The heart (p2) Flashcards
What are some key differences in the physiological properties of cardiac muscle and skeletal muscle?
Skeletal muscle:
- long
- multinucleate
- cylindrical
- no gap junctions
- SR elaborate (has terminal cisterns)
- abundant amt of T-tubules
- motor units stimulated individually
- source of calcium is only SR
- no pacemaker cells
- tetanus is possible
- aerobic and anaerobic
Cardiac muscle:
- short
- one or two nuclei
- branched
- gap junctions present
- functional syncytium (bc of gap junctions)
- fewer and wider T-tubules
- less elaborate SR (no terminal cisterns)
- pacemaker cells present -> heart can beat on its own
- tetanus is not possible
- aerobic only
Both striated, and calcium binds to troponin
What are the 2 types of cell junctions contained in intercalated discs?
1) Gap junctions - electric coupling to create a functional syncytium
So that the atria and ventricles can contract as a functional syncytium
2) Desmosomes - strong cell to cell adhesion during contraction
Strengthens the walls of the heart
What is heart contraction stimulated by? How does this relate to muscle twitches?
Stimulated by action potentials
AP = signal
Muscle twitch = response
What are pacemaker cells?
Specialized cardiac cells that are capable of spontaneous depolarization
What occurs as a result of an influx of Ca2+ in the heart? Where does the calcium come from?
Calcium from ECF triggers further calcium release from SR
From slow channels - a ‘jump start’ of calcium is needed to support and start contraction
Why is it important that the cardiac absolute refractory period is longer compared to that of skeletal?
Important that cardiac is a longer duration so that the possibility of having tetanic muscle contractions is not allowed (tetanus possible in skeletal but not cardiac muscle)
This forces the cardiac muscle to be refractory and to completely refract to only be able to be stimulated again until they have had a chance to relax
- until ventricles have had a chance to fill again before you stimulate them to contract and push blood out into the pulmonary and systemic circulations
Describe the action potential of contractile cardiac muscle cells, what phases do they undergo?
1) Depolarization
- due to Na influx through fast channels
- reverses the membrane potential
2) Plateau phase
- due to Ca influx through slow channels
- keeps cell depolarized bc of few K channels opened
3) Repolarization
- due to Ca channels inactivating and K channels opening
- K effflux, bringing membrane potential back to resting voltage
How long (approx) is the absolute refractory period? What does this duration allow for?
Almost equals the duration of a muscle twitch
Allows the heart to fill again before further contraction
What is heart rate? What is this determined by?
Heart rate = electrical activity in the heart because of spontaneous depolarization in the SA node
Heart rate determined by sinus rhythm
What are pacemaker potentials?
Authorhythmic cells have unstable RMPs due to funny Na channels that open at negative membrane potentials (usually Na channels only open when threshold is reached)
K channels are closing as well but slowly
This allows a drift towards threshold
What do pacemaker potentials lead to?
Action potentials
What are APs due to in autorhythmic cells?
Voltage gated calcium channels
Influx of calcium is responsible for the spike of depolarization, not the influx of Na (skeletal)
This means they dont ever have a steady RMP unlike skeletal muscle
Which autorhythmic cell is the pacemaker cell? Why?
The sinoatrial node (SA)
- depolarizes the fastest, the farther you get from it, the more the autorhythmic cell will depolarize slower
- overrides all other authorhythmic nodal tissue
- sets the pace for heart rate
Describe the electrical activity of autorhythmic cardiac muscle cells, whwat are the different phases?
1) Pacemaker potential
- slow depolarization
- due to both Na channel opening and K channel closing
2) Depolarization
- AP begins once threshold is reached
- due to Ca influx
3) Repolarization
- due to Ca channels inactivate and K channels opening
- allows K efflux bringing the membrane potential back to most negative voltage
In which direction do each of the following ions travel (generally); sodium, potassium, calcium.
Na = IN
K = OUT
Ca = IN
What is the order in which an AP generated by the SA node undergoes?
1 - SA node
2- AV node
3 - AV bundle after a short delay
4 - right and left bundle branches
5 - Subendocardial conducting network (purkinje fibers)
Why is there a bottleneck from atria to ventricles?
AV node is the only pathway to reach the ventricles from the atria causing a short delay
What are the influences of the parasympathetic NS and sympathetic NS on cardiac function?
