Physiology Flashcards
(69 cards)
1
Q
What are the 5 steps of the cardiac cycle?
A
- Passive Filling
- Atrial Contraction
- Isovolumetric Ventricular Contraction
- Ventricular Ejection
- Isovolumetric Ventricular Relaxation
2
Q
Describe what happens in the cardiac cycle during passive filling
A
- Blood flows into atria as atrial pressure is lower than venous pressure
- AV valves open
- Venous return enters the ventricles
- Ventricles are ~80% filled
3
Q
Describe what happens in the cardiac cycle during atrial contraction
A
- Atria depolarise and contract
- This adds a small volume that completes EDV (~130ml)
4
Q
Describe what happens in the cardiac cycle during isovolumetric contraction
A
- Ventricles depolarise and ventricular pressure increases greatly
- AV valves shut when ventricular pressure exceeds atrial pressure, producing the first heart sound
5
Q
What is meant by isovolumetric contraction?
A
Tension rising around the closed volume of the ventricle
6
Q
Describe what happens in the cardiac cycle during ventricular ejection
A
- Aortic and pulmonary valves open due to increased ventricular pressure
- Stroke volume is ejected by each ventricle, leaving ESV
- The ventricles repolarise and relax, so ventricular pressure starts to fall
7
Q
Describe what happens in the cardiac cycle during isovolumetric relaxation
A
- Aortic and pulmonary valves shut when ventricular pressure falls below aortic and pulmonary arterial pressure, producing the second heart sound
- When ventricular pressure falls below atrial pressure the AV valves open and a new cycle starts
8
Q
What is meant by isovolumetric relaxation?
A
Tension falling around the closed volume of the ventricle
9
Q
What is the dicrotic notch? When does it occur?
A
- A bump in the aortic pressure curve caused by aortic valve vibration
- It occurs during isovolumetric relaxation following the closure of the aortic valve
10
Q
What causes the first heart sound (S1)? When does this occur in the cardiac cycle?
A
Closure of the mitral and tricuspid (AV) valves
During isovolumetric contraction
11
Q
What does S1 signify?
A
The beginning of systole
12
Q
What causes the second heart sound (S2)? When does this occur in the cardiac cycle?
A
Closure of the aortic and pulmonary valves
During isovolumetric relaxation
13
Q
What does S2 signify?
A
The end of systole and the beginning of diastole
14
Q
When can splitting of S2 be physiological?
A
If it only occurs during inspiration
15
Q
Why can inspiration cause physiological splitting of S2?
A
Inspiration reduces intrathoracic pressure which increases venous return to the right side of the heart
Increased EDV in the right ventricle means that the pulmonary valve closes a fraction of a second after the aortic valve does
16
Q
What are some causes of pathological splitting of S2? (3)
A
Pulmonary stenosis, mitral regurgitation, right bundle branch block
17
Q
Where is physiological splitting of S2 best auscultated?
A
The pulmonary area -> 2nd intercostal space, left sternal border
18
Q
When does S3 occur and how is it described?
A
- Occurs immediately after S2
- Described as an early diastolic, low frequency filling sound
19
Q
What causes S3?
A
Acceleration and deceleration of blood during early passive filling of the ventricle
20
Q
Can S3 by physiological?
A
May be physiological in healthy children and young adults
21
Q
What are some pathological causes of S3? (3)
A
LV failure
Mitral regurgitation
Constrictive pericarditis
22
Q
Where is S3 best heard?
A
At the apex with the bell of the stethoscope
23
Q
When does S4 occur and how is it described?
A
- Occurs shortly before S1
- Described as a late diastolic, low frequency filling sound
24
Q
What causes S4?
A
Atrial contraction causing rapid blood flow into a less compliant (stiff) ventricle
25
Can S4 be physiological?
Usually not
| It's almost always pathological
26
What are some causes of S4? (3)
Myocardial ischaemia
Hypertension
Aortic stenosis
27
Where is S4 best heard?
At the apex with the bell of the stethoscope
28
Which neurotransmitter increases heart rate and force? Which receptor does it act on?
Noradrenaline acting on beta-1 adrenoceptors
29
Which neurotransmitter reduces heart rate? Which receptor does it act on?
