Cardiovascular physiology Flashcards

1
Q

What is valve regurgitation

A

Blood leaks back into chambers; occurs when a valve does not close tightly

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2
Q

How are the left and right atria separated

A

By fibromuscular wall - Atrial (interatrial) septum

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3
Q

Where does the Left Atria receive blood from

A

Pulmonary vein

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4
Q

Where does the right Atria receive blood from

A

Superior and Inferior Vena Cava

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5
Q

Why does the left ventricle have a thicker muscular wall than the right ventricle

A

A high pressure is required to eject blood from the LV, through the aortic valve, into the aorta

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6
Q

Which ventricle pumps deoxygenated blood

A

Right ventricle

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7
Q

What is the cardiac afterload

A

The pressure the heart must eject blood against

-Left Ventricle
Afterload is relative to the aortic pressure

-Right Ventricle
Afterload is relative to that of the pulmonary artery pressure

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8
Q

What allows blood to flow between right atria and right ventricle

A

Tricuspid valve

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9
Q

How does blood flow from left atrium to left ventricle

A

Mitral (bicuspid) valve

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10
Q

What are papillary muscles

A

Muscular projections of the ventricular walls connected to valve cusps by fibrous Chordae Tendineae
Function to prevent backflow of blood and limits valve cusp movements

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11
Q

Why do valves not lift open when under pressure

A

When valves fill up with blood and close the valve, papillary muscles anchor the valve to chordae tendineae allowing the valves to remain closed under pressure preventing cusps from lifting open

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12
Q

What are the semilunar valves of the heart called and where are they situated

A

Pulmonary valve - permits blood flow between right ventricle and pulmonary artery (right)

Aortic valve - permits blood to flow between the left ventricle and aorta (left)

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13
Q

What forces the semilunar valves closed

A

The pressure difference between the artery and the ventricle

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14
Q

How are the heart sounds generated

A

Sound one -AV vales closing (LUB)

Sound two - Semilunar valves closing (DUB)

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15
Q

What is valve stenosis

A

Thickening/stiffening of valve cusps
Prevents the heart valve from opening fully; not enough blood can flow through

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16
Q

When might a third heart sound be heard

A

Due to oscillation of blood flow into the ventricle or various disease states (e.g. heart valve defect)

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17
Q

What are congenital heart defects

A

Often pulmonary / aortic valves that do not form properly during development

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18
Q

What is the flow of blood during the cardiac cycle

A

Superior/inferior Vena Cava
Right Atrium
Tricuspid valve
Right Ventricle
Pulmonary valve
Pulmonary artery
Lungs
Pulmonary veins
Left Atrium
Mitral valve
Left Ventricle
Aortic valve
Aorta
Tissues of body systems

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19
Q

What is systole

A

A phase of the cardiac cycle which involves contraction of the myocardium

ATRIAL SYSTOLE
-atrial contraction to eject blood into ventricles

VENTRICULAR SYSTOLE
-ventricular contraction to eject blood into aorta (LV) and pulmonary artery (RV)

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20
Q

What is Diastole

A

Relaxation of the myocardium which facilitates re-filling of ventricles between contractions

ATRIAL DIASTOLE
-relaxation of atrial muscle, to allow refilling (masked by ventricular systole)

VENTRICULAR DISTOLE
-ventricular relaxation

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21
Q

How does rapid ventricular ejection occur (blood leaves heart)

A

-Pressure in the ventricles exceeds pressure in the aorta and pulmonary artery
-Semi-lunar valves open and blood is ejected from LV into aorta and from RV into pulmonary artery
-Volume of blood ejected from ventricle during systole = stroke volume (SV)

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22
Q

What is stroke volume

A

The volume of blood pumped from the left ventricle per contraction

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23
Q

What is isovolumetric ventricular contraction

A

‘no change in volume’ contraction
when contracting is starting but not enough to force valves open to eject blood

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24
Q

What is EDV end diastolic volume

A

Volume of blood in the ventricle prior to contraction

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25
Q

What does ESV end systolic volume refer to

A

Volume of blood remaining in ventricle after each ejection as ventricles are not fully emptied during systole

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26
Q

What is the ejection fraction

A

The volume of blood ejected by the ventricle with each contraction, as percentage of end diastolic volume (what systole begins with)

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27
Q

What is cardiac output and the equation

A

Volume of blood ejected in one minute
Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)

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28
Q

What percentage ejection fraction indicates a severely impaired LV

A

<35%

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29
Q

How is heart rate determined

A

By the rate which the cardiac pacemaker (sino-atrial node) fired action potentials to stimulate contraction of the cardiac muscle

