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Cardiovascular > Circulation > Flashcards

Circulation Flashcards

1
Q

Parasympathetic preganglionic fibres

A

Arise either in brainstem and leave CNS in the cranial nerves or arise in sacral portion of spinal cord and leave through 3rd or 4th sacral spinal roots

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2
Q

Sympathetic preganglionic fibres

A

Arise in cord between first thoracic segment and second or third lumbar segment and leave through thoracolumbar nerve roots

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3
Q

Preganglionic fibre neurotransmission

A

Synapse with postganglionic fibres in autonomic ganglia
ACh binds nicotonic ACh receptors on postganglionic fibres
In PSNS ganglia lie close to organs
In SNS ganglia lie close to spinal cord

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4
Q

Postganglionic fibre neurotransmission

A

PSNS release ACh which bind muscarinic ACh receptors on target organs
SNS release noradrenaline which bind adrenergic receptors on target organs

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5
Q

Cholinergic neurotransmission

A

ACh synthesised in cytoplasm, stored in vesicles
Vesicles fuse with membrane, release ACh into synaptic cleft
ACh diffuses across and binds cholinergic receptor of postsynaptic membrane (nerve or tissue)
ACh inactivated by AChE

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6
Q

Cholinergic receptors

A

Nicotinic: found in autonomic ganglia (Nn receptors) and on neuromuscular endplate in skeletal muscle (Nm receptors)
Muscarinic: found on cell membranes of organs innervated by postganglionic parasympathetic fibres

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7
Q

Atropine

A

Muscarinic receptor antagonist

Increases heart rate and prevents salivation

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8
Q

5 main types of adrenergic receptors

A

a1: vasoconstriction
a2: neurotransmitter inhibition
b1: increased cardiac rate and force
a2: bronchodilation
b3: lipolysis

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9
Q

Examples of adrenergic agonists

A

a1: phenylephrine
a2: clonidine
b1: dobutamine
b2: salbutamol

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10
Q

Examples of adrenergic antagonists

A

a: prazosin
b: beta blockers (atenolol)

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11
Q

Heart rate decrease in response to increased PSNS

A

ACh release, binds muscarinic cholinergic receptors
Receptors open potassium channels through stimulatory G proteins, close funny channels and T-type calcium channels through inhibitory G proteins
Hyperpolarisation of membrane potential and slower spontaneous depolarisation
AP frequency decreases, HR decreases

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12
Q

Heart rate increase in response to increased SNS

A

NAdr binds B1 receptors on SA nodal cells activating cAMP which opens funny channels and T-type channels
Slope of spontaneous depolarisation
AP frequency in SA node increases resulting in HR increase

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13
Q

Control of stroke volume

A

Sympathetic neurons release NE which binds B1 adrenergic receptors
Adenylate cyclase activated, cAMP produced
Increased intracellular calcium, increased contractility, faster calcium removal and faster relaxation

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14
Q

Baroreceptor reflex

A

Buffers rapid change in arterial pressure and ensures adequate perfusion of vital organs
Afferent input from carotid and aortic receptors increases arterial pressure resulting in increased baroreceptor firing
Increase in activity results in increase in vagal activity and inhibition of sympathetic activity

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15
Q

Chemoreceptor reflexes

A

Responds to change in oxygen carbon dioxide and pH levels in blood
Sinus and aortic nerves innervate carotid and aortic bodies in response to hypoxia, hypercapnia and low pH
Increase BP, decrease HR

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16
Q

CNS ischaemic response

A

When blood flow to the brain is very low, very large increase in sympathetic activity occurs causing increased peripheral resistance

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17
Q

Diving reflex

A

Oxygen conserving response
Stimulation of cranial nerve V and peripheral chemoreceptors
Apnea, bradycardia, peripheral vasoconstriction and increased BP
Blood flow directed to heart and brain

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18
Q

Respiratory sinus arrhythmia

A

Heart rate increases when we breathe in and decreases when we breathe out
Reflects changes in vagal tone