Acetylcholine acting on muscarinic M2 receptors
30
Describe phases 0-4 of the ventricular myocyte action potential
Phase 0: Rapid Na+ influx
Phase 1: Transient K+ efflux and closure of Na+ channels
Phase 2: Mainly Ca2+ influx through L-type Ca2+ channels
Phase 3: Rapid K+ efflux and closure of Ca2+ channels
Phase 4: Resting membrane potential (Na+/K+ ATPase)
31
Describe the 3 phases (0, 3 and 4) of the pacemaker cell action potential
Phase 0: Rapid Ca2+ influx through L-type Ca2+ channels
Phase 3: Rapid K+ efflux and closure of Ca2+ channels
Phase 4: Pacemaker potential (slow Na+ influx via HCN channels - funny current)
32
What is blood pressure?
Outwards hydrostatic pressure exerted by the blood on the blood vessel walls
33
How is blood pressure measured using a sphygmomanometer and stethoscope?
- Sphygmomanometer is tightened until no sound is heard
- Pressure is slowly released
- The pressure where the first sound appears is taken as SBP
- The pressure where the sound disappears is taken as DBP
34
What are Korotkoff sounds? When are they heard?
Blood pressure heard using a sphygmomanometer and stethoscope
They are heard when the cuff pressure is between SBP and DBP
35
What is the normal range for pulse pressure (SBP - DBP)?
30-50 mmHg
36
What is a normal range for MAP?
70-105 mmHg
37
What is the minimum MAP required to perfuse the vital organs?
60 mmHg
38
Which factor plays the biggest role in a vessels resistance to blood flow?
Its radius
39
What is vagal tone?
The constant domination of the vagus nerve acting on the SA and AV nodes to reduce heart rate
40
What is vasomotor tone?
Tonic discharge of sympathetic nerves at vascular smooth muscle leading to constant, partial constriction of vessels
41
What type of nerve supply mainly supplies vascular smooth muscle?
Sympathetic nerve fibres (there is no significant parasympathetic supply to vascular smooth muscle)
42
Which neurotransmitter do sympathetic fibres release in vascular smooth muscle and what is its receptor?
Noradrenline binds to alpha receptors to cause vasodilation
43
How does the hormone adrenaline act on the heart?
It binds to beta-1 receptors on cardiac muscle to increase HR, SV and SVR
44
List some metabolic factors that cause relaxation of arteriole smooth muscle and vasodilation (6)
- Decreased PO2
- Increased CO2
- Decreased pH (increased H+)
- Increased extracellular K+
- Increased osmolality of ECF
- Adenosine release from ATP
45
List some local chemicals that can be released by an organ during injury or inflammation to cause vasodilation of arteriolar smooth muscle (3)
- Histamine
- Bradykinin
- Nitric oxide
46
When is nitric oxide produced by vascular endothelium? How does it produce it?
- NO is produced continuously by vascular endothelium from the enzymatic action of nitric oxide synthase (NOS) acting on the amino acid L-arginine
47
What happens after NO is produced in the vascular epithelial cells?
- NO diffuses into adjacent smooth muscle cells
- There it activates the formation of cGMP whcih acts as a second messenger in the signalling of smooth muscle relaxation
48
List some local chemicals that can be released by an organ to cause vasoconstriction of arteriolar smooth muscle
- Serotonin
- Thomboxane A2
- Leukotrienes
- Endothelin
49
Endothelial-produced vaso-? are anti-thrombotic, anti-inflammatory and anti-oxidant
Vasodilators
50
Endothelial-produced vaso-? are pro-thrombotic, pro-inflammatory and pro-oxidant
Vasoconstrictors
51
Why does cerebral blood flow remain constant over a range of MAP values?
