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CVS Physiology Flashcards

(85 cards)

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1
Q

What is the CVS system made up of

A

Heart
Vessels
Blood

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2
Q

What is the function of the CVS system

A

Transport 02 and C02
Transport nutrients and metabolites
Hormones
Heat

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3
Q

What is the cardiac output of the heart

A

5l / minute

CO = SV x HR

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4
Q

What is 02 consumption compared to cardiac output

A

Organs use similar %02 to cardiac output
Kidney’s get more cardiac output
Heart gets 4% CO but uses 10% of the 02 so more prone to disease

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5
Q

What is flow through vessels determined by

A

Pressure difference (MAP - central venous pressure)
High in artery to low in venous system
Resistance of vessels

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6
Q

How is the heart and vascular system wired

A

R+L in series so both outputs equal
Vascular beds parallel so flow at same time
Hypothalamus + pituitary, gut + liver = series as need blood flow after each other

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7
Q

How should flow through CVS system be

A

At any point should be the same

Vary throughout day / clinical situation as arteries constrict and alter resistance

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8
Q

What is the aorta

A

Elastic artery
Very low resistance
High pressure blood to pump through higher pressure of arterioles
Dampens pressure variation in between systole + diastole as energy stored in wells so blood keeps coming out

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9
Q

What are arteries made up like

A

Muscular and non elastic
Wide lumen
Low resistance

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10
Q

What are arterioles made up like

A

Muscular wall with narrow lumen
Constrict to control total peripheral resistance and blood flow to organs
Pressure falls as goes through vascular tree
Small drop through artery but large drop through arterioles as high resistance

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11
Q

What are capillaries made up like

A

Exchange vessels
Very narrow lumen and thin wall
BP very low

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12
Q

What are veins made up like

A

Low resistance so blood can get back to the heart
Wide lumen
2/3 of blood stored in veins = capacitance vessels

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13
Q

What is MAP determined by

A

Cardiac output and total peripheral resistance

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14
Q

How is arteriolar resistance controlled

A

Extrinsic neural control
Extrinsic hormonal control
Intrinsic control - individual tissue

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15
Q

What is extrinsic control

A

Sympathetic release noradrenaline which binds to A1 receptors on smooth muscle
Cause contraction
Para has no effect

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16
Q

What is arteriolar resistance at rest

A

Largely high as tissue don’t require as much 02

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17
Q

What is hormonal control of resistance

A

Epinephrine binds to A1 receptor = constriction
Can also bind to B2 receptor = dilation if tissue needs 02
Angiotensin II = constriction
Vasopressin = constriction
ANP + BNP = dilatation

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18
Q

What is intrinsic control measures of controlling resistance

A

Active hyperaemia
Pressure auto regulation
Reactive hyperaemia
Injury response

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19
Q

What is active hyperaemia

A

When activity increase metabolites released from tissue - H, Co2, K, lactate etc.
EDRF released causing dilatation to match needs
When metabolites decrease tone goes back to normal

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20
Q

What is pressure autoregulation

A

If pressure goes down flow will decrease and metabolites will increase
Cause dilatation to maintain blood supply despite changes in MAP
Body can do to certain extent but if drops too low will fail

