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Anaesthetic FRCA Primary - eLFH Physiology > eLFH - Cardiovascular Physiology Part 2 > Flashcards

eLFH - Cardiovascular Physiology Part 2 Flashcards

1
Q

12 Lead ECG electrode placement

A
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2
Q

ECG lead categorisation

A

Limb leads (Bipolar)

Augmented limb leads (Unipolar)

Chest leads (unipolar)

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3
Q

Limb leads

A

Read potential difference between 2 active electrodes

Form borders of Einthoven’s triangle

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4
Q

Augmented limb leads

A

Record potential difference between one active limb electrode and a composite reference electrode formed by the average of signals from the other limb leads

Readings have lower amplitude so are augmented

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5
Q

Chest leads

A

Aka precordial leads

Record electrical activity perpendicular to limb leads in ‘horizontal plane’

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6
Q

Standard ECG recording speed

A

25 mm/s

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7
Q

Standard ECG calibration

A

1 mV/cm

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8
Q

Normal cardiac axis

A
  • 30 degrees to + 90 degrees
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9
Q

Time represented by one small ECG square

A

0.04 s

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10
Q

ECG changes associated with Posterior STEMI

A

ST depression V1-4

Upright T waves in V1-2

R>S wave in V1-2

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11
Q

ECG electrode position to pick up posterior STEMI

A

V7-9 continue posteriorly along same horizontal plane from V6

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12
Q

CM5 electrode position

A

Red over Manubrium
Yellow in V5 position
Green is neutral and can go anywhere, but often placed on left clavicle

Hence name CM5:
Clavicle
Manubrium
V5

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13
Q

CM5 use

A

Good view of left ventricle and very sensitive at detecting left ventricular ischaemia (>80%)

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14
Q

Most common Atrial flutter ventricular rate

A

150 bpm

2:1 conduction ratio most common with atrial rate of 300

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15
Q

Ways in which valvular lesions result in increased work for the heart

A

Volume

Pressure

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16
Q

Volume changes leading to increased work for the heart in valvular lesions

A

Regurgitant lesions allow backflow

Increase volume load in the heart chamber preceding the valve

Leads to distension and dilatation

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17
Q

Pressure changes leading to increased work for the heart in valvular lesions

A

Stenotic pathology reduces cross sectional area of valve

Therefore higher resistance against flow and pressure load

Chamber preceding the valve develops higher pressure to eject blood past the narrowed valve

Leads to hypertrophy

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18
Q

Two most common valvular pathologies

A

Aortic stenosis

Mitral regurgitation

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19
Q

Most common causes of acute mitral regurgitation

A

Ruptured chordae tendinae
Post MI
Trauma

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20
Q

Most common causes of chronic mitral regurgitation

A

Mitral valve prolapse
Rheumatic fever
Connective tissue diseases
Dilated cardiomyopathy

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21
Q

Effects of chronic mitral regurgitation on cardiac function

A

LA volume increases due to backflow during systole

Can lead to AF

Progressive dilatation of left heart as LAEDV increases so greater volume delivered to LV

If muscle fails and stroke volume falls, LA and LV pressure increases as LVESV and LVEDV increase

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22
Q

Clinical features of chronic MR

A

Initially asymptomatic

As left heart failure develops then get symptoms of SOB, orthopnoea, etc

Palpitations if AF develops

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23
Q

Cardiac auscultation with MR

A

Pansystolic murmur
Maximal at apex
Radiation to axilla

3rd heart sound

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24
Q

ECG changes with MR

A

P mitrale due to LA enlargement
AF
LVF

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25
Q

CXR findings with MR

A

Cardiac enlargement
Straightening of left heart border
Pulmonary oedema

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26
Q

Grading of MR severity

A

Functional capacity of pt - NYHA functional class III or IV

Measurement of regurgitant fraction

Degree of LV dysfunction

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27
Q

Measurement of regurgitant fraction in MR

A

Measures flow into left atrium : Flow into aorta

Value > 0.3 indicates mild MR
Value > 0.6 is severe MR

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28
Q

Anaesthetic management changes for patient with MR for optimal cardiac output

A

Avoid bradycardia - bradycardia increases time for regurgitation

Minimise vasoconstrictor use - dilated peripheral system needed for good forward flow

