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Physiology > CVS > Flashcards

CVS Flashcards

0
Q

How much of the blood volume remains in the systemic system?

A

84%

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1
Q

Where are serial and parallel systems located?

A

Serial: Heart and lungs
(Local- kidney and liver)
Parallel: at periphery

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2
Q

What makes up the systemic system

A

Arteries, arterioles, micro circulation, venues and veins.

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3
Q

What is the most elastic vessel and the most muscular?

A

Elastic- aorta

Muscular- terminal arterioles

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4
Q

What is ohms law

A

Q= ΔP/R vol/time

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5
Q

Name the 2 types of blood flow and explain

A

Laminar- low Reynolds in small vessels

Turbulent- high Reynolds in large vessels causes sound

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6
Q

What is the ideal blood flow

A

5L/min

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7
Q

How is Reynolds worked out

A

(Density x diameter x velocity) / viscosity

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8
Q

What is the equation for velocity

A

V(m/s) = Q/crossectional area

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9
Q

Describe the velocity in serial and parallel vessels

A

Parallel- large A to small A –> velocity increases

Parallel- a increases–> velocity decreases

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10
Q

Where is velocity at it’s lowest?

A

Capillaries

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11
Q

What is viscosity? And what is it’s relationship to Q?

How is the bloods viscosity determined?

A

Q= 1/η
It is the physical properties of fluids due to size and density of particles that can effect resistance and velocity.
Determined by the haematocrit

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12
Q

How is mean pressure calculated

A

[(2x diastolic p) + (1x systolic p)]/ 3

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13
Q

What does pulse pressure show? And how is it calculated?

A

Shows: arterial compliance and stroke volume

Systolic p- diastolic p

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14
Q

Which vessels have the largest:
total area? (Cm^2)
Blood pressure? (MmHg)

Which have the lowest velocity?(cm/s)

A

Area- capillaries
Pressure- aorta and large arteries
Velocity- capillaries

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16
Q

What is the mean pressure determined by? And what parameter does it control?

A

Determined by CO and peripheral resistance

It’s determines flow

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17
Q

How is arterial pressure measured? And explain.

A

With a auscultation cuff. 1. Inc pressure above 120mmHg so no blood flow

  1. Graduate lower unti eventually systolic p can over come the cuff pressure— turbulent flow causes Korotkoff sound
  2. When cuff pressure is below diastolic p of 80mmHg flow is laminar so no sound
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18
Q

What is the main parameter that determines blood flow? How is this parameter calculated?

A

Resistance=(η x L)/ r^4

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19
Q

What determines resistance and how? What effects does it have on flow?

A

Arterioles serial vessels have the highest resistance… Determine flow due to their radius.
Resistance is inversely proportional to diameter.. 1/r^4

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20
Q

What is starlings hypothesis about filtration?

A

Hydrostatic p- Oncotic p

Ie. outward force should be greater than inward force

Out ward force: (hydrostatic p of cap + Oncotic p of interstitial fluid)

Inward force: (hydrostatic p of interstitial fluid + Oncotic p of capillaries)

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21
Q

What is the normal Oncotic p?

A

25mmHg

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22
Q

What happens if arterial pressure drops?

A

Vasomotor reflex: Pressor reflex inc–> symp activities. Inc vascular tone (vasoconstriction) to increase resistance. increase HR, contractility and stroke volume to increase CO. This increase pressure

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23
Q

What is the dominant pacemaker? What is the secondary pace maker?
What is the tertiary pacemaker?
How many APs met mum for each?

A

1- SAN 100AP/min
2- AVN 40-60/min
3- ectopic anywhere else below 40

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24
Q

describe the SAN and Ventricular APs and what ions are involved in depolarisation

A

SAN- slow AP spontaneous and no stable resting membrane pot
I funny Na channels - depolarise spontaneously
L and T type Ca channels for depolarisation

Ventricles- fast depolarisation and AP, small depolarisation initially, plateau
Depolarisation: fast voltage gated Na and Ltype Ca channels

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25
Q

Explain a cardiac ap and it’s contraction

A

Beats rhythmically
Had a slow long plateau AP
Contraction occurs during AP
Relaxation starts as Ca goes off and finishes before membrane potential is normal so causes and effective absolute refractory period to ensure no tetanus

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26
Q

What is the main cause is Sudden death syndrome

A

Channel opathies

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27
Q

Name drugs that target sodium, calcium and potassium channels to control arrhythmias and hypertension

A

Na- lidocaine and procainamide
Ca- verapamil and nifedipine
K- dofetelide and ibutilide

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28
Q

How to arrhythmia and hypertension drugs work

A

Dec frequency by blocking spontaneous AP depolarisation.

