Week 5 - Anesthesia for Valvular Disease Flashcards
Why is the atrial kick important?
- 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)
What is the difference between concentric hypertrophy and eccentric hypertrophy?
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
What do broad and/or notched P waves on an EKG inticate?
left atrial enlargement seen in mitral regurgitation
What changes to an EKG can be seen with Left of Right Ventricular Hypertrophy?
L/R axis deviation and high voltage R waves
What is mitral regurgitation characterized by?
Decreased forward left ventricular stroke volume and associated increased left atrial pressures
*as much as 50% of the SV can be regurgitant
What are the common etiologies of mitral regurgitation?
-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
How does the heart compensate for mitral regurgitation?
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
How does acute mitral regurgitation present clinically?
Presents as cardiogenic shock and/or pulmonary edema
What are the signs and symptoms of mitral regurgitation?
- Dyspnea and dyspnea on exertion
- Fatigue
- Orthopnea (due to backing up into pulmonary system)
- Angina
- Palpitations
- Congestive heart failure
What type of murmur is heard with mitral regurgitation?
Holosystolic apical murmur radiating to the axilla
What echo findings are seen in mitral regurgitation?
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
What are the hemodynamic anesthetic goals for a patient with mitral regurgitation?
“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)
What type of anesthetics are good for patients with mitral regurgitation?
- 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)
What supportive medications are a good choice for patients with mitral regurgitation?
Inotropes and Chronotropes to maintain contractility and HR (Dopamine/Dobutamine, Milrinone)
Nitroprusside, Nitroglycerine (careful as it can reduce preload) for reduction in afterload
What vasopressor should you avoid using in patients with mitral regurgitation? Why?
Phenylephrine
- increases SVR which increases regurgitant flow
- causes reflex bradycardia
What is the most common cause of mitral stenosis?
Rheumatic heart disease
What is the pathophysiology of mitral stenosis?
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)
What effect does mitral stenosis have on the pulmonary system?
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
Why is mitral stenosis associated with vocal hoarsness?
An enlarged left atrium can cause pressure on the left recurrent laryngeal nerve
How do 90% of mitral stenosis patient present clinically?
In A-fib with congestive heart failure
*risk of embolus with undiagnosed a-fib
What are the signs and symptoms of mitral stenosis?
- Dyspnea/Dyspnea on exertion
- Fatigue
- Chest Discomfort (15-20% develop chest pain)
- Palpitations/A-fib
- Hemoptysis
- TIA/CVA (due to associated A-fib emboli)
What type of murmur is heard with mitral stenosis?
Rumbling diastolic murmur that is heard at the apex and the characteristic opening snap occurring in early diastole
How much is the mitral valve orifice decreased in mitral stenosis when pts normally become symptomatic?
Decreased by at least 50% (normally 4-6 cm^2)
What EKG changes do you see with mitral stenosis?
Broad, notched P waves
*due to left atrial enlargement
What are the hemodynamic anesthetic goals for patients with mitral stenosis?
- 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
What are the regional anesthetic considerations for patients with mitral stenosis?
Epidural preferred to Spinal due to gradual onset of sympathetic blockade and less systemic vascular dilation
What medications are preferred for treating the following in pts with mitral stenosis?
- tachycardia
- hypotension
- acute hypertension
- pulmonary HTN
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
What are the anesthetic considerations in patients with mitral stenosis?
- 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
What are the post op considerations for patients with mitral stenosis?
Careful prevention of hypoxia, hypercarbia, acidosis, hypoventilation
Mechanical ventilation in the ICU is a prudent decision based upon MS severity
What are the common causes of aortic regurgitation?
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
What does aortic regurgitation cause?
- 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
What two variables does the magnitude of the regurgitant fraction in aortic regurgitation depend on?
- Time available for backflow of blood (length of diastole) — tachycardia reduces regurgitant volume
- Pressure gradient across the aortic valve during diastole – HTN worsens regurgitation
Why can angina occur in the absence of coronary artery disease in patients with aortic regurgitation?
- 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
What are the signs and symptoms of aortic regurgitation?
- 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
What murmur is heard with aortic regurgitation?
Characteristic diastolic murmur heard along the left sternal border
What are the hemodynamic anesthetic goals for patients with aortic regurgitation?
- 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)
what are regional anesthetic considerations for patients with aortic regurgitation?
Spinal and Epidural anesthesia are acceptable provided the intravascular volume is maintained
*epidural may be slightly preferred due to less abrupt/severe sympathectomy
What are the anesthetic considerations for aortic regurgitation?
-Induction/maintenance with IV or inhaled agents of preference – afterload reduction is good
What are the preferred medications to treat the following in patients with aortic regurgitation?
- hypertension
- bradycardia
- hypotension
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
What are the two main factors associated with the development of aortic stenosis?
- 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)
What is the most common cause of aortic stenosis?
Calcification of the aortic leaflets, preventing them from opening correctly
What type of hypertrophy is caused by aortic stenosis?
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
Why can angina pectoris occur in the absence of CAD in patients with aortic stenosis?
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
How much does CO decrease with the loss of atrial kick in aortic stenosis?
Loss of atrial kick will decrease ventricular filling and could lead to a 40% reduction in CO
How does aortic stenosis impair coronary perfusion?
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
What is the classic triad of symptoms for aortic stenosis?
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
What type of murmur is heard with aortic stenosis?
Systolic murmur heard at the right 2nd intercostal space with transmission into the neck when severe (carotid bruit)
Fill in the ?
Answer
What are the hemodynamic anesthetic goals for aortic stenosis?
- 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)
What are the anesthetic considerations for patients with aortic stenosis?
- 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
What are the preferred medications to treat the following in aortic stenosis?
- Hypotension
- Tachyarrhythmias
- Bradycardia
- Tachycardia
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)
What is hypertrophic cardiomyopathy?
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
What increases the LVOT obstruction in hypertrophic cardiomyopathy? (3)
Increased Contractility (catecholamines)
Decreased Preload
Decreased Afterload
What decreases the LVOT obstruction in hypertrophic cardiomyopathy? (3)
Decreased Contractility
Increased Preload
Increased Afterload
What are the signs and symptoms of hypertrophic cardiomyopathy?
- 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
What EKG changes are seen with hypertrophic cardiomyopathy?
EKG shows left ventricular hypertrophy, ST and T wave abnormalities, Q wave, and LA enlargement (high amplitude P wave)
What are the hemodynamic anesthetic goals for hypertrophic cardiomyopathy?
- 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
What are the anesthetic considerations for hypertrophic cardiomyopathy?
- 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
What valve disease does this pressure-volume loop show?
Aortic Regurgitation
What valve disease does this pressure-volume loop show?
Aortic Stenosis
What valve disease does this pressure-volume loop show?
Mitral Regurgitation
What valve disease does this pressure-volume loop show?
Mitral Stenosis
In which valvular diseases would you want to maintain a decrease in SVR?
Aortic Insufficiency (Regurgitation)
Mitral Regurgitation