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19
Q

Heart rate control

A

Medullary respiratory centre senses change in intrathoracic pressure or sends signal straight to medullary cardiac vagal centre
Change in intrathoracic pressure triggers stretch receptors which sense change in lung volume or cause change in venous return
Change in venous return causes change in arterial pressure or bainbridge reflex
Change in arterial pressure triggers baroreceptor reflex
Change in lung volume due to stretch receptors, baroreceptor reflex and bainbridge reflex send signal to medullary cardiac vagal centre
Medullary cardiac vagal centre causes change in heart rate

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20
Q

Bainbridge reflex

A

Atrial reflex

Increased heart rate due to increase in central venous pressure

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21
Q

Systolic pressure

A

Peak pressure

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22
Q

Diastolic pressure

A

Minimum pressure

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23
Q

Pulse pressure

A

Systolic pressure - diastolic pressure

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24
Q

Mean arterial pressure calculation

A

Diastolic pressure + 1/3 pulse pressure
Because ventricles spend 1/3 of their time in systole
ΔMAP = CO x TPR

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25
Q

Arterial compliance

A

The more compliant the vessel the smaller the pulse
Blood not stored during systole when arteries are rigid causing systolic pressure to increase and diastolic pressure to decrease therefore overall pulse pressure increases

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26
Q

Stroke volume and systolic pressure

A

Stroke volume = change in arterial volume

As stroke volume increases, systolic pressure increases

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27
Q

Blood pressure techniques

A

Palpation: allows systolic pressure to be estimated
Auscultatory: allows systolic and diastolic pressure to be estimated

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28
Q

Auscultatory method of blood pressure

A

High pressure in cuff means artery is completely occluded therefore no flow and no sound - above systolic
No pressure in cuff means artery is completely open therefore laminar flow and no sound - below diastolic
Partially occluded arteries allow blood to spurt through the gap causing turbulence and causing sound (Kortokoff sounds) - between systolic and diastolic

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29
Q

Effects within seconds in response to decreased arterial pressure

A

Baroreceptors, chemoreceptors and nervous system ischaemic mechanism cause rapid vasoconstriction of veins which pushes blood back into the heart
Increased heart rate and contractility and constriction of most peripheral arteries to impede flow out of arteries

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30
Q

Effects within minutes in response to decreased arterial pressure

A

Changes in perfusion of the kidney cause Ang II to increase, causing vasoconstriction
Fluid shift through capillaries increases to readjust blood volume

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31
Q

Effects within hours or days in response to decreased arterial pressure

A

Kidneys via RAAS vital to ensure blood pressure regulation is restored without dependence on salt

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32
Q

Distribution of blood volume

A 
Systemic veins and venules: 60%
Capillaries: 5%
Systemic arteries and arterioles: 15%
Pulmonary blood vessels: 12%
Heart: 8%
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33
Q

3 key points about pressure vs cross sectional area of vessels

A

1) major pressure drop across small arteries and arterioles
2) inverse relationship between blood flow velocity and cross sectional area
3) maximal cross sectional area and minimal flow rate in capillaries

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34
Q

Relationship between pressure, flow and resistance

A

Q = ΔP / R
Q measured in mL/min
Therefore CO = MAP/TPR

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35
Q

Assumption of CO = MAP/TPR

A

MAP = P(arterial) - P(venous)
In healthy inviduals, venous pressure is almost 0 therefore we can disregard it and just measure arterial pressure, however in individuals with heart failure, venous pressure is higher and can’t be ignored

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36
Q

Poiseuilles equation

A

R = (8nL) / (pi x r^4)
Where n = viscosity
L = tube length
r = radius

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37
Q

Poiseuilles assumptions

A

Steady laminar flow - only in periphery, near the heart flow is pulsatile
Rigid vessels - Larger arteries and veins are compliant and collapsible
Newtonian fluid - viscosity actually not independent of flow rate, blood not always homogeneous

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38
Q

4 determinants of blood viscosity

A

Temperature - viscosity rises when it’s cold
Haematocrit - viscosity rises when Hct rises (increased resistance)
Shear rate - slow blood flow causes cell aggregation which increases viscosity
Vessel diameter - small vessels have decreased viscosity blood

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39
Q

Autoregulation of blood vessels

A

Compensate for changes in arterial pressure to maintain flow at constant rate
Therefore blood flow not directly proportional to pressure gradient