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30
Q

What is the resting heart rate

A

60-100 bpm

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31
Q

What determines the rate of action potential firing and heart rate

A

Activity of the Autonomic nervous system

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32
Q

What do these terms mean:
A-Chronotropy
B-Inotropy
C-Lusitropy
D-Dromotropy

A

A-Increases heart rate
B-Strength of myocardial contraction
C-Rate of myocardial relaxation
D-Conduction speed in AV node

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33
Q

What cardiac effects does the sympathetic nervous system have

A

Positive chronotropy
Positive inotropy ​
Positive lusitropy
Positive dromotropy

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34
Q

What cardiac effects does the parasympathetic nervous system have

A

Negative Chronotropy
Negative inotropy
Negative lusitropy in atria
Negative dromotropy

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35
Q

Why does the parasympathetic system have these effects

A

Cholinergic nerves derived from the vagus nerve​

Release neurotransmitter Acetylcholine (Ach) ​

Binds to M2 muscarinic receptors in cardiac muscle, particularly at the SA & AV nodes​

Activates inhibitory G-protein​

Blocking cAMP pathway and allows K+ efflux from cell​

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36
Q

what is the membrane potential

A

-Potential difference between intra and extra cellular sides of the membrane
-Generated by ion gradients across the cell membrane
-Dependent on ionic gradients across membrane and ionic permeability

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37
Q

What is depolarisation

A

Potential (electrical) difference across the cell membrane becomes ‘less negative’

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38
Q

What is repolarisation

A

Potential difference across sarcolemma returns to resting Vm following depolarisation (becomes ‘more negative’)

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39
Q

What happens during contraction of a cardiomyocyte

A

-T tubules takes signal deep into cell​
-Calcium induced calcium released, small influx triggers greater release of calcium​
-Falls during diastole​
-Calcium is removed by sodium channel or by ATPsse ​
-Action potential triggers the calcium induced calcium release allowing calcium to bind to contractile apparatus ​

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40
Q

What does an increase in calcium within cardiac myocyte cytosol do

A

Increase the force of myocardial contraction of the cell due to excitation - contraction coupling

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41
Q

How can the force of cardiac contraction be influenced

A

By the length of the heart muscle cell
Level of calcium within the cardiac myocyte cytosol

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42
Q

What is Starling’s Law

A

The force of muscle contraction increases as the muscle is stretched in response to an increased filling of the heart’s chambers.​
-Heart muscle must respond to stretching in this way​
-As otherwise circulation of blood would fail.​
-This response is intrinsic to the heart​

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43
Q

What is Cardiac preload

A

Initial stretching of cardiac myocytes to contraction indicated by ventricular end - diastolic volume because stretching of cardiac myocytes cannot be determined in intact heart muscles

The magnitude of the stretch (preload) predicts the strength of contraction

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44
Q

What is an echocardiogram

A

A type of ultrasound scan used to assess structure and function of heart at high temporal resolution (2D)

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45
Q

What can an echocardiogram aid detection of

A

Impaired cardiac contractility e.g as a results of myocardial infarction (heart attack)

Congenital heart disease; birth defects that impact cardiac function

Cardiomyopathy: enlargement of ventricular walls

Endocarditis: infection of endocardium that damages heart valves

Heart Failure: heart is unable to adequately pump blood to meet metabolic demands of the body

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46
Q

What is myocardial infarction

A

Heart attack

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47
Q

What is endocarditis

A

Infection of endocardium that damages heart valves

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48
Q

What happens in a doppler echocardiogram

A

Erythrocytes reflect ultrasound waves which are used to meassure the blood flow through the heart

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49
Q

What does ECG stand for

A

Electrocardiogram

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50
Q

What is the purpose of an ECG

A

Detects phasic change in potential difference between two electrodes

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51
Q

Where are the electrodes placed in an electrocardiogram

A

On limbs and the surface of the chest

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52
Q

What does bradycardia mean

A

Slow heart rate

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53
Q

What does tachycardia mean

A

Fast heart rate

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54
Q

What rhythms are detected by an ECG

A

Sinus rhythm
Sinus bradycardia
Atrial fibrillation
STEMI (S-T Elevated myocardial infarction)

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55
Q

What is the driving force for blood flow through organs

A

Mean arterial blood pressure

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56
Q

When is the arterial blood pressure greatest and lowest

A

On waking and sleeping

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57
Q

How is the arterial blood pressure measured

A

With a Sphygmomanometer

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58
Q

What is a result of the difference between systole and diastole

A

Pulse pressure

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59
Q

What is the systolic blood pressure

A

The pressure in the arteries (aorta) during myocardial contraction (systole)

