Cardiac Surgery Flashcards
What is Ohm’s law and what is its relevance in relation to cardiology?
Q = (P1 - P2)/R.
In relation to cardiology, states that pressure differences (delta P) are the driving force for blood flow (Q) and that increased resistance (R) of vessels will deter blood flow (Q).
Consider: BP = CO x SVR, where BP = P, CO = Q, SVR = R.
Aka if you rearrange it, CO = BP/SVR or Q = P/R (Ohm’s law)
What is Poiseuille’s law and what is its relevance to cardiology?
Q = (P2 - P1)pir^4 / 8nl.
Translation: blood flow (Q) is exponentially (power of 4) proportional to the radius (r) of the vessel. I.e. 4 cm vessel has 16x flow rate of 1 cm vessel. Alt, small decreases in radius (r) will result in very large resistances to flow.
Blood flow (Q) is inversely proportional to vessel length (l) and viscosity (n).
Applications: If you need to resuscitate someone, use a large bore (big r) IV that is short (decrease l).
What is the Law of Laplace and how does it relate to cardiology?
Wall stress (T) = Pr / 2*wall thickness P = LV pressure. r = LV radius. Wall thickness = LV wall thickness.
Stress on the wall of the L ventricle is proportional to the P in the ventricle and increases with ventricle radius and is reduced by a factor of 2 with increased wall thickness.
Clinical applications:
1) An aneurysm will increase LV wall stress by increasing radius and decreasing wall thickness.
2) Wall stress increases with afterload (increased LV P). The heart will try to compensate by remodeling to increase wall thickness. This in turn increases oxygen demand to the heart.
3) Reducing wall stress can decrease oxygen demand of heart.
Major vessels of coronary anatomy.
RCA –> posterior descending artery. Supplies RV, atrium, AV and SA nodes.
L main CA –> L circumflex and L anterior descending. L circumflex provides oxygen to lateral and back of heart. L anterior descending provides oxygen to anterior L heart.
Define: CO, Cardiac Index, EF, Pulm Artery Wedge P, CVP
CO: vol of blood ejected per min.
Cardiac Index: = CO/BSA. Vol of blood pumped by heart divided by BSA. Relates heart performance to the size of the individual.
EF: SV/EDV. Considered systolic dysfunction once <40%.
Pulmonary Artery Wedge P: Indicator of LV end-diastolic vol (and thus preload). P within the pulmonary arterial system when catheter tip is wedged into the tapering branch of one of the pulmonary arteries.
CVP: measure of RA P/SVC. Measures filling pressure of the R side of the heart. Indicates the amt of blood returning to the heart.
Determinants of myocardial oxygen supply vs demand
Oxygen Demand: HR, contractility, myocardial wall stress.
Oxygen Supply: blood flow, oxygen content. Requires fxnal lungs, adequate blood O tension, fxnal hgb.
Causes of cardiac ischemia.
Ischemia: inadequate blood flow (worse than hypoxia, which does not always result in ischemia.
Thrombosis (atherosclerotic CAD), embolism, spasm, dissection, ostial narrowing due to aortitis, Syndrome X (microvascular coronary disease), HOCM, Ao stenosis, Aortic insufficiency, anemia, hypoxia.
ACS: what, RF, presentation, mgmt.
Stenosis: >70% stenosis is enough to create significant blockage and warrants revascuarlization for ischemia.
Presentation: Use CCS/NYHA for severity of angina. May be stable or unstable.
RF: HTN, DM, high chol, smoking, famHx CAD, vascular disease (TIA, stroke).
Medical mgmt: acutely– ASA, BB, ACEi, nitrate, heparin. Long term– ACEi, statin.
PCI: indicated for severe obstruction, high risk for CABG complications.
CABG: Indicated for L main artery stenosis >50%, 3 system disease or 2 system disease with significant proximal stenosis. Use L internal mammary artery for graft.
Signs of acute cardiac tamponade, investigations, tx
Beck’s triad: distended neck veins, muffle heart sounds, hypoTN.
Also: tachyardia, altered ECG.
Do cardiac sonogram (part of FAST scan).
Tx: immediate decompression via needle pericardiocentesis, pericardial window or thoracotomy with manual decompression.
Aortic Stenosis: what, etiology, pathophys, SS, investigations, mgmt
What: incomplete AV opening causing fixed LV obstruction. Restricts blood flow out of LV.
Etiology: congenital– bicuspid aortic valve, sub/supra-valvular aortic stenosis. Acquired– degenerative AS or rheumatic.
Pathophysiology: obstruction to LV outflow -> increased LV P -> increased LV wall stress. Causes concentric hypertrophy resulting in less compliant LV and eventual diastolic dysfunction. Increased end-diastolic pressures cause impaired maximal coronary flow. Increased oxygen demand with now impaired supply.
SS: Syncope, angina, dyspnea. Fatigue, decreased exercise tolerance, GI bleeding. Once symptoms manifest, survival drops rapidly.
On PEx, prominent a wave at JVP, carotid bruits, small volume and delayed carotid pulse, systolic crescendo-decrescendo murmur at RUSB. Delayed S2 or single/paradoxically split S2. Brachio-radial delay, carotid-apical delay.
Investigations: ECHO
Mgmt: No medical options. For congenital causes of AS, can do PBV or TAVR. For other causes, aortic valve replacement with either mechanical or bioprosthetic valve.
Pro’s/con’s of mechanical or bio-prosthetic valves.
Mechanical: lasts longer but requires use of warfarin which can potentially cause birth defects. Need to have discussion re: risks with pre-menopausal women.
Bioprosthetic: no warfarin needed but doesn’t last as long (~10 yrs). Good for older individuals (don’t wear out valves as quickly) and for young women who plan to have children.
5 causes of congenital cyanotic heart disease
Tetralogy of Fallot: overriding aorta, pulmonary artery stenosis, RV hypertrophy, VSD.
Transposition of the great arteries.
Truncus arteriosus.
Tricuspid atresia (no connection between RA and RV, blood moves form RA via PFO).
Total anomalous pulmonary venous return.
