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Exam Prep Tutorials (Physiology) > Cardiovascular Physiology 2 > Flashcards

Cardiovascular Physiology 2 Flashcards

1
Q

What ECG leads are referred to as bipolar?

A

The limb leads.

These record the potential difference between 2 active electrodes.

I, II, and III - these form the borders of Einthoven’s triangle

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2
Q

What are the unipolar limb leads?

A

The augmented (because they’re lower amplitude than the standard and chest leads) limb leads.

They record the potential difference between one active limb electrode and a “composite reference” electrode formed by an average of the signals from the other limb leads.

aVL = left arm

aVR = right arm

aVF = left leg

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3
Q

What are the unipolar chest leads?

A

These are the precordial leads.

They’re in a horizontal plane across the chest and are placed at anatomically defined positions, V1-6.

They record electrical activity perpendicular to the limb leads - ie view the heart from a horizontal plane.

V1-2 = right ventricle

V3-4 = interventricular septum

V5-6 = anterolateral aspect of LV

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4
Q

What changes on an ECG would indicate a posterior infarct?

A
  • ST depression in V1-4
  • R > S wave in V1-2
  • upright T waves in V1-2
  • reflection of the trace would produce the more expected ECG changes of an infarction
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5
Q

What is the CM5 ECG placement?

A
  • provides an excellent view of the left ventricle
  • very sensitive at detecting left ventricular ischaemia (>80%)
  • lead I is displayed
  • right arm electrode (red) over manubrium
  • left arm electrode (yellow) in V5 position
  • left leg electrode (green) is neutral and can be placed anywhere, but often placed on clavicle
  • CM5 = clavicle, manubrium and V5
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6
Q

What are the characteristics of AF?

A
  • irregularly irregular rhythm
  • HR is variable and depends on how many atrial impulses are transmitted from the atria to the ventricles
  • no P waves
  • P waves replaced by fibrillatory waves ~f waves
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7
Q

What is this?

A

Atrial flutter

  • usually regular but can be irregular
  • HR is variable and depends on how many atrial impulses are transmitted from atria to ventricles
  • no P waves
  • P waves replaced by saw tooth flutter waves
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8
Q

What is this?

A

SVT

  • narrow QRS complexes
  • rate approaching 200bpm
  • regular
  • may be due to:
    • AV nodal re-entry tachycardia (AVNRT) - re-entry circuit next to or within AV node
    • AVRT (AVRT) AV re-entrat tachycardia - re-entry circuit formed from AV node and an abnormal accessory pathway linking atria and ventricles (eg Wolff-Parkinson-White with accessory pathway)
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9
Q

What is this?

A

Ventricular tachycardia.

Characterized by:

  • monomorphic ventricular tachycardia
  • may be pulsed or pulseless
  • wide morphology as ventricular tachyarrhythmia
  • can deteriorate into VF
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10
Q

What is this?

A

Torsades de pointes

Characterized by:

  • polymorphic VT
  • twisting axis
  • may be due to SEs from drugs +/- structural heart disease
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11
Q

What is this?

A

2nd degree heart block, Mobitz 2

  • PR interval is constant but not all beats are conducted
  • repeating pattern of conducted: non conducted impulses (eg 2:1 conduction, a P-QRS-T will then be followed but just a P wave and alternate beats are conducted)
  • may also see 3:1 block etc
  • this can deteriorate into complete (3rd degree) heart block
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12
Q

What is this?

A

1st degree heart block

  • PR interval > 0.2 seconds (5 small squares on ECG)
  • PR interval is measured from start of P wave to start of QRS complex
  • represents an AV conduction delay
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13
Q

What is this?

A

Complete heart block (3rd degree)

  • dissociation between atrial and ventricular conduction
  • regular atrial rate (some P waves concealed in QRS complexes)
  • slow ventricular rate (~40 bpm) set by ventricular pacemaker cells as escape rhythm
  • dangerous rhythm - needs immediate pacing
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14
Q

What is this?

