Case 88 - CV system Flashcards
What are etiologies of RV failure?
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RV failure = structural or functional disorder
- RV unable to eject blood into pulmonary circulartion
Structural
- Wall stress, pump mechanism
- RV ischemia
- cardiac tamponade
- inadequate myocardial protection
- myocardial stunning
- coronary air embolism
Functional
- L side heart failure
- pulm valve stenosis
- chronic pulm HTN from lung disease (cor pulmonale)
- PE
- tension pneumothorax
- hypoxemia, acidosis, hypercarbia, hypothermia
- TRALI
- Sepsis
patient with pre-existing pulm htn presents to surgery for mitral valve repair 2/2 mitral regurg. Patient weaned off bypass on epi drip. post op patient in ICU, patient weaned of epi, and given large fluid bolus to maintain presure. CVP increases but no change in systemic pressure, and patient began to deteriorate. What is happening?
RV failure
- pre-existing pulm HTN –> chronic afterload will increase RV wall tension –> inc O2 demand
- cross-clamping of aorta and bypass -> dec coronary blood flow –> ischemia
- LV function depressed immedietly after MV repair –> pre-existing LV chamber is dilated due to chronic increase end-diastolic volume.
- after MV repair, dilated LV cannot eject blood into low resistance MV to LA chamber. Has to eject blood against a higher afterload (aorta) only. –> reduced EF
What is law of Laplace? what does it do?
Wall Stress = (LV pressure x radius) / 2 x LV wall thickness
- Left ventricular wall stress is the force acting against the myocardial cells.
- directly proportional to the left ventricular pressure and radius (inc O2 demand)
- LV pressure - states that increase “afterload” of the heart including systemic hypertension and aortic valve stenosis.
- LV radius - valvular heart disease (especially aortic regurgitation) or cardiomyopathies causing systolic heart failure.
- Wall stress is indirectly proportional to two times the wall thickness (dec O2 demand)
- LV wall thickness increases (compensatory mech) in order to minimize increase in wall stress –> therefore decreasing oxygen demand (since the stress will be distributed over a larger mass)
what is the impact of chronic pulm HTN on RV function?
- chronic pulm HTN = Increase Afterload
- increase afterload -> increase wall stress of RV
- RV compensate –> inc wall thickness (RVH)
- RVH casuses flattening of interventric septum –> decrease diastolic filling of LV (reduce LV chamber size)
- prolong Pulm HTN –> hypertrophy to dilation of RV –> dec cardiac output –> tricuspid annular dilation –> TR –> CHF
How is RV failure diagnosed?
- cardiac MRI
- asses RV structure and function
- Cardiac cath
- look at PVR
-
ECHO
- measure RVEF
- tricuspid annular plane systolic excursion (TAPSE)
How can RV dysfunction lead to LV dysfunction?
-
RVH or RV dilation leads to bowing of RV septum toward LV
- this results in decrease LV compliance, decrease LV filling chamber size –> LV Diastolic dysfunction
How do you treat RV failure?
Goals:
1) maintain preload
- provide volume, do not overdistend RV
2) decrease PVR
- PDE inhibitor - milrinone
- pulm vasodilators - nitric oxide, prostaglandin E1 (iloprost)
3) Maintain SVR
- end organ perfusion + CPP
4) support LV and RV contractility
- inotropic support - epi, milrinone
- RVAD
- IABP
What are the benefits and complications of PAC?
PAC benefits
- CO by thermodilution
- right-sided filling pressur (CVP)
- left-sided fillinge pressure (pulm artery diastolic pressure or pulmonary capillary wedge pressure)
-
calculate SVR, PVR
- can help guide use of vasoconstrictor or dilators
-
calculate ventricular stroke work
- can help guide inotrope therapy
PAC complications
- arrythmias (heart block in pre-exist bifascicular block)
- air embolism
- endocardial damage
- valvular damage
- pulm A rupture
- pulmary infarction (decrease blood flow to pulmonary tissue due to mech obsruction of PAC)
What are normal intracardiac pressures? (Right atrium all the way till LV systolic pressure/LVEDP)
Right atrium
- 1-12 mmHg (mean 6)
RV (systolic/diastolic)
- 15-30 / 2-8 (mean 25/5)
PA pressure systolic
- 15-30 (mean 20)
PA pressure diastolic
- 5 - 15 (mean 10)
mean PA pressure
- 10 - 20 (mean 15)
PCWP/LA pressure / LVEDP
- 4-15 (mean 10)
LV systolic pressure
- 90-140 (mean 120)
what is normal CO, CI, SV?
- CO: 4-6 L/min
- CI: (CO/BSA): 2.8 - 4.2 L/min/m2
- SV: 50-100 mL
how do you calculate SVR and PVR, what are their normal values?
SVR
- SVR = { (MAP - CVP) / CO } x 80
- normal 800 - 1200 dyne sec cm -5
PVR
- PVR = { (MPAP - PCWP) / CO } x 80
- mPAP = mean pulm artery pressure
- normal 150 - 250 dyne sec cm -5
