0
Q
Where does excitation of the heart normally originate?
A
Sino-atrial node
1
Q
Define autorhythmicity
A
The hearts ability to beat rhythmically in the absence of external stimuli
2
Q
Where is the Sino-atrial node found?
A
Upper right atrium
3
Q
A heart controlled by the Sino-atrial node (as is normal) is said to be in what rhythm?
A
Sinus rhythm
4
Q
How is the SA node able to cause cardiac excitation?
A
They have spontaneous pacemaker potential
5
Q
What causes the slow depolarisation membrane potential to a threshold in the heart (pacemaker potential)
A
Decrease in K+ efflux and a slow Na+ influx (funny current) causing build up of positive charge (depolarization)
6
Q
Once threshold is reach what causes the rising action potential (depolarization) in the heart?
A
Activation of L-type voltage activated Ca2+ channels resulting in Ca2+ influx
7
Q
What causes the falling action potential in the heart (repolarization)?
A
Activation of K+ channels causing K+ efflux coupled with a decreased influx of Ca2+ causing the cell to become more negative
8
Q
What is the pathway of spread of excitation across the heart?
A
SA node to AV node by cell-to-cell conduction
Then to bundle of His
Then left and right branches
Finally along the purkinje fibres to the ventricles
9
Q
What junctions allow excitation to spread across the heart?
A
Gap junctions - allow cell to cell current flow
10
Q
What happens to the spread of excitation in the AV node and why?
A
The conduction is delayed to allow atrial systole to precede ventricular systole
11
Q
What is the resting membrane potential in the ventricle?
A
-90mV
12
Q
What causes depolarization of the ventricle?
A
Fast Na+ influx
13
Q
What is the membrane potential in the ventricles after depolarization?
A
+30mV
14
Q
What is the depolarization phase of the ventricle also known as?
A
Phase 0
15
Q
What causes the plateau phase in ventricular muscle action potential and what else can this be called?
A
It is when the membrane potential in the ventricle stays constant. It is caused mainly by an influx of Ca2+ which is superimposed on a decrease in Na+ influx which balance each other out (Phase 2)
16
Q
What causes the rapid repolarization in the ventricular muscle action potential and what phase is this?
A
Closure of Ca2+ channels stopping Ca2+ influx and activation of K+ channels causing K+ efflux resulting in an overall decrease in membrane potential (phase 3)
17
Q
What is phase 4 of the ventricular muscle action potential?
A
Resting membrane potential
18
Q
What effect does Vagal stimulation have on heart rate and how?
A
Slows heart rate from 100 to about 70 by increasing AV nodal delay. Does this by causing the cell to hyperpolarize meaning it takes longer to reach threshold (slope of pacemaker potential decreases)
19
Q
What areas do cardiac sympathetic nerves supply?
A
SA node
AV node
Myocardium
20
Q
What is it called when something has an effect that causes an increased heart rate?
A
Positive chronotropic effect
21
Q
What is the P wave on an ECG?
A
Atrial depolarization
22
Q
What does the QRS complex show on an ECG?
A
Ventricular depolarization
23
Q
What happens to the atrial repolarization on an ECG?
A
Masked by QRS complex
24
What is the T wave on an ECG?
Ventricular repolarization
25
What is the PR interval on ECG?
Largely AV nodal delay
26
What is the ST segment on ECG?
Ventricular systole
27
What is the TP interval on ECG?
Diastole
28
What is 1,2,K a memory aid for?
Spontaneous pacemaker potential:
Sodium in until threshold
calcium in causing depolarization
potassium out causing repolarization
29
Describe the cardiac muscle
Striated
No neuromuscular junctions
Cardiac myocytes are electrically coupled by gap junctions
30
What junction provides mechanical adhesion between adjacent cardiac cells?
Desmosomes
31
What is each cardiac muscle fibre made up of? (What are the contractile units)
Myofibrils
32
What are myofibrils made up of?
Actin - thin light coloured filaments
| Myocyin - thick dark coloured filaments
33
What is the name for the arranged actin and myocin?
Sarcomeres
34
How is cardiac muscle tension and force produced?
Sliding of actin filaments on myocin filaments
35
Is ATP required for contraction, relaxation, both or neither of the heart muscles?
Both
36
Where is the calcium for heart muscles released from?
