Valvular Disorders reduced Flashcards
Valvular disease
preop evaluation
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History and Physical Examination
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Assessment of the
- severity of the cardiac disease;
- degree of impaired myocardial contractility;
- presence of associated major organ disease,
- development of compensatory mechanisms for maintaining cardiac output
- increased sympathetic nervous system activity
- cardiac hypertrophy
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Elicit the following information:
- Exercise tolerance is useful for evaluating cardiac reserve
- Anxiety, diaphoresis, and resting tachycardia may reflect a compensatory increase in sympathetic nervous system activity.
- Cardiac dysrhythmias, especially atrial fibrillation, are common.
- Angina pectoris may be due to increased cardiac muscle mass that exceeds the ability of even normal coronary arteries to deliver adequate amounts of oxygen.
- Congestive heart failure (CHF), manifesting as dyspnea, orthopnea, and fatigue, is a frequent companion of chronic valvular heart disease
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Assessment of the
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Drug Therapy
- Digitalis (Digoxin) - Given to increase contractility and slow the ventricular rate in those with a-fib
- Diuretics - May be given for excess intravascular fluid volume, but resultant hypokalemia can place at risk for digitalis toxicity
- Prophylactic** **Antibiotics - Recommended for the protection against the development of sub-acute bacterial endocarditis
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Laboratory Data
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Doppler Echo
- valve movement, flow and pressure gradients
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Cardiac cath
- measure the severity of valvular heart disease
- valve movement, flow and pressure gradients
- ABG→decreased PaO2 and V/Q mismatch
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Doppler Echo
Pathophysiology of mitral stenosis
- Most common in females
- Primary cause = rheumatic fever (slow development over 20-30 years)
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Valvular manifestations:
- fusion of mitral valve leaflets at the commisures
- calcification of annulus an leaflets
- Senosis with a valve <1cm2 (normal 4-6cm2)
- this requires a mean left atrial pressure of about 25 mmHg is necessary to maintain an adequate resting cardiac output
- Stenosis over time will lead to
- Left atrial enlargement
- Pulm HTN
- RV enlargement and RF failure
- Left atrial enlargement predisposes to atrial fibrillation
- Stasis of blood in the distended LA predisposes to the formation of thrombi
- may be receiving chronic anticoagulant therapy.
- Stasis of blood in the distended LA predisposes to the formation of thrombi
Mitral Stenosis
Anesthetic Management
GOALS
SLOW, TIGHT, and FULL → prevention and treatment of events that decrease CO or cause pulmonary edema
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Slow HR (50-60):
- <strong>AVOID</strong> tachycardia or a-fib with RVR (both decreases CO and cases pulmonary edema d/t increased RA pressure)
- Keep it in sinus!
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Tight controll of blood volume:
- Tight fluid administration, give <strong>blood</strong> or <strong>colloids</strong>.
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Full:
- Maintain preload→<strong>avoid marked increases</strong> in<strong> </strong>blood volume from <strong>over-transfusion</strong> or <strong>head-down positions</strong> →still need adequate pressures to overcome the stenosed valve.
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Maintain afterload → Large decreases in SVR will drop preload.
- <strong>More importantly -</strong> the <strong>compensation </strong>for decreased SVR→<strong>baroreceptor reflex</strong>→<strong>increases HR which will generate a LOW CO in this patient!</strong> (avoid NTG, and high MAC techniques→IAs will drop SVR).
- Maintain full contractility
(also avoid arterial hypoxemia/hypoventilation that may exacerbate PulmHTN→leading to right ventricular failure)
MITRAL STENOSIS
Induction - pharmacologic considerations
- Etomidate is ideal (if you must use propoflol use it with phenylephrine, also give esmolol prior to DVL)
- Goal = ventricular rate controll!