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40
Q

2 things that control contractile state of vascular smooth muscle

A

1) myogenic mechanism

2) vascular endothelial cells (shear stress)

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41
Q

Shear stress

A

Tangential force of flowing blood on endothelial surface of blood vessels
As flow increases, shear stress increases
Causes NO release and vasodilation
Can cause damage to the endothelium and aggravate atherosclerotic process

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42
Q

Reynolds number

A

Indicates whether blood flow is laminar or turbulent

When value is more than 2000-3000, flow is turbulent

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43
Q

4 Factors that influence reynolds number

A

Vessel diameter
Flow rate
Viscosity
Density

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44
Q

Bernoullis principle: 3 factors

A

Pressure
Gravity
Velocity

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45
Q

Transmural pressure

A

Pressure difference across wall of vessel

Pressure inside vessel - pressure outside vessel

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46
Q

Laplace equation purpose

A

Relationship between transmural pressure and circumferential rension in vessel wall

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47
Q

Capacitance

A

Measure of the volume to rpesure relationship over the entire P/V curve
Change in volume for change in pressure over whole curve
Veins have a large capacitance reflecting their role as storage vessels

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48
Q

Compliance

A

Stretchability at various points along P/V curve

Change in volume for a given change in pressure at one point

49
Q

Arteriole function

A

Control distribution of vascular pressure and flow with a thick continuous layer of smooth muscle in walls allowing changes in vascular resistance

50
Q

Metarteriole function

A

Same as arterioles but without the continuous layer of smooth muscle
Often branch at right angles to arterioles

51
Q

Precapillary sphincter function

A

Act as gates with a cuff of smooth muscle at the entrance to many capillaries
Open or close to determine number of capillaries open and this determine distribution of capillary blood flow

52
Q

Precapillary sphincter control

A

Controlled by local mechanisms, not neural influence

53
Q

Precapillary resistance vessels

A

Arterioles, metarterioles and precapillary sphincters

54
Q

Capillary function

A

Uniquely suited for rapid exhchange of water and solutes due to high surface area to volume ration and very thin walls

55
Q

Capillary walls

A

Made up entirely of endothelium, mostly lipid membrane with an outer coating of mucopolysaccharide basement membrane
Allow lipid soluble molecules to cross through the endothelial cell membrane, whereas lipid insoluble molecules have to pass through holes in the membrane

56
Q

Shunt vessels

A

AKA arteriovenous anastamoses
Allow flow to bypass exchange vessels
In skin, blood can be redirected to rediate heat

57
Q

Venules

A

Similar to capillaries but some have smooth muscle

58
Q

Postcapillary resistance vessels

A

Venules and small veins

59
Q

Neural regulation of blood flow

A

Most arterioles receive innervation from sympathetic nerves
Increased sympathetic activity acts via a1-adrenergic receptors to cause vasoconstriction of b2-adrenergic receptors to cause vasodilation

60
Q

Metabolic regulation of blood flow

A

In most tissues increasing metabolic rate increases blood flow

61
Q

Factors that promote dilation of vascular smooth muscle

A 
Decreased tissue oxygen levels
Increased CO2 and H+
Lactic acid generation
Adenosine, prostaglandins and NO
Increased local temperature
62
Q

Reactive hyperaemia

A

Increase in blood flow that occurs in tissue when blood flow has been interrupted for a short period, ensuring oxygen is restored

63
Q

Autoregulation of local blood flow

A

Return of blood flow towards normal within a few minutes after change in arterial flow, despite change in pressure
Result of changes in circulation metabolites and myogenic mechanism

64
Q

Myogenic mechanism

A

When small blood vessels stretch the smooth muscle in the wall contracts

65
Q

Myogenic mechanism initiation

A

Initiated by stretch-induced vascular depolarisation which then rapidly increases calcium entry into the cell causing them to contract

66
Q

Main transcapillary exchange processes

A

Diffusion
Filtration
Large molecule movement

67
Q

Flow limited transcapillary transport

A

Transport of small rapidly diffusing molecules limited by rate of delivery of material to vessel

68
Q

Diffusion limited transcapillary transport

A

Transport of large molecules limited by pore size

69
Q

Diffusion vs filtration

A

Diffusion is dependent on concentration gradient whereas filtration is dependent on hydrostatic and osmotic pressure differences

