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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)


Forms of ventricular dysfunction

  1. Systolic and diastolic HF
  2. Acute and chronic HF
  3. Left and right sided HF
  4. Low output or high output HF


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


Why does the body activate the SNS in HF?

It's all about maintaining 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


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
  2. Orthopnea/ orthopneic cough -
  3. Paroxysmal noctural dyspnea
  4. Fatigue Weakness at rest
  5. Tachycardia
  6. Oliguria
  7. Edema
  8. Atrial fibrillation due to dilation
  9. Tachypnea
  10. Lung Rales
  11. S3 gallop
  12. Hypotension
  13. 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


The presence of __ is the single most important risk factor for predicting perioperative cardiac morbidity and mortality

Heart failure 


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


What is cardiomyopathy?

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


Manifestations of Hypertrophic Cardiomyopathy

  1. Asymmetric myocardial hypertrophy
  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 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 


What should you assume if your patient has a long-standing history of ETOH abuse?

They have dilated cardiomyopathy


What do the ventricles look like in dilated cardiomyopathy?

Large, dilated chambers with normal LV thickness


What are two examples of high-output HF

  1. Pregnancy
  2. anemia


pathophysiologic manifestations of 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 the Frank-Starling relationship - what do the curves mean?

  1. relationship of an increased SV that will accompany an increased LV end diasotic volume and presure
  2. Up/Left- Good, more stretch, more contractility (early, acute, compensated HF)
  3. Down/Right- Bad, too much/too little stretch leads to decreased contractility (later, decompensated HF)


Explain the role of natriuretic peptide in Heart failure 

  1. To promote BP controll and protect for the effects of VOLUME and PRESSURE overload
  2. 2 types - Brain and Atrial (BNP & ANP)
  3. Promotes: 
    • Diuresis
    • Naturesis
    • Vasodilation
    • Anti- inflammation
    • Inhibition of RAaS, SNS, and cardiac remodeling


Myocardial remodeling

  • Bad. Big, hypertrophied heart (pressure load)
    • results from long term activation of compensatory mechanisms for HF
  • Myocardial dilation, wall thinning (volume load) Interstitial collagen deposition increased (inflammation) 
    • leads to fibrosis/scarring and stiffening of the heart


Tests to diagnose Heart failure

  1. CXR
  2. Elevated BNP
  3. Echo
  4. MRI


What does orthopnea really indicate physiologically?

The inability of the failing LV to andle the increased venous return in the supine position


Anesthetic Management of Heart failure

  1. Normal to high Heart Rate
    • ​​very rate dependent
    • Have Atropine, Ehedrine, and Glycopyrolate ready
  2. Keep in a Normal Sinus Rhythm
  3. Normal to high  Preload
    • to increase folow back to the heart, but dont overload 
  4. Low Afterload
    • Vasodilating agents
    • NTG, Isopril
    • Epi, NE - to increase contractility and decrease afterload
  5. Increase Contractility
    • Epi, NE - to increase contractility and decrease afterload
    • Be very careful of high MAC anesthesia


Other management considerations in HF

  1. Maintain medication regime (esp. BB) unless contraindicated (ACE inhibitors)
  2. Treat hypotension judiciously- ephedrine, phenylephrine, vasopressin are all good
  3. May need to decrease general anesthetic dose→ balanced approach is advised
  4. Positive pressure ventilation beneficial
  5. Regional is ok
  6. Avoid fluid overload, keep track of fluids
  7. +/- A-line