Avoid large preload increase - can decompensate the heart

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29
Q

Aide memoir of anaesthetic management changes in MR

A

‘Fast and Loose’

Higher HR, Avoid vasoconstrictors

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30
Q

Categories of Aortic Stenosis

A

Congenital

Acquired

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31
Q

Most common causes of congenital Aortic stenosis

A

Bicuspid or Unicuspid valve

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32
Q

Most common causes of acquired aortic stenosis

A

Rheumatic heart diseases

Degenerative calcification

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33
Q

Risk factors for degenerative calcification of aortic valve

A

HTN
High cholesterol
Diabetes
Smoking

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34
Q

Effects of Aortic Stenosis on cardiac function

A

Valve area decreases

Outflow obstruction leads to increased LV systolic pressure

Compensatory concentric LV hypertrophy - initially preserves function but leads to decreased compliance and diastolic dysfunction

Reduced passive filling due to reduced compliance - increased LA systole contribution

Increased myocardial O2 demand

Increased LV pressure reduces coronary blood flow due to transmitted LV diastolic pressure acting as a Starling resistor

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35
Q

Area particularly vulnerable to ischaemia with AS causing reduced coronary blood flow

A

Subendocardium

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36
Q

Clinical features of chronic AS

A

Develops gradually - often 10-15 year asymptomatic period

Triad of:
-Exertional SOB
- Chest pain
- Syncope

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37
Q

Why are exertional symptoms classical for AS

A

Heart is unable to adequately increase cardiac output during exercise due to outflow tract obstruction

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38
Q

Auscultation of AS

A

Coarse ejection systolic murmur
Maximal over aortic area
Radiation to carotids

Quiet 2nd heart sound

39
Q

Clinical examination finding with AS

A

Narrow pulse pressure

40
Q

CXR findings for AS

A

Cardiac enlargement
Aortic valve calcification

41
Q

ECG findings for AS

A

LVH

Can develop 1st or 2nd degree HB if calcification extends to conducting system

42
Q

ECG findings with LVH

A

Voltage criteria

Left axis deviation

T wave inversion in V5 or V6 +/- ST depression (this indicates a ‘strain’ pattern)

Can also get widened QRS

43
Q

Voltage criteria for LVH on ECG

A

R wave in either V5 or V6 exceeds 25 mm

OR

Sum of tallest R wave in V5 or V6 and deepest S wave in V1 or V2 exceeds 35 mm

44
Q

Grading of AS severity

A

Functional capacity

Echo assessment - mean gradient and aortic valve area

45
Q

Mean gradient and Aortic valve area grading of AS severity

A
46
Q

Aortic valve area in healthy adult

A

2.5 - 3.5 cm^2

47
Q

Anaesthetic management changes for patient with AS for optimal cardiac output

A

Avoid tachycardia as it shortens diastolic time for coronary flow

Maintain SVR - preserves gradient for coronary filling

Maintain preload

Maintain sinus rhythm - onset of AF will decompensate

Avoid vasodilation with induction drugs as can create negative spiral

48
Q

Negative spiral that can be seen in AS patients if vasodilation not avoided with induction of anaesthesia

A

Reduced SVR

Reduced aortic diastolic pressure

Reduced coronary perfusion

Myocardial ischaemia

Further reduction in cardiac output

Cardiogenic shock

49
Q

Aide memoir of anaesthetic management changes in AS

A

‘Slow and tight’

50
Q

Effect on BP of moving from supine to standing

A

Initial increased pooling of blood to legs

Reduces Preload / venous return to heart

Immediate drop in stroke volume by Frank-Starling mechanism

Cardiac output and BP therefore fall

51
Q

Mechanisms to restore cardiac output to compensate for drop in BP from standing from supine

