0
Q
Aorta
A
- receives blood from left ventricle
- large elastic component allows for distention and continuous flow
1
Q
Cardiac cellular structure
A
- large dilated T-tubules arranged in diads containing glycocalyx
- Ca induced Ca release (contractility)
- functional syncytium
- maximal force is developed when sarcomere is 2-2.4 micrometers (big heart isn’t always a strong heart)
2
Q
Arteries
A
- higher systolic pressure than aorta but lower diastolic so MAP is essentially the same
- frictional resistance is low so pressure remains high (spikes in arterioles where pressure drops sharply)
- significant muscle component
3
Q
Arterioles
A
- resistance vessels: large drop in BP and velocity
- from pulsatile -> steady
- regulates flow into capillary bed
4
Q
Capillary beds
A
- high cross sectional area
- very slow flow (important for exchange)
- O2 sat post ex: 50-80%
5
Q
Venules
A
- 20 micrometers
- increased velocity
- no smooth muscle
6
Q
Veins
A
- largest container of blood volume
- pressure continues to drop as they get near the heart
- they do contain smooth muscle (unlike venules)
7
Q
Pulmonary O2 sat
A
94-98% after exchange
- 18 to 20 mls O2/100 mls blood
8
Q
Phases in myocytes contraction
A
Phase 0: rapid depol; fast - Na influx, slow - Ca influx
Phase 1: partial depol; K efflux (only in fast)
Phase 2: plateau - balance of Ca in, K eff
Phase 3: repol - Keff predominates
Phase 4: resting/pacemaker potential
9
Q
Fast vs slow ap
A
- fast response occurs in ventricles (propagating through thicker tissue)
> resting potential more negative
> amplitude of wave is determined by Na channels - slow occurs in SA/AV nodes
> higher resting membrane potential
> Ca channel regulated
10
Q
Overdrive suppression
A
- fastest pacemaker takes control
11
Q
Bidirectional block
A
- no ap is conducted through particular region
- either intense vagal stimulation or cell damage (ischemia)
12
Q
Unidirectional block
A
- Anterograde block, retrograde propagation
- may result in reentry arrythmias
- elevated extracellular K, extracellular lactic acid
- trt by speeding up or slowing down conduction to induce bi directional block (lido slows down by blocking Na channels)
13
Q
Depolarization and Ca release
A
- Ca induced Ca release
- glycocalyx has a charge that holds Ca close
- ryanodine receptors close to Ca channels so release is significant and local from SER
- pH effects release significantly (basic pH induces, acidic pH inhibits) maximal at 7.4
14
Q
Preload
A
- stretching the elastic element (end diastolic volume)
- increasing preload will increase contraction up to maximal response
15
Q
Afterload
A
- the pressure the ventricle must work over come to eject (aortic pressure
- increased afterload will increase pressure during isovolumetric contraction
16
Q
Velocity and force of contraction
A
- inverse: no load = highest velocity
- in isotonic contraction muscle is preloaded and after loaded
- elastic first with no shortening of external length
17
Q
Contractility
A
- aka ionotropic state
- performance at given pre and afterload
- EF is a good index for contractility
18
Q
Frank-Starling mechanism
A
- In an isolated heart, as preload increases so does contraction
- maximal contraction reqs optimal stretching (not too full, not too empty)
- increasing afterload will initially decrease SV, heart will compensate the following beat and increase force of contraction maintaining CO, but at greater energy cost
19
Q
Ficks principle
A
- CO = O2 consumed /(PVO2-PAO2)
- computed over several beats
- can be used to measure O2 consumption in a single organ
20
Q
Dilution measurement of CO
A
- CO = amt Dye injected/(time when dye [] = 0 - time first injected)
- recirculation is a problem
- lare central vein/rt side of heart
21
Q
Thermodilution
A
- measures CO based on ice cold saline in vein, temp measured in pulmonary artery
22
Q
Echo Doppler
A
- non-invasive! But expensive…
- CO = x-section of aorta multiplied by velocity
23
Q
Fluid movement (starling equation)
A
- flow = K [(Pc+PiIF) - (Pic+PiIF)]
24
aortic pressure curve follows decreased trajectory (similar pattern but less extreme and lower over all) ejection also happens with greater velocity
- aortic stenosis
25
Normal pressure curve but reduced overall with increased atrial pressure (but overall increased)
- mitral stenosis
26
Normal ventricular and atrial pressure curve but aortic pressure curve drops sharply after ejection
- aortic regurgitation
27
Decreased overall pressure curve, left atrial pressure spikes in diastole
Mitral regurgitation
28
A murmur that increases on inspiration
Right side defect
| - inspiration increases venous return delaying pulmonic valve closure such that it is more easily discerned
29
Murmurs increasing on expiration
- increases volume of blood ejected from left ventricle increasing mitral and/or pulmonic opening
30
Left 3rd IC space
Erbs point
| - best to auscultation S2 split
31
Phospholambam
- seriously....?
- modifies speed of Ca pump in SER sequesting Ca
- when phosphorylated cAMP protein Kinase it activates speeding up sequestration
32
Reynolds number
- measure of viscosity and velocity
> low velocity and high viscosity = higher Reynolds number
> Nr ~ 2500 you start to see turbulence
> most likely in ascending aorta
- conditions like anemia and polycythemia affect significantly
33
Fahraeus-Lindquist effect
- fastest Lamina in blood flow pulls blood cells toward it and plasma is pushed peripherally and moves slower allowing for the transfer of nutrient and gas exchange
34
Plat vs. Pdyn
- dynamic pressure is the kinetic force and represents ~ 95%
- In vessels with atherosclerosis, velocity is increased to the Plat is decreased and the smaller collateral vessels can be compromised
- in a dilated vessel, velocity drops and P lat increases compromising the already damaged intima
35
Pulse pressure
Pp = Psys - Pdyn
| - hardened arteries show increases PP, less accommodating of pressure change
36
Effect of Loss of compliance on MAP
- diastole drops (weighted) dropping MAP more than the increase raises it.
- TPR increases to maintain MAP
- TPR increase -> increase afterload
37
First heart sound
Closure of AV valves (lub)
38
Second heart sound
AP valves closing
| - split may be heard on inspiration or with right AV block
39
Third heart sound
Blood hitting incompliant ventricles in early/mid diastole
- low frequency
- only common in young; adult 3rd sound is pathological
40
Fourth heart sound
Filling of ventricle which cannot expand by atrial systole
| - not normally heard
41
Opening snap
Blood hitting residual volume in diastole
42
Increase in blood volume (decrease in TPR) on a starling venous return chart
- clockwise rotation of the venous return curve
| * Not actually TPR: arteriodilation without venodilation increases venous return
