Valves Flashcards Preview

Coexisting 2016 > Valves > Flashcards

Flashcards in Valves Deck (35)
Loading flashcards...

Drug therapy for valvular disease

  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


Tests for valvular heart disease? what will they tell us?

  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 2 (normal 4-6cm2) need 25 mmHg to generate adequate cardiac output
  5. Stenosis over time will lead to 
    • ​Left atrial enlargement
    • Pulm HTN
    • RV enlargement and RF failure


What are some complications associated with Left atrial enlargement?

  • Left atrial enlargement - Predisposes to a-fib
  • A-fib→stasis and development of thrombi 
  • Anticoagulants are needed


Severe Mitral stenosis can lead to



Mitral Stenosis

Anesthetic Management GOALS

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)
  2. Tight controll of blood volume:
    • Tight fluid administration, give blood or colloids.
  3. Full:
    • manitain 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 hgh MAC techniquesIAs will drop SVR). 
    • ​​​Manitain full contractility 

(also avoid arterial hypoxemia/hypoventilation that may exacerbate PulmHTNleading to right ventricualr failure)


Induction for MITRAL STENOSIS 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 HRNO KETAMINE, No anticholinergics (glyco or atropine), 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


Patho of mitral regurgitation

  1. Usually d/t rheumatic fever and is almost always associated with mitral stenosis.
  2. Causes decreased forward LV Stroke volume and retrograde flow during ventricular contraction - resulting in LA fluid volume overload
  3. Can be caused by RA, MI, ruptured chordae tendonae, ischemia to the papillary muscles, congenital disorders


Appearance of mitral regurgitation:

  1. On PCWP tracing
  2. x-Ray
  3. EKG

  1. Reguritant flow = V wave on PCWP tracing
    • (Size of the V wave correlates with the magnitude of regurgitant flow)
  2. X-ray shows cardiomegaly
    • (eccentric hypertrophy over time to compensate for decreased CO)
  3. EKG shows ​Left atrial and left ventricular hypertrophy
    • ​​(Atrial = notched broad P wave)


 Mitral regurgitation anesthetic management GOALS

Fast, Full, Forward

Goal = improve LV forward stroke volume and decrease the regurgitant fraction:

  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
  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 
  4. Maintain contractility -
    • low MAC - balanced techniques - high opioids,
    • inotropes


Causes of of aortic stenosis

Associated size and pressure?

  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 <1 cm2 and a transvalular gradient of >50mmHg.


Explain the pathology of angina associated with Aortic stenosis

What is the classic symptom triad with Aortic Stenosis

  1. Angina is often present without CAD
  2. The specific contributers to angina
    • LV concentric hypertrophy increases oxygen requirements  
    • Increased myocardial work to overcome stenosis
    • decreased O2 delivery d/t compression of the subendocardial vessels
  3. Classic triad = Angina, Dyspnea on Exertion, Syncope
    • (75% who are symptomatic will die w/ in 3 years if they do not have a valve replacement!)


Aortic Stenosis anesthetic management GOALS from class

Prevent hypotension and any hemodynamic change that will decrease cardiac output

  1. MUST Maintain NSR: Low/normal (60-90)→avoid sudden decreases in HR (worse) AND tachycardia
    • BP is HR 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


Induction in a patient with Aortic Stenosis

Method? Drugs?

  1. GENERAL ANESTHESIA is preferred over regional (because regional causes sympathectomy and drop in SVR)
  2. Good choice is something that DOES NOT decrease SVR
    • Etomidate is best
    • High opioid technique if poor LV function
    • Etomidate + Benzos
    • Propofol + Phenylephrine??
  3. AVOID: Ketamine - it causes tachycardia 


Causes of aortic regurgitation

  1. Acute
    • Infective endocarditis
    • Dissection of thoracic aortic aneurysm
  2. Chronic
    • ​​Rheumatic fever
    • Chronic HTN
    • Marfans
    • idiopathic aortic root dilation
    • bicuspid aortic valve


Causes and management of Tricuspid Regurgitation

  1. Usually due to pulmonary HTN.
  2. RV becomes dilated (usually a functional problem and well tolerated) 
  3. Leads to RV Volume overload
  4. GOALS
    1. maintain fluid volume→preload dependent
    2. avoid a drop in venous return (make sure PPV allows for adequate VR)
    3. Avoid increase in PA pressure 
      • Avoid N2O
      • increased PA pressure can cause a right to left shunt if the pt has a PFO
  5. Tricuspid regurge is common in seasoned atheletes


How do we treat a-fib with RVR?