Inhibit ventricular contraction to dec cardiac output

And the cause vasodilation to dec peripheral resistance

Thus dec in Bp

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29
Q

Outline the mechanism of action of an ECG

A

The area of the Heart that gives an AP is positive inside compared to the outside, unlike an area with no AP generating a potential difference at different area of the heart, the potential is propagated to the body’s surface and is measured. The ECG records fluctuations of electrical potential in the chest reflecting cardiac AP. A galvanometer is used. The heart is positioned in a Einthoven triangle. right arm lead (- -) left arm (+ -) and left leg (++)

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30
Q

What does the time between p and q represent?

A

AP tracking to AVN

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31
Q

What so ectopic pacemakers cause?

A

Arrhythmias. Paroxysmal tachycardia

32
Q

What indicated AVN block?

A

A PQ duration longer than 0.2s

33
Q

What causes 3rd degree AVN blocks?

A

Ectopic nodes

34
Q

What does ECG AF look like?

A

No constant QRS intervals

35
Q

Describe a normal axis Einthoven triangle

A

All leads are positive
Lead II has the largest amplitude
The arrow point down to lead III

36
Q

Describe the Einthoven triangle of right axis shift and it’s cause

A

Lead I is negative and lead III has the highest amplitude
The arrow point down towards lead II
Pulmonary hypertension causes right ventricle hypertrophy so the direction is diverted to the right

37
Q

Describe left axis shift of an Einthoven triangle and it’s cause

A

Lead III is negative
Lead I has highest amplitude
The arrow is horizontal and points to lead III
systemic hypertension causes left ventricle hyper trophy

38
Q

How long do systole and diastole last

A

Sys- o.3s

Dia- 0.5s

39
Q

Explain the sequence of events that occur durning systole

A

Ventricles contract inc pressure higher than atria so mitral valves close
Aorta is closed as the pressure is lower in aorta than in ventricles
Both valves shut= isovolumatric contraction
Pressure in vents exceeds aorta and opens valves
Blood is ejected rapidly, then slowly as blood leaves

40
Q

Explain the diastole sequence of events

A

Vent pressure is below aorta during relaxation, so valves close. The mitral valves are closed = isovolumetric relaxation
When vent pressure is below atria, the atrioventricular valves open, blood rapidly flows in then slows = diamesis

41
Q

Define CO and give the equation

A

The quantity of blood pumped into the aorta each minute by the heart

CO = HR x Stroke Volume

42
Q

Define HR and Stroke volume

A

HR- no of systole a per min

SV- quantity of blood pumped out by a ventricle during systole

43
Q

What are the determinants of CO

A

BMR
If the individual is exercising
Age
And size of body

44
Q

What is the normal cardiac index of an individual

A

3L/min/m^2

45
Q

How is CO measured

A

Ficks Principle: flow=O2consumed➗ (aterial- venous 02 conc)

46
Q

How much 02 is consumed per min

A

250ml

47
Q

Name the cardiac factors that control CO

A

NS: controlling HR and contractility(stroke volume)

48
Q

Name the coupling factors that effect CO

A

Preload: starling laws - venous return
Afterload: ohms law -peripheral resistance

49
Q

What are the hypothesises behind starlings law of venous return

A
  1. As more blood enter the heart, the muscle fibres are stretched, causing the sarcomeres to increase in length, this allowing more cross links to form and bring about a more forceful contraction
  2. The extra blood entering the heart pre- stretches the muscle fibres this increases Ca conc and it’s affinity for troponin C ensuring that troponin I is relaxed more cross bridges form thus giving a more forceful contraction
50
Q

How does preload effect the CO

A

Preload is the right atrial pressure that influences: venous return and filling
During diastole the pressure gradient is: vein > atria > ventricle
Inc atrial pressure :decreases venous return but inc ventricle filling (valves open)

51
Q

How does after load affect CO

A

During diastole ventricle pressure > artery pressure

An increase in artery pressure would increase resistance during ejection this decreasing strove volume and CO

52
Q

True/false: the NS only effects the HR and contractility directly. Explain

A

False: has direct and indirect effect- on preload and after load

53
Q

Vagus nerves and sympathetic that effect the heart are due to which type of ganglia

A

Vagus- pre ganglionic

Syp- post ganglionic

54
Q

Explain the vagus nerves mode of action

A

Releases ach to m2 receptors so increase k+ permeability causing hyper polarisation
This is a tonic inhibition acting on the SAN alone

55
Q

Describe the syp nerves mode of action on the heart

A

Nor ad released to act on β adrenergic receptors all over the heart act via GPCR inc cAMP and PKA this increasing HR and contractility
cAMP can activate Ca channels And can phosphorylate troponin I allowing Ca to bind to troponin C

56
Q

What drugs affect the PSY and SY nerves action and how?