A

2nd degree heart block, Mobitz type 1

  • Wenckebach
  • progressive lengthening of the PR interval until a QRS complex is not conducted and a P wave is seen with no QRS this then repeats
    • seen in high vagal tone in athletes or post MI
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15
Q

What is the effect of regurgitant lesions?

A
  • allow backflow of blood and hence increase volume load in the heart chamber preceding the valve
  • this leads to distension and ultimately chamber dilatation
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16
Q

What is the effect of stenotic valves?

A
  • reduces the cross-sectional area of the valve
  • causes higher resistance against flow and hence increased pressure is required to eject blood past the narrowed valve
  • this ultimately leads to hypertrophy
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17
Q

How common is mitral regurgitation?

A

5 in 10,000

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18
Q

What are the most common causes of acute MR?

A
  • ruptured chordae tendinae
  • post MI
  • trauma
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19
Q

What are the most common causes of chronic MR?

A
  • mitral valve prolapse
  • rheumatic fever
  • connective tissue diseases
  • dilated cardiomyopathy
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20
Q

What are the effects of chronic MR on cardiac function?

A
  • during systole, some blood flows back into the LA and LA volume increases
  • LA dimensions can increased by 4x to accommodate the regurgitant volume - may lead to development of AF
  • LA end diastolic volume increases, and hence a larger volume is delivered to the LV - progressive dilatation of left heart
  • if cardiac muscle dysfunction develops then SV falls, this elevates end-systolic volue and end diastolic volume - this increases LA and LV pressure
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21
Q

What are the clinical features of chronic MR?

A
  • initially asymptomatic
  • as systolic dysfunction develops then symptoms of fatigue, SOB on exertion, orthopnoea and reduced exercise tolerance
  • palpitations (if AF occurs)
  • pansystolic murmur (max at apex, radiates to axilla) and 3rd heart sound
  • ECG shows P mitrale, AF and voltage criteria for LVH
  • CXR shows cardiac enlargement, straightened L heart border and pulmonary oedema
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22
Q

What are the ways of grading severity of MR?

A
  • functional capacity of patient (NYHA functional class)
  • measurement of regurgitant fraction (flow into LA: flow into aorta) - value of >0.3 indicates mild regurg, value >0.6 = severe regurgitation
  • degree of left ventricular dysfunction
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23
Q

How should you anaesthetise patients with MR?

A

To optimise CO:

  • avoid bradycardia - this increases the time for regurgitation, aim for faster HR to minimize this
  • minimize use of vasoconstrictors (to achieve good forward flow, a dilated peripheral circulation is required)
  • avoid a large increase in preload, this can decompensate the heart

Fast and loose

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24
Q

What are the congenital causes of AS?

A
  • bicuspid
  • unicuspid valve
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25
Q

What are the acquired causes of AS?

A
  • rheumatic heart disease
  • degenerative calcification (progressive calcification of valve leaflets can extend and involve the conduction system leading to conduction defects)
    • associated with hypertension
    • hypercholesterolaemia
    • diabetes mellitus
    • smoking
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26
Q

What are the effects of AS on cardiac function?

A
  • as valve area decreases, resistance to systolic ejection increases and a systolic pressure gradient develops between LV and aorta
  • this outflow obstruction causes increased LV systolic pressure
  • as a compensatory mechanism LV wall thickness increases by concentric hypertrophy
    • this leads to decreased compliance and diastolic dysfunction
  • decreased compliance reduces passive filling of LV, so atrial systole makes a significant contribution
  • myocardial O2 demand is increased
  • increased LV pressure reduces blood flow through the coronary arteries
  • the subendocardium is particularly vulnerable to iscahemia
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27
Q

What are the clinical features of chronic AS?

A
  • 10-15 yr asymptomatic period
  • exercise induced symptoms are classic, because the heart can’t increase it’s CO during exertion due to the outflow obstruction
  • exertional dyspnoea/fatigue most common initial complaint
  • classic triad - chest pain, heart failure, syncope eventually
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28
Q

What findings would you expect on examination of an AS patient?

