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Systems 1a Revision Decks > CVS Physiology > Flashcards

CVS Physiology Flashcards

1
Q

What planes may a standard limb lead perceive events in?

A

Frontal or vertical

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2
Q

What structures are associated with the following SSLs:

SLL1
SLL2
SLL3

A

SLL1 - Right arm with respect to left arm

SLL2 - Left leg with response to right arm

SLL3 - Left leg with respect to left arm

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3
Q

What two basic principles are essential to understanding and ECG blip?

A
  • Approaching depolarisation causes and upward blip (visa versa)
  • Fast events are transmitted better than slow events
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4
Q

What is the most important SLL and why?

A

SLL2 - the main wave of depolarisation passes down the axis of the ventricles

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5
Q

What is represented by a P-wave?

A

Atrial depolarisation

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6
Q

What is represented by the QRS complex?

A

Ventricular depolarisation

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7
Q

What is represented by the T-wave?

A

Ventricular repolarisation

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8
Q

What is the PR intervals and what is its typical duration?

A

The length of time between atrial and ventricular depol. usually 0.12-0.2 seconds

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9
Q

What is the typical duration of the QRS complex

A

.08 s

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10
Q

What is the QT interval and what is its typical duration?

A

Time spend while ventricles are depolarised about 0.42 seconds

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11
Q

Why can’t we see atrial depolarisation on an ECG?

A

Hidden by QRS complex

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12
Q

Outline the components of the QRS complex

A

Q - Septal depolarisation
R - Bulk depolarisation
S - Upper part of the inter-ventricular septum depolarisation

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13
Q

What pathologies may cause axis deviation of the heart?

A

Rotation, hypertrophy of left/atrophy of right side of the heart

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14
Q

What do augmented limb leads tell you?

A

Gives another aspect of the heart

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15
Q

What do precordial leads give you?

A

Horizontal view of events in the heart

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16
Q

What kind of blips do the precordial chest leads produce?

A

Negative until about V3/4 then positive

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17
Q

What does the rhythm strip tell you?

A

Heart rate and regularity, PR interval, , QRS complex width, QT interval and the relationship between a P-wave and QRS complex

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18
Q

What is a STEMI, how does it differ from a NSTEMI?

A

ST- elevated MI

Non-ST-Elevated MI

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19
Q

How is heart rate regulated?

A

Neural control

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20
Q

How is stroke volume regulated?

A

Preload/afterload and neural control

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21
Q

What is the collective effect of regulation of heart rate and stroke volume?

A

Regulation of cardiac output

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22
Q

How does the sympathetic nervous system regulate heart rate?

A

Noradrenaline and circulating adrenaline from the adrenal glands act on Beta-1 receptors on the SA node - increasing the slope of the path maker potential and increasing heart rate

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23
Q

How does the parasympathetic nervous system regulate heart rate?

A

Vagus nerve releases ACh and acts on muscarinic receptors of the S node, hyperpolarising cells and decreasing heart rate

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24
Q

What does Starlings law state?

A

The force of cardiac contractility is proportional to the initially length of the cardiac muscle fibre