Sarcoplasmic reticulum
37
What activates the release of calcium from the Sarcoplasmic reticulum?
Extra-cellular calcium. It is a calcium induced calcium release
38
Define the refractory period
A period following an action potential in which it is not possible to elicit another potential
39
What is responsible for the refractory period in the ventricular muscle
a) during the plateau phase
b) during the repolarization phase?
a) Plateau phase - Na+ channels are in depolarised closed state
b) Repolarization phase - K+ channels are open and the membrane cannot be depolarised due to rapid repolarization that is taking place
40
Define the stroke volume
Volume of blood ejected by each ventricle per heart beat
41
What is the equation for stroke volume?
End diastolic volume - end systolic volume
42
Define intrinsic controls in the heart
Within the heart muscle itself
43
Define extrinsic controls to do with the heart
Nervous and hormonal control
44
What causes intrinsic control of stroke volume?
Venous return determines the end diastolic volume.
The end diastolic volume then determines the length (stretch) of myocardial fibres.
This determines the stroke volume
45
What is preload and what determines it?
Preload is the stretching of the ventricle cardiac muscle.
| It is determined by end diastolic volume.
46
What does the frank-starling curve show?
That the greater the end diastolic volume the greater the stroke volume
47
When is the cardiac muscle at optimal length?
When Stretched
48
Define after load
The resistance into which the heart is pumping (forces working against the ejection of blood such as the aortic pressure)
49
What effect does an increased after load have?
The heart is unable to eject optimal stroke volume so Residual blood in ventricle is added to next EDV resulting in greater volume. Process repeats, stretching ventricle further each time leading to hypertension and LVH.
50
What happens if increased after load persists? (Untreated hypertension)
the ventricular muscle mass increases to overcome the resistance (ventricular hypertrophy)
51
What part of the ANS supplies the ventricle?
Sympathetic (parasympathetic has nothing to do with ventricle)
52
What is an positive inotropic effect and what causes it?
Increased force of contraction and it is caused by stimulation of sympathetic nerves
53
What effect does stimulation of the sympathetic nerves have on the frank-starling curve and why?
It is shifted to the left as a greater stroke volume is achieved as there is a stronger force of contraction pumping a greater percentage of the EDV out of the ventricle.
54
What two things are plotted on a frank-starling curve?
Stroke volume (y axis) against End Diastolic Volume (x axis)
55
What is a negative inotropic effect?
Decreased ventricular force of contraction
56
Where are adrenaline and noradrenaline released from when considering the heart?
Adrenal medulla
57
What effect do adrenaline and noradrenaline have in the heart?
Inotropic and chronotropic
58
What is the equation for cardiac output?
SV x HR
59
When do heart valves usually produce a sound?
When they shut
60
At a heart rate of 75 beats/min how long to diastole and systole take?
Diastole - 0.5 seconds
| Systole - 0.3 seconds
61
What are the 5 steps of the cardiac cycle?
```
Passive filling
Aortic contraction
Ventricular contraction
Ventricular ejection
Ventricular relaxation.
```
62
During passive filling what is the pressure in the atria and ventricles?
Close to zero
63
Why is the aortic valve closed during passive filling?
Because the pressure in the aorta is around 80mmHg so it greater than that in the ventricle
64
What is the difference between filling of the left and right ventricles?
The right side happens at a lower pressure
65
How full (%) do ventricles become by passive filling?
80%
66
What causes the first heart sound and what is the sound?
The closure of the AV valve after the pressure in the ventricle exceeds that of the atria. This produces a LUB sound
67
What causes the aortic valve to open?
The tension in the ventricle rises (isovolumetric contraction) increasing the pressure until it exceeds that of the aorta causing the valve to open.
68
What causes the second heart sound?
The pressure in the ventricle falls below that in the artery, as majority of blood has been ejected, closing the aortic/pulmonary valve. DUB
69
What happens during isovolumetric relaxation of the ventricles?
The ventricle relaxes reducing the pressure until it is lower than that in the atria which causes the AV valve to open starting a new cycle
70
What valves close in the first heart sounds and what sides are they on?
Mitral - left AV valve
| Tricuspid - right AV valve
71
What valves close in the second heart sound and what side are they on?
Aortic - left
| Pulmonary - right
72
When do you hear the heart sounds in relation to systole and diastole?