Myogenic response
52
Describe the myogenic response in autoregulating cerebral blood flow
- Increase in MAP causes constriction of resistance vessels to limit flow to the brain
- Decrease in MAP causes dilation of resistance vessels to increase flow to the brain
53
What effects does activation of beta-1 adrenoceptors by adrenaline/noradrenaline in the heart have? (7)
- Increased heart rate (+ve chronotropic effect)
- Increased myocardial contractility (+ve inotropic effect)
- Increased automaticity
- Increased Na+/K+ ATPase activity
- Decreased duration of systole (+ve lusitropic effect)
- Reduced AV nodal delay (+ve dromotropic response)
- Cardiac hypertrophy
54
What happens inside the cell when adrenaline/noradrenaline binds to beta-1 adrenoceptors?
- The beta-1 adrenoceptor is a GPCR, so Gs is activated and goes on to activate adenylyl cyclase in the cell membrane
- Adenylyl cyclase increases conversion of ATP to cAMP
- cAMP is a second messenger that can carry out cellular responses
55
What does cAMP act on to increase cardiac contractility?
Protein kinase A (PKA)
56
How does protein kinase A increase cardiac contractility? (2)
- PKA phosphorylates L-type Ca2+ channels, resulting in increased Ca2+ influx which causes more CICR from the sarcoplasmic reticulum. This increased Ca2+ can act on the actin-myosin contractile apparatus
- PKA also phosphorylates part of the actin-myosin contractile apparatus to make it more sensitive to Ca2+
57
How does protein kinase A aid in relaxation after systole?
PKA phosphorylates phospholamban on the SR, allowing Ca2+ ATPase to pump Ca2+ back into the SR more efficiently
58
Describe excitation-contraction coupling during systole
- L-type Ca2+ channels open during phase 2 of the ventricular action potential, allowing Ca2+ to enter the cell
- As Ca2+ concentration increases, it can occupy RyR2 (ryanodine) receptors on the sarcoplasmic reticulum
- This leads to CICR and a large Ca2+ influx into the cytosol
- Ca2+ binds to troponin C and moves tropomyosin out of the actin cleft
- This allows the actin-myosin cross-bridge to form and the muscles contract
59
Describe excitation-contraction coupling during diastole
- L-type Ca2+ channels are closed during phases 3 and 4 of the ventricular action potential, causing Ca2+ influx to cease
- NCX1 couples the inward movement of 3Na+ to move Ca2+ out of the cell
- Ca2+ release from the SR ceases and it is actively pumped back into the SR by the active transport system Ca2+ ATPase
- When Ca2+ concentration returns to its basal level, Ca2+ dissociates from troponin C and the actin-myosin cross-bridge breaks, allowing the muscles to relax
60
What effects does activation of M2 muscarinic receptors by acetylcholine in the heart have? (3)
- Decreased heart rate (-ve chronotropic effect)
- Decreased atrial contractility (-ve inotropic effect)
- Increased AV nodal delay (-ve dromotropic effect)
61
What happens inside the cell when acetylcholine binds to M2 muscarinic receptors?
- M2 muscarinic receptors are GPCR's so the G protein is activated
- The alpha subunit goes on to inhibit adenylyl cyclase which reduces conversion of ATP to cAMP which will lead to cellular responses
- The beta-gamma subunit activates GIRK channels which causes K+ efflux from the cell. This also leads to various cellular responses
62
What are myofibrils?
Contractile units within muscle fibres
63
What are myofibrils made up of?
Alternating segments of actin (thin) and myosin (thick) protein filaments
64
What are sarcomeres?
The arrangement of actin and myosin in myofibrils
| They are the functional unit of muscle i.e., the smallest unit that can generate contractile force
65
What is required for myosin to form a cross-bridge with actin?
In the presence of ATP and Ca2+, myosin becomes energised and is able to form a cross-bridge with actin
66
Why is Ca2+ required to form the actin-myosin cross-bridge?
It binds to troponin C to detach the troponin-tropomyosin complex from the myosin cross-bridge binding site on actin
67
How is the Ca2+ for contraction supplied to the actin and myosin filaments?
Due to CICR from the sarcoplasmic reticulum
68
What triggers CICR from the sarcoplasmic reticulum?
Influx of Ca2+ during the plateau phase of the cardiac myocyte action potential
69
Why does the heart muscle relax when the action potential has passed?
Ca2+ influx ceases so Ca2+ is reabsorbed by the sarcoplasmic reticulum by Ca2+ ATPase