BBs, CCBs, amiodarone, or digoxin.


Preop eval

Syncope, fainting, compensation?

Major end organ disease?

Cardiac hypertrophy, increased SNS output for compensation?

How bad is the CV disease?


One of the single best questions for many CV assesments

Exercise tolerance


Common symptoms of CHF with valve disease

Dyspnea, orthopnea, fatigue

CHF is a common conpanion with valvular disease


what is a common arrythmia associated with valvular disease?

Atrial Fibrilation - due to left atrial enlargement


What are the sighns and symptoms associated with Left atrial enlargement?

  1. dispnea on exertion
  2. orthopnea
  3. paroxysmal nocturnal dyspnea


with mitral stenosis CO is usually maintained by an increase in atrial pressure - what situations cause CO to drop?

  1. Stress induced tachycardia
  2. A-fib - when there is a loss in atrial contraction


Induction of anesthesia for Mitral Regurgitaion

Remember: Fast, Full and Forward - choices should be based on avoiding bradycardia and avoiding an increase in SVR

  1. 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??


Mirtal Regurgitation Maintinence and of Anesthesia drug considerations

Maint.Determined by the degree of LV dysfunction

  1. Absence of severe LV dysfunction use Nitrous + volitile
  2. Use a Lower MAC - VAs attenuate increases in BP and SVR that accompany surgical stimulation
  3. Opioids → Class = minimizes likelyhood of drug induced myocardial depression (stoelting says to use caution with high doses becasue of the decrease in HR and myocardial depression)
  4. Isoflurane - decreases SVE and prevents increases in BP d/t surgical stimulation - Sevo and Des do as well, OK choices
  5. SNP, Hydralazine, (NTG???) intra op to decrease BP - they all decrease afterload


Monitor considerations for Mitral Reurgitation and Mitral Stenosis.

  1. Invasive monitoring depends on the
    • surgical procedure
    • extent of  phydiologic impairment 
    • presence end organ dysfunction
  2. CVP (MR used to monitor V-wave)
  3. +/- a-line
  4. +/- swan
  5. consider TEE if undercoing major fluid shift surgeries (MS may require post op intubation d/t CHF/pulmonary edema - need time to equilibrate)


Explain why Normal Sinus Rhythm MUST be maintainded in  Aortic Stenosis

HR determines 3 things

  1. Time for ventricualr filling
    • (increased HR = decreased LV filling = decreased CO)
  2. Volume of ejected SV
  3. Coronary Profusion→coronaries fill in diastole  
    • (increased HR = decreased coronary blood flow→ ischemia and further LV deterioration)

They are reliant on atrial kick to have adequate LVEDV

  • a junctional rhythm or a-fib = dramatic decrease in SV and BP
  • Decreased BP = Decreased coronary blood flow = Ischemia
    • ​Hypotension should be treated with Phenylephrine - b/c it WILL NOT increase HR

AS requires aggressive treatment of hypotension to prevent cardiogenic shock 

  • it is hard to get a BP back because the force required to overcome the stenotic valve is too high and adequate SV cannot be attained. For this same reason CPR is ineffective in these patients


Maintinence of anesthesia in a patient with Aortic Stenosis (key points, drugs and likely complications)

  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 ventricualar arrythmias- ALWAYS have Lidocaine, Amioderone and a Defibrilator Availible


Intraoperative monitoring for aortic stenosis MUST consist of this

5 lead EKG that is capable of detecting myocardial ischemia


Explain the basis of the valvular disease that has the highest perioperative risk

  1. Aortic stenosis has the highest risk of intraoperative cardiac complications, increased mortality and increased risk of perioperative myocardial infarction
  2. The risk for myocardial ischemia in aortic stenosis is INDEPENDENT of their assoiated risk attributed to CAD