A
  • coarse ejection systolic mumur
    • max over aortic area and radiates to carotid arteries
  • quiet 2nd heart sound
  • narrowed pulse pressure on BP measurement
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29
Q

What findings would you expect on CXR of aortic stenosis?

A
  • enlarged heart
  • aortic valve calcification (usually from 65yrs unless congenital biscuspid - 30yrs)
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30
Q

How do you find the aortic valve on a lateral CXR?

A

Draw a line from the carina to the junction of the diaphram with the anterior chest wall the aortic valve will be above this, mitral valve below.

31
Q

What would you expect to find on an ECG of someone with aortic stenosis?

A

LVH in 85% of patients with aortic stenosis.

If calcification extends into the conduction system, you might see 1st or 2nd degree heart block.

32
Q

What are the features of LVH on ECG?

A
  • if an R wave in either V5/6 exceeds 25mm or if the sum of the tallest R wave in V5/6 with the deepest S wave (in V1/2) exceeds 35mm
  • left axis deviation
  • T wave inversion in V5-6 with or without ST depression indicates “strain” pattern
  • prolonged QRS interval
33
Q

What size is a normal adult aortic valve area?

A

2.5 - 3.5cm2

34
Q

How is aortic stenosis graded with respects to the transvalve gradients?

A

Mild - <25 mmHg

Moderate - 25-40 mmHg

Severe - >40 mmHg

Critical - >80 mmHg

35
Q

How is aortic stenosis graded based on aortic valve area?

A

Mild - >1.5 cm2

Moderate - 1 - 1.5 cm2

Severe - <1 cm2

Critical - < 0.5cm2

36
Q

How should you anaesthetise a patient with aortic stenosis?

A

Slow and tight

  • avoid tachycardia - this shortens diastolic time for coronary flow
  • avoid significant bradycardia- this decreases CO
  • maintain SVR to preserve gradient for coronary filling
  • maintain preload
  • maintain SR -onset of AF will cause decompensation, will need cardioversion
  • avoid vasodilation caused by anaesthetic induction agents - this can create a negative spiral
37
Q

What is the normal cardiac axis?

A

Between -30 degrees to +90

(0° is taken as the lead I viewpoint). Anything <-30° represents left axis deviation. Anything >+90° is termed right axis deviation.

38
Q

What are J waves associated with?

A

Hypothermia - characterized by a dome in the terminal portion of the QRS complexes

The size of J wave usually corresponds to degree of hypothermia.

Also seen in hypercalcaemia, massive head injury and SAH.

39
Q

Why does the pulse pressure become wide in aortic regurgitation?

A

Because regurgitant flow across the aortic valve into the LV causes a reduced diastolic pressure.

Aortic stenosis is associated with a narrowed pulse pressure.

40
Q

What are the degrees associated with Leads I, II and III in the axial referencing system?

A

Lead I = 0°

Lead II = 60°

Lead III = +120°

41
Q

What is NYHA functional class IV?

A

Symptoms occur at rest and the patient can’t carry out any physical activity without discomfort.

Implies severe heart failure.

42
Q

What is Class III NYHA heart failure?

A

Moderate - marked limitation of physical activity and les than ordinary activity causes fatigue, palpitations or dyspnoea

43
Q

Why do 30% of patients with aortic stenosis and normal coronary arteries have angina?

A

Because there’s an increased myocardial O2 demand due to increased wall tension - coronary blood flow doesn’t increase in proportion to the hypertrophied muscle mass and subendocardial ischaemia despite normal coronaries.

44
Q

How much pressure must a true Valsalva manoeuvre generate?

A

40 mmHg of intrathoracic pressure

45
Q

Where does the adrenal medulla recieve sympathetic stimulation from?

A

Directly from a pre-ganglionic nerve fibre.

This releases ACh, which acts on nicotinic receptors to stimulate the adrenal gland to release adrenaline and noradrenaline into the blood stream.

46
Q

What happens when a person goes from lying supine to standing?

A
  • pooling of blood in dependent capacitance veins in legs due to gravity
  • reduces venous return to heart
  • immediate fall in SV
  • because CO = HR x SV
    • both CO and BP fall
47
Q

What is Class I haemorrhage?