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60
Q

What is the diastolic blood pressure

A

The pressure in arteries (aorta) during myocardial relaxation (diastole)
-when ventricles are refilling

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61
Q

How does control and regulation of blood pressure occur

A

Through rapid regulation of blood pressure
-nerves
-hormones

Long term regulation
-Blood volume

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62
Q

What are Baroreceptors

A

Mechanoreceptors that detect the degree of stretch of blood vessel walls and monitor blood pressure

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63
Q

Where are baroreceptors most abundant

A

In the aortic arch and carotid sinus

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64
Q

Why does mechanical stretch (circumferential stress) in arteries arise

A

Due to pulsatile blood flow
-directly related to blood pressure
-Increases during systole
-Gradually reducing during diastole

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65
Q

Where are baroreceptors found

A

Carotid sinus
Aortic arch
BOTH REQUIRED

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66
Q

How are the carotid sinus baroreceptors innervated

A

By the sinus nerve of Hering

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67
Q

How are the aortic arch baroreceptors innervated

A

By the aortic nerve (combines with vagus nerve)

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68
Q

Why are aortic arch baroreceptors less sensitive to changes in stretch than carotid sinus baroreceptors

A

They have a higher threshold pressure

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69
Q

How to identify the carotid sinus

A

The artery wall is thinner and contains a large number of branching nerve endings

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70
Q

Which cranial nerve is the sinus of Herring a branch of

A

IX - Glossopharyngeal nerve

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71
Q

What happens when baroreceptors detect a decrease in arterial pressure

A

There is a reduction in the action potential firing from baroreceptors

Stimulation travels along afferent neurons

To the medullary Cardiovascular Centre

Increased stimulation of sympathetic neurons to heart/arterioles/veins

Decreased stimulation of parasympathetic neurons (vagus nerve) to heart

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72
Q

Where is the Medullary Cardiovascular centre

A

In Medulla Oblongata

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73
Q

When the baroreceptors detect an increase in arterial pressure what occurs

A

Increased action potential firing from baroreceptors

Stimulation travels along afferent neurons

To the medullary Cardiovascular Centre

Decreased stimulation of sympathetic sympathetic neurons to heart/arterioles/veins

Increased stimulation of Parasympathetic neuros to heart/arterioles/veins

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74
Q

What is the Valsalva manoeuvre

A

The attempt to expire against a closed glottis
(exhaling when mouth & nose are closed)

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75
Q

What is the physiological response to the Valsalva manoeuvre

A

-Increased intrathoracic pressure
-Raising blood pressure; normal LV contraction + (1): increased baroreceptor firing
-Heart rate falls transiently - impending return of blood to heart
-Fall in CO and MAP
-As MAP decreases, HR rises and (w/TPR), stabilises blood pressure

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76
Q

What occurs when the glottis is re-opened after the Valsalva manoeuvre

A

slows fast heart rate
-Intrathoracic pressure falls
-BP falls initially
-Venous return is rapidly restored
-EDV & CO increase, raising BP
-Increased BP is sensed by baroreceptors results in reflex bradycardia (slowing of HR)

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77
Q

Within blood pressure regulation what does blood volume influence

A

Venous pressure
Venous return
End - diastolic volume
Stroke volume
Cardiac output

An increased blood volume increases arterial pressure

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78
Q

How does an increased arterial pressure reduce blood plasma volume

A

Via increasing renal excretion of salt & water

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79
Q

What are arterioles

A

Small diameter muscular walled blood vessels

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80
Q

What causes capillary fluid shift

A

Occurs due to venous dilators
Caused by reduced proximal capillary hydrostatic pressure

Most vasodilators have effects on both arteries and veins

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81
Q

Mechanisms that locally regulate long term blood pressure originate via:

A
  • Renin - Angiotensin - Aldosterone System (RAAS)
    -Blood vessels (myogenic or endothelial factors)
  • Maintenance of constant blood flow
  • Blood volume and fluid regulation
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82
Q

What is hypertension

A

Clinic blood pressure of 140mmHg systolic and 90mmHg diastolic (140/90) or higher

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83
Q

Risk of hypertension is raised by what

A

Age
Cigarette smoking
High salt intake
Lack of exercise
Being overweight
Regularly drinking excess alcohol
Stress
Genetic predisposition
Family history

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84
Q

How common is hypertension the result of an underlying health condition or medication

A

1 in 20 cases

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85
Q

What is secondary hypertension

A

Hypertension as the result of an underlying health condition or taking certain medicine