- USE: ß-blockers, CCB
- AVOID: tachycardia →decreases left ventricualr filling and increases left atrial pressure! a drop in SV
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AVOID things that increase HR→
- NO KETAMINE
- No anticholinergics (glyco or atropine)
- NO histamine releasing drugs
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AVOID things that abruptly decrease SVR
- Better to chose a high opioid techniqe over IAs , Propofol, NTG
- USE: Phenylephrine (pure vasoconstrictor) and Vasopressin (does NOT effect the pulmonary vasculature) to treat/avoid decreased SVR
- Possiblly avoid nitrous → it increases pulmonary vascular resistance which may potentiate pulmonary edema
- Desflurane → not a good choice it decreases SVR and causes increased HR and BP transiently when increased - ISO = slow ∆ abd time for body to adapt
MITRAL STENOSIS
Maintenance
Goal = minimize the likelihood of marked and sustained changes in HR, SVR, PVR, and myocardial contractility.
- Keep BP within 20% of their norm
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Useful drugs:
- ß-blockes and CCB (maintain HR)
- Phenylephrine (maintian SVR w/ little rise in HR)
- Use of invasive monitoring depends on the complexity of the operative procedure and the magnitude of physiologic impairment produced by mitral stenosis.
- Consider A-line, TEE, PA cath
mitral regurgitation
Patho
- Usually d/t rheumatic fever and is almost always associated with mitral stenosis.
- Can be caused by RA, MI, ruptured chordae tendonae, ischemia to the papillary muscles, congenital disorders
- Causes decreased forward LV Stroke volume and retrograde flow during ventricular contraction - resulting in LA fluid volume overload
- Causes LA elnargement over time
- Regurigitant flow is responsible for the V wave present on the recording of the PAOP
- The size of the V wave correlates with the magnitude of the regurgitant flow
Mitral regurgitation
anesthetic management GOALS
Fast, Full, Forward = avoid decreases in CO
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Fast HR: (80-100 bpm)
- Avoid sudden decreases in HR
- Keep a NSR!
- Full tank: Manitain Preload
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Forward: Decreased/Normal Afterload
- Avoid sudden increases in SVR
- Maintain contractility
- Minimize drug induced myocardial depression
(Not on slide)
Goal = improve LV forward stroke volume and decrease the regurgitant fraction = avoid decreases in CO
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Fast HR: (80-100 bpm)
- Avoid sudden decreases in HR - (Bradycardia cuases severe LV volume overload and allows more time for blood to flow backwards)
- Maintain NSR
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Full tank: Preload remains the same
- Increase = more regurgitaion
- Decrease = Less CO (NTG = bad choice)
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Forward: Decreased/Normal Afterload
- Decreased SVR promotes forward flow
- Nitropruside → decreases afterload and allows for more effective cardiac pumping
- Hydralazine (arterial dialator)
- Regional may be a good choice to decrease SVR
- Avoid: sudden increases in SVR, which would promote backward flow
- Monitor the size of the V wave as a reflection of regurgitant flow
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Maintain contractility - Minimize drug-induced myocardial depression
- low MAC - balanced techniques - high opioids,
- inotropes
Mitral Regurgitation
Induction
Remember: Fast, Full and Forward
choices should be based on avoiding bradycardia and avoiding an increase in SVR
Maintain fast HR:
- Pancuronium = stimulates the ganglion and causes tachycardia
- Have Atropine ready, maybe give at induction
- Etomidate = minimal changes in HR, SVR and CO
- Propofol + Ephedrine??
Mitral Regurgitation
Maintenance
Is influenced by the degree of LV dysfunction
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In the absence of severe LV dysfunction: maintenance of anesthesia is often with nitrous oxide + volatile anesthetic
- <strong>isoflurane</strong> is an attractive choice because of its hemodynamic effects - decreases SVR and prevents increases in BP d/t surgical stimulation
- Sevo and Des do as well, OK choices
- When LV dysfunction is severe: the use of an opioid technique that minimizes the likelihood of drug-induced myocardial depression may be a consideration.
- Use of invasive monitoring depends on the complexity of the operative procedure and the magnitude of the physiologic impairment produced by mitral regurgitation (a-line, CVP PA, TEE?)
Aortic Stenosis
Patho
- Calcification developed over time (develops around 60-80 years)
- Bicuspid Aortic Valve instead of a Tricuspid Aortic valve (develops around 30-50 years)
- Congenital abnormality
- Rheumatic heart disease or Endocarditis
- Normal valve area is 2.5-3.5cm2
- Significant AS is associated with valve area of <1cm2 and a transvalular gradient of >50mmHg.