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21
Q

What is reactive hyperaemia

A

Occlusion of blood = metabolites increase

Extreme form of auto regulation

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22
Q

What is the injury response

A

C fibres release action potential stimulates substance P

Acts on mast cells = histamine + dilatation

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23
Q

What are special circulations

A

Coronary
Cerebral
Pulmonary
Renal

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24
Q

What happens in coronary

A

Blood is interrupted by systole

Has excellent active hyperaemia with B2 receptors

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25
What is special about cerebral
Excellent pressure auto regulation so perfusion maintained if pressure drops
26
What is special about pulmonary
If 02 decreased = constriction so blood will go to well ventilated area
27
What happens win renal circulation
Filtration is dependent on MAP | Arterioles constrict and dilate depending on how much absorption is needed
28
What is Raynaud's an example of
Reactive hyperaemia Blood flow decreased so increase in metabolites Dilate to wash out metabolites When blood flow returns resistance is very low
29
Cardiac output
SV X HR
30
How is HR controlled and what achieves tonic control
The Autonomic Nervous System | Parasympathetic - sit at 60bpm
31
How do you increase your HR
Decrease para and increase sympathetic Sympathetic - noradrenaline on B1 on SA node + AVN Spreads up depolarisation Also increase contractility (inotropic affect)
32
How do you decrease HR
Increase parasympathetic input Vagus nerve release Act acts on muscarinic 2 receptor on SA + AVN Hyperpolaries cell
33
What causes a tachycardia
``` Anxiety Infection Hypoglycaemia Hypovolaemia Hyperthyroidism Problems with conductance in the heart ```
34
What type of conductance issues can you get
Wide Complex Tachy - broad QRS - Ventricular tachy - Wolff parkinson white Narrow complex tachy - Sinus tachy - AF and flutter
35
How do you treat wide complex and narrow complex
Wide - Amiodarone - DC conversion if unstable Narrow - Vagal manouvere - IV adenosine - DC conversion if unstable - AF = BB to control rate + anti-coagulant
36
What is the stroke volume
The amount of blood expelled by the heart in a cardiac cycle Determined by filling of heart in diastole and how easy it is to be expelled in systole EDV + ESV Contractility and inotropy In HF these compensatory mechanism fail so can't maintain CO
37
What affects stroke volume
Central venous pressure - if increases then increases filling of ventricles in diastole Total peripheral resistance - decreases so easier for blood to be expelled ESV Contractility Afterload
38
What affects contractility of heart
Para little effect | Sympathetic - Na on B1 of mycoytes
39
What does sympathetic do to calcium
More calcium from ECF = more forceful contraction Also increases Ca-ATPase on sarcoplasmic retinaculum Ca removed faster so shorter contraction
40
What else affects contractility
Inotropes - epinephrine, Hypercalcaemia Thyoid hormones Glucagon
41
What decreases contractility
``` Ach by vagus nerve on m2 Hypocalcaemia Ischaemia - hypoxia Hyperkalaemia Barbituarates ```
42
What is Starling's Law
The more the heart fills e.g. EDV, the harder it will contract and the larger the SV Therefore a rise in central venous pressure will increase SV This only occurs up to a certain point
43
What is pre-load
The degree of myocardial stretch (due to venous filling) before contraction
44
What determines preload
The end diastolic volume - the volume of blood in the heart at the end of diastole Venous return and filling time
45
Sum this up
``` Increased venous return Increased EDV Increases Preload Increased SV Increased CO Self regulating mechanism summing up Starling's law ```
46
What factors affect venous return
Skeletal muscle pump - exercise Respiratory pump - inspiration decrease pressure so more blood drawn in Sympathetic - contract veins and increase return (venomotor tone) Systemic filling pressure from ventricle Gravity - orthostatic hypotension as decreased EDV when lying flat
47
What decreases preload
``` Decreased thyroid Decreased calcium High or low K / Na Low body temp Hypoxia Abnormal pH Drugs - CCB ```
48
What is after load
The load against which myocardial cells have to contract If TPR increases then aorta at higher pressure so ventricle needs to work harder SV decreases
49
SO
Resistance vessels affect after load | Capacitance veins affect pre-load
50
What happens in exercise
CO increases 4-6x HR and contractility increases due to sympa Venous return increases to maintain preload by sympa causing contraction TPR falls due to dilatation so decreased after load
51
How does the heart compensate for reduced pumping ability
Works with increases EDV | Results in lower ejection fraction and reduced exercise capacity
52
What is the ejection fraction
Stroke volume / EDV
