Chest Pain Flashcards
Flux (J)
=KD[^C/^x]
Fick equation
VO2 = CO x (arterialO2-venousO2)
Cardiac output equation
CO = HR x SV
Left side of the heart
systemic circulation
Right side of the heart
pulmonary circulation
Pulmonary and systemic circulation systems are in?
Series
Organs are in?
Parallel, each organ gets freshly, fully oxygenated blood, flow to one organ can be changed without affecting flow to other organs
Hemodynamic Ohm’s Law equivalent
Q = ^P/R
Resistance =
^P/CO = (MAP-CVP)/CO
MAP normal?
95mmHg
CVP normal?
2mmHg
CO normal?
5-6L/min
Blood flow is proportional to?
Pressure difference
Pressures of heart chambers
RA = 2mmHg RV = 25/10mmHg LA = 8-9mmHg LV = 130/80mmHg
Responses to drop in pressure?
- Reduced outflow (increase R) controlled by SNS 2. Increase inflow by increasing HR and contractility 3. Increase volume (short term - venous return, long term - salt and water retention increase BV)
Depolarization of the heart
SA, AV, septum (left to right), His/Purkinje system, ventricular muscle (endo to epicardium)
Fast APs vs Slow APs of heart
contracting regions (atrial and ventricular muscles), fast conduction (His, Purkinje), Left side pacemaking (SA) and slow conduction (AV) right side
Fast AP Phases
0 - rapid depol due to activation of inward Na+ current 1 - initial repol due to inactivation of Na+ channels and activation of transient outward K+ channels (Ito) 2 - plateau phase due to slow activating inward Ca++ currents, triggers CICR 3 - repol due to inactivation of Ca++ currents and activation of several different K+ currents (Iks, Ikr) 4 - resting membrane potential due to inward-rectifying K+ channels (Ik1)
Slow AP Phases
0 - slow depol due to activation of slowly-acting Ca++ channels 1 - absent 2 - absent 3 - repol due to Ca++ channel inactivation and activation of K+ channels 4 - slowly depolarizing resting potential (If - nonselective cation channel - HCN)
Absolute refractory period for fast v slow AP
Fast - Na inactivation Slow - Ca inactivation
Spontaneous depol of Slow AP
imbalance between outward K channels (Ik,ach, or Igirk) and inward current of not selective cation channel (If)
Parasympathetic stimulation on AP
PNS releases ACh, binds to muscarinic ACh receptors, increasing Igirk, reducing rate of phase 4 depol, negative chronotropic effect
Sympathetic stimulation on AP
SNS release norepi, epi, binds to b1 adrenergic repectors, increase both If and Ica, increasing phase 4 depol, positive chronotropic effect
Intrinsic rate of SA node, AV node, and His/Purkinje systems
SA = 100bpm AV = 40-60bpm His/Purkinje = 30-40bpm
Dromotropic effects
Positive dromotropic effect - increases AP conduction, SNS Negative dromotropic effect - decreases AP conduction, PNS
P-wave
atrial depolarization, speed of propagation throughout the atria
PR-segment
movement of the AP through the AV node
QRS-complex
ventricular depolarization
Q-wave
left side of the septum depolarizes before the right, resulting in small downward deflection
R-wave
depolarization spread from endo to epicardium, large muscle mass involved, large amplitude
S-wave
last part of ventricle depolarization is near the atrium, gives brief negative deflection
Bundle-branch block
widening of QRS
ST-segment
interval between ventricular depolarization and repolarization
T-wave
ventricular repolarization
Interval between P-waves
‘sinus rhythm’, HR, tachycardia, bradycardia
Lead I, II, aVf, III, aVr, aVL
0, +60, +90, +120, -150, -30
Right and left axis deviations
Right - MEA moves right, clockwise, pulmonary HTN Left - MEA moves left, counterclockwise, systemic HTN
Normal MEA
between +100 and -30
First degree heart block
P-waves are all followed by QRS, but PR-interval is increased
Second degree heart block
PR interval lengthened so much that not every P-wave is followed by QRS
Third degree heart block
P-wave and QRS depolarize independently with ventricle depol driven by latent pacemaker
Atrial flutter
P waves are too fast, driven by atrial pacemaker, but QRS is normal
Atrial fibrillation
atria are not driven by SA node, but instead by local currents, result in uncoordinated atrial firing and no P waves are detected
Ventricular tachycardia/flutter
ventricular rate is greater than atrial rate, due to ectopic pacemaker
Ventricular fibrillation
electrical activity is completely uncoordinated, lethal condition that must be corrected within minutes
Spontaneous AP in ventricular cells
abnormal QRS complex
ST segment depression/elevation
MI occurred recently
S4
Atrial gallop usually due to ventricular hypertrophy, occurs in late diastole, never normal to hear
S3
Ventricular gallop heard during ventricular filling, common in children and young adults, due to supple ventricle, but sign of dilated cardiomyopathy in an adult
Compliance
volume changes with pressure
SV
CO = SV x HR
Normal EF
>55%
Increasing Preload of the heart?