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86
Q

What therapeutics (medication) can increase Hypertension risk

A

Contraceptive pill
Non-steroidal anti-inflammatory drugs (NSAIDS)
Recreational drugs

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87
Q

Which health conditions can raise Hypertension risk

A

Kidney conditions
-Chronic kidney disease
-Narrowing of arteries that supply blood to kidneys / renal hypertension
-Long-term kidney infections
-Glomerulonephritis

Diabetes
Obstructive sleep apnoea
Hormone problems

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88
Q

What is sleep apnoea and what does is increase the risk of

A

Stop breathing during sleep causing you to wake up increasing risk of hypertension

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89
Q

What does an under/over active thyroid cause

A

Hormone problems

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90
Q

Why are baroreceptors ineffective monitors of absolute pressure of blood in carotid arteries to the brains and only short term regulators of blood pressure

A

When the arterial blood pressure is elevated for prolonged periods the threshold for baroreceptor activity rises to a higher value and baroreceptor activity adapts over time and heart rate will increase at the same level

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91
Q

When does the resetting of baroreceptor sensitivity occur

A

During exercise - Maintains Cardiac output as heart rate does not fall in response to increase in BP accompanying exercise

Hypertension - Aids buffering of acute fluctuations in BP at new higher BP level

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92
Q

What are some damages caused by prolongs hypertension

A

Aneurysms in cerebral arteries
Left Ventricular hypertrophy (LVH)
Thickening of arteries
Atherosclerosis Deterioration

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93
Q

What is atherosclerosis deterioration

A

A condition where the arteries become narrowed and hardened due to build up of plaque (fats) in the artery wall.

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94
Q

What can atherosclerosis deterioration, Thickening of arteries and Left ventricular hypertrophy all lead to

A

Renal disease
Development of heart failure due to myocardial adaptation to compensate for LVH
Malignant Hypertension
Angina or myocardial infarction
Stroke

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95
Q

What does HMOD stand for

A

Hypertension-mediated organ damage

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96
Q

What does SCORE stand for

A

Systematic coronary risk evaluation

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97
Q

When are endogenous catecholamines released

A

Due to pain/stress

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98
Q

What is Hypotension

A

Systolic = 90mmHg
Diastolic = 60 mmHg
(90/60mmHg)

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99
Q

What is another name for postural hypotension

A

Orthostatic hypotension

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100
Q

What is postural/orthostatic hypotension

A

An abnormal drop in blood pressure when individuals stand up after sitting or lying down

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101
Q

What are the symptoms of postural hypotension

A

Dizziness
Light head
Fainting
Possible fall

102
Q

Who is orthostatic hypotension most commonly found in

A

Older people and those with certain underlying conditions that affect the sympathetic or parasympathetic nervous systems ex Parkinson’s disease or diabetes

103
Q

What is the P-Q interval

A

The time for the impulse to travel from the sino-atrial node to the ventricular muscle

104
Q

Why might the Q wave (slight decrease before upstroke) be hard so see

A

Baseline noise

105
Q

What does the QRS section on an ECG show

A

The time requires for depolarisation to spread throughout the ventricles

106
Q

What can the duration of ventricular systole be denoted as on an ECG

A

Q-T interval

107
Q

What does the ECG record

A

Total electrical activity (action potentials) produced by the heart muscle

108
Q

What can the ECG tell us about the strength of force of the heart’s contraction

A

Nothing

109
Q

How many electrode combinations will a full clinical ECG use

A

12

110
Q

What causes the P wave on an ECG

A

Depolarisation of the atrial muscle

111
Q

What does the T-wave represent

A

The repolarisation phase of the ventricular action potentials

112
Q

How can the mean arterial pressure be calculated

A

Diastolic BP + 1/3 Pulse pressure

Cardiac Output x Total peripheral
resistance

113
Q

What does the pulse pressure represent

A

The force the heart generates with each contraction to overcome arterial resistance​

114
Q

What is afterload

A

The force (pressure) against which the heart must contract to eject blood into the arteries

115
Q

What factors can influence pulse pressure

A

Stroke Volume
Ejection velocity of stoke volume
Arterial compliance

116
Q

What happens to stroke pressure if stroke volume or ejection velocity increases

A

Increases

117
Q

What happens to stroke volume if the arteries are more compliant

A

Decrease

118
Q

What are the major branches of the aorta

A

Subclavian
Common carotid
Iliac

119
Q

What are some muscular arteries

A

Coronary and renal arteries (smaller branches of aorta)

