Physiology Flashcards
(126 cards)
1
Q
Where does excitation originate in the heart?
A
SA node
2
Q
Where is the SA node located
A
Upper right atrium (close to SVA entry)
3
Q
When the heart is controlled by the SA node, init is said to be in what time of rhythm?
A
Sinus rhythm
4
Q
What is the pacemaker potential due to?
A
- Decrease in funny current
- Background current of potassium influx (lb)
- Transient Ca2+ influx
5
Q
What happens when the pacemaker potential reaches threshold ?
A
L-type calcium channels open allowing for calcium influx
6
Q
What are the 2 main causes of the falling phase in a nodal action potential?
A
- Inactivation of L-type Ca2+ channels
2. Activation of delayed rectifier outward potassium channels
7
Q
What permits the spread of excitation between myocardial cells?
A
Gap junctions
8
Q
Where is the AV node located?
A
At the base of the right atrium just above the atrium/ ventricular junction
9
Q
What is the purpose of the AV nose?
A
To allow conduction to spread to the ventricles from the atria
10
Q
What attributes of the AV node allows for heart contraction and coordination?
A
It has a low conduction velocity allowing there to be a delay between atrial and ventricular contraction
11
Q
What is the bundle if His?
A
This is a bundle of nerve fibres which carries the impulse from the AV node to the ventricles where the impulse passes upwards via Purkinje fibres in the ventricles
12
Q
What is the resting potential of a myocardial cells?
A
-90mV
13
Q
In a myocardial action potential, what is phase 0?
A
Rapid depolarisation from -90 mV to +20mV due to Na+ influx
14
Q
In a myocardial action potential, what is a phase 4
A
Resting membrane potential is achieved (-90mV)
15
Q
In a myocardial action potential, what is phase 3?
A
Closure of Ca2+ channel influx and K+ efflux begins
16
Q
In myocardial action potential, what is phase 2?
A
L-type Ca2+ channel influx
17
Q
In a myocardial action potential, what is phase 1?
A
Closure of Na+ channels and transient K+ channels
18
Q
What is the plateau phase and what causes it?
A
Maintained during phase 2 of a myocardial AP. Due to Ca2+ influx through L-type channels. Maintains peak AP
19
Q
How does the sympathetic system affect heart rate?
A
Increases
20
Q
How does the parasympathetic system affect heart rate?
A
Decreases
21
Q
What is vagal tone?
A
Continuous influence of the vagus nerve on SA node lowering heart rate to normal levels
22
Q
What is the normal range for heart rate?
A
60-100bpm
23
Q
What is the term for low heart rate (<60bpm)?
A
Bradycardia
24
Q
What is the term for high heart rate (>100bpm)?
A
Tachycardia
25
On which receptors does acetylcholine from the vagus nerve act?
Type 2 muscarinic
26
What type of drug is atropine and what may it be used for?
Competitive acetylcholine inhibitor
| Treats brachycardia by speeding up heart rate
27
What three effects does sympathetic stimulation have on the heart?
1. Increase HR
2. Decrease Av node delay
3. Increase contractile force
28
Noradrenaline from the sympathetic system acts on which receptors in the heart?
B1
29
What is a chronotropic effect?
Something which influences heart rate e.g. positive chronotropic increases HR
30
In an ECG what does the P wave represent?
Atrial depolarisation
31
In an ECG what does the QRS complex represent?
Ventricular depolarisation
32
In an ECG what does the T wave represent ?
Ventricular repolarisation
33
In an ECG what does the PR interval represent ?
AV node delay
34
In an ECG what does the ST segment represent ?
Ventricular systole
35
In an ECG what does the TP interval represent ?
Diastole
36
How long does the cardiac cycle normally last?
0.8s
37
What 5 events comprise the cardiac cycle?