53
How do capillaries work
Allow gas exchange One cell thick so quick diffusion Individual high resistance but in parallel so reduces
54
What are the types of capillaries
Continuous - no clefts or channels e.g. in brain so anything polar is stuck inside Fenetrated - contains cleft and channels e.g. intestine Discontinous - cleft and massive channels e.g. in liver 02 nd C02 able to freely diffuse across
55
What affects diffusion rate
Concentration gradient Distance SA of area receiving
56
What forces control movement across capillaries
Blood hydrostatic - forces fluid out Blood osmotic - pressure exerted by proteins which can't get out so pulls fluid in Interstitial hydrostatic - forces fluid back into capillary Interstitial osmotic - pulls fluid out of capillary
57
Whats bulk flow mechanism
Hydrostatic pushes fluid out of capillary Oncotic pressure builds up as protein conc increases Draws fluid back in Capillary hydrostatic vs ISF hydrostatic Capillary oncotic vs ISG oncotic
58
What volumes of blood move in and out of the capillaries
20l 17l regained 3l picked up by lymphatics
59
What do lymph capillaries do
Same structure but no return valves so fluid goes to the heart
60
What causes oedema
Excess fluid caused by lymph obstruction, raised CVP, huypopoteinaemia (no oncotic to pull water in), increased capillary permeability
61
What is shock
Inadequate blood flow
62
What can cause shock
Cardiogenic - pump failure reduces CO so decreased MAP, CVP may be normal or raised, Mechanical - pump doesn't fill, e.g. cardiac tamponade, high CVP and low MAP Hypovolaemic - loss of blood volume Distibutive - uncontrollable fall in TPR Toxic shock - endotoxins released in infection = vasodilation and drop in TPR
63
What are typical symptoms of shock
Tachycardia Rapid and shallow breathing Reduced BP Fluid resus and treat cause
64
What is systolic blood pressure
The pressure during ventricular systole / heart contraction
65
What is diastolic BP
The pressure during ventricular diastole / after contraction but before the next
66
What is the mean arterial pressure MAP
CO x TPR The driving force of blood through the circulation Pulse pressure + 1/3 of your diastolic
67
What controls short term regulation of BP
Autonomic nervous system
68
What detects change in BP
Baroreceptor in aortic arch + carotid sinus
69
What happens when there is an increase in BP
Increased MAP = greater stretch which baroreceptor detect Send AP to medullary CVS control centre Parasympathetic acts to reduce BP
70
What does aortic arch baroreceptor stimulate and carotid sinus
Aortic arch = vagus | Carotid sinus = glossopharyngeal
71
What are other inputs to short term control
Cardiopulmonary - in low pressure areas of heart and lung which fire if high volume Central chemoreceptors - if low O2 Muscle chemoreceptors - increased metabolites Joint receptors - movement
72
What is the valsalva manouvre
Forced expiration against a closed glottis
73
What happens in the valsalva manoeuvre
Increase in thoracic pressure transported to vessel Decreased venous return Decreased EDV, SV, CO + MAP Common when you strain and go to toilet Decreased MAP detected by baroreceptors which work to increase BP
74
What is the reflex
Deceased vagal = increased HR + CO Increased sympa = Increased HR, CO, contractility, venoconstriction so increased VR, arteriolar constriction so increased TPR
75
What is the long term control of BP
Renin-angiotensin system (RAAS)
76
Where is renin produced
JG of kidney
77
What triggers renin production
Activation of sympathetic ( reduced MAP post JG) Decreased distention of afferent / blood flow Decreased delivery of NACL detected by macula densa
78
What does renin do
Converts angiotensinogen to ANG 1 | ANG1 - ANG2 by ACE
79
What does ANG2 do
Release of aldosterone from adrenal cortex Na reabsorption in proximal tubule Increased release of ADH from PP Potent vasoconstrictor so increases TPR
80
What does aldosterone do
Increase NA reabsorption in distal tubule so increased volume
81
What does ADH do (Vasopressin)
Increased water permeability of collecting duct | Increased thirst
82
What else triggers ADH
Decrease in blood volume - cardiopulmonary | Increased osmolarity
83
What does ANP do
Released from myocardial cells when increased distension Inhibits renin Dilates afferent arterioles so increased GFR Increases NA excretion Decreases MAP
84
What is the link between respiratory system + CVS
If hypoxia / hypercapnia = often pulmonary hypertension (constrict) + R heart failure (due to hypertension as increased after load) Initially compensate but won't get enough 02 in vessels Leads to L HF and further pulmonary hypertension Increased hydrostatic pressure so fluid out = pulmonary oedema Decreased gas exchange as increased distance CO2 decreases respiratory drive
85
What do prostaglandins do
Local vasoconstrictor to increase GFR and reduce Na reabsorption

CVS (30 decks)

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