120
Q

What size would a small artery be

A

<2mm diameter

121
Q

What is haematocrit

A

The proportion of red blood cell total volume

122
Q

What does increase haematocrit indicate

A

Dehydration

123
Q

When does skeletal muscle have a greater demand for O2

A

During exercise than at rest. Thus during exercise, blood flow to skeletal muscle must increase.​

124
Q

When does the GI system have a greater demand for O2

A

Following ingestion of food and so following a meal, blood flow to GI system must increase. ​

125
Q

How does altered blood flow to specific organs/tissues occur

A

By changing arteriolar resistance

126
Q

What is intrinsic control

A

Local
-Matches blood flow to metabolic requirement of tissue system​
-Direct action of metabolites on arteriolar resistance

127
Q

What is extrinsic control

A

Neural/hormonal
-Action of sympathetic nervous system on vascular smooth muscle ​
-Action of vasoactive substances (histamine, bradykinin, prostaglandins)​

128
Q

What are the specific needs of the tissues for blood flow

A

Delivery of oxygen to tissues and nutrients (glucose, amino acids, fatty acids)​

Removal of carbon dioxide and hydrogen ions​

Maintenance of ion concentrations in tissues​

Transport of hormones​

129
Q

What are the three mechanisms of intrinsic control

A

Autoregulation
Active hyperaemia
Reactive hyperaemia

130
Q

What are factors that determine resistance to blood flow

A

Vessel diameter
Vessel length
Viscosity of blood

131
Q

What is autoregulation

A

Maintenance of constant blood flow while arterial pressure changes

If coronary arterial pressure decreases, immediate compensatory vasodilatation of coronary arterioles to decrease coronary vasculature resistance, will attempt to maintain constant blood flow in this coronary artery.​

132
Q

What occurs during active hyperemia

A

Blood flow to tissues is
proportional to its metabolic
activity

Increased blood flow when metabolic activity increases (exercising skeletal muscle increased O2 consumption / ATP demand)​

Increased arteriolar dilation.​

133
Q

What is reactive hyperemia

A

Increase in blood flow in response to a prior period of decreased blood flow
e.g., following period of arterial occlusion, an O2 dept accumulates – longer the arterial occlusion, greater O2 debt, greater the increase in blood flow (above pre-occlusion levels) until the O2 dept reversed.​

134
Q

When does the viscosity of blood not remain within a narrow range

A

During changes in haemocrit

135
Q

What can cause increases in viscosity

A

Dehydration, immobility in which blood flow is reduced and there is a risk of deep vein thrombosis

136
Q

What does Poiseuille’s equation describe

A

How flow is related to perfusion pressure, radius, length and viscosity

137
Q

What happens to velocity as viscosity increases

A

The velocity of flow increases to a maximum at the centre of the tube (blood vessel)

138
Q

What happens to the velocity if flow in a vessel has a negligible resistance

A

It is the same across the tube

139
Q

What does the venous system transport

A

Blood from tissues systems/ organs back to the heart

140
Q

Why are venous valves orientated towards the heart

A

To maintain blood flow in one direction

141
Q

How does exercise aid in venous return

A

During exercise, venous return is aided as intrathoracic pressure becomes more negative – deeper and more frequent respirations increase the pressure gradient between abdominal and thoracic veins.​

142
Q

What is preload

A

Venous return to the right ventricle

143
Q

What occurs if preload increases

A

The heart will have to work harder to pump the blood out and this can be a problem in coronary artery disease and heart failure

144
Q

What are the types of circulation

A

Coronary
skeletal muscle
Cerebral

145
Q

What is coronary circulation

A

Facilitates perfusion of
myocardium
Maintains high basal rate of O2 supply to cardiac muscle

146
Q

What percentage of cardiac output does the heart receive

A

5% (<0.5% of total body weight)

147
Q

What supplies the entire myocardium

A

Right and left coronary arteries

148
Q

Where do the coronary arteries originate

A

From root of aorta, behind cusps of the aortic valve

149
Q

What does the left coronary artery divide into

A

Left coronary artery divides close to its origin into left circumflex artery – branching to the LA & LV and the left anterior descending artery, descending to the apex – branching to supply interventricular septum and portion of right and left ventricles.​

150
Q

What are the circulations with specialised local control

A

Pulmonary circulation​
Skin circulation​
Renal circulation​
Coronary circulation
Skeletal muscle circulation
Cerebral circulation

151
Q

Where do the epicardial veins transport blood to

A

Coronary sinus

152
Q

What does the coronary sinus do

A

Empty blood into the right atrium

153
Q

What does the thesbian veins do

A

Drain deoxygenated blood from capillary networks in ventricular wall directly into the cardiac chambers

