Cardiovascular Flashcards
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
Major determinants of cardiac demand
- Basal 02 needs
- LV wall tension (↑ preload or ↑ afterload → ↑ tension)
- HR
- contractility
Why do you need a PA cath to measure Sv02?
-Because different organs extract different amounts of 02, a true mixed venous sample must contain blood returning from the SVC, IVC, and coronary sinus. The only place blood from all 3 of these sources mixes is in the pulmonary artery.
MR/MI
“Fast full forward” sort of…
HR: ↑ normal with NSR
↑ Preload: some SV lost to LA, ↑ preload helps compensate.
(PAOP overestimates LVEDP)
Afterload: ↓ helps promote forward flow
Weird causes you might not think about: muscular dystrophy, scoliosis
AR/AI
Fast, full, forward
Can be caused by RA, Marfan’s
MS
Full, slow, tight
HR: low-normal with NSR
Preload: maintain, LV chronically underfilled, but don’t make it too much, hypervolemia → ↑ LAP → ↑ pulm congestion
Afterload: maintain (rapid ↓ SVR → baroreceptor mediated ↑ HR = not good), phenylephrine is ideal
Aortic stenosis
HR: 70-80, NSR: properly timed atrial contraction imperative
Preload: ↑ : adequate LVEDP to fill noncompliant LV
SVR: maintain or ↑ (phenylephrine usually good)
How to think about valvular lesions in the context of pressure volume loops
- Stenotic valves cause pressure overload → change HEIGHT of PV loop
- Regurgitant values cause volume overload → change WIDTH of PV loop
How long should elective surgery be delayed after stent placement?
- DES: 6 months
- BMS: 30 days
Types of AAAs that involve the ascending aorta
DeBakey 1 and 2
Stanford type A
-All are surgical emergencies
AV often involved so consider AI in your anesthetic plan
Contraindications to aortic balloon pump
- Severe AI
- Descending aortic disease
- Severe PVD
- Sepsis
Systolic and diastolic murmurs
Systolic: MR, AS
Diastolic: MS, AR
AoX application: what ↑, what ↓ ?
↑ c application:
venous return (blood volume shifts proximal to clamp)
MAP, SVR, PAOP, coronary flow, Sv02 (less consumed so more leftover)
↓ c application:
Renal blood flow (even if clamp is infrarenal), CO, total body V02
AoX removal: What ↑, what ↓ ?
↑ c removal: PVR, total body V02
↓ c removal: CO, MAP, SVR, venous return, renal blood flow, coronary flow, Sv02
Only drugs that can reverse myocardial remodeling
ACEIs (-pril)
Aldosterone inhibitors
→ of enhanced cardiac silhouette on CXR
Pericardial effusion
cardiomegaly
Cardiac aneurysm
In an MI/02 supply-demand imbalance situation, which parts of the heart fail in which order?
Diastolic dysfunction (↓ ventricular compliance) occurs first.
Systolic dysfunction occurs second. → wall motion abnormalities, usually correlates with ↓ EF. TEE is an excellent monitor of systolic function.
EKG changes occur after systolic dysfunction.
Clinical symptoms after all these.
Which 4 conditions WORSEN LVOT in HOCM
- ↓ preload
- ↓ afterload
- ↑ HR
- ↑ contractility
Want to volume load, depress myocardium a little, lower HR, and dilate them
LCA
Gives rise to circumflex and anterior interventricular arteries
RCA
Gives rise to PDA and marginal
Hyperkalemic EKG signs of pending cardiac arrest needing IMMEDIATE intervention
P wave flattening/disappearing
QRS prolongation
QRS → sine wave pattern, then VF, then arrest