Rate of SA node depolarizattion is regulated by the ANS
1) PNS - Decreases depolarization rate
- slows down rate threshold is reached
- at rest, PNS dominates your heart rate
2) SNS - Increases depolarization and repolarization rates
- fight/flight system, wanting to increase heart rate -> blood circluates faster and there is a higher rate of spontaneous depolarization
What is bradycardia?
Having a slower than normal heart rate
> 55bpm
What is tachycardia?
Having a faster than normal heart rate
<100bpm
What does an electocardiogram (ECG) do?
Records electrical changes during heart activity and relies on the conductive activity of body fluids
A normal ECG means you can assume the person has a normal beating herat
What is the order following atrial depolarization?
Atrial depolarization → ventricular depolarization after a short delay
1) P-wave = atrial depolarization
2) QRS complex = ventricular depolarization (not called a wave but rather a complex because it has a dip and a spike
3) T-wave = ventricular repolarization
Where is atrial repolarization?
Occurs at the same time as ventricular depolarization, contributes to the different and fairly complex shape of the QRS complex
- however its most ventricular depolarization
What is a systole? Diastole? What is teh relation to a cardiac cycle?
Systole = contraction of heart (pumping OUT)
Diastole = relaxation of herat (filling)
Cardiac cycle = atrial systole + diastole → ventricular systole + diastole
Describe theperiod of ventricular filling
Mid to late diastole (when both atria and ventricles are relaxed)
- pressure is low but atria (p) > ventricles (p)
- AV valves open, SL valves closed
- after ~70% ventricular filling, AV valves begin to close → P-wave and atrial systole
- atrial P increases, remaining ~30% blood enters ventricles → end diastolic volume (EDV) and atrial distole for rest of cycle
Describe ventricular systole
QRS complex and T-waves
- ventricles begin to contract
- increased pressure closes AV valves
- period of isovolumetric contraction (volume is constant in a closed system)
- increased pressure opens SL valves
- Ventricular ejection phase (aortic pressure up), blood ejected from ventricles → aorta
Describe isovolumetric relaxation
Early diastole
- ventricles relax
- pressure rapidly decreases
- backflow of aortic/pulmonary blood closes SL valves (dicrotic notch)
Ventricles in a closed system = isovolumetric relaxation
What is the quiescent period?
When both atria and ventricles are in diastole
What are the 2 features that drive the cardiac cycle?
a) Blood flow through heart controlled entirely by pressure changed
b) blood flows from high → low pressure through any avail. opening
Electrical activity of left and right hearts = almost simultaneous
What are heart sounds?
2 distinguishable sounds that can be heard through a stethoscope
a) first heart sound = closure of AV valves = beginning of systole
b) second heart sound = closure of SL valves = end of systole
Due to vibrations of the heart/chest due to valve closure
What are heart murmurs? How do they differ from heart sounds
Heart murmurs = abnormal blood sounds
1) Valvular stenosis = high velocity jet of blood through narrow opening → high pitch
2) Valvular insuffieciency = leakage of blood back causes sounds where there should be silence
What is cardiac output (CO)?
CO = volume of blood pumped from each ventricle per minute
How is stroke volume (SV) calculated?
SV = EDV-ESV
SV - volume of blood pushed out with each heart beat
EDV = end diastolic volume
ESV = end systolic volume
How can cardiac output (CO) be calculated?
CO = HR x SV
HR = heart rate
SV = stroke volume
What factors of spontaneous depolarization of the SA node determines heart rate?
Daily occurence:
- autonomic fibers innervating SA node
- circulating hormones (epinephrine)
Less often:
Kept in a smaller range, but can still interfere with the spontaneous depolarization
- plasma electrolyte concentrations (Ca++, Na+, K+, H+)
- body temperature
What effect does norepinephrine in the sympathetic NS have on spontaneous depolarization?
NE increases rate of spontaneous depolarization → increased heart rate
What effect does acetylcholine in the parasympathetic NS have on spontaneous depolarization?
ACh decreases rate of spontaneous depolarization → hyperpolarizes pacemaker cells → decreases heart rate
What is vagal tone?
When under resting conditions the parasympathetic NS is dominant
- dominant effect of the vagus nerve on the SA node to slow down heart rate
What is extreme tachycardia?
Extremely fast heart rate, can occur is someone experiences a serious injury
Leads to reduced cardiac output because heart is working very hard but the ventricles are hardly filling - you are not moving around very much blood per unit of time (min.)