154
Q

When does perfusion of the myocardium from the coronary arteries occur

A

During early diastole

155
Q

What percentage of left coronary blood flow occurs during diastole

A

80%

156
Q

what is the maximal cardiac work

A

300-400ml/min/100g

157
Q

Why does ventricular mass increase in exercise training

A

To meet physiological demands of prolonged exercise training

158
Q

What is an athletic heart

A

Physiological adaptation of structural and functional remodelling in response to exercise training.​

159
Q

What is blood flow coupled to

A

Exercise intensity

160
Q

How is blood flow regulated at rest

A

Sympathetic innervation

161
Q

What are some local vasodilators in skeletal muscle

A

Lactate
Adenosine
Potassium ions

162
Q

What does muscle capillary density depend on

A

Muscle function

163
Q

What does Alpha 1 adrenoreceptor activation cause

A

Vasoconstriction: increased resistance, decreasing blood flow

164
Q

Which vasoconstriction primarily dominates

A

Alpha-1 induced

165
Q

What does Beta-2 adrenoreceptor activation cause

A

Vasodilation: decreased resistance, increased blood flow

166
Q

Where is adrenaline released

A

Adrenal gland

167
Q

What is a special adaption of skeletal muscle contraction

A

Adrenaline causes vasodilation

168
Q

Where does tonic sympathetic vasoconstriction continue

A

In feed arteries and proximal resistance vessels

169
Q

What arteries account for 50% of vascular resistance

A

Cerebral arteries

170
Q

What forms the circle of Willis

A

Basilar and internal carotid arteries enter the cranial cavity and anastomose

171
Q

What does the circle of Willis do

A

Can help to preserve cerebral perfusion if carotid artery obstruction occurs

172
Q

What can lead to cerebral vasodilation

A

Local hypoxia

173
Q

What is cerebral autoregulation

A

Cerebral resistance vessels dilate
to maintain perfusion when
arterial blood pressure falls below arterial blood pressure of -60mmHg, cerebral blood flow steeply declines

174
Q

What can reduce cerebral perfusion (dizziness)

A

Hyperventilation

175
Q

What is hypercapnia

A

Prescence of higher than normal level of carbon dioxide in the blood

176
Q

What does hypercapnia cause

A

Cerebral vasodilation, mediated by endothelial NO
And cerebral vasoconstriction

177
Q

What are cerebral resistance vessels highly sensitive to

A

Local hypoxia and arterial CO2

178
Q

Why are capillary walls normally 1 cell thick

A

Allow optimal exchange between blood and tissues via fenestrations

179
Q

What layer do capillaries lack

A

Tunica media
Tunica adventitia

180
Q

What size are the veins lumens relative to arteries

A

Larger diameter and lumen with thinner vessel walls

181
Q

At low blood pressure what percentage of total blood volume do veins contain

A

70%

182
Q

What doe venous valves do

A

Prevent backflow of blood due to lower pressure flowing through vessels

183
Q

What could occur if venous walls or valves lost their elasticity

A

Leads to weakening of these structures resulting in turbulent blood flow within the vessel and can result in development of varicose veins as the vessel wall becomes distended

184
Q

What is the 3 layer wall structure that blood vessels share (aside from capillaries)

A

Tunica intima
Tunica media
Tunica Adventitia

185
Q

What is the structure of the tunica intima

A

Consists of endothelial cells attached to a basement membrane

Underlying layer of extracellular matrix

Separated from media by internal elastic lamina

186
Q

What is the structure of the tunica media

A

Layers of elastin fibres and smooth muscle cells - proportion dependent on vessel function e.g. whether elastic or muscular artery

High elastin content enables vessel wall expansion during systole and recoil during diastole

187
Q

What is the external layer on blood vessels

A

Tunica adventitia

188
Q

What is the structure of the tunica adventitia

A

Often separated from media by external elastic lamina

Thick connective tissue -elastic and collagen fibres

Contain network of nerve fibres, lymphatics and in larger arteries, vasa vasorum perfuse the outer media

189
Q

What fibres does the tunica adventitia contain

A

Collagen and elastic

190
Q

What do larger blood vessels contain in the tunica adventitia

A

Vasa vasorum (small arterioles) which perfuse the outer media (are vessels of the vessels)

191
Q

What is compliance in relation to blood vessels

A

The ability of a blood vessel wall to passively expand and recoil in response to changes in pressure​

192
Q

How is compliance calculated

A

Change in volume/ Change in pressure

193
Q

What occurs during arterial compliance

A

Arterial wall will expand to accommodate the
ventricular stroke volume allowing large arteries to act as pressure reservoir