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Signs and symptoms
- Classic triad = Angina, Dyspnea on Exertion, Syncope
The rest is NOT on the slides
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Angina - often present without CAD d/t:
- LV concentric hypertrophy increases oxygen requirements
- Increased myocardial work to overcome stenosis
- decreased O2 delivery d/t compression of the subendocardial vessels
- 75% who are symptomatic will die w/ in 3 years if they do not have a valve replacement!
Aortic Stenosis
anesthetic management GOALS
Prevent hypotension and any hemodynamic change that will decrease cardiac output
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MUST Maintain NSR
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Low/normal HR (60-90)→avoid sudden decreases in HR (worse) AND tachycardia
- BP is HR dependent & atrial kick dependent
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Low/normal HR (60-90)→avoid sudden decreases in HR (worse) AND tachycardia
- Maintain Preload→Optimize intervascular fluid volume to maintain venous return and LV filling
- Maintain Afterload→Avoid sudden decreases in SVR→decreased coronary filling
- Maintain contractility
General anesthesia is often selected in preference to epidural anesthesia or spinal anesthesia to minimize the likelihood of an undesirable decrease in SVR.
Use of A-line and PA catheter depends on the magnitude of the surgery and the severity of the aortic stenosis.
Aortic Stenosis
Maintenance of anesthesia
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Anestheisa maintained
- with N2O + opioids or
- if they have significant LV dysfunction a High Opioid Technique
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NMB - w/o CV side effects
- Roc, Vec, Cis-atra)
- Bad Choice = Pancuronium - stimualtes Ganglion and increases HR
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Hypotension: treat with an alpha agonist
- Phenylephrine (it DOES NOT increase HR)
- Treat Junctional Rhythm/Bradicardia
- Glycopyrolate, Atropine, Esmolol →BP is HR dependent
- SVT - treat promptly with cardioversion
- Aortic Senosis has a propensity to develop ventricular arrhythmias
- __ALWAYS have Lidocaine, Amiodarone and a Defibrilator Available
Aortic regurgitation
Patho
May be:
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Acute:
- Infective endocarditis
- Dissection of thoracic aortic aneurysm
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Chronic
- Rheumatic fever
- Chronic HTN
- Marfans
- idiopathic aortic root dilation
- bicuspid aortic valve
Not on slides
(volume regurgitant into the left ventricle→eccentric hypertrophy (difficulty contracting)→dialated heart that doesnt function well)
Aortic Regurgitation Anesthetic Management GOALS
Goal: maintain forward LV stroke volume
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High/normal HR→ 80-100 bpm
- AVOID sudden decreases in HR
- Maintain Preload
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Decreased/normal Afterload→
- AVOID sudden increases in SVR
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Maintain contractility →
- minimize drug induced myocardial depression
Not on slides
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High/normal HR→ 80-100 bpm
- Avoid sudden decreases in HR
- High HR = less regurgitant volume (decreased diasotlic time where refurgitation can occur)
- If HR falls below 80 → volume overload and LV failure
- Have Robinul (glyco) and atropine on hand
- Maintain Preload
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Decreased/normal Afterload→
- AVOID sudden increases in SVR→it will precipitate LV failure
- Use of a vasodialator to decrease afterload
- SNP, hydralazine, nifedipine
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Maintain contractility → delicate balance
- minimize drug induced myocardial depression
- lower MAC, use of opioids or high opioid technique
(IF LV failure develops tx with vasodialator to reduce afterlaod and inotropes to increse contractility → ie dobutamine + SNP)
Aortic regurgitation
INDUCTION anesthetic management.
Goal: Avoid decreases in HR below 80, maintain forward LV stroke voume.
- DOC is usually Etomidate
- Choose a NMB that does not decrease HR
- Roc, Vec, Cis-Atricurium
- Pancuronium - stimulates ganglion = increases HR
- Have atropine and glyco READY! (treat brady promptly)