HEART FAILURE, CARDIOMYOPATHIES Flashcards

1
Q

HF definition

A

inability of the heart to fill with or eject blood at a rate appropriate to meet tissue requirements

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2
Q

s/s HF

A

dyspnea
fatigue
s/s circulatory congestion OR s/s end-organ hypoperfusion

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3
Q

causes of HF

A
  • impaired myocardial contractility
  • cardiac valve abnormalities
  • systemic HTN
  • pericardial diseases
  • pulmonary HTN (cor pulmonale)
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4
Q

systolic vs. diastolic HF

A
systolic = decreased ventricular systolic wall motion
diastolic = abnormal ventricular relaxation & reduced compliance
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5
Q

acute vs. chronic HF

A

acute = change in the s/s HF that requires emergency therapy (hypotension)

  • worsening chronic HF
  • new onset HF (ie valve rupture, MI, severe HTN)
  • terminal HF (refractory to therapy)

chronic = long-standing cardiac disease; venous congestion, but BP is maintained

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6
Q

left vs. right HF

A

left = high LVEDP –> pulmonary congestion

right = high RVEDP –> systemic congestion (usually a product of LVF)

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7
Q

compensatory mechanisms to HF to help maintain a normal CO

A
  • frank starling relationship
  • SNS activation
  • alterations of inotropy, HR, afterload
  • humoral-mediated responses
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8
Q

preoperative evaluation & management of the pt w HF

A

HF = single most important risk factor for predicting perioperative cardiac morbidity & mortality
- all precipitating factors should be noted & aggressively treated pre-op

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9
Q

intraoperative management of pt w/ HF (not IHSS)

A

High/normal HR, high/normal preload, low afterload, increase contractility

  • opioids
  • PPV (decrease pulmonary congestion)
  • art line
  • CVP +/- or PA cath
  • TEE
  • regional = usually helpful bc decreases SVR, but can also be unpredictable/hard to control
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10
Q

hypertrophic cardiomyopathy: definition & pathophysiology

A

def = LV hypertrophy in absence of other cardiac disease

  • myocardial hypertrophy
  • LV outflow tract obstruction (assymetrical hypertrophy, anterior movement of the MV & MR)
  • diastolic dysfunction
  • myocardial ischemia
  • dysrhythmias
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11
Q

hypertrophic cardiomyopathy: what increases outflow obstruction?

A
  1. increased myocardial contractility (B stim, dig)
  2. decreased preload (hypovolemia, vasodilators, tachycardia, PPV)
  3. decreased afterload (hypotension, vasodilators)
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12
Q

hypertrophic cardiomyopathy: what decreases outflow obstruction?

A
  1. decreased myocardial contractility (BB, volatiles, CCB)
  2. increased preload (hypervolemia, bradycardia)
  3. increased afterload (HTN, a stim)
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13
Q

hypertrophic cardiomyopathy: anesthetic management goals

A

minimized LV outflow tract obstruction

  • low contractility
  • high preload
  • high afterload
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14
Q

hypertrophic cardiomyopathy: induction

A
  • avoid sudden decreases in SVR (will compensate w/ increased HR/contractility)
  • modest myocardial depression is good
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15
Q

hypertrophic cardiomyopathy: anesthetic management (maintenance)

A
  • keep full, low inotropy (volatile good)
  • be careful w/ PPV (decreases preload) - try high rr, low Tv, avoid PEEP
  • consider TEE
  • tx hypotension w/ alpha-agonist (avoid beta stim = inotropy)
  • promptly replace fluid/blood loss
  • no vasodilators if hypertensive
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16
Q

dilated cardiomyopathy: definition

A

LV or biventricular dilation
systolic dysfunction
normal LV wall thickness

17
Q

dilated cardiomyopathy: anesthetic management

A

same as HF (since it is a cause of HF)

  • normal/high HR
  • normal/high preload
  • low/normal afterload
  • increase contractility
18
Q

cor pulmonale: definition

A
  • RV enlargement (hypertrophy and/or dilation) that may progress to RVF
  • caused by dz that induces pulmonary HTN
19
Q

preoperative management of cor pulmonale

A
  • eliminate & control acute & chronic pulmonary infections
  • reverse bronchospasm
  • improve clearance of airway secretions
  • expand collapsed or poorly ventilated alveoli
  • hydration
  • correct electrolyte imbalances
20
Q

intraoperative management of cor pulmonale

A
  • avoid bronchospasm (make sure they’re deep before DL)
  • use a volatile (good bronchodilator); avoid large doses of opioids (vent depression post-op)
  • avoid histamine releasers (sux, some NDNMR)
  • PPV
21
Q

effects of SNS activation in HF

A
  1. arteriolar constriction = maintains BP despite CO decrease, redirects BF to coronary & cerebral systems
  2. venous constriction = increases preload, helps maintain CO (Frank)
  3. RAAS activation 2/2 decrease in RBF –> increased blood volume & ultimately CO
  4. HR increases
22
Q

clinical features of HF

A
  • dyspnea (orthopnea, PND)
  • fatigue
  • weakness at rest
  • tachycardia
  • oliguria
  • edema
  • afib (2/2 dilation)
  • tachypnea
  • lung rales
  • S3 gallop
  • hypotension
  • JVD
23
Q

pathogenesis of HF

A
  1. decreased contractility
  2. ventricle dilated to increase contractility from stretched muscle fibers
  3. increase ventricular radius = increased cardiac work
  4. increased O2 consumption & increased cardiac work
  5. CO falls
  6. increased SNS outflow to increase HR/SVR
  7. SV falls