Week 5 - Anesthesia for Valvular Disease Flashcards

1
Q

Why is the atrial kick important?

A
  • Up to 20% of ventricular preload acting as a priming force for the ventricle – increases efficiency of ventricular ejection due to the acutely increased preload
  • Progressively more important with increasing heart rate (tachy leads to less time in diastole for passive filling)
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2
Q

What is the difference between concentric hypertrophy and eccentric hypertrophy?

A

Concentric: caused by prolonged exposure of the cardiac ventricular muscle to increased afterload (ie. HTN and Aortic stenosis)
-actually causes remodeling of the sarcomeres = thicker ventricular wall while intra-ventricular volume remains unchanged initially

Eccentric: prolonged exposure to excessive amounts of intravascular volume (ie. renal failure)
-ventricular wall thickness is unchanged while intra-ventricular volume increases causing dilation of the ventricle

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3
Q

What do broad and/or notched P waves on an EKG inticate?

A

left atrial enlargement seen in mitral regurgitation

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4
Q

What changes to an EKG can be seen with Left of Right Ventricular Hypertrophy?

A

L/R axis deviation and high voltage R waves

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5
Q

What is mitral regurgitation characterized by?

A

Decreased forward left ventricular stroke volume and associated increased left atrial pressures

*as much as 50% of the SV can be regurgitant

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6
Q

What are the common etiologies of mitral regurgitation?

A

-Myocardial ischemia, infarction, ineffective endocarditis, and chest trauma

  • Chronic: usually rheumatic fever, incompetent valve or annulus destruction
  • Acute: generally from ischemia/infarction and destruction of the chordae tendinae
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7
Q

How does the heart compensate for mitral regurgitation?

A

The left ventricle dilates to increase end-diastolic volume

  • this allows the forward stroke volume to be maintained even as the regurgitant volume increases
  • leads to eccentric LV hypertrophy (regurgitant volume can exceed the forward SV)

Reduced atrial compliance can cause pulmonary congestion

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8
Q

How does acute mitral regurgitation present clinically?

A

Presents as cardiogenic shock and/or pulmonary edema

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9
Q

What are the signs and symptoms of mitral regurgitation?

A
  • Dyspnea and dyspnea on exertion
  • Fatigue
  • Orthopnea (due to backing up into pulmonary system)
  • Angina
  • Palpitations
  • Congestive heart failure
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10
Q

What type of murmur is heard with mitral regurgitation?

A

Holosystolic apical murmur radiating to the axilla

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11
Q

What echo findings are seen in mitral regurgitation?

A

Mild Symptoms: 20-30% Regurgitant Fraction (RF) and/or < 3 Jet Area (JA)
Moderate Symptoms: 30-60% RF and/or 3-6 JA
Severe Symptoms: >60% RF and/or > 6 JA (pulm vein flow reversal)

  • RA = % of blood volume flowing back through the mitral valve
  • JA = square cm as measured on color doppler
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12
Q

What are the hemodynamic anesthetic goals for a patient with mitral regurgitation?

A

“Full, Fast, Forward”

  • Maintain an upper normal HR (80-100) – brady worsens regurgitant flow/can result in severe LV overload
  • Normal sinus rhythm (A-fib is common in chronic MR - loss of coordinated atrial contraction increases RF)
  • Adequate preload maintenance (excessive fluids causes LV decompensation and worsen regurgitation, hypovolemia causes inadequate CO)
  • Decrease afterload (promotes forward blood flow, sudden increase in SVR can cause LV decompensation and worsen regurgitation – ie giving phenylephrine)
  • Maintain contractility
  • Prevent increased Pulmonary Vascular Resistance
  • Allow time for venous filling (I;E ratio/prevention of increased RR of vent)
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13
Q

What type of anesthetics are good for patients with mitral regurgitation?

A
  • Spinal and Epidural anesthesia is well tolerated (maintain preload in careful balance, associated increase in HR is ok if intravascular volume is maintained appropriately)
  • Inhaled anesthetics are good (decrease SVR and have relatively minimal myocardial depression)
  • Severe MR pts benefit from opioid based anesthetic (take care to avoid bradycardia, treat with glyco or atropine)
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14
Q

What supportive medications are a good choice for patients with mitral regurgitation?

A

Inotropes and Chronotropes to maintain contractility and HR (Dopamine/Dobutamine, Milrinone)

Nitroprusside, Nitroglycerine (careful as it can reduce preload) for reduction in afterload

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15
Q

What vasopressor should you avoid using in patients with mitral regurgitation? Why?

