CV Physiology Flashcards
1
Q
What are key features of the myocardium?
A
- comprises 95% of the heart
- responsible for pumping action
- striated, involuntary muscle
- fibres swirl diagonally around heart in bundles
- heart “wrings” blood out of ventricles
2
Q
What is functional syncytium? What facilitates this?
A
- muscles all work together
- path of innervation going through the muscle where there is no motor end plate at each tissue (unlike skeletal muscle)
- intercalated discs are at junction between muscle cells and contain gap junctions and desmosomes
- gap junctions allow the flow of a signal between cells, desmosomes connect cells
3
Q
Describe cardiac conduction
A
- beat is initiated at SA (sinoatrial) node; autorhythmic, self-excites, beats at 100bmp
- action potential propogates through the atrium to the AV node (atrioventricular) located in interatrial septum
- AV node has smaller fibres and less gap junctions so it causes a slowing of the electrical signal as it moves through the heart
- signal moves through AV bundle (bundle of his) and moves through the interventricular septum through the right and left bundle branches
- as signal moves to the sides of the ventricles, it moves through the Purkinje fibres
- fibrous skeleton electrically insulates the atria and ventricles so that atria and ventricles don’t contract at the same time
4
Q
Describe the conduction of an AP in a ventricular contractile fibre
A
- RMP is -90mV
1. Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open - RMP increases and channels become inactive
- slight delay between the start of the depolarization and the start of the contraction
2. Plateau phase: maintain depolarization due to influx of Ca2+ when voltage gated slow Ca2+ channels open, also triggers release of Ca2+ from sarcoplasmic reticulum - Ca2+ allows contraction to happen
- some outflow of K+ at the same time
- strength of contraction is influenced by substances which alter movement of Ca2+ (inotropes- eg. epinephrine which increases force of contraction)
3. Repolarization: closure of Ca2+ channels, K+ outflow, MP back to negative - can not get tetanny with cardiac muscle (sustained contraction)
- need alternating contraction between atria and ventricles in order for blood to move
- refractory period>contraction period
5
Q
What does an ECG show?
A
- composite record of action potentials and the electrical activity of the entire heart
- detected at body surface through placing of electrodes
- tells us whether heart is functioning well
- P wave: first wave, representing atrial contraction (atrial systole)
- QRS complex: representing ventricular contraction (ventricular systole)
- during QRS phase, also having atrial relaxation but since ventricular contraction is so strong you don’t see the atrial relaxation on the ECG
- T wave: ventricular relaxation wave
6
Q
Describe the production of waves and contractions on ECG
A
- depolarization of atrial contractile fibres produces p wave
- SA node generates initial signal which travels to the atria
- after p wave forms, atria contract
- at the AV node, the signal slows between atria and ventricles
- depolarization of ventricular contractile fibres produces QRS complex followed by ventricular systole (contraction continues in S-T segment)
- repolarization of ventricular contractile fibres produces T wave
- after t wave, ventricular diastole
7
Q
Describe the pressure diagram
A
- increase in pressure during atrial systole
- another increase happens when bicuspid valve closes then atrial pressure starts to go down during ventricular systole period
- ventricular systole; pushes blood up to aorta, pressure rises while bicuspid valve and aortic semilunar valve are still closed, when pressure in ventricle>pressure in aorta semilunar valve opens
- aortic and ventricular pressures mirror each other
- at the end of the contraction, ventricular pressure falls and valve closes
- dicrotic wave is produced when semilunar valve closes
- ventricular pressure drops during ventricular relaxation
8
Q
Describe the 4 primary heart sounds
A
S1: associated with closure of atrioventricular valve
S2: closure of semilunar valves
S3: ventricular filling
S4: atrial contraction
9
Q
Describe volume of blood during cardiac cycle
A
- atrial systole: extra contribution of blood moving down into ventricles
- isovolumetric contraction; all 4 valves are closed, volume is the same, muscles have the same tension, haven’t started active contraction yet
- ventricular ejection; blood moves from the ventricles to great vessels
- isovolumetric relaxation
- AV valves open and get ventricular filling
10
Q
Describe the end diastolic volume, stroke volume, and end systolic volume
A
- volume left in ventricles at the end of the relaxation period
- whatever is left after the ejection from the ventricles is the end systolic volume (ventricles don’t fully empty)
- stroke volume is the difference between the two (how much blood is being ejected per stroke)
SV (mL/beat)=EDV-ESV
*same amount of blood is ejected on the left and right sides
11
Q
What is cardiac output?
A
-volume of ejected blood from the left ventricle (or RV) to the aorta (or pulmonary trunk) each minute
CO (mL/min)= HR x SV
12
Q
What factors affect stroke volume?
A
- Preload: the degree of stretch on the heart before it contracts
- Contractility: forcefulness of contraction of individual ventricular muscle fibres
- Afterload: pressure ventricles must overcome before the semilunar valves open
13
Q
What is the Frank-Starling law of the heart?
A
- heart muscle is stretched during the diastolic filling
- as it fills, it impacts force of contraction which impacts force of blood going into aorta
- more stretch=greater the force of the contraction=increased volume in aorta
- increase stroke volume because you can eject more blood
- proportional to EDV
14
Q
What things can change preload?
A
- duration of ventricular diastole: blood starts to flow in ventricles, if you shorten filling time you will have less blood flowing in ventricles and lower stroke volume ejected (high heart rate), lower heart rate you increase filling time and increase preload
- venous return: if this decreases (eg. cut in leg less blood flowing to heart) would decrease preload, increase in venous return (eg. exercise) would increase preload
15
Q
How is contractility changed?
A
- contractility is strength of contraction at any given preload and is due to changes in influx of calcium from extracellular fluid and sarcoplasmic reticulum
- increases with positive inotropes (epinephrine, thyroxine)
- decreases with negative inotropes (hypoxia, acidosis)
19
Q
What area of the brain houses the cardiovascular centre?
A
-medulla oblongata