increases EDV, SV, CO no affect on aortic pressure
Heart Failure
decreased CO triggers increased BV, PL, EDV, SV and CO, but this is only a short term compensatory mechanism, decreases starling curve/inotropy
Law of LaPlace
wall stress (sigma) = [P x r]/2h Pressure, chamber radius, wall thickness
Increasing Afterload of the heart?
force that heart has to overcome to force blood into the aorta, afterload is wall stress, very close to aortic pressure increases aortic pressure that ventricle must contract against to open valve, and valve closes at higher pressure, ESV Decreasing fiber shortening velocity, SV, CO
Aortic stenosis
left ventricular emptying is impaired because of narrowing of the aortic valve, flow through aortic valve generates additional sounds between S1 and S2
Increasing Inotropy of the heart?
Shifts ESPVR curve to the left and increases line slope, increases velocity of shortening, decreases ESV, increasing SV and CO
Blood flow (Q) =
Q = V x a = P/R
Poiseulle’s equation
Q = [P(Pi)r^4]/8Ln(viscosity)
Changes to viscosity
- life at high altitudes, increased viscosity 2. polycythemia vera, increased viscosity 3. severe dehydration, increased viscosity 4. sickle-cell anemia, increased viscosity
Parallel arrangement has the highest resistance
FALSE - LOWEST
Normal MAP
95mmHg
TPR =
[MAP-CVP]/CO
Normal TPR
15-18mmHg/l/min or 15-18 HRUs or Wood units
PP
Pulse pressure = SBP - DBP
MAP =
DBP + [PP/3]
Septic shock is associated with?
Large drop in TPR, only form of shock that is associated with decrease, rather than increased TPR
Factors that affect Poiseuille’s law
- turbulent flow 2. viscosity of blood changes with velocity 3. compliance of blood vessels
Reynold’s Number
Nr = vdp/n velocity, diameter, density, viscosity Nr>2000 = turbulent flow
Korotkoff sounds
partial occlusion of brachial artery with pressure cuff that reflects blood spurting at high velocity through the constriction
compliance =
[^V] / [^P]
capacitance vessels
thin walled vessels with minimal resistance to stretching by filling pressures
Hydrostatic pressure
pushing fluid out
Osmotic pressure
sucking fluid in
Starling’s Law of the Capillary
Q = k[(Pc+[Pi]i)-(Pi+[Pi]c)] Q = k [force in - force out] k is dependent on type of capillary, increasing with leakiness
Hydrostatic v Osmotic pressure for: renal system, pulmonary circulation, CHF, Nutritional Edema
Renal system - H > O, fluid moves out of cap, urine Pulmonary circulation - H < O, fluid moves into cap, dry alveoli CHF - H > O, fluid moves out of cap, edema Nutritional Edema - H > O, fluid moves out of cap, because lower osmotic pressure because no albumin, ascites
Local control
independent of CNS, metabolic waste build-up (adenosine, lactate, CO2, H+, K+) and myogenic (autoregulation) to keep blood flow consistent
Central control
CNS makes final decision, humoral mechanisms (ANP, AngII, Epi, NO, ET-1) or neural mechanisms (targeted to certain organs)
Phases Wiggers diagram
- Atrial systole 2. Isovolumetric contraction 3. Rapid Ejection 4. Reduced Ejection 5. Isovolumetric relaxation 6. Rapid Filling 7. Reduced Filling
When and what time is S1 heard?
Isovolumetric contraction at 0.1sec
When and what time is S2 heard?
Isovolumetric relaxation at 0.4sec
Changes in inotropy are dependent on sarcomere length
FALSE - INDEPENDENT
Ventricular hypertrophy increases or decreases compliance?
Decreases
typical EF?
60%
HR equation
=60/R-R interval (#blocks x 0.04sec)
Cardiac impulse through AV node plus bundle
0.13sec (0.09 AV, 0.03 His)
SA node to epicardium
0.22sec
Normal Q-T interval
0.35-0.40sec
Normal QRS
0.12sec
Right bundle branch block cause
Pulmonary hypertension
Left bundle branch block cause
Systemic hypertension, aortic valve stenosis and regurgitation
Normal PR interval
0.12-0.20sec
