MAP
(1/3 x SBP) + (2/3 x DBP)
Or
[(CO x SVR) / 80] + CVP
~depends which variables you’re given in the question
→ directly affected by: CO, SVR
SVR
[(MAP - CVP) / CO] x 80
Normal is 800-1500 dynes/sec/cm^5
PVR
[(MPAP- PAOP) / CO] x 80
Normal = 150-250 dynes/sec/cm^5
Law of Laplace
Wall stress = (intraventricular pressure x radius) / ventricular thickness
Which 3 conditions set afterload proximal to the systemic circulation?
- AS
- Hypertrophic cardiomyopathy
- Coarctation aorta
Coronary perfusion pressure equation
Aortic DBP - LVEDP
Which TEE view is best for diagnosing myocardial ischemia?
Midpapillary muscle in short axis
Which region of heart is most susceptible to ischemia?
LV subendocardium - best perfused during diastole -
Resting membrane potential of cardiac myocyte
-Myocyte membrane is permeable to K+, but not other electrolytes or proteins. K+ is the primary determinant of RMP
→ when K+ ↓, RMP → more negative, myocytes harder to depolarize (hypokalemia = harder to depolarize)
→ when K+ ↑, RMP → more positive, myocytes easier to depolarize (hyperkalemia=easier to depolarize, why hyperkalemia → vtach/vfib etc)
Cardiac action potential: SA node
4 - 0 - 3
4: spontaneous depolarization = Na+ in, lf or “funny current”
0: depolarization = Ca2+ in
3: repolarization = K+ efflux
Cardiac action potential: ventricle
0=depolarization=Na+ in
1=initial repolarization = Cl- in, K+ out
2=plateau = Ca2+ in
3=repolarization = K+ out
Autonomic innervation of the heart
At rest, PNS > SNS
PNS: R vagus nerve innervates SA node, L vagus innervates AV node
SNS: cardiac accelerator fibers T1-T4
Normal values: Ca02, D02, V02, Cv02
Ca02=arterial 02 content: 20mL/02/dL
D02=delivery: 1000mL/min
V02=consumption: 250mL/min
Cv02=venous 02 content: 15mL/dL
Mechanical/valvular events of systole
Isovolumetric contraction:
- S1, MV closed, AV closed.
- LV pressure ↑, LV volume constant.
Ventricular ejection:
- MV closed, AV open → SV ejected into aorta.
- most of SV ejected during first 1/3 of systole.
Diastole: mechanical, valvular events
Isovolumetric relaxation:
- S2. MV closed, AV closed
- LV pressure ↓, LV volume constant.
Rapid ventricular filling:
- MV open, AV closed
- LV pressure constant, LV volume ↑
DIASTASIS or reduced ventricular filling:
- MV open, AV closed
- LV filling still happening, but slows down a lot.
Atrial systole:
- MV open, AV closed =
- LA contraction = AV ‘kick”
- contributes last 20% filling
- end of atrial systole = EDV
Primary determinants of end systolic volume
Afterload (SVR)
Contractility
End systolic volume directly affects: SV, CO
Primary determinants of end diastolic volume or preload
- Filling pressure
- Compliance
ESV or preload directly affects: SV, CO
Conditions in which PAOP overestimates LVEDP? Underestimates it?
OVERESTIMATES:
- Impaired LV compliance (ischemia)
- Mitral valve diseas (MS or MI)
- L → R shunt
- Tachycardia
- PPV, PEEP
- COPD
- pulm HTN
- PA cath tip placed outside West zone III
UNDERESTIMATES:
-Aortic insufficiency
BP measurement change with height differences
- For every 10 cm change, BP changes by 7.4mmHg
- For every inch change, BP changes by 2mmHg
Which leads monitor the CxA?
Which area of the myocardium does this correspond to?
- LATERAL wall
- I, aVL, V5, V6
Which leads monitor the RCA?
Area of myocardium?
INFERIOR wall
-II, III, avF
Which leads monitor the LAD?
Area(s) of myocardium?
- SETPAL:V1, V2
- ANTERIOR: V3, V4
02 delivery
D02 = Ca02 x CO x 10
When is the EKG not an effective intraoperative monitor of myocardial ischemia?
- LV hypertrophy
- conduction abnormalities
- V-pace dependent
