Valvular Disorders reduced Flashcards Preview

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Flashcards in Valvular Disorders reduced Deck (18):

Valvular disease

preop evaluation

  1. History and Physical Examination
    1. 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
    2. 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
  2. Drug Therapy
    1. Digitalis (Digoxin) - Given to increase contractility and slow the ventricular rate in those with a-fib
    2.  Diuretics - May be given for excess intravascular fluid volume, but resultant hypokalemia can place at risk for digitalis toxicity
    3. Prophylactic Antibiotics - Recommended for the protection against the development of sub-acute bacterial endocarditis
  3. Laboratory Data
    1. Doppler Echo 
      • ​valve movement, flow and pressure gradients
    2. Cardiac cath
      • measure the severity of valvular heart disease
      • valve movement, flow and pressure gradients
    3. ABG→decreased PaO2 and V/Q mismatch


Pathophysiology of mitral stenosis

  1. Most common in females
  2. Primary cause = rheumatic fever (slow development over 20-30 years)
  3. Valvular manifestations:
    • fusion of mitral valve leaflets at the commisures
    • calcification of annulus an leaflets
  4. 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
  5. Stenosis over time will lead to 
    • ​Left atrial enlargement
    • Pulm HTN
    • RV enlargement and RF failure
  6. 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.


Mitral Stenosis

Anesthetic Management


SLOW, TIGHT, and FULL → prevention and treatment of events that decrease CO or cause pulmonary edema 

  1. Slow HR (50-60):  
    • AVOID tachycardia or a-fib with RVR (both decreases CO and cases pulmonary edema d/t increased RA pressure)
    • Keep it in sinus!
  2. Tight controll of blood volume:
    • Tight fluid administration, give blood or colloids.
  3. Full:
    • Maintain preloadavoid marked increases in blood volume from over-transfusion or head-down positions →still need adequate pressures to overcome the stenosed valve.
    • Maintain afterload → Large decreases in SVR will drop preload.
      • More importantly - the compensation for decreased SVR→baroreceptor reflexincreases HR which will generate a LOW CO in this patient! (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)



Induction - pharmacologic considerations

  1. Etomidate is ideal (if you must use propoflol use it with phenylephrine, also give esmolol prior to DVL)
  2. Goal = ventricular rate controll!
    • USE: ß-blockersCCB
    • AVOID: tachycardia →decreases left ventricualr filling and increases left atrial pressure! a drop in SV
    • AVOID things that increase HR
      • No anticholinergics (glyco or atropine)
      • NO histamine releasing drugs
    • 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 
  3. Possiblly avoid nitrous → it increases pulmonary vascular resistance which  may potentiate pulmonary edema
  4. 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




Goal = minimize the likelihood of marked and sustained changes in HR, SVR, PVR, and myocardial contractility. 

  1. Keep BP within 20% of their norm
  2. Useful drugs:
    • ß-blockes and CCB (maintain HR)
    • Phenylephrine (maintian SVR w/ little rise in HR)
  3. 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


  1. 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
  2. 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

  1. Fast HR: (80-100 bpm)
    • Avoid sudden decreases in HR 
    • Keep a NSR!
  2. Full tank: Manitain Preload 
  3. Forward: Decreased/Normal Afterload
    • ​​Avoid sudden increases in SVR
  4. ​Maintain contractility 
  5. Minimize drug induced myocardial depression

(Not on slide)

Goal = improve LV forward stroke volume and decrease the regurgitant fraction = avoid decreases in CO

  1. 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
  2. Full tank: Preload remains the same
    • Increase = more regurgitaion
    • Decrease = Less CO (NTG = bad choice)
  3. 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
  4. Maintain contractility - Minimize drug-induced myocardial depression
    • low MAC - balanced techniques - high opioids,
    • inotropes


Mitral Regurgitation


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


Is influenced by the degree of LV dysfunction

  • In the absence of severe LV dysfunction: maintenance of anesthesia is often with nitrous oxide + volatile anesthetic
    • isoflurane 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


