Cardiac Pathophysiology + Valvular Heart Disease Flashcards
Aortic Valve: Location and Timing of the Sound
Location: 2nd intercostal space, right sternal border
Timing of the Sound: Aortic valve is heard here during S2
Tricuspid Valve: Location and Timing of the Sound
Location: 5th intercostal space, left sternal border
Timing of the Sound: Tricuspid valve is heard here during S1
Mitral Valve: Location and Timing of the Sound
Location 5th intercostal space, midclavicular line
Timing of the Sound Mitral valve is heard here during S1
Pulmonary Valve: Location and Timing of the Sound
Location 2nd intercostal space, left sternal border
**Timing of the Sound **Pulmnary valve is heard here during S2
Preoperative Evaluation PEARLS for cardiac patients
**History **
Symptoms related to ventricular function
Medications
Atrial fibrillation
Neurologic symptoms
Physical Examination
S3 gallop or pulmonary rales, JVD, hepatojugular reflux, hepatosplenomegaly, and pedal edema
Laboratory Findings
Routine labs, LFTs, ABGs,
Special Studies
ECG, CXR, Echo, ETT, and cardiac catheterization
Valvular Aortic Stenosis Symptoms
Symptoms
Fatigue
Dyspnea on exertion (DOE)
Angina
Exertional Syncope
Heart Failure (HF)
Sudden Cardiac Death (SCD)
Normal valve = ____
Tricupsid
(people who come for valve replacements have a bicuspid valve)
SVR and afterload… are they the same?
No!!!
SVR can create afterload
Afterload = LV workload
The higher the SVR, the harder the ventricle has to work.
SVR does not equal afterload
LV to AO gradient.. what is it?
If your LV to AO gradient is 80, this means that if your systemic SBP is 140, the pressure in the ventricle is 220.
Meaning, in aortic stenosis that ventricle has to develop a pressure of 220 to get the blood past the valve and out into the systemic circulation.
With aortic stenosis the afterload is ___.
Fixed
What would happen if you decreased the SVR for patients with aortic stenosis?
They won’t get enough preload to satisfy the higher pressure requirement they need to overcome the stenosed valve.
What is the patho of aortic stenosis?
Obstruction to LV ejection
Pressure overload on the LV
Concentric ventricular hypertrophy
* Wall thickness increases
* Chamber radius decreases
Stroke volume can be maintained with adequate preload
Etiology of Aortic Stenosis
* Sub-valvular
* Supravalvular
* Valvular (Most common)
Anesthetic Considerations for Aortic Stenosis
Maintain Normal Sinus Rhythm
* Dependent on atrial “kick” for ventricular filling
* Tachycardia will lead to ischemia
* Bradycardia (CO may be rate dependent)
Afterload
AFterload = Fixed (decreasing SVR is not helpful)
Preload
If decreased = reduction in CO and hypotension
Aortic Insufficiency/Regurgitation is an issue of _____.
volume not pressure
Aortic Insufficiency/Regurgitation
Basically you have an insufficient aortic valve where blood goes back into the LV.
Increasing LVEDV
* leads to Eccentric hypertrophy (stretching of the heart)
LV chamber dilates and wall stress increases
* Ventricular contractility becomes impaired
Increase heart rate is questionable
* Minimizes time for regurgitant flow back into the heart
Aortic Insufficiency/Regurgitation Anesthetic Considerations
(the key to these ones is that this valve is just “floppy” not stenosed, so different consideration).
Increased venous return will volume overload the heart (pulmonary vasculature)
* Lack of compensatory hypertrophy - wall stress rises - forward stroke volume falls
Modest reductions in afterload
* Increase forward CO
Maintain preload at adequate level
Maintain high normal HR, we don’t want bradycardia!
Mitral valve: normal and diseased measurements
The normal mitral valve orifice is 4 – 6 cm2
Severe disease is present with
* Valve area < 2 cm2
* LAP gradient > 10 mmHg
* PA systolic > 50 mm Hg
With mitral stenosis (Mitral valve area of <2 cm2), what are some of the consequences?
Pressure gradient develops
LA pressure increases to maintain CO
Increased LA pressure transmits to pulmonary vasculature
Reduction in pulmonary compliance
Increased lung stiffness
Increased work of breathing
LA enlargement
Atrial dysrhythmias
PCWP rises
Definition of pulmonary hypertension
mean pulmonary artery presure of 20
Which drugs are most likely to contribute to hemodynamic instability in the patient who is symptomatic from severe MS? (directly from slide)
- Ephedrine (avoid tachycardia, their HR needs to be slow enough that whatever is in that atrium will be able to be ejected into the ventricle)
- Nitrous oxide (will increase PVR- avoid this, we want their pulmonary artery pressures low)
When the patient with mitral stenosis goes into Atrial fibrillation, we need to consider ___.
rate control
Mitral stenosis is a disorder of ___.
pressure
they are not as volume sensitive
Anesthetic Considerations for Mitral Stenosis
Filling of LV through a restricted orifice requires increase driving pressure and increased time = YOU NEED THE HR SLOWER.
* Rapid ventricular rates are poorly tolerated
Strict control of HR
May use beta blockers
Rapid AFib requires DC cardioversion
Preload is especially important
Maintain adequate volume gradient across valve
Marked increase of central blood volume may exacerbate RV failure
Avoidance of the following:
Hypoxia, hypercarbia, hypothermia, acidosis and catecholamine release BECAUSE WE ARE TRYING TO AVOID INCREASES IN PVR
Select the BEST treatment for the hypotensive patient with Mitral Stenosis?
Vasopressin (no receptors in the pulmonary vasculature) or 2nd choice = Phenylephrine (will increase SVR but possibly slow the heart)
Mitral Stenosis
(impaired LV filling)
Aortic Stenosis
(LV emptying impairment, massive contraction trying to get by aortic valve)
Aortic Insufficiency
(LA and insufficient aortic valve)
Mitral regurgitation
(large SV, d/t increased blood leaving the LV)
falsely large stroke volume