1. Passive filling
2. Atrial contraction
3. Isovolumetric ventricular contraction
4. Ventricular ejection
5. Isovolumetric ventricular relaxation
38
Describe passive filling
Pressure in the atria is slightly higher than ventricles allowing for passive filling of the ventricles with blood
39
Passive filling accounts for what percentage of ventricular filling?
80%
40
Describe how atrial contraction contributes to ventricular filling
The final 20% of ventricular filling is achieved by atrial contraction
41
Describe isovolumetric ventricular contraction
Ventricular pressure rises past atrial pressure upon contraction causing the AV valves to close. Semilunar valves remain closed so pressure builds around a closed volume
42
Describe ventricular ejection
Ventricular pressure exceeds aortic/pulmonary valve pressure causing ejection of stroke volume
43
What is the end systolic volume
This is the amount of blood left behind in the ventricles after contraction
44
How is stroke volume calculated?
SV= EDV-ESV
45
When do the semilunar valves close?
When ventricular pressure falls after contraction
46
What causes the first heart sound?
Closing of the AV valves during isovolumetric ventricular contraction
47
What causes the second heart sound ?
Closing of semilunar valves after ventricular ejection
48
What causes the dicrotic notching the pressure curve?
Valve vibration
49
What does isovolumetric ventricular relaxation involve?
The closing of aortic and pulmonary valves
50
What causes the third heart sound(S3)?
Occurs after the 2nd heart sound- due to acceleration and deceleration of blood into the ventricles- can signify cardiac disease
51
What causes the fourth heart sound (S4)?
Occurs shortly before the first heart sound- due to rapid blood flow into less compliant ventricles (usually left) causing turbulence
52
Where are the S3 and S4 heart sounds best heard?
Apex
53
Where is the aortic area?
2nd intercostal space right parasternal
54
Where is the pulmonary area?
2nd intercostal space left parasternal
55
Where is the tricuspid area?
4th intercostal space left parasternal
56
Where is the mitral area?
5th intercostal space left parasternal
57
For which two reasons does arterial pressure never fall to zero?
1. Contractile of arterial muscle
| 2. Retraction of elastic fibres
58
What is blood pressure?
Hydrostatic (outward) pressure exerted on vessels by blood flow
59
What is the upper limit of blood pressure before treatment?
140/90 mmHg
60
What is the term used to describe blood flowing without turbulence?
Laminar blood flow
61
What are Korotkoff sounds?
```
There are 5 and they are heard when blood pressure is taken
phase 0- silence
phase 1- Tapping sound
phase 2 - soft swishing sound
phase 3- crisp sound
phase 4 - blowing sound
phase 5 - silence
```
62
At which Korotkoff sound is diastolic pressure measured and why?
5
At sound 5, the change is more easily heard as any sound heard changes to silence
Technically the fourth Korotkoff sound is where diastolic pressure occurs
63
What drives blood circulation ?
The pressure gradient between aorta and right atrium
64
How is mean arterial blood pressure (MABP) calculated? (3)
1. MABP= (2x diastolic + systolic)/3
2. MAP = 1/3 (systolic- diastolic) + diastolic
3. MABP = CO x TPR
65
What is pulse pressure?
This is the difference between systolic and diastolic pressure
66
What is the range for MABP?
70- 105 mmHg
67
What is the minimum requirements of MABP to perfuse organs?
60 mmHg
68
What can happen if MABP is too high?
Damage to organs, vessels and extra strain is placed on the heart
69
What is TPR?
Total peripheral resistance
| The sum of all the resistance is systemic and peripheral circulations
70
What are the main resistance vessels and what evidence is there for this?
Arterioles
| The blood pressure drops the most after entering these vessels
71
What effect does parasympathetic stimulation have on the cardiovascular system?
1. Decreases heart rate
2. Decreases cardiac output
3. Decreases MABP
72
What effect does sympathetic stimulation have on the cardiovascular system?
1. Increases heart rate
2. Increases contractile strength
3. Increases cardiac output (increased stroke volume)
4. Increases MABP
73
What are baroreceptors ?