194
Q

What does the decline in arterial compliance due to age affect

A

Can increase pulse pressure

195
Q

What is arteriosclerosis

A

Age related arterial stiffness due to calcification of elastin, collagen and the extracellular matrix

196
Q

Why are endothelial cells arranged along the axis of blood vessel walls

A

To minimise shear stress by providing a friction free surface for blood flow

197
Q

What role to endothelial cells play in cardiovascular function

A

-Regulate platelet function and fibrinolysis
-Promote angiogenesis and vessel remodelling
-Regulate permeability of blood vessels (form a selective barrier between blood and tissues)
-Form inner lining of entire blood vessel (tunica intima) system and the heart

198
Q

What is angiogenesis

A

Process of new capillaries forming out of pre-existing blood vessels

199
Q

What do SMCs secrete

A

An extracellular matrix which gives cells their elastic properties

200
Q

What is vasoconstriction

A

Contraction of vascular smooth muscle to narrow vessel lumen and reduce radius

201
Q

What is vasodilation

A

Relaxation of vascular smooth muscle to widen vessel lumen and increase radius

202
Q

What is the appearance of SMCs

A

Mononucleated spindle shaped non-striated myocytes

203
Q

How is peripheral resistance determined

A

Autonomic activity
Pharmacologic agents
Blood viscosity

204
Q

What does Local control refer to (BP)

A

The mechanism of altering small artery and arteriolar resistance in organs and tissues
-self regulation of blood flow
-regulation by autocrine and paracrine substances

205
Q

How does adrenaline aid in local control

A

Released from adrenal medulla, circulates in blood and binds (mostly) to beta 2 adrenoreceptors leading to vasodilatation via increase in cAMP and reduced sensitivity for SMC contraction

206
Q

When does adrenaline cause vasoconstriction

A

At high conc adrenaline binds to alpha 1 adrenoreceptors on arteriolar smooth muscle causing contraction

207
Q

What does ANP stand for

A

Atrial Natriuretic Peptide

208
Q

How does ANP influence BP

A

A potent vasodilator and influences BP due to regulation of Na+ balance and blood volume

209
Q

What does Angiotensin II do

A

Constricts arterioles and is important as part of RAAS (renin - angiotensin - aldosterone system)

210
Q

What is the RAAS

A

Reduced blood flow to kidney is sensed by receptors in juxta – glomerular apparatus in kidney, causing release of Renin from juxta – glomerular cells.​

Renin acts on circulating Angiotensinogen (produced by liver) to convert it to Angiotensin I​

Angiotensin I is converted by angiotensin converting enzyme (ACE) – released from endothelial cells – in the lungs and kidney to Angiotensin II​

Angiotensin II is a potent vasoconstrictor

211
Q

How does angiotensin II increase intravascular volume

A

Stimulates Na and water reabsorption and stimulates
release of aldosterone from
adrenal cortex​

Aldosterone acts on distal convoluted tubule (DCT) and collecting duct (CD) of kidney to increase sodium and water retention therefore increasing intravascular volume. ​

212
Q

What stimulates the release of aldosterone from the adrenal cortex

A

Angiotensin II

213
Q

How does Angiotensin II increase water reabsorption

A

Angiotensin II stimulates antidiuretic hormone (ADH) release from posterior pituitary gland ​

ADH release causes increased water via aquaporin – 2 channels in DCT and CD of kidney and vasoconstriction of blood vessels via V1 receptors on vascular SMCs.​

214
Q

How do many drugs lower blood pressure

A

By acting on the RAAS pathway

215
Q

Which nervous system does the RAAS pathway affect

A

Autonomic nervous system
(sympathetic)

216
Q

What are some vasodilators

A

Nitric Oxide (NO)​
-Produced by Nitric Oxide Synthase (NOS) from L – arginine in vascular endothelial cell​
-NO diffuses into SMC and induces relaxation via cGMP activation of guanylate cyclase.​
-NO release occurs in response to factors such as binding of endothelium dependent vasodilators (e.g. acetylcholine, ATP and bradykinin) to receptors on surface membrane of endothelial cells and shear stress.​

Prostaglandin I2 (Prostacyclin)​
-Eicosanoid produced in endothelial cells​
-Activates adenylate cyclase to increase cAMP production, activating protein kinase A (PKA)​
-Leads to vasodilation​

217
Q

What are some vasoconstrictors

A

Endothelin – 1 (ET – 1)​
-Belongs to endothelin family of peptide agents​
-Secreted by endothelial cells in response to stimuli such as pulsatile stretch, sheer stress, neurohormones and cytokines​

Acts on ETA receptor on vascular smooth muscle cells to initiate vasoconstriction​