  1. Calcification developed over time (develops around 60-80 years)
  2. Bicuspid Aortic Valve instead of a Tricuspid Aortic valve (develops around 30-50 years)
  3. Congenital abnormality 
  4. Rheumatic heart disease or Endocarditis
  5. Normal valve area is 2.5-3.5cm2
    • ​​Significant AS is associated with valve area of <1cm2 and a transvalular gradient of >50mmHg.
  6. Signs and symptoms
    1. Classic triad = Angina, Dyspnea on Exertion, Syncope

The rest is NOT on the slides

  1. 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
  2. 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

  1. MUST Maintain NSR
    • ​Low/normal HR (60-90)→avoid sudden decreases in HR (worse) AND tachycardia
      • BP is HR dependent & atrial kick dependent
  2. Maintain Preload→Optimize intervascular fluid volume to maintain venous return and LV filling
  3. Maintain Afterload→Avoid sudden decreases in SVR→decreased coronary filling
  4. 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

  1. Anestheisa maintained
    • with N2O + opioids or 
    • if they have significant LV dysfunction a High Opioid Technique
  2. NMB - w/o CV side effects
    • ​​Roc, Vec, Cis-atra
    • Bad Choice = Pancuronium - stimualtes Ganglion and increases HR
  3. Hypotension: treat with an alpha agonist
    • Phenylephrine (it DOES NOT increase HR)
  4. Treat Junctional Rhythm/Bradicardia
    • ​​Glycopyrolate, Atropine, Esmolol →BP is HR dependent
  5. SVT - treat promptly with cardioversion
  6. Aortic Senosis has a propensity to develop ventricular arrhythmias
    • ​​ALWAYS have Lidocaine, Amiodarone and a Defibrilator Available


Aortic regurgitation


May be:

  1. Acute
    • Infective endocarditis
    • Dissection of thoracic aortic aneurysm
  2. 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

  1. High/normal HR→ 80-100 bpm
    • AVOID sudden decreases in HR
  2. Maintain Preload
  3. Decreased/normal Afterload 
    • ​​AVOID sudden increases in SVR
  4. Maintain contractility → 
    • minimize drug induced myocardial depression

Not on slides

  1. 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
  2. Maintain Preload
  3. Decreased/normal Afterload
    • ​​AVOID sudden increases in SVR→it will precipitate LV failure
    • Use of a vasodialator to decrease afterload
      • SNP, hydralazine, nifedipine
  4. 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. 

  1. DOC is usually Etomidate
  2. Choose a NMB that does not decrease HR
    • Roc, Vec, Cis-Atricurium
    • Pancuronium - stimulates ganglion = increases HR
  3. Have atropine and glyco READY! (treat brady promptly)


Aortic Regurgitation

Maintenance of Anesthesia

  1. In the absence of LV dysfunction:
    • N2O + volitile anesthetic  
    • Ususally Iso(minimal cardiac depression, CO maintained, preservation of baroreceptor reflex
    • Des and Sevo ok as well
    • N2O + Opioids may unmask  myocardial dysfunctction
  2. With significant LV dysfunction:
    • High opioid technique BUT there is a risk for bradycardia - treat promptly with atropine
  3. If hypotension occurs DOC is Ephedrine - increases HR
  4. Mantain volume status, propmt replacement of blood loss to maintain LV SV
  5. Treat high SBP with SNP


Tricuspid Regurgitation


  1. Usually funtional, due to pulmonary HTN.
  2. RV becomes dilated (usually a functional problem and well tolerated) 
  3. Leads to RV Volume overload
  4. Usually well tolerated
  5. common in seasoned atheletes


Tricuspid Regurgitation

Management of Anesthesia


  • maintain fluid volume→preload dependent
  • avoid a drop in venous return
    • make sure PPV allows for adequate venous return
  • Avoid hypoxia and hypercarbia
    • Avoid increase in PA pressure 
    • increased PA pressure can cause a right to left shunt if the pt has a PFO
  • Avoid N2O