Pressure receptors
74
Where is the control centre located for baroreceptors ?
The medulla
75
What are the effectors for the baroreceptors ?
The heart and blood vessels
76
Where are the two groups of baroreceptors located?
1. Aortic arch
| 2. Carotid sinus (bifurcation)
77
Which cranial nerves allow signals to be sent from baroreceptors to the brain?
9 and 10
(IX and X)
(Glossopharyngeal and Vagus)
78
How do blood vessels "react" to increased carotid sinus afferent nerve fibre firing?
Vasodilate
79
How do blood vessels "react" to cardiac vagal nerve efferent nerve fibres?
Vasodilation
80
Explain the process baroreceptors go through when a person stands up quickly after lying down
1. Venous return decreased duet o a drop in blood pressure
2. Firing rate of baroreceptors decreases
3. Vagal tone of the heart decreases as the sympathetic system increases heart rate and stroke volume to attempt a blood pressure increases
4. Sympathetic constrictor tone increases TPR which increases venous return and stroke volume correcting the low MABP and increasing it
81
What happens to the baroreceptor response when blood pressure is maintained over a long period of time?
The baroreceptor response is designed for response to acute changes
The response sets a new baseline value to an acute change, if this change is maintained it will become the new "normal"
82
How is MABP controlled long term?
Blood volume
83
Total body fluid is made up of which two components?
1. Extracellular volume
| 2. Intracellular volume
84
What two components make up extracellular fluid volume?
1. Plasma volume
| 2. Interstitial fluid volume
85
What happens in order to balance a full in plasma volume?
Compensatory mechanisms shift fluid from the interstitial fluid volume
86
Blood volume and MABP are controlled by mechanisms regarding ______ _____ ____
Extracellular Fluid volume (ECFV)
87
Which two main factors affect ECFV?
1. Water excess or deficit
| 2. Na+ excess or deficit
88
Which three systems are involved in regulating ECFV?
1. Renin Angiotensin Aldosterone system
2. Atrial Naturiuretic Peptide
3. Antidiuretic hormone (vasopressin)
89
How does the RAAS regulate MABP?
By regulating TPR and plasma volume
90
Where is renin produced and what is its function?
Kidneys (juxtaglomerular apparatus)
| Stimulates formation of angiotensin I in the blood from angiotensinogen (from liver)
91
What happens to angiotensin I?
It is converted to angiotensin II by angiotensin converting enzyme (ACE, produced in pulmonary vascular endothelium)
92
What does angiotensin II stimulate?
1. Release of aldosterone from adrenal cortex
2. Causes systemic vasoconstriction increasing TPR
3. Stimulates thirst and ADH release (contributes to increasing plasma volume)
93
What does aldosterone do?
Acts on kidney to increase sodium and water retention to increase plasma volume and hence MABP
94
What can stimulate renin release form the juxtaglomerular apparatus in the kidneys?
1. Renal artery hypertension
| 2. Stimulation of renal sympathetic nerves]3. Decreased (Na+) in renal tubular fluid (sensed my macradensa)
95
What are the macra densa?
```
Can detect (Na+) in renal tubular fluid
Specialised renal tulles composed of extraglomerular mesangial and granular cells (which release renin)
```
96
What is atrial natriuretic peptide (ANP) and when is it released?
Atrial myocytes synthesise a 28- amino acid peptide (ANP)
| Released in response to atrial distension (stretch) in hypervolaemic states
97
What does ANP do?
Causes release of water and Na+ in urine
The system reduces MABP and causes vasodilation and reduced renin release
This is counter regulatory mechanisms for RAAS
98
What is ADH?
Anti-diuretic hormone (vasopressin)
| A peptide hormone
99
Where is ADH produced?
Precursor formed in hypothalamus and stored in posterior pituitary
100
What will stimulate ADH secretion?
Reduced ECFV or increased extracellular fluid osmolarity
101
What monitors plasm osmolarity?
