)


Explain Adaptive responses to HF

In the failing heart, these mechanisms are initiated to help improve CO:

  • Frank-Starling Relationship
  • SNS activation

(in reaction to decreased SV--> RAAS activated which stimulates SNS to increase HR, SV -->when actually worsens HF)

  • Alterations in contractility, HR, and afterload
  • Humoral responses (heart produces endocrine peptide mediators)
  • When these mechanisms become maladaptive, it leads to myocardial remodeling. (at this point there is no reversal except for transplant)


What is myocardial remodeling?

Changes in

  1. size 
  2. shape
  3. structure
  4. physiology

of the heart after injury to the myocardium


Initially, how does the body  compensate for HF?

Activation of the SNS


Heart failure and activation of SNS

It's an adaptive response to maintain BP and CO

  1. Arteriolar constriction
    • Maintains BP (increases SVR) despite decrease in CO
    • Redirects blood flow to coronary and cerebral systems (shunt to important systems!)
  2. Venous constriction
    • ​​Increase preload - Attempt to increase CO via frank starling
  3. RAAS
    • Activated d/t decrease in RBF from shunting to vital organs and decreased SV
    • Increased blood volume (sodium and water retention) --> increases CO 
  4. HR is increased (trying to increase CO) Eventually this system will poop out because the increase in SVR increases workload


Adaptive mechanisms in heart failure

to increase CO:

  1. Increased contraction velocity
  2. Reduced afterload
  3. Increase HR

to promote BP control and protect from effects of volume and pressure overload:

  1. diuresis
  2. natriuresis
  3. vasodilation
  4. anti-inflammatory
  5. inhibition of RAS and SNS an dcardiac remodeling


Types of Myocardial remodeling - what does it lead to?

  1. Hypertrophy
  2. Dilation and wall thinning
  3. Increased interstitial collagen deposition (leads to ineffective pumping which then leads to fibrosis)
  4. Fibrosis and scar formation

(Remodeling = increased O2 requirements = more at risk for ischemia)


S/S of HF

  1. Dyspnea
    • Orthopnea/ orthopneic cough
    • Paroxysmal noctural dyspnea
  2. Fatigue Weakness at rest
  3. Tachycardia
  4. Oliguria
  5. Edema
  6. Atrial fibrillation due to dilation
  7. Tachypnea
  8. Lung Rales
  9. S3 gallop
  10. Hypotension
  11. JVD


Pharmacologic Management of HF

  1. ACE Inhibitors/ ARBs - Decrease afterload by interfering with RAAS to cause peripheral vasodilation
  2. Aldosterone antagonists - Aldosterone production is increased in HF d/t activation of the RAAS. Causes Na+ retention and K+ excretion. Diuretics - Decrease preload (thiazide and loop)
  3. Digoxin - Increases contractility and treats a-fib
  4. Inotropes - Increase contractility (dobutamine and milrinone)
  5. ß- blockers - Inhibit the SNS. Slow HR and lowers BP. Shown to reverse remodeling.
  6. Vasodilator therapy - Decreases afterload (hydralazine and isosorbide)
  7. Biventricular pacing - improves ventricular function and reverses remodeling
  8. Nesiritide - Synthetic BNP. Decreases preload by stimulating natriuresis, and decreases afterload via vasodilation
  9. Assist devices - IABP / LVAD
  10. Transplant


Patho of Heart failure in a nutshell

  1. Decreased contractility →Ventricle is dilates to increase contractility from stretched muscle fibers
  2. Results in an increased ventricle radius which increases cardiac work
  3. Increased work = increased O2 consumption and demand
  4. CO falls
  5. SNS outflow to increase HR and SVR
  6. SV falls d/t decreased contractility and more fluid, and then repeat the cycle


Heart Failure - Anesthetic management


The goal is to prevent and avoid myocardial depression:

  1. Heart rate  -  normal to elevated
    • keep atropine, glycopyrolate, epherdine handy
  2. Preload  -  normal to high
  3. Afterload  -  low
  4. Contractility - increase
    • consider use of dobutamine or isoprel if needed)

Systolic heart failure: beat the horse (inotropes) and unload the wagon (pharmacologically induced afterload reduction or IABP)


Heart Failure - Anesthetic management


  • ›Maintain medication therapy, esp. beta blockers
  • ›Hypotension treated with ephedrine, phenylephrine, vasopressin
  • ›General anesthetic doses may be decreased
  • ›Positive pressure ventilation beneficial
    • decreases pulmonary congestio & improves oxygenation 
  • ›Regional anesthesia ok
  • ›Avoid fluid overload
  • +/- A-line


What is cardiomyopathy?

