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 (collaerals 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

Forms of ventricular dysfunction

Answer 3

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

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 size, shape, structure and 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

Why does the body activate the SNS in HF?

Answer 7

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

Question 8

Adaptive mechanisms in heart failure to increase CO

Answer 8

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

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
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

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. 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

Question 12

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

Answer 12

Heart failure

Question 13

Patho of Heart failure in a nutshell

Answer 13

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 14

What is cardiomyopathy?

Answer 14

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

Question 15

Manifestations of Hypertrophic Cardiomyopathy

Answer 15

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

Question 16

S/S of hypertrophic cardiomyopathy

Answer 16

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)

Question 17

Treatment of hypertrophic cardiomyopathy

Answer 17

Treat the underlying cause using ß-Blockers or CCBs

Question 18

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

Answer 18

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 19

Factors that IMPROVE outflow in hypertrophic cardiomyopathy

Answer 19

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 20

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

Answer 20

They have dilated cardiomyopathy

Question 21

What do the ventricles look like in dilated cardiomyopathy?

Answer 21

Large, dilated chambers with normal LV thickness

Question 22

What are two examples of high-output HF

Answer 22

1. Pregnancy
2. anemia

Question 23

pathophysiologic manifestations of Heart failure

Answer 23

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 24

Explain the Frank-Starling relationship - what do the curves mean?

Answer 24

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)

Question 25

Explain the role of natriuretic peptide in Heart failure

Answer 25

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

Question 26

Myocardial remodeling

Answer 26

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

Question 27

Tests to diagnose Heart failure

Answer 27

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

Question 28

What does orthopnea really indicate physiologically?

Answer 28

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

Question 29

Anesthetic Management of Heart failure

Answer 29

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

Question 30

Other management considerations in HF

Answer 30

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

Question 31

Types of cardiomyopathy

Answer 31

1. Hypertrophic 2. Myocarditis 3. Peripartum 4. Toxic myopathies (ETOH, cocaine, chemo) 5. Dialated cardiomyopathy 6. Sarcoidosis - from inflammation 7. Acromegaly (endocrine)

Question 32

What is thought to be the root cause of hypertrophic CM? Who does it typically occur in?

Answer 32

1. Ca++ channel abnormalities (symptoms typically seen in young children during exertion. Often leads to sudden death).

Question 33

Explain Cor pulmonale

Answer 33

1. **RV enlargement** with either hypertrophy and/or dilation 2. May progress to **right HF** 3. Typically caused by **pulm HTN** and **chronic alveolar hypoxia** (long standing lung disease such as COPD)

Question 34

Pharmacologic therepies that decreases afterload - and MOA

Answer 34

1. **ACE-I and ARBS** - interfere with RAAS which results in peripheral vasodilation 2. **Vasodilators** - hydralzine and Isosorbide - arterial dilation \> venous

Question 35

Heart failure pharmacologic therapy that decreases preload

Answer 35

1. Aldosterone antagonists - decrease fluid volume 2. Diuretics - also decrease fluid volume 3. Nesiritide- decreases both preload and afterload by stimulating diuresis

Question 36

Effects of Isopril with nitroglycerine

Answer 36

Increase in HR and decrease in SVT - will maintain forward flow (good for heart failure)

Question 37

Hypertrophic Cardiomyopaty anesthestic management **GOALS**

Answer 37

Goal is to minimize LV outfolwo obstruction and have minimal effects on preload and afterload 1. **Maintain Heart Rate** * ß-blockers - counteract SNS activation w/DVL 2. **Keep in a NSR** - but may see a-fib 3. **Increased Preload** * ​​Give fluids! #1 4. **Increase Afterload** * ​​Pure Vasoconstrictors #2 (phenylephrine)

Question 38

Dilated Cardiomyopathy anesthetic management **GOALS**

Answer 38

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 39

Cor Pulmonale Anesthetic Mangament **GOALS**

Answer 39

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