A

1) Baroreceptors

2) Afferent pathways

3) Vasomotor centres

4) Sympathetic tone

5) Efferent pathway

6) Effect of sympathetic stimulation

52
Q

Baroreceptor pathway

A

Stretch receptors which increase or decrease firing rate according to stretch detected

Negative feedback mechanism to vasomotor centre
I.e. High firing rate, inhibits vasomotor centre vs Low firing rate, less inhibition of vasomotor centre

53
Q

Baroreceptor location

A

Walls of carotid sinus, aorta and heart

Carotid sinus baroreceptors most sensitive to BP alterations

54
Q

Afferent pathway

A

From carotid sinus baroreceptors to the CNS
Via Hering branch of Glossopharyngeal nerve (CN IX)

Aortic and cardiac baroreceptors relay signals to CNS via vagus nerve

55
Q

Sensory nucleus for CN IX and CN X that connects baroreceptor afferent pathways to vasomotor centres

A

Nucleus tractus solitarius

56
Q

Vasomotor centre pathway

A

Pressor centre:
Tonic output to maintain background vascular smooth muscle tone

Depressor centre:
Inhibits the pressor centre and directly inhibits sympathetic outflow at spinal level

57
Q

Pressor centre of vasomotor centre location

A

Ventrolateral medulla

58
Q

Depressor centre of vasomotor centre location

A

Caudal and medial to pressor centre in medulla

59
Q

Sympathetic tone pathway

A

Set by balance of pressor centre and depressor centre signals

Also affected by central and peripheral chemoreceptors triggered by changes to PaCO2 and pH

60
Q

Location of central chemoreceptors

A

Medulla

61
Q

Location of peripheral chemoreceptors

A

Carotid and aortic bodies

Have more effect on respiratory centre but some effect on BP

62
Q

Cushing reflex

A

Hypertension
Bradycardia
Irregular breathing

Triggered by massive sympathetic outflow in aim of maintaining cerebral perfusion pressure

63
Q

Efferent pathway

A

Sympathetic outflow is via pre-ganglionic nerves

Majority of these nerves synapse in paravertebral chain with long post-ganglionic nerves

Efferent pathways go to heart and blood vessels

Pre-ganglionic nerve fibres also stimulate adrenal medulla using cholinergic transmission

64
Q

Features of pre-ganglionic sympathetic nerves

A

Short
Myelinated
ACh neurotransmitter

65
Q

Features of post-ganglionic sympathetic nerves

A

Long
Unmyelinated
Noradrenaline neurotransmitter

66
Q

Effect of sympathetic stimulation

A

Peripheral vasoconstriction - increases SVR

Peripheral venoconstriction - increases venous return to heart

Increased heart rate - accelerates pre-potential decay in cardiac pacemaker cells

Increased cardiac contractility - increased Ca2+ release from sarcoplasmic reticulum in cardiac myocyte

All the above ultimately increase cardiac output

67
Q

Classification of haemorrhage

A

Class I

Class II

Class III

Class IV

68
Q

Class I haemorrhage blood loss

A

< 15%
750 ml

69
Q

Class I haemorrhage signs

A

Minimal signs of shock
HR slightly raised possibly
BP stable

70
Q

Class II haemorrhage blood loss

A

15 - 30%
750 - 1500 ml

71
Q

Class II haemorrhage signs

A

Tachycardia
Tachypnoea
Narrow pulse pressure
UO < 0.5 ml/kg/hour

72
Q

Class III haemorrhage blood loss

A

30 - 40%
1500 - 2000 ml

73
Q

Class III haemorrhage signs

A

Marked tachycardia
Fall in BP
CNS impairment
UO severely compromised

74
Q

Class IV haemorrhage blood loss

A

> 40%
2000 ml

75
Q

Class IV haemorrhage signs

A

Life threatening
Weak thready pulse
Significant hypotension
Anuria
Mottled with CRT > 5s

