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Year 1 Systems (JBR) > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

What does auto-rhythmicity mean?

A

That the heart can generate it’s own heart beat

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2
Q

What is meant by a heart that is in sinus rhythm?

A

Electrical signals coming from the SA node are controlling the rhythm

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3
Q

Parasympathetic stimulation acts via _____ on which receptors on the heart?

A

acetylcholine

M2 muscarinic receptors

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4
Q

What is the effect of parasympathetic stimulation of the heart?

A

Increase potassium efflux, decrease Na and Ca influx, increase AV node delay

Decrease slope of pacemaker potential
Decrease HR

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5
Q

Vagal tone lower to HR from _____ to ______

A

100 to 70

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6
Q

Sympathetic stimulation acts via ______ on beta-1-adrenoreceptors

A

noradrenaline

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7
Q

What is the normal MAP range?

A

75-105

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8
Q

What is defined as hypertension?

A

BP above 140/90

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9
Q

How is MAP calculated?

A

((2 x diastolic) + Systolic) / 3

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10
Q

The pressure gradient (MAP-CVP) pushes blood around the body. What is the main resistance vessel to this?

A

Arterioles

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11
Q

What are the (5) Korotkoff sounds?

A
  1. Peak systolic
    2-3. Intermittent sounds due to turbulent flow
  2. Minimum diastolic pressure (last sound)
  3. No sound due to laminar flow
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12
Q

Short-term BP changes are controlled by?

A

The Baroreceptor Reflex

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13
Q

Outline the baroreceptor reflex?

A

Pressure sensor in aortic arch (CNX), central in carotid sinus (CNIX)
Firing reduced when BP low
Causes decreased vagal and increased sympathetic tone
HR increases
Baroreceptor reflex increases TPR

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14
Q

What can occur as a consequence of the baroreceptor reflex in elderly patients with a worn out baroreceptor reflex?

A

Postural hypotension

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15
Q

Which hormones/systems are involved in longterm control of BP?

A

RAAS
APN
ADH

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16
Q

Explain how RAAS influences BP

A

Renin released from kidneys
ACE converts angiotensin I to 2 stimulating aldosterone from adrenal cortex
Vasoconstriction, increased TPR and ADH
Conserves water

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17
Q

What stimulates RAAS?

A

Renal hypotension
Renal sympathetic nerve stimualtion
Decreased sodium concentration in tubular fluid

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18
Q

Which sensor detects decreased sodium concentration in tubular fluid?

A

Macula densa

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19
Q

Where is APN synthesised and stored?

A

Atrial myocytes

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20
Q

When is APN released?

A

In Hypervolaemia

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21
Q

What does APN result in?

A

Excretion of salt (and therefore water) by the kidneys + decreased renin release

Acts as a vasodilator (counteracts RAAS)

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22
Q

What is the main condition where ADH (vasopressin) is significant?

A

Hypovolaemic Shock

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23
Q

Where is ADH synthesised?

A

Hypothalamus

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24
Q

Where is ADH stored and released?