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25
In vivo, what variable effects preload?
End diastolic volume
26
What effect does an increased venous return have on stroke volume?
Increases EDV, therefore increases stroke volume
27
What effect does a decreased venous return have on stroke volume?
Decreases preload therefore decreases stroke volume
28
What is afterload?
The load of blood against which the muscle tries to contract
29
What is TPR?
Total peripheral resistance - a measure of how easy it is for blood to get through the aorta
30
An increased after load will decrease stroke volume - how?
- TPR increases - Aortic pressure increases - More energy required to open aortic valves - Less energy available to eject blood - Decreased stroke volume
31
Describe the neural effect on stroke volume?
Noradrenaline/circulating adrenaline increase contractility of myocytes by acting on Beta-1 receptors
32
What effect does the parasympathetic system have on regulation of stroke volume?
Very little because vagus nerve does not innervate ventricles
33
What pathologies have an effect on regulations of stroke volume?
- Hypercalcaemia - Hypocalcaemia - Ischaemia
34
What effect does hypercalcaemia have on stroke volume/EDV graph?
Shifts up and left
35
What effect does hypocalcaemia and ischaemia have on the stroke volume/EDV graph?
Shifts down and right
36
Where would you find capillaries with no clefts and no channels?
The brain
37
What is a capillary cleft?
Gap between adjacent epithelial cells
38
What is a capillary fenestration?
Circular pore in capillary
39
Where would you find a capillary with clefts only?
Muscles
40
Where would you find fenestrated capillaries?
Intestines
41
What are discontinuous capillaries and where would you find them?
Large open pores, also known as sinusoidal capillaries, can be found in the liver and kidneys
42
What two components to a blood clot must occur?
Platelet plug and fibrin clot
43
What is a platelet plug?
Aggregation of platelets to an exposed area of damage
44
What is a fibrin clot?
Protein mesh that caps the platelet plug
45
What ways can the endothelium prevent clotting?
- Production of prostacyclin and NO - Expresses thrombomodulin and heparin - Secretes t-PA (tissue plasminogen activator)
46
What are the causes of oedema?
Imbalance of Starling forces due to: - Lymphatic obstruction - Raised CVP - Hypoproteinaemia - Increased capillary permeability
47
What are the Starling forces?
The balance between hydrostatic and oncotic pressures of tissue fluid and blood vessels
48
What laws of haemodynamics regulate arteriolar resistance?
Darcy's and Poiseulle's Laws
49
How do you calculate MAP?
CO x TPR
50
How do autonomic nerves have extrinsic control of arteriolar resistance?
Sympathetic - norepinephrine act on alpha-1 receptors and cause vasoconstriction Parasympathetic - no effect
51
How does epinephrine have extrinsic control of arteriolar resistance?
Acts on alpha-1 cells causing vasoconstriction | Some skeletal and cardiac muscles have beta-2 receptors which cause vasodilation
52
What other hormones have extrinsic control on arteriolar resistance?
Angiotensin II - constriction Vasopressin - constriction Atrial and brain natriuretic peptide - dilation
53
What local intrinsic controls are there?
Active hyperaemia Pressure flow auto regulation Reactive hyperaemia
54
What is active hyperaemia?
Increased activity causes metabolite build up - triggers EDRF causing dilation
55
What is EDRF?
Endothelium derived relaxing factor
56
What is pressure autoregulation?
Decreased MAP causes metabolites to accumulate - causing EDRF release
57
What is reactive hyperaemia?
Occlusion of flood supply causes increase in blood flow (extreme pressure auto regulation)
58
What is special about the arteriolar regulation of the coronary arteries?
Blood supply is interrupted during systole Show excellent pressure active hyperaemia Expresses many B2 receptors to keep it dilated
59
What is special about cerebral circulation?
Needs to be kept stable so demonstrates excellent pressure autoregulation
60
What is special about renal circulation?
Main function is filtration - relies on good autoregulation of pressure to function
61
What is meant by intrinsic effects?
Local
62
What is meant by extrinsic effects?
Distant - concerned with TPR of whole body
63
What are Korotkoff sounds?
Auscultated sounds of the heart
64
What are Korotkoff sounds used to measure?
Arterial pressure
65
Atrial pressure wave are affected by what four variables?
- Stroke volume - Velocity of ejection - Elasticity of arteries - Total peripheral resistance
66
What is considered to be a normal arterial pressure?
120/80mmHg
67
What effect does age have on pulse pressure?
Increases
68
Veins are distensible and collapsable; what five factors can effect this?
- Gravity - Skeletal pump - Respiratory pump - Venomotor tone - Systemic filling pressure
69
What is mean arterial pressure?
The main force driving blood through the circulation
70
What happens if MAP is too low?
Syncope
71
What happens if MAP is too high?
Hypertension
72
What two locations for baroreceptors are there in the body in terms of blood pressure?
Aortic arch and carotid sinus
73
What nerve transmits impulses from the aortic baroreceptors?
Sensory branch of the vagus nerve
74
What nerve transmits impulses from the carotid sinus baroreceptors?
The glossopharyngeal nerve
75
Where do both the vagus and glossopharyngeal nerve transmit impulses to in the brain?
The cardiac regulatory centre in the medulla
76
Outline the motor side of regulation of blood pressure?
Vagus nerve innervates the SA node, causes hyper polarisation and the speed of depolarisation decreases therefore so does heart rate Sympathetic has opposite effect
77
What else occurs during activation of sympathetic nervous system?
Release of epinephrine from adrenal glands Ventricles innervated to increased contractility Vasoconstriction
78
What effect does activation of central chemoreceptors have on the CVS?
Increases both heart rate and strength of contraction to accommodate increased PaO2
79
Increased use of joints/muscles causes what?
Receptors to be activated to effect CVS
80
What function do higher centres serve?
Feed-forward system to prepare body for physical activity
81
What are the two reflexes occur to produce an increased blood pressure?
Decrease vagal tone and increase sympathetic tone
82
What is the Valsalva manoeuvre?
Forced expiration against a closed glottis
83
Outline the mechanics of the Valsalva manoeuvre?
Increase in thoracic pressure transmitted through pulmonary veins Reduces venous return and decreases EDV Produces weaker strength of contraction Lowers MAP Baroreceptors detect decrease in pressure and triggers reflex
84
What is probably not the main gringo in long term blood pressure control?
The arterial baroreflex
85
What three hormone systems are involved in long term blood pressure control?
RAAS Antidiuretic hormone Atrial natriuretic peptide
86
What factors effect long term control of blood pressure?
Blood volume
87
Where is renin produced?
Juxtaglomerular cells in the kidneys
88
What triggers the release of renin?
Activation of the sympathetic nerves to the juxtaglomerular apparatus Decreased distention afferent arterioles to glomerulus Decreased delivery of Na+ and Cl- to kidneys
89
What are the three triggers of renin production indicative of?
Decreased MAP
90
What does renin do?
Causes angiotensinogen to be converted to angiotensin I
91
What does angiotensin II do?
Vasoconstriction and stimulates the release of aldosterone and reduces diuresis
92
What kind of system is the RAAS?
Negative feedback
93
Where is ADH produced?
Pre-synthesised in the hypothalamus then released from the posterior pituitary gland
94
What triggers ADH release?
Reduced MAP, Angiotensin II and increased osmolarity of interstitial fluid
95
What does ADH do?
Causes water retention and vasoconstriction
96
Where is ANP produced?
Myocytes of the atria
97
What stimulates ANP release?
Increased distention of the atria
98
What does ANP do?
Increases natriuresis, inhibits the release of renin and acts on CV centres in the medulla to reduce MAP
99
What percentage of hypertensive patients are classed as secondary?
5-10%
100
What pharmacological approach to management of blood pressure are there?
CCBs Beta-blockers Thiazide type diuretics ACE inhibitors

Systems 1a Revision Decks (22 decks)

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