3 - CV Physiology Flashcards
Myocardium (key points)
- 95% of the heart
- responsible for pumping
- cardiac muscle (involuntary)
- fibers swirl diagonally around the heart
Cardiac muscle tissue (structural components of cell connections)
- sarcolemma (cell wall)
- cells connect at intercalated discs (1) containing:
- gap junctions (allow cells to communicate)
- desmosomes (keep fibers connected)
1-thickened sarcolemma
quiz on:
cardiac conduction system
see goodnotes
Sinoatrial (SA) node
(electrical signal)
fires constantly (100 times/min) which would translate to our bpm if nothing controlled it
cardiac conduction system anatomy
- sinoatrial (SA) node
- atriventricular (AV) node
- bundle of HIS
- right and left bundle branches
- purkinje fibers
Action potential phases in ventricular myocyte
RMP roughly -90mV (1)
rapid depolarization (+20mV)
- Na+ channels open
- Na+ inflow depolarizes the cell
plateau (+10mV)
- Ca2+ inflow
- some K+ outflow
repolarization (90mV)
- Ca2+ channels close
- K+ outflow
refractory period (2) from depolarization to mid repolarization
contraction starts right after RP and ends right before
1-voltages are just examples, 2-cardiac AP cannot trigger
Electrocardiogram (ECG) 3 waves
(draw + label)
also called ECG or EKG, see goodnotes for graph
in order:
- P wave: small wave (+0.1mV/0.1s)
- QRS complex: 3 spikes (0.2,+1,-0.4mV/0.1s)
- T wave: large wave (+0.2mV/0.2s)
- U wave: tiny wave (not visible on most graphs)
voltages and times are just example values
info on how ECG functions is on avenue, not neccessary
Events corresponding to sections of the ECG graph
- P: atria depolarize (action potential at SA node)
- flat: atrial systole (1)
- QRS: ventricles depolarize
- flat: ventricular systole
- T: ventricles repolarize
- flat: ventricles relax
1-contraction
average values for adult:
- cardiac cycle length
- native bpm
- stroke volume
- blood pressure
- 0.8s
- 75bpm
- 70mL
- < 120/80 mmHG
Pressure waves vs ECG
(draw wave + label valve changes)
see goodnotes for graph
pressure waves: aortic, V, A
- AV close: R spike, first dip in LV/LA P
- SL open: QRS end, start of 1st wave for aortic P, 2nd wave peak LA
- SL close: mid T, dip in aortic P
- AV open: T end, end of wave in LV and aortic P, small wave in LA
systole –> increased pressure
aortic valve pressure wave
(notable points)
- aortic valve opens
- aortic valve closes
- dicrotic wave due to rebound off valve closure
heart sounds
loudest
- S1: AV valves close
- S2: SL valves close
- S3: ventricles fill (much quieter
- S4: atrial systole (almost silent)
Pressure phases (cardiac cycle) in order
- atrial contraction (AV open)
- isovolumetric contraction (all closed)
- ventricular ejection (SL open)
- isovolumetric relaxation (all closed)
- ventricular filling (AV open)
- atrial contraction (AV open)…
Ventricular volume curve
(draw + label)
- end diastolic volume (V systole start)
- end systolic volume (V systole end)
- stroke volume = EDV - ESV (∆volume in a V)
Cardiac output
(definition + equation)
volume of blood ejected from a ventricle into it’s respective vessel each minute
CO = HR x SV
heart rate x stroke volume
cardiac reserve
(definition + equation)
difference between our maximum HR and our resting HR
CR = HR(max) - HR(rest)
Factors regulating stroke volume
(names + definitions)
increased x will increase SV:
- preload: stretch on heart before contracts
- contractility: contraction force of muscle fibers
increased x will decrease SV:
- afterload: pressure in V required to open SL valves
Frank-Starling Law
stroke volume (SV) is proportional to muscle stretch and end diastolic volume (EDV)
only to a point, muscle can’t stretch indefinitely
what affects preload?
- duration of ventricular diastole
- increase leads to slower HR
- venous return
- eg: increased by exercise, decreased by hemorrhage
increase in either leads to increased preload
what affects contractility?
changes in cytosolic Ca2+
altered by inotropes:
- positive (increase C) eg: epinephrine
- negative (decrease C) eg: hypoxia(1)
1-low O2 levels in body tissues
what affects afterload?
- blood pressure
- high BP –> increased afterload
- vessel structure
- vasoconstriction –> increased afterload
qualities of the conductive fibers in the heart
- autoarithmic: will depolarize spontaneously (act as pacemakers)
- SA node is fastest and will set the pace
- if preceding structures are impaired, the next structure sets a slower pace (eg: damaged SA node will lead to slower pace set by AV node)
Factors regulating HR
- Autonomic NS (+ symp. -parasymp.)
Chemical:
- Hormones ( +E&NE +Thyroxine)
- Cations (+Ca -Na -K)
- Hypoxia (-less oxygen)
- Acidosis (-excess H+)
- Alkalosis (-high pH)
Other:
- Age (+infants -older)
- Body Temp (+high T -low T)
Nervous system control of the heart
Input:
- proprioceptors (monitor movement)
- chemoreceptors (measure blood chemistry)
- baroreceptors (monitor blood pressure)
Processing:
- cardiovascular center in medulla oblongata
Output:
- cardiac accelerator nerves (sympathetic) - increase HR and stroke volume
- vagus nerves (CN X, parasympathetic) - decrease HR
remember: SNS - adrenergic receptors, PSNS - cholinergic receptors