A

Atropine- blocks m2 receptors so imce HR

Propranolol- blocks β adrenergic receptors causing a slight dec in HR

57
Q

What are the control mechanisms of circulation and BP, explain each and what they act on

A

Local- maintains flow Accoring to metabolism and against change in BP

Global- maintains BP (perfusion pressure), redistributes blood flow to diff areas of the body, and inc/dec pumping of the heart

Both act on arterioles

58
Q

How does the action of local and global mechanisms on the arterioles maintain blood circulation

A

Vasodilation- inc flow and dec BP

Vasoconstriction - dec flow and inc BP

59
Q

How does local adaptation to inc metabolism arise?

A

Vasodilation occurs
Theory 1. Vasodilator theory: tissue hypoxia, vasodilator substances (co2, adenosine, k+, h+)
Theory 2. Lack of oxygen: low po2 opens pre capillary sphincters, unlike low po2 that closes them. So hypoxia inc flow

60
Q

Explain auto regulation of blood flow and BP

A

At low pressure there is a linear relationship between P and Q (ohms law: Q=p/R) as P and Q increases vasodilator substances are washed out causing vasoconstriction.
Vessels react to pressure change and stabilise Q.
P increases, vessel distends, myogenic contraction response, inc resistance and thus restores blood Q

61
Q

What is the primary factor that effects coronary perfusion

A

Aortic pressure

62
Q

When is coronary flow greatest

A

Early diastole

63
Q

Explain local regulation of flow in coronary circulation as metabolic regulation

A

Myocardial metabolic rate sets myocardial O2 demand. If O2 supplied ( from aterial po2 and coronary blood flow) is less than that used by myocardium ADENOSINE vasodilator is released (k+ has transient effects) to increase coronary flow

64
Q

Explain local regulation of blood flow in the brain as metabolic regulation

A

Co2 vasodilator from neural tissue maintains circulation between 60-200mmHg
Dec flow, means that co2 is retained to vasodilates vessels
And increase flow means that co2 is washed away so vessels vasoconstrict

65
Q

What contributes to the global mechanism of control of BP

A

ANS and the vasomotor cortex: Pressor (SY) and depressor areas(PSY)

66
Q

How many APs does the SY nerve stimulate at resting, vasoconstriction and vasodilation?

A

Resting- 5/s
Con- 25/s
Dila- 1/s

67
Q

What causes vasoconstriction (NT and receptors)

A

SY- norad, binds to α1 of smooth muscle - GPCR Gq–> phospholiapse C , Ip3, Ca = contraction

68
Q

Where is the one exception of NA and adrenaline action that causes vasodilation vs. vasoconstriction
Explain

A

Skeletal muscles- lack α1 and NA and adrenaline bind to β2–> cAMP inc myosin light chain kinase–> motor cortex–> vasod to increase flow

69
Q

Explain the effects of SY on the heart

A

SY releases NA and binds to β1 acts on GPCR–> Gs–> cAMP–> PKA–> inc Ca–> inc HR contractility and CO

70
Q

Where are baroreceptors and what do they sense (within what range)

A

In the carotid sinus and aorta wall sense change in BP within 80-130mmHg (not sensitive below 60mmHg)

71
Q

True/false: baroreceptors are sensors, vasomotor is a comparator and vessels/smooth muscle/heart are effectors

A

True

72
Q

Explain the baroreceptor reflex

A 
Stand up
Dec venous return
Dec CO (starling and preload)
Arterial BP dec
Baroreceptor firing dec
Pressor reflex: reduced PSY to SAN (tachycardia), vasoconstriction of veins, inc myocardial tone (inc stroke work) 
BP returned to normal 120/80
73
Q

Where are chemoreceptors and at which range do they work in maintaining global regulation of BP, and how?

A

In the carotid/aortic (peripheral) body and brain stem (central)
Work below 60mmHg
They sense po2 and pco2
In these inc–> Pressor reflex to inc BP

74
Q

What determines long term regulation of BP

A

Blood volume. Altering blood volume increase venous return as to increase CO and BP

75
Q

How is effective circulating volume EVC (vol that perfuses the blood) maintained

A

By the renin angiotensin mechanism. renin from kidneys combined with angiotensinogen from the liver causes angiotensin 1, with the aid of enzymes from the Lungs this is converted to angiotensin 2–> a) vasoconstriction and inc BP b) acts on adrenal cortex to release aldosterone, increasing h2o reabsorption and inc BP

76
Q

What determines BP

A

Cardiac Output, peripheral resistance (mean pressure)
And
Arterial compliance, Stoke volume
(Pulse pressure)

Physiology (3 decks)

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