Thromboxane A2​
-Eicosanoid​
-Activated by tissue injury and inflammation​

218
Q

What is shear stress

A

Force that blood flow exerts on the vessel wall

219
Q

Why does shear stress occur

A

Due to blood travelling at different velocities within a blood vessel

220
Q

What can lead to physiologic adaptation of disease of the blood vessel wall

A

Alterations in the homeostatic conditions:
-exercise
-pregnancy
-growth
-hypertension
-flow reduction
-flow overload

221
Q

What is the primary site for exchange of fluid, electrolytes and gases

A

Capillary system

222
Q

What are the spaces separating endothelial cells of the capillary walls

A

Intercellular clefts

223
Q

What are the 3 structural classifications of capillaries

A

Continuous
Fenestrated
Discontinuous

224
Q

What are the properties of continuous capillaries

A

Continuous basement membrane with tight intercellular clefts
Continuous capillaries have the lowest permeability

225
Q

Where are continuous capillaries found

A

Muscle
Skin
Pulmonary system
CNS

226
Q

Where are fenestrated capillaries found

A

Exocrine glands
Renal glomeruli

227
Q

What are fenestrated capillaries

A

Possess perforations or fenestrations in endothelium
Enables relatively high permeability

228
Q

Where can discontinuous capillaries be found

A

In liver

229
Q

Which capillaries are the most permeable

A

Discontinuous due to large intercellular clefts and gaps in the basement membrane

230
Q

What are metarterioles

A

Terminal arterioles that do not contain a continuous layer of smooth muscle, instead smooth muscle fibres encircle the vessel at intermittent points along its length

231
Q

What do metarterioles do

A

Connect arterioles and venules and branch off to capillaries

232
Q

Why is blood through capillaries not continuous

A

Vasomotion

233
Q

What is vasomotion

A

Spontaneous oscillation in tone of blood vessel walls, independent of heart beat, innervation or respiration

234
Q

What is the ring of smooth muscle surrounding branch sites of capillaries

A

Pre-capillary sphincters which contract and relax in response to local metabolic factors.

235
Q

Which are lower:
Pulmonary hydrostatic pressures or systemic hydrostatic pressures

A

Pulmonary hydrostatic pressures

236
Q

What is pulmonary oedema

A

Excess fluid in the lungs that collects in the alveoli

237
Q

How might pulmonary oedema be induced

A

-Heart failure​
-Left side heart failure – capillary hydrostatic pressure is increased, particularly in extremities​
-Right sided heart failure ​
-High altitude exposure​
-Lung damage due to severe infection​
-Adult respiratory distress syndrome​
-Following major injury​

238
Q

What does the lymphatic system play a role in controlling

A

Concentration of proteins in interstitial fluids

Volume of interstitial fluids

Interstitial fluid pressure

239
Q

What does increasing the interstitial fluid pressure result in

A

Increase in the rate of lymph flow, which caries interstitial fluid volume and protein that accumulates in interstitial away

240
Q

What is the purpose of the lymphatic system

A

Acts as an overflow mechanism to return excess fluid volume from tissue spaces to the circulation

241
Q

How does increasing colloid osmotic pressure in interstitial fluid promote fluid filtration

A

Shifts the balance of forces at the membrane of blood capillaries in favour of fluid filtration​

242
Q

What exists under normal conditions of most capillaries

A

A state of near equilibrium

243
Q

What is a near state of equilibrium within capillaries

A

The amount of fluid filtering outward from arterial end
is almost exactly equal to fluid returned to the circulation by absorption

244
Q

How does disequilibrium occur within capillaries

A

Fluid returned to the circulation via the lymphatic system

245
Q

What is the structure of the lymphatic system

A

A network of small lymph nodes and lymphatic vessels through which lymph flows

246
Q

What is lymph

A

A fluid derived from interstitial fluid

247
Q

What does hydrostatic pressure do

A

Tends to force fluid and dissolved substances through capillary intercellular spaces to the interstitial spaces

248
Q

What causes osmotic pressure

A

Plasma proteins

249
Q

What forces fluid movement from interstitial space to the blood via capillary intercellular spaces

A

Osmotic pressure

250
Q

What happens to hydrostatic pressure as blood pressure drops from arterial to venous system

A

Decreases

251
Q

Why does fluid move out of capillaries at the arterial end and in at the venous end

A

Hydrostatic pressure drops from arterial to venous system and the colloid osmotic pressure remains constant forcing fluid out at the arterial end and providing an osmotic gradient at the venous end with a high conc of proteins which are too big to pass out of capillaries