76
Q

Compensatory mechanisms to sudden loss of circulating volume
(detected by baroreceptors and volureceptors in RA and great veins)

A

Immediate responses:
- Redistribution of CO
- Catecholamine release
- Recruitment of effective circulating volume

Later responses

77
Q

Redistribution of cardiac output following sudden loss in circulating volume

A

Maintains blood flow to key organs

Muscle blood flow decreases
Renal vasoconstriction reduces CO to kidneys (usually 25%) - also reduces fluid lost in urine

Cerebral blood flow preferentially maintained

78
Q

Catecholamine release following sudden loss in circulating volume

A

Sympathetic outflow increases and adrenal medulla releases catecholamines into circulation

Increases:
- HR
- Cardiac contractility
- Vasoconstriction
- Venoconstriction

79
Q

Recruitment of effective circulating volume following sudden loss in circulating volume

A

Venoconstriction mobilises blood from liver, muscle and lung reservoirs

Fluids translocated from interstitium to plasma

Renin secretion due to reduced renal perfusion - RAAS activated

ADH released from pituitary following fall in atrial stretch receptor stimulation

80
Q

Mechanism by which fluid translocates from interstitium to plasma in response to haemorrhage

A

Haemorrhage leads to drop in hydrostatic pressure in capillaries

Generates Starling forces gradient favouring translocation of fluid from interstitium into intravascular space

Ultimately fluid will shift from intracellular space to replenish interstitium and then into plasma again

81
Q

Volume of fluid that can be re-absorbed from interstitium into plasma following haemorrhage

A

0.25 ml/kg/min

82
Q

Later response mechanisms to compensate for fall in circulating volume following haemorrhage

A

Increased plasma protein synthesis - takes few days

Increased erythropoietin production - initially results in high reticulocyte count before Hb and RBCs restored

83
Q

Compensatory mechanisms following rapid IV crystalloid infusion in euvolemic patient

A

Venodilation

Fluid redistribution - increased hydrostatic pressure so fluid moves to interstitium via Starling forces mechanism

Diuresis - inhibition of ADH release

84
Q

Valsalva manoeuvre definition

A

Forced expiration against a closed glottis

85
Q

Intrathoracic pressure change with Valsalva manoeuvre

A

Rise in intrathoracic pressure by 40 mmHg

86
Q

Graph with phases of autonomic changes in BP and HR during Valsalva manoeuvre

A

Phase 1 - onset of strain
Phase 2 - continued strain
Phase 3 - release of strain
Phase 4 - strain still off

87
Q

Phase 1 of Valsalva - Onset of strain

A

Squeeze on intra-pulmonary vessels
Return of more blood to left atrium
Increased preload results in increased stroke volume
Direct transmission of intra-thoracic pressure onto aorta

88
Q

Phase 2 of Valsalva - Continued strain

A

Impaired return of blood to thorax
Reduced CO and BP
Baroreceptors sense reduced BP
Sympathetic compensation increases HR and peripheral vasoconstriction

89
Q

Phase 3 of Valsalva - Release of strain

A

Loss of squeeze on intra-pulmonary vessels
Calibre of intra-pulmonary vessels increases
Temporarily reduces return of blood to heart - BP falls
Too brief an interval for any HR changes

90
Q

Phase 4 of Valsalva - Strain still off

A

Venous return to LA normalises
CO now delivered to vasoconstricted peripheral circulation
Overshoot of BP sensed by carotid sinus baroreceptors
Reflex vagal slowing of HR

91
Q

Clinical uses of Valsalva manoeuvre

A

Assess autonomic function

Cardiovert SVT

92
Q

Valsalva ratio calculation

A
93
Q

Use of Valsalva ratio

A

Ratio > 1.5 indicates competent functioning of autonomic cardiac control

94
Q

Effect of age on Valsalva ratio

A

Ageing blunts baroreceptor response
Therefore reduced Valsalva ratio

Anaesthetic FRCA Primary - eLFH Physiology (13 decks)

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