A

Phenylephrine

  • increases SVR which increases regurgitant flow
  • causes reflex bradycardia
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16
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease

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17
Q

What is the pathophysiology of mitral stenosis?

A

Thickening and calcification of the mitral valve leaflets causes a mechanical obstruction to the left ventricle increasing left atrial volume and pressure

*slow process (most pts don’t become symptomatic for 20-30 years post rheumatic infection)

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18
Q

What effect does mitral stenosis have on the pulmonary system?

A

Left atrial dilation causes an increase in pulmonary venous pressure leading to transudation of fluid into pulmonary interstitial space causing:

  • decreased pulmonary compliance
  • increased work of breathing leading to progressive dyspnea on exertion
  • pulmonary edema (generally associated with episodes of Afib, pain, pregnancy, sepsis/infection)

*pulmonary deterioration causes RV failure – increased PVR creates increased RV afterload

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19
Q

Why is mitral stenosis associated with vocal hoarsness?

A

An enlarged left atrium can cause pressure on the left recurrent laryngeal nerve

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20
Q

How do 90% of mitral stenosis patient present clinically?

A

In A-fib with congestive heart failure

*risk of embolus with undiagnosed a-fib

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21
Q

What are the signs and symptoms of mitral stenosis?

A
  • Dyspnea/Dyspnea on exertion
  • Fatigue
  • Chest Discomfort (15-20% develop chest pain)
  • Palpitations/A-fib
  • Hemoptysis
  • TIA/CVA (due to associated A-fib emboli)
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22
Q

What type of murmur is heard with mitral stenosis?

A

Rumbling diastolic murmur that is heard at the apex and the characteristic opening snap occurring in early diastole

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23
Q

How much is the mitral valve orifice decreased in mitral stenosis when pts normally become symptomatic?

A

Decreased by at least 50% (normally 4-6 cm^2)

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24
Q

What EKG changes do you see with mitral stenosis?

A

Broad, notched P waves

*due to left atrial enlargement

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25
Q

What are the hemodynamic anesthetic goals for patients with mitral stenosis?

A
  • HR maintained at slow to normal (60-80) (allows for diastolic filling)
  • Maintain sinus rhythm (if a-fib is present keep ventricular rate <100)
  • Euvolemia (hypervolemia overloads the right atrium promoting pulmonary edema/htn and right ventricle failure – hypovolemia can cause precipitous drop in SV and CO)
  • Maintain normal SVR (increased LV afterload worsens stenotic effects at MV level)
  • Maintain contractility
  • Prevent increased PVR (hypoxia, hypercarbia, acidosis, excessive PIP/PEEP) – lung protective ventilation
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26
Q

What are the regional anesthetic considerations for patients with mitral stenosis?

A

Epidural preferred to Spinal due to gradual onset of sympathetic blockade and less systemic vascular dilation

27
Q

What medications are preferred for treating the following in pts with mitral stenosis?

  • tachycardia
  • hypotension
  • acute hypertension
  • pulmonary HTN
A

Tachycardia: beta blockers (Esmolol/Metoprolol)

Hypotension: phenylephrine preferred over ephedrine and norepi due to lack of beta adrenergic activity

Acute HTN: nitroprusside (fast acting vasodilator)

Pulmonary HTN: pulmonary vasodilators – Flolan, Nitric Oxide

28
Q

What are the anesthetic considerations in patients with mitral stenosis?

A
  • Avoid ketamine on induction due to propensity to increase HR
  • Maintenance: avoid myocardial depressants and changes in vascular resistance (nitrous/narcotic, minimizing volatile)

*sympathetic stimulation from surgical stimulation can precipitate cardiovascular decompensation

29
Q

What are the post op considerations for patients with mitral stenosis?

A

Careful prevention of hypoxia, hypercarbia, acidosis, hypoventilation

Mechanical ventilation in the ICU is a prudent decision based upon MS severity

30
Q

What are the common causes of aortic regurgitation?

A

Caused either by disease of the leaflets or the aortic root:

  • Leaflet Origin: infective endocarditis, rheumatic fever, bicuspid valve, anorexigenic drugs
  • Aortic Root Origin: marfan syndrome, EDS, aortic root dilation, annuloaortic ectasia, rheumatoid and psoriatic arthritis, and ankylosing spondylitis

*acute aortic regurg is most commonly a result of infective endocarditis, trauma, or aortic dissection

31
Q

What does aortic regurgitation cause?