70
Q

5 factors affecting filtration across the capillary membrane

A

1) filtration coefficient
2) capillary hydrostatic pressure
3) interstitial fluid hydrostatic pressure
4) colloid osmotic pressure of the plasma
5) colloid osmotic pressure of the interstitial fluid

71
Q

Filtration coefficient

A

How permeable the capillary wall is to water

Variable between and within tissues

72
Q

Capillary hydrostatic pressure

A

Blood pressure in capillary
Variable along capillary
Dependent on pre and post capillary resistance vessels

73
Q

Interstitial fluid hydrostatic pressure

A

Normally small but can increase in some cases where oedema is present

74
Q

Colloid osmotic pressure of the plasma

A

Due to large plasma proteins (albumin and globulin) in high concentrations in the blood which are not able to freely move across the membrane
Determined by number of molecules in solution
The proteins suck and hold water in their space to maintain intravascular volume

75
Q

Colloid osmotic pressure of the interstitial fluid

A

Created by proteins that have leaked out of circulation

76
Q

Large molecule movement

A

Can occur by vesicular transport or directly through fenestrations

77
Q

Functional organisation of lymphatic drainage

A

Widely distributed network of closed-ended, highly permeable lymph capillaries
Similar in appearance to blood capillaries with large gaps between endothelial cells
One way valves and muscle pumping activity directing flow towards heart

78
Q

Composition of lymph

A 
Water
Proteins
Coagulation factors
Electrolytes
Lipids
Cells (especially lymphocytes)
Red blood cells when capillary damage has occurred
79
Q

Lymphatic system function

A

Lymph allows return of blood components to circulation
Plays a role in absorption from the gut, removal of RBCs form tissues and removing bacteria from tissues and isolating it to nodes

80
Q

4 factors that determine cardiac output

A 
The cardiac factors:
Heart rate
Myocardial contractility
The coupling factors:
Preload
Afterload
81
Q

Venous return is dependent on:

A

The pressure gradient (venous tone) and vascular resistance (arteriolar)

82
Q

Venous return vs mean right atrial pressure

A

VR = CO (input = output)
As MRAP falls, return gradient increases, therefore more flow
At low atrial pressures the curve levels off - large intrathoracic veins collapse, increasing resistance, therefore no further increase in VR

83
Q

Increased venous tone/blood volume vs MSFP

A

Increased venous tone/blood volume causes increase in MSFP
Normal conditions: 5 L/min blood volume at 7 mmHg
Small increase volume = large increase MSFP

84
Q

MSFP

A

Mean systemic filling pressure

Basically the same as mean circulatory filling pressure because pulmonary circulation only contains 10% blood volume

85
Q

Effect of transfusion on MSFP

A

MSFP increases due to increased venous tone

More flow at given MRAP therefore venous return curve shifts up

86
Q

Effect of haemorrhage on MSFP

A

MSFP decreased due to decreased venous tonie

Less flow at given MRAP therefore venous return curve shifts down

87
Q

Effect of increased arteriolar constriction on venous tone

A

Reduction of venous return at any given RAP

No major effect on MSFP

88
Q

Effects of increased sympathetic tone

A

Increased arteriolar resistance and MSFP

89
Q

Effect of blood transfusion on cardiac function/venous return curves

A

Doesn’t directly affect cardiac function therefore no change in cardiac function curve
Venous return curve shifted uo as MSFP increases

90
Q

Effect of sympathetic stimulation on cardiac function/venous return curves

A

Cardiac function curve shifts up and to the left as a result of increased heart rate and inotropy
Venous return curve shifts up due to increased venous tone and resistance

91
Q

Effect of supine to erect movement on cardiac function/venous return curves

A

Upon standing up, increase in venous capacity due to venous pooling, drop in venous pressure at heart causing VR curve to shift down and CO to drop

92
Q

Effect of exercise on cardiac function/venous return curves

A

CO curve shifts up due to increased inotropic drive, increased HR and decreased afterload
VR curve shifts up due to increase venous tone, increase rate and depth of respiration and skeletal muscle pumping blood back
Both changes contribute to greatly increased intersection of curves