LUB - systole - DUB - diastole
73
What is the normal length of the QRS complex?
<0.1 seconds
74
Normal length of PR interval?
0.12-0.2 seconds
75
Normal P length?
0.08-0.1 seconds
76
How do you work out rate on ECG with regular whythm?
300/number of large squares between R-R interval
77
What are the 7 steps to interpreting an ECG rhythm strip?
1.Is electrical activity present?
2.Rhythm regular or irregular?
3.What is the heart rate?
4.P waves present?
5.What is the PR interval?
6.Is each P wave followed by QRS?
7.Is QRS duration normal?
Then look at individual limb leads
78
What leads show the inferior heart?
II
III
aVF
79
What leads show an anteroseptal MI?
V1-V4
80
What leads show an anterior MI?
V1-V6
81
What leads show an anterolateral (extensive anterior) MI?
I
AvL
V1-V6
82
What leads show a lateral MI?
I
| AvL
83
Which coronary arteries are affected in an inferior MI and an anterior MI?
Inferior - right coronary artery
| Anterior - left coronary artery
84
What is the only point of electrical contact between the atria and ventricles?
The AV node
85
Where does the vagus nerve supply in the heart?
SA node and AV node
86
What reaction must take place to allow the cross bridge formation between myosin and actin (movement in myofibrils)
Ca2+ must bind to troponin so that myosin can bind to actin forming the cross bridge allowing this to shorten and cause contraction
87
What prevents myosin binding to actin and how?
Troponin is bound to the actin and blocks the myosin from binding preventing the formation of the cross bridge
88
Describe how ventricular diastole is achieved?
Intracellular Ca2+ is re-up taken by the Sarcoplasmic reticulum stopping the calcium induced calcium release preventing contraction.
89
What enzyme is responsible for the re-uptake of calcium into the Sarcoplasmic reticulum?
Ca2+ ATPase
90
What effect does increased ventricular myocardial stretch have on the actin myosin cross-bridge?
As the cardiac muscle is stretched it naturally wants to contract so affinity of Ca2+ for troponin increases allowing greater actin and myosin binding resulting in a huge contraction
91
Explain the effect of sympathetic stimulation on the ventricle
Force of contraction increases because of increased Ca2+ influx causing increased ventricular pressure. Therefore decreasing duration of both systole and diastole
92
Define cardiac output
Volume of blood pumped by each ventricle per minute
93
What is the cardiac cycle?
All events that occur between the beginning of one heart beat and the next
94
What happens in ventricular contraction?
SV is ejected by each ventricle and ESV is left behind and the aortic pressure rises
95
How do you work out the heart rate if the it is irregular?
Count number of QRS in 30 big squares and multiply by 10.
96
If no rhythm is indicated what lead should you use?
Lead II
97
At what korotkoff sound is systolic BP taken?
Sound 1
98
At what korotkoff sound is diastolic BP taken?
5
99
What is pulse pressure?
The difference between systolic BP and diastolic BP
100
What is the normal range of MAP?
About 70-105mmHg
101
What is the minimum MAP needed to perfuse the coronary arteries, brain and kidneys?
60mmHg
102
What is the equation for MAP?
CO x TPR
So: SV x HR x TPR
103
What are the major resistance vessels?
Arterioles
104
Explain the basic baroreceptor reflex
Baroreceptors detect sudden change from normal blood pressure , signal medulla (control centre) to stimulate change at effector (heart and blood vessels)
105
Where are the Baroreceptors and what nerves do they use to send signals to the medulla?
Carotid sinus - glossopharengeal nerve
| Aortic arch - vagus nerve
106
What effect does increased BP have on Baroreceptors?
Increased rate of afferent signal firing
107
What effect does decreased BP have on Baroreceptors?
Decreased
108
What is postural hypotension?
Decreased BP when moving from horizontal to vertical position due to failure of Baroreceptors response to gravitational shifts in blood.
109
What happens if high BP is sustained?
Baroreceptor firing decreases and Baroreceptors reset at a new higher steady state limit. (Hypertension)
110
How does the RAAS system detect a change in blood pressure?
In the renal arteries
111
What does detection of a decreased BP in the renal arteries cause?
Release of rennin from the jucto glomerular apparatus in the kidneys
112
What does rennin do?