A
  • Regurgitation from the aorta back to the LV during diastole results in a combined pressure and volume overload of the LV
  • Reduction in effective SV and thus CO
  • Overtime the LV retains a larger and larger regurgitant volume and there is no room for the atrium to empty
  • Eccentric LV Hypertrophy due to volume overload
  • Pulmonary congestion can occur as well due to back up of blood through the left heart
32
Q

What two variables does the magnitude of the regurgitant fraction in aortic regurgitation depend on?

A
  • Time available for backflow of blood (length of diastole) — tachycardia reduces regurgitant volume
  • Pressure gradient across the aortic valve during diastole – HTN worsens regurgitation
33
Q

Why can angina occur in the absence of coronary artery disease in patients with aortic regurgitation?

A
  • Increased myocardial oxygen demand in response to muscular hypertrophy/dilation
  • Reduction of blood supply to the cardiac muscle related to a drop in diastolic pressures
34
Q

What are the signs and symptoms of aortic regurgitation?

A
  • Initial symptoms include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea
  • Peripherally there will be hyper-dynamic circulation with widened pulse pressure and bounding pulses
  • Decreased diastolic pressure
  • Can progress to combination with mitral regurgitation
  • chronic disease can be symptomless for 20 years – minimal symptoms as RF remains <40% of SV and severe symptoms being when RF is >60% of SV
  • chronic AR presents classically as CHF
35
Q

What murmur is heard with aortic regurgitation?

A

Characteristic diastolic murmur heard along the left sternal border

36
Q

What are the hemodynamic anesthetic goals for patients with aortic regurgitation?

A
  • Maintain a therapeutic increase in HR (80-100) – decrease diastolic time minimizing RF while preserving CO
  • Sinus Rhythm promotes forward flow of blood
  • Adequate preload maxes the hearts ability to maintain forward flow
  • Reduce afterload (aids by increasing SV and CO, reduces RF by decreasing diastolic pressure gradient – too much reduction can precipitate coronary ischemia w/ or w/o concomitant CAD)
  • Adequate contractility to preserve SV and CO (be careful of myocardial depressant drugs)
37
Q

what are regional anesthetic considerations for patients with aortic regurgitation?

A

Spinal and Epidural anesthesia are acceptable provided the intravascular volume is maintained

*epidural may be slightly preferred due to less abrupt/severe sympathectomy

38
Q

What are the anesthetic considerations for aortic regurgitation?

A

-Induction/maintenance with IV or inhaled agents of preference – afterload reduction is good

39
Q

What are the preferred medications to treat the following in patients with aortic regurgitation?

  • hypertension
  • bradycardia
  • hypotension
A

HTN: aggressive treatment with peripheral vasodilators (Nitroprusside, Nitroglycerine, Hydralazine, Alpha blockers)

Bradycardia: aggressive treatment with atropine/glyco

Hypotension: should be treated with ephedrine to avoid reflex bradycardia seen with phenylephrine

  • if tachyphylaxis occurs, norepi in lower doses is beneficial
  • dopamine and dobutamine are also helpful in preserving HR and CO
40
Q

What are the two main factors associated with the development of aortic stenosis?

A
  • Degeneration and calcification of the aortic leaflets
  • Presence of a bicuspid rather than tricuspid aortic valve (congenital and develops earlier in life, 30-50yo, compared w/ pts with tricuspid, 60-80yo)
41
Q

What is the most common cause of aortic stenosis?

A

Calcification of the aortic leaflets, preventing them from opening correctly

42
Q

What type of hypertrophy is caused by aortic stenosis?

A

Concentric hypertrophy - result of the increased afterload on the LV

*aortic stenosis related obstruction is gradual which allows the LV to compensate and maintain an adequate to normal SV and CO

43
Q

Why can angina pectoris occur in the absence of CAD in patients with aortic stenosis?

A

Increased myocardial oxygen demand related to the concentric remodeling of the LV (more myocytes, thicker ventricular walls)

Increase in myocardial work due to the increase in afterload

44
Q

How much does CO decrease with the loss of atrial kick in aortic stenosis?

A

Loss of atrial kick will decrease ventricular filling and could lead to a 40% reduction in CO

45
Q

How does aortic stenosis impair coronary perfusion?

A

Due to low aortic diastolic pressures

-makes pts with aortic stenosis at high risk of MI even if they have normal coronary arteries, especially if aortic regurgitation and hypertrophy also exists

46
Q

What is the classic triad of symptoms for aortic stenosis?

A

Chest Pain
Syncope
Orthostatic or Exertional Dyspnea

  • generally significant symptoms dont develop until 30-60 years of age
  • symptom onset correlates with time of death – 75% succumb within 3 years w/o surgical intervention
47
Q

What type of murmur is heard with aortic stenosis?