93
Q

Effect of heart failure on cardiac function/venous return curves

A

Heart’s ability to eject blood impaired causing CO drop, increased venous pressure and kidneys retain fluid
Venous return curve shifts up due to hypervolaemia

94
Q

3 clinical signs of increased venous pressure

A

Raised JVP
Pulmonary oedema
Peripheral oedema (ankles and feet)

95
Q

5 ket interventions for heart failure

A 
Diuretics
ACE inhibitors
Beta blockers
Postive inotropes
Diet
96
Q

Diuretics in heart failure

A

Lower venous pressure
Reduce ventricular size and therefore wall stress
Reduce pulmonary and systemic congestion

97
Q

ACE inhibitors in heart failure

A

Vasodilators

Reduce remodelling

98
Q

Beta blockers in heart failure

A

Reduce energy demand and improve survival

99
Q

Positive inotropes in heart failure

A

Improve contractility

Controls associated atrial fibrillation

100
Q

Diet in heart failure

A

Reduce salt to help control blood volume

101
Q

Symptoms of LHF

A 
Lung crackles
Tachycardia
Low oxygen levels
Paroxysmal nocturnal dyspnoea
GI disturbances
Weight gain (ascites)
Poor blood flow to extremities
102
Q

Symptoms of RHF

A

Jugular vein distension
Liver engorgement
Ascites
Peripheral oedema

103
Q

Heart failure key general symptoms

A 
SOB
Lower extremity oedema
Decreased exercise tolerance
Orthopnoea
Unexplained confusion or fatigure
Nausea or abdominal pain (due to ascites or hepatic engorgement)
104
Q

Abnormal findings in heart failure

A

Tachycardia
Third heart sound (due to floppy ventricles)
Laterally displaced apical pulse
Irregular pulse

105
Q

Investigations for heart failure

A

ECG
Brain natriuretic peptide
Chest xray
Echocardiogram

106
Q

Ejection fraction in heart failure

A

Either preserved or reduced
Preserved: patients experiencing symptoms with EF higher than 50% (arbitrary value)
Reduced: patients experiencing symptoms with EF lower than 40%
EFs 40 - 50% = borderline

107
Q

Heart failure with preserved ejection fraction

A

Diastolic dysfunction

Impaired ability to fill heart, elevated left ventricular diastolic pressures

108
Q

HFpEF cause

A

Consequence of concentric remodelling where the muscle cells become wider secondary to increased afterload
Common primary causes include systemic hypertension and aortic stenosis

109
Q

HFpEF patients

A

Most often in older hypertensive women

110
Q

Heart failure with reduced ejection fraction

A

Systolic dysfunction

Imparied ability of heart to contract with increased EDV

111
Q

HFrEF cause

A

Dilated cardiac myopathy

Muscle cells increase in length secondary to remodelling after myocardial infarction

112
Q

Dilated remodelling

A

Myocytes get longer resulting in increased stretch but inefficient contraction

113
Q

Concentric remodelling

A

Thicker cells causing smaller lumen

114
Q

Risk factors for HFrEF

A 
Male
Obesity
Smoking
Old age
MI
115
Q

Risk factors for HFpEF

A 
Female
Obesity
Old age
Renal dysfunction
Urinary albumin loss
Atrial fibrillation
116
Q

Neurohumoral response to heart failure

A

Increased in restricted stroke volume due to compensation for impaired cardiac performance
Increased SNS activity increases sodium and water retention, peripheral resistance and inotropy to allow maintenance of CO
Over time, causes additional damage by increasing energy expenditure in energy starved areas causing further remodelling

117
Q

MI remodelling cycle

A 
MI
Decreased ventricular performance
Decreased cardiac output
Increased sympathetic activity
Neurohumoral activation
Cardiotoxicity and remodelling
Increased demand on heart
Increased chance of another MI
118
Q

Treatment of heart failure

A

Weigh every day to monitor fluid
Dieretics
Restrict fluid and salt
Exercise (even though exercise intolerance is common)
Digoxin and antiarrhythmics
Nitrates to decrease afterload and prevent excess heart modelling

Cardiovascular (6 decks)

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