Heart Mechanism Flashcards
Aorta
- receives blood from left ventricle
- large elastic component allows for distention and continuous flow
Cardiac cellular structure
- 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)
Arteries
- 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
Arterioles
- resistance vessels: large drop in BP and velocity
- from pulsatile -> steady
- regulates flow into capillary bed
Capillary beds
- high cross sectional area
- very slow flow (important for exchange)
- O2 sat post ex: 50-80%
Venules
- 20 micrometers
- increased velocity
- no smooth muscle
Veins
- largest container of blood volume
- pressure continues to drop as they get near the heart
- they do contain smooth muscle (unlike venules)
Pulmonary O2 sat
94-98% after exchange
- 18 to 20 mls O2/100 mls blood
Phases in myocytes contraction
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
Fast vs slow ap
- 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
Overdrive suppression
- fastest pacemaker takes control
Bidirectional block
- no ap is conducted through particular region
- either intense vagal stimulation or cell damage (ischemia)
Unidirectional block
- 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)
Depolarization and Ca release
- 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
Preload
- stretching the elastic element (end diastolic volume)
- increasing preload will increase contraction up to maximal response
Afterload
- the pressure the ventricle must work over come to eject (aortic pressure
- increased afterload will increase pressure during isovolumetric contraction
Velocity and force of contraction
- inverse: no load = highest velocity
- in isotonic contraction muscle is preloaded and after loaded
- elastic first with no shortening of external length
Contractility
- aka ionotropic state
- performance at given pre and afterload
- EF is a good index for contractility
Frank-Starling mechanism
- 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
Ficks principle
- CO = O2 consumed /(PVO2-PAO2)
- computed over several beats
- can be used to measure O2 consumption in a single organ
Dilution measurement of CO
- CO = amt Dye injected/(time when dye [] = 0 - time first injected)
- recirculation is a problem
- lare central vein/rt side of heart
Thermodilution
- measures CO based on ice cold saline in vein, temp measured in pulmonary artery
Echo Doppler
- non-invasive! But expensive…
- CO = x-section of aorta multiplied by velocity
Fluid movement (starling equation)
- flow = K [(Pc+PiIF) - (Pic+PiIF)]
aortic pressure curve follows decreased trajectory (similar pattern but less extreme and lower over all) ejection also happens with greater velocity
- aortic stenosis
Normal pressure curve but reduced overall with increased atrial pressure (but overall increased)
- mitral stenosis
Normal ventricular and atrial pressure curve but aortic pressure curve drops sharply after ejection
- aortic regurgitation
Decreased overall pressure curve, left atrial pressure spikes in diastole
Mitral regurgitation
A murmur that increases on inspiration
Right side defect
- inspiration increases venous return delaying pulmonic valve closure such that it is more easily discerned
Murmurs increasing on expiration
- increases volume of blood ejected from left ventricle increasing mitral and/or pulmonic opening
Left 3rd IC space
Erbs point
- best to auscultation S2 split
Phospholambam
- seriously….?
- modifies speed of Ca pump in SER sequesting Ca
- when phosphorylated cAMP protein Kinase it activates speeding up sequestration
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
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
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
Pulse pressure
Pp = Psys - Pdyn
- hardened arteries show increases PP, less accommodating of pressure change
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
First heart sound
Closure of AV valves (lub)
Second heart sound
AP valves closing
- split may be heard on inspiration or with right AV block
Third heart sound
Blood hitting incompliant ventricles in early/mid diastole
- low frequency
- only common in young; adult 3rd sound is pathological
Fourth heart sound
Filling of ventricle which cannot expand by atrial systole
- not normally heard
Opening snap
Blood hitting residual volume in diastole
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