A

Pituitary gland

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25
When is ADH secreted?
If ECFV is decreased or ECF osmolarity is increased
26
What is the effect of ADH?
Acts on kidney tubule to increase tubular reabsorption (antidiuresis - more concentrated uric) Increased ECF and plasma volume Increased CO and BP
27
Which cell junctions allow for low resistance conductance and tension spread in striated muscles?
Conductance = Gap junctions | Tension spread - Desmosomes
28
Contraction and relaxation of myocytes requires?
ATP | Calcium
29
What is Stroke Volume?
The volume of blood ejected by each ventricle per heart beat = EDV - ESV
30
What are intrinsic regulators of SV? (5)
``` Length of myofibrils EDV Stretch Venous return Afterload ```
31
What are extrinsic regulators of SV? (2)
Sympathetic - calcium influx - via noradrenaline (inotropic + chronotropic) Parasympathetic (affects rate not force) via acetylcholine
32
What is the Frank-Starling Law?
The greater the EDV the greater the SV until maximal force by optimal fibre length is reached
33
What is after load?
Resistance into which the heart is pumping
34
Persistent increase in after load can lead to?
LVH
35
How is the AP in the SA node generated (3)
Decrease in K efflux, increase in Na Influx (funny current) Once @threshold, Ca influx raises to AP K efflux results in fall of membrane potential
36
The Bundle of His and Purkinje fibres spread excitation to the _____?
Ventricles
37
The AV node ___ the pulse slightly
delays
38
Outline the AP in Ventricular Myocytes
``` 0 - Fast Na influx 1 - close Na, transient K efflux 2 - Ca influx - plateau 3 - K efflux 4 - resting membrane potential (-90) ```
39
What are the approximate duration times of diastole and systole?
Diastole - 0.5 | Systole - 0.3
40
What are the 5 stages of the cardiac cycle?
``` Passive filling Atrial contraction Isovolumetric contraction Ventricular ejection Isovolumetric relaxation ```
41
What happens during passive filling?
No pressure All valves open 80% of filling
42
What happens during atrial contraction?
Remaining blood enters ventricles
43
What happens during isovolumetric contraction
AV valves shut, S1 Pressure in ventricles > atria Tension rises around ventricles
44
What happens during ventricular ejection?
Pressure in ventricles > aorta/pulmonary A/P valves open SV ejected (ESV remains)
45
What happens during isovolumetric relaxation?
Ventricles repolarise and pressure falls - A/P shut, S2 | Tension falls and ventricular pressure < atrial pressure
46
JVP occurs right after and mimics the ____________
atrial pressure wave
47
What is Shock?
Abnormality in the circulatory system resulting in inadequate tissue perfusion and oxygenation leading to cellular failure
48
The body can compensate BP until more than __% of blood volume is lost
30
49
Hypovolaemia is classified into which 4 severity categories?
I - <15 II - <30 III - <40 IV - >40
50
Hypovolaemic shock refers to?
Lowered volume due to haemorrhage / non-haemmorhage
51
How is hypovolaemic shock treated?
Ideally blood transfusion; can maintain for a wee while with fluids
52
How does the body compensate for hypovolaemic shock?
Decreased SV - Tachycardia | Decreased CO - increased sympathetic vascular resistance
53
What is the cause of carcinogenic shock?
Heart can't contract
54
What is the cause of obstructive shocK?
Tension on the heart (e.g. tamponade) means it can't pump
55
What is the cause of distributive shock?
Neurogenic - loss of sympathetic tone | Vasoactive
56
How is shock treated?
ABCDE | Then treat the cause
57
When do the coronary arteries get blood from the base of the aorta?
During diastole
58
Coronary arteries are drained by...?
The coronary sinus
59
What are intrinsic adaptations of the coronary circulation?
high oxygen extraction Adenosine and decreased PO2 dilate vessels Adrenaline dilates by beta 1
60
What are extrinsic adaptations of the coronary circulation?
Metabolic hyperaemia matches flow to demand
61
What are adaptations of the cerebral circulation?
Circle of Willis (anastomoses btw. basilar and carotid arteries) Raised MABP - constriction vs. reduced - dilation Regulators: PCO2 (increase = vasodilation), regional hyperaemia, changes in ICP (increase = decreased perfusion)
62
What are adaptations of the pulmonary circulation?
Low resistance/pressure protects against oedema | Hypoxia - vasoconstriction
63
What are adaptations of the skeletal circulation?
Low resting blood flow because of sympathetic vasoconstrictor tone Exercise: local metabolic hyperaemia > sympathetic tone + circulating adrenaline (via beta-2) = vasodilation Skeletal muscle pump increases venous return
64
Blow flow through capillaries depends on __________ in terminal arterioles
pre capillary sphincters
65
Forces favouring filtration
Capillary hydrostatic pressure | Interstitial fluid osmotic pressure
66
Forces opposing filtration
Interstitial fluid hydrostatic pressure | Capillaryy osmotic pressure
67
What prevents oedema under normal conditions?
Lymphatic drainage
68
Oedema forms under which conditions?
Raised capillary pressure Reduced plasma pressure Lymphatic insufficiency Permeability --> Reabsorption is bad

Year 1 Systems (JBR) (21 decks)

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