Osmoreceptors
102
How does ADH function?
Acts on kidney tulles to increase water reabsorption allowing for increased blood volume and MABP
It will stimulate vasoconstriction to increase TPR and MABP
103
What is shock?
An abnormality of the circulating system resulting in inadequate tissue perfusion
104
What is the pathway for shock?
1. Inadequate tissue perfusion
2. Inadequate tissue oxygenation
3. Anaerobic metabolism
4. Waste product build up
5. Cellular failure and death
105
Which two factors are essential for there to be adequate tissue perfusion?
Adequate cardiac output and blood pressure
106
Which three factors can affect the stroke volume?
1. Preload
2. Myocardial contractility
3. Afterload
107
What is preload?
The preload is the amount of blood in the ventricles before systole - it is the EDV
108
What is after load?
This is the amount of blood left in the ventricles after systole- provides resistance for contracting heart muscle during the next contraction
109
Why does hypovolaemic shock occur?
Loss in blood volume
110
Why does hypovolaemic shock lead to inadequate tissue perfusion?
1. Loss in blood volume
2. Venous return/ EDV reduced
3. Stroke/ cardiac volume reduced
4. Blood pressure is lowered
5. Inadequate tissue perfusion
111
In response to hypovolaemic shock, which way does the Frank- Starling curve shift and why?
```
To the right
Decreased EDV (sub-optimal fibre length) hence stroke volume is reduced
```
112
What is cardiogenic shock?
Occurs when the heart cannot pump enough blood around the body duet o decreases cardiac contractility
113
How does cardiogenic shock lead to inadequate tissue perfusion?
1. Decreased contractility
2. Decreased stroke volume
3. Decreased cardiac output
4. Reduced blood pressure
5. Inadequate tissue perfusion
114
How does cardiogenic shock affect the Frank- Starling curve?
Shifts very far to the right- more than heart failure alone
115
What is obstructive shock?
Due to increased Intrathoracic pressure which decreases venous return
(e.g. pneumothorax)
116
Why does tissue perfusion become inadequate in obstructive shock?
1. Decreased venous return and EDV
2. Decreased stroke volume
3. Decreased cardiac output
4. Reduced blood pressure
5. Decreased tissue perfusion
117
What does neurogenic shock involve?
Loss of sympathetic tone causing massive vasodilation
118
Why does neurogenic shock lead to a lack in tissue perfusion?
1. Massive vasodilation
2. Reduced venous return and EDV
3. Reduced stroke volume
4. Reduced cardiac output and blood pressure
5. Inadequate tissue perfusion
119
What is vasoactive shock?
The release of vasoactive mediators causing massive vasodilation and increased capillary permeability
120
Why is capillary permeability a relevant factor to vasoactive shock?
This can lead to a decreased blood volume and cause hypovolaemic shock
121
How does vasoactive shock lead to inadequate tissue perfusion?
1. Massive vasodilation
2. Decreased venous return and EDV
3. Decreased stroke volume and cardiac output
4. Lowered blood pressure
5. Inadequate tissue perfusion
122
How should shock be treated?
1. ABCDE approach
2. High flow oxygen- makes most of tissue perfusion that does occur
3. Increased blood volume
4. Use of positive inotropes e.g. adrenaline for anaphylaxis
5. In septic shock, vasopressors can be used to cause mass vasoconstriction and increases MABP
123
What are the two main causes of hypovolaemic shock?
1. Haemorrhage (trauma, surgery etc)
| 2. Vomiting, diarrhoea, excessive sweating (decreases ECFV)
124
How is haemorrhage shock characterised ?
Tachycardia- baroreceptor reflex
| Small volume pulse - cardiac output is lowered
125
What is the myogenic (Bayliss) effect?
This involves the control of vessel dilation/ contraction to ensure blood flow remains constant where there is fluctuating blood pressure
It prevents damage to areas such as the brain
126
What are the first vessels to arise from the aorta?
Left and right coronary arteries