Converts angiotensinogen (which is produced in the liver) to angiotensin I
113
What happens to angiotensin I in the RAAS system?
ACE in the lung vascular endothelium converts it to angiotensin II
114
What does angiotensin II do?
Causes vasoconstriction, increased ADH secretion and increased thirst all of which increase BP.
AND stimulates the adrenal cortex to release aldosterone
115
What does aldosterone do?
Causes increased sodium and water reabsorption in the kidneys.
Which causes increased plasma volume and therefore increased BP
116
What is the rate limiting step in the RAAS system?
Rennin
117
What is the role of Atrial Natriuretic Peptide (ANP)?
Released in response to atrial distension (caused by hypervolaemia).
Causes excretion of salt and water in the kidneys (decreased blood volume so decreased BP).
Acts as vasodilator
Decreases rennin release so acts as a counter-regulatory mechanism of the RAAS
118
Where is ADH (aka vasopressin) produced and stored?
Synthesised by the hypothalamus and stored in the posterior pituitary
119
What stimulates the secretion of ADH?
Reduced extracellular fluid
| Increased extracellular fluid osmolarity
120
Where is plasma osmolarity monitored and by what?
By osmoreceptors mainly in the brain in close proximity to the hypothalamus
121
What does ADH do?
Acts on kidney tubules to increase reabsorption of water
| It also acts as a vasoconstrictor small effect in normal people but important in hypovalaemic shock (haemorrhage)
122
What is the relationship between resistance to blood flow; blood viscosity; length of blood vessel and radius of blood vessel?
R = (n x L)/r4
```
R = resistance to flow
n = blood viscosity
L = length of blood vessel
r = radius of blood vessel
```
123
Define the vasomotor tone
That blood vessels are partially constricted at rest
124
Where are the only places that parasympathetic innervation has an effect on arterial smooth muscle?
The penis and clitoris
125
Where are alpha receptors predominately found?
In skin, gut and kidney Arterioles because release of adrenaline to alpha receptors causes vasoconstriction and blood is not needed at these areas during fight or flight
126
Where are beta receptors found predominantly?
The cardiac and skeletal muscle because adrenaline caused vasodilation and this is where you need blow to flow for fight or flight
127
What are the intrinsic control mechanisms of vascular smooth muscles?
They include local chemical and physical factors.
128
What are the intrinsic factors causing relaxation of arterial smooth muscle leading to vasodilation?
```
Decreased local PO2
Increased local CO2
Increased local H+ (decreased pH)
Increased extra-cellular K+
Increased osmolarity of ECF
Adenosine release (from ATP)
```
129
What humoral agents that cause intrinsic vasodilation of arterial smooth muscle?
Histamine
Prostaglandins
Bradykinin
Nitric oxide - continuously released by endothelial cells of arteries and Arterioles
130
How does NO cause vasodilation?
NO is a potent vasodilator. It diffuses from the vascular endothelium into the adjacent smooth muscle cell where it activates the formation of cGMP which is a secondary messenger for signalling smooth muscle relaxation.
131
How is NO made? (There are a number of different ways)
1. Continuously produced by the vascular endothelium from amino acid L-arginine which is acted upon NOS.
2. Shear stress causes releases of Ca2+ which activates NOS
3. Histamine, bradykinin, prostaglandin induce receptor stimulated NO formation.
132
What humoral agents cause vasoconstriction when released?
Serotonin
Thromboxane A2
Leukotrienes
Endothelin
133
What stimulates production of endothelin?
Angiotensin II
| Vasopressin
134
What are the physical factors that have an effect on intrinsic control of vascular smooth muscle?
Temperature
Myogenic response - increased MAP causes resistance vessels (muscles) to constrict which reduces blood flow to the artery lowering the MAP (and same for reverse).
Sheer stress - dilatation of Arterioles causes sheer stress in the arteries upstream (greater blood flow to Arterioles causes high BP in artery) so these also dilate increasing blood flow to metabolically active tissues
135
What is Myogenic response of vascular smooth muscles particularly important in?
Protection of brain and kidneys against excessively high MAP
136
What is hypercapnia and what effect does it have on cerebral blood flow?
Too much CO2 in the blood causing vasodilation resulting in increased cerebral flow (over-perfusion)
Physiology
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