Heart Failure and Cardiomyopathy

Question 1

What is heart failure?

Answer 1

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

Question 2

What usually causes heart failure?

Answer 2

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)

Question 3

Patho - Heart Failure

Answer 3

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)}

Question 4

Explain Adaptive responses to HF

Answer 4

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)

Question 5

What is myocardial remodeling?

Answer 5

Changes in

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

of the heart after injury to the myocardium

Question 6

Initially, how does the body compensate for HF?

Answer 6

Activation of the SNS

Question 7

Heart failure and activation of SNS

Answer 7

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

Question 8

Other adaptive mechanisms in heart failure

Answer 8

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 and cardiac remodeling

Question 9

Types of Myocardial remodeling - what does it lead to?

Answer 9

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)

Question 10

S/S of HF

Answer 10

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

Question 11

Pharmacologic Management of HF

Answer 11

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.
3. Diuretics - Decrease preload (thiazide and loop)
4. Digoxin - Increases contractility and treats a-fib
5. Inotropes - Increase contractility (dobutamine and milrinone)
6. ß- blockers - Inhibit the SNS. Slow HR and lowers BP. Shown to reverse remodeling.
7. Vasodilator therapy - Decreases afterload (hydralazine and isosorbide)
8. Biventricular pacing - improves ventricular function and reverses remodeling
9. Nesiritide - Synthetic BNP. Decreases preload by stimulating natriuresis, and decreases afterload via vasodilation
10. Assist devices - IABP / LVAD
11. Transplant

Question 12

Patho of Heart failure in a nutshell

Answer 12

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

Question 13

Heart Failure - Anesthetic management

Goal

Answer 13

The goal is to prevent and avoid myocardial depression:

1. Heart rate - normal to elevated
   
   • keep atropine, glycopyrolate, ephedrine 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)}

Question 14

Heart Failure - Anesthetic management

Considerations

Answer 14

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

Question 15

What is cardiomyopathy?

Answer 15

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

Question 16

Hypertrophic Cardiomyopathy

Patho

Answer 16

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
6. Sudden death

Question 17

S/S of hypertrophic cardiomyopathy

Answer 17

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

Question 18

Treatment of hypertrophic cardiomyopathy

Answer 18

Treat the underlying cause using ß-Blockers or CCBs

Question 19

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

Answer 19

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)

Question 20

Factors that IMPROVE outflow in hypertrophic cardiomyopathy

Answer 20

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

Question 21

Hyperthrophic Cardiomyopathy Anesthetic Management

Goals

Answer 21

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)

Question 22

Hyperthrophic Cardiomyopathy Anesthetic Management

Considerations

Answer 22

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

Question 23

Dilated Cardiomyopathy

Answer 23

›Myocardial disease with:

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

Question 24

Dilated Cardiomyopathy anesthetic management

GOALS

Answer 24

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

Question 25

Cor Pulmonale

Patho

Answer 25

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

Question 26

Cor Pulmonale Anesthetic Management

GOALS

Answer 26

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

Question 27

Cor Pulmonale - Management

Answer 27

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