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CVS Flashcards

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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
Explain a cardiac ap and it's contraction
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
26
What is the main cause is Sudden death syndrome
Channel opathies
27
Name drugs that target sodium, calcium and potassium channels to control arrhythmias and hypertension
Na- lidocaine and procainamide Ca- verapamil and nifedipine K- dofetelide and ibutilide
28
How to arrhythmia and hypertension drugs work
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
29
Outline the mechanism of action of an ECG
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 (++)
30
What does the time between p and q represent?
AP tracking to AVN
31
What so ectopic pacemakers cause?
Arrhythmias. Paroxysmal tachycardia
32
What indicated AVN block?
A PQ duration longer than 0.2s
33
What causes 3rd degree AVN blocks?
Ectopic nodes
34
What does ECG AF look like?
No constant QRS intervals
35
Describe a normal axis Einthoven triangle
All leads are positive Lead II has the largest amplitude The arrow point down to lead III
36
Describe the Einthoven triangle of right axis shift and it's cause
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
Describe left axis shift of an Einthoven triangle and it's cause
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
How long do systole and diastole last
Sys- o.3s | Dia- 0.5s
39
Explain the sequence of events that occur durning systole
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
Explain the diastole sequence of events
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
Define CO and give the equation
The quantity of blood pumped into the aorta each minute by the heart CO = HR x Stroke Volume
42
Define HR and Stroke volume
HR- no of systole a per min | SV- quantity of blood pumped out by a ventricle during systole
43
What are the determinants of CO
BMR If the individual is exercising Age And size of body
44
What is the normal cardiac index of an individual
3L/min/m^2
45
How is CO measured
Ficks Principle: flow=O2consumed➗ (aterial- venous 02 conc)
46
How much 02 is consumed per min
250ml
47
Name the cardiac factors that control CO
NS: controlling HR and contractility(stroke volume)
48
Name the coupling factors that effect CO
Preload: starling laws - venous return Afterload: ohms law -peripheral resistance
49
What are the hypothesises behind starlings law of venous return
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
How does preload effect the CO
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
How does after load affect CO
During diastole ventricle pressure > artery pressure | An increase in artery pressure would increase resistance during ejection this decreasing strove volume and CO
52
True/false: the NS only effects the HR and contractility directly. Explain
False: has direct and indirect effect- on preload and after load
53
Vagus nerves and sympathetic that effect the heart are due to which type of ganglia
Vagus- pre ganglionic | Syp- post ganglionic
54
Explain the vagus nerves mode of action
Releases ach to m2 receptors so increase k+ permeability causing hyper polarisation This is a tonic inhibition acting on the SAN alone
55
Describe the syp nerves mode of action on the heart
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
What drugs affect the PSY and SY nerves action and how?
Atropine- blocks m2 receptors so imce HR | Propranolol- blocks β adrenergic receptors causing a slight dec in HR
57
What are the control mechanisms of circulation and BP, explain each and what they act on
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
How does the action of local and global mechanisms on the arterioles maintain blood circulation
Vasodilation- inc flow and dec BP | Vasoconstriction - dec flow and inc BP
59
How does local adaptation to inc metabolism arise?
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
Explain auto regulation of blood flow and BP
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
What is the primary factor that effects coronary perfusion
Aortic pressure
62
When is coronary flow greatest
Early diastole
63
Explain local regulation of flow in coronary circulation as metabolic regulation
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
Explain local regulation of blood flow in the brain as metabolic regulation
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
What contributes to the global mechanism of control of BP
ANS and the vasomotor cortex: Pressor (SY) and depressor areas(PSY)
66
How many APs does the SY nerve stimulate at resting, vasoconstriction and vasodilation?
Resting- 5/s Con- 25/s Dila- 1/s
67
What causes vasoconstriction (NT and receptors)
SY- norad, binds to α1 of smooth muscle - GPCR Gq--> phospholiapse C , Ip3, Ca = contraction
68
Where is the one exception of NA and adrenaline action that causes vasodilation vs. vasoconstriction Explain
Skeletal muscles- lack α1 and NA and adrenaline bind to β2--> cAMP inc myosin light chain kinase--> motor cortex--> vasod to increase flow
69
Explain the effects of SY on the heart
SY releases NA and binds to β1 acts on GPCR--> Gs--> cAMP--> PKA--> inc Ca--> inc HR contractility and CO
70
Where are baroreceptors and what do they sense (within what range)
In the carotid sinus and aorta wall sense change in BP within 80-130mmHg (not sensitive below 60mmHg)
71
True/false: baroreceptors are sensors, vasomotor is a comparator and vessels/smooth muscle/heart are effectors
True
72
Explain the baroreceptor reflex
``` 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
Where are chemoreceptors and at which range do they work in maintaining global regulation of BP, and how?
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
What determines long term regulation of BP
Blood volume. Altering blood volume increase venous return as to increase CO and BP
75
How is effective circulating volume EVC (vol that perfuses the blood) maintained
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
What determines BP
Cardiac Output, peripheral resistance (mean pressure) And Arterial compliance, Stoke volume (Pulse pressure)

Physiology (3 decks)

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