A

Systolic murmur heard at the right 2nd intercostal space with transmission into the neck when severe (carotid bruit)

48
Q

Fill in the ?

A

Answer

49
Q

What are the hemodynamic anesthetic goals for aortic stenosis?

A
  • Normal HR (70-80) – optimizes myocardial oxygen utilization for ischemia prevention
  • Avoid bradycardia (<60) – SV is “fixed” due to stenotic lesion so bradycardia can cause a precipitous decrease in CO
  • Maintenance of sinus rhythm is extremely important (tachycardia can precipitate myocardial demand ischemia, loss of atrial kick can have profound impact on CO)
  • Avoid decreased afterload (maintain or allow slight increase)
  • Adequate contractility to help preserve ventricular function (avoid myocardial depression)
  • Monitor for intra-op ischemia (think demand ischemia if ST changes are noted or decreased afterload)
50
Q

What are the anesthetic considerations for patients with aortic stenosis?

A
  • General anesthesia is most often selected over neuraxial
  • Spinal/Epidural is contraindicated in severe AS
  • Opioid anesthetic or Ketamine/Benzo or Etomidate for induction
  • Maintenance with low dose volatile or N2O/narcotic
  • Arterial line placement awake
  • Consider TEE intraop
51
Q

What are the preferred medications to treat the following in aortic stenosis?

  • Hypotension
  • Tachyarrhythmias
  • Bradycardia
  • Tachycardia
A

Hypotension: phenylephrine bolus (consider prophylactic infusion depending on anesthetic choice)

SVT/Ventricular Tachyarrhythmias: amiodarone

Bradycardia: atropine (if refractory use epinephrine in small boluses or low dose infusion)

Tachycardia: Esmolol (can also be used as an infusion 0-300 mcg/kg/min)

52
Q

What is hypertrophic cardiomyopathy?

A

Hypertrophy of the left ventricular tissue, particularly the interventricular septum below the aortic valve

  • blocks the outflow of blood from the LV to the aorta through the LVOT
  • obstruction peaks in mid to late systole
  • as systole occurs and blood rushes through the narrowed LVOT the mitral valve is drawn out due to the venturi effect
  • most common cause of sudden death in pts younger than 30
  • most common genetic cardiovascular disease that affects all ages and has an autosomal dominant inheritance
53
Q

What increases the LVOT obstruction in hypertrophic cardiomyopathy? (3)

A

Increased Contractility (catecholamines)

Decreased Preload

Decreased Afterload

54
Q

What decreases the LVOT obstruction in hypertrophic cardiomyopathy? (3)

A

Decreased Contractility

Increased Preload

Increased Afterload

55
Q

What are the signs and symptoms of hypertrophic cardiomyopathy?

A
  • Dyspnea on Exertion
  • Angina that is relieved by lying down
  • Fatigue
  • Syncope
  • Tachydysrhythmias (both supraventricular and ventricular arrhythmias are common due to ventricular remodeling)
  • Congestive Heart Failure
56
Q

What EKG changes are seen with hypertrophic cardiomyopathy?

A

EKG shows left ventricular hypertrophy, ST and T wave abnormalities, Q wave, and LA enlargement (high amplitude P wave)

57
Q

What are the hemodynamic anesthetic goals for hypertrophic cardiomyopathy?

A
  • MINIMIZE SYMPATHETIC ACTIVATION
  • Maintain preload (1st line defense for hypotension)
  • Increased afterload (2nd line defense w/ hypotension – Phenylephrine)
  • Decreased contractility (inotropic drugs can precipitate cardiovascular collapse, increased contractility exacerbates the narrowing of the LVOT further worsening CO) – Avoid EPI
58
Q

What are the anesthetic considerations for hypertrophic cardiomyopathy?

A
  • No neuraxial blocks (catastrophic decrease in preload and afterload)
  • Phenylephrine is the ideal vasopressor because it doesn’t affect inotropy
  • Beta blockade can be crucial in counteracting sympathetic activation and maintaining LVOT patency
59
Q

What valve disease does this pressure-volume loop show?

A

Aortic Regurgitation

60
Q

What valve disease does this pressure-volume loop show?

A

Aortic Stenosis

61
Q

What valve disease does this pressure-volume loop show?

A

Mitral Regurgitation

62
Q

What valve disease does this pressure-volume loop show?

A

Mitral Stenosis

63
Q

In which valvular diseases would you want to maintain a decrease in SVR?

A

Aortic Insufficiency (Regurgitation)

Mitral Regurgitation