Diseases of the myocardium associated with mechanical and/or electrical dysfunction with inappropriate hypertrophy or dilation


Hypertrophic Cardiomyopathy


  1. Asymmetric myocardial hypertrophy (IHHS)
  2. LV outflow tract obstruction caused by 
    • Asymmetric septal hypertrophy (superior hypertropht interferes with valve function) 
    • Systolic anterior movement (SAM) of the mitral valve and resultant mitral regurgitation
  3. Diastolic dysfunction
    • increased LVEDP
  4. Ischemia can occur
  5. Dysrhythmias
  6. Sudden death


S/S of hypertrophic cardiomyopathy

  1. Angina (releved by rest and laying down)
  2. Fatigue
  3. Syncope (cannot maintain SV- happens ezpecially when they are exercising)
  4. Tachydysrhythmias (SVT, a-fib)
  5. HF
  6. Sudden death (in young, healthy, undiagnosed patients)


Treatment of hypertrophic cardiomyopathy

Treat the underlying cause using ß-Blockers or CCBs


Factors that WORSEN the hypertrophic cardiomyopathy outflow obstruction and the pharmacologic implications

  1. Increasing Myocardial Contractility
    • Avoid digoxin
    • Avoid ß-adrenergic stimulation
  2. Decreasing Preload
    • Avoid hypovolemia
    • Avoid vasodilators
    • Avoid tachycardia
    • Avoid positive pressure ventilation
  3. Decreaseng LV afterload
    • ​​Avoid hypotension
    • Avoid vasodilators
    • NO nitrates, digoxin or diuretics!!!!!

(produce decrease ventricular volume that brings the anterior Mitral Valve leaflet closer to the interventricular septum)


 Factors that IMPROVE outflow in hypertrophic cardiomyopathy

  1. Decrease contractility:
    • Beta-adrengeric blockade  
    • Calcium channel blockers (improve diasotolic relaxation as well)
    • Volatile anesthetics - HIGH MAC case!!
  2. Increase preload:
    • 1st line!
    • Hypervolemia
    • Bradycardia
  3. Increase afterload:
    • 2nd line
    • Alpha-adrenergic stimulation (phenylephrine)
    • Hypertension 


Hyperthrophic Cardiomyopathy Anesthetic Management


Anesthetic Goals = avoid SNS stimulation, avoid HYPOtension & maintain SVR - ›Minimize LV outlet obstruction

  1. Maintain preload
  2. Reduce HR & contractility
  3. Maintain normal to high-normal SVR (to counter high ejection velocity)


Hyperthrophic Cardiomyopathy Anesthetic Management


  1. ›Volatile anesthetics good
  2. ›A-line
  3. ›Treat hypotension with alpha adrenergic agonists (phenylephrine) and VOLUME
  4. ›Beta adrenergic agonists are contraindicated
    • due to drug-induced increased contractility and heart rate
    • ex: ephedrine, dopamine, dobutamine
  5. ›Prompt replacement of blood and fluids
    • for maintaining preload and BP

  6. ›Avoid vasodilators
    • due to the decrease in systemic vascular resistance will accenuate LV outflow obstruction

  7. ›Maintain NSR
    • treat arrhythmias promptly


Dialted Cardiomyopathy

›Myocardial disease with:

  • LV or biventricular dilation
  • systemic dysfunction, and
  • normal LV thickness


Dilated Cardiomyopathy anesthetic management


THe goal is to prevent and avoid myocardial depression

  1. High to Normal Heart  Rate
    • ​​HR dependent because of compensatory measures 
  2. High to Normal Preload
    • CVP, Foley, A-line, propper fluid volume calculation
    • replace blood with colloid to keep in vaculature
    • judicious fluids replacement
  3. Low to Normal Afterload
    • low normal is to promote forward flow
  4. Increase Contractility
    • ​​Avoid full 1 MAC, balanced technique with opioids


Core Pulmonale


  • ›Right ventricular enlargement with hypertropy and/or dilation, that may progress to right heart failure
  • ›Caused by pulmonary hypertension and chronic alveolar hypoxia


Cor Pulmonale Anesthetic Mangament GOALS

  1. Oxygenation
  2. Avoid Bronchospasm!
    • NO histamine releasing drugs - morphine, demerol, thiopental, mivacurium, atricurium, curare
    • Keep anesthesia deep to avoid - bronchodilator and less likly to react to stimuli
  3. A-line very useful 
  4. TEE for monitoring RV function
  5. High level block should be avoided - they are dependent on accessory muscles for breathing


Cor Pulmonale - Management

  • ›Eliminate any infection
  • ›Reverse bronchospasm
  • ›Improve expectoration
  • ›Maintain good oxygenation, hydration and lung mechanics
  • ›Correct electrolyte imbalance