A

Up to 15% (750ml)

  • patient may be anxious
  • pulse may be slightly elevated but usually <100 bpm
  • BP and pulse pressure normal
48
Q

What is Class II haemorrhage?

A

15-30% (750-1500 ml)

  • anxiety
  • tachycardia
  • tachypnoea
  • narrowed pulse pressure
  • urine OP < 0.5ml/kg/hr
49
Q

What is Class III haemorrhage?

A

30-40% (1500-2000ml)

  • tachycardia
  • tachypnoea
  • fall in sys BP
  • CNS impairment (drowsiness/confusion)
  • urine OP severely compromised
50
Q

What is Class IV haemorrhage?

A

>40% ( > 2000ml)

  • life-threatening
  • urgent fluid resus required
  • weak thready pulse
  • significantly low sys BP
  • anuria
  • cold peripheries
  • cap refill >5s
  • reduced consciousness
51
Q

What happens when the body suddenly loses 1 litre of blood?

A
  • fall in BP and circulating volume sensed by baroreceptors in the carotid sinus and volureceptors in RA and great veins
  • immediately :
    • redistribution of CO to preserve flow to core areas
    • muscle blood flow decreases
    • renal vasoconstriction to minimize fluid loss through urine
    • cerebral blood flow is prioritized due to autoregulation, baroreceptor and chemoreceptor reflexes
  • catecholamines released by adrenal medulla
    • increases HR, cardiac contractility
    • vasoconstricts and venoconstricts
  • recruitment of effective circulating volume
    • venoconstriction mobilizes blood from liver, lungs and muscle beds into circulating volume
    • fluid translocated from interstitium into plasma
    • reduced renal perfusion pressure = increased renin secretion from JGA, results in ingreased angiotensin II (potent vasoconstrictor) and increased aldosterone (renal retention of Na)
    • ADH released from pituitary due to fall in stimulation from atrial stretch receptors -triggers thirst
      • also promotes renal H2O conservation in collecting ducts
      • also a potent vasoconstrictor at high concentrations
52
Q

What is the effect on Starling forces in haemorrhage?

A

Capillary hydrostatic pressure falls in haemorrhage - which generates a Starling forces gradient favouring translocation of fluid from interstitium to plasma.

Up to 0.25 ml/kg/min of fluid can be reabsorbed.

Fluid shifts from intracellular compartment to replenish the interstitium then plasma.

53
Q

What are the later responses to haemorrhage?

A
  • increased plasma protein synthesis in the liver (takes a few days to restore plasma protein levels)
  • increased EPO restores red cell and Hb levels and initially there is a high reticulocyte count because immature RBCs are released into the circulation from bone marrow
54
Q

What compensatory mechanisms does the body have if you infuse 1 litre of 0.9% saline into a normovolaemic adult?

A
  • Venodilation
    • carotid baroreceptors sense an increase in BP - increased firing - inhibits vasopressor centre
    • peripheral venodilation decreases venous return and reduces CO - BP normalises
  • Fluid redistribution
    • increased capillary hydrostatic pressure causes extrusion of fluid into the interstitium
    • presence of Na+ (charged) limits distribution of the IV fluids, this type of fluid is limited to ECF (made of intravascular fluid and interstitial fluid)
    • ISF 75%, IVF 25%
      • 1 litre of 0.9% saline = 750mls ISF and 250mls IVF
  • increased BP leads to pressure diuresis and natriuresis
    • volureceptors have a threshold of 8-10%, if this is exceeded then ADH is inhibited and diuresis promoted
    • osmoreceptors may be stimulated, change of 1-2% is required for threshold to be exceeded, so if osmolality falls - ADH is inhibited to promote diuresis and normalisation of serum osmolality
55
Q

How will 1 litre of 5% glucose be distributed in the normovolaemic adult?

A

The glucose is taken up by the cells and metabolized. The remainder is free water which distributes across all fluid compartments.

ICF - 66%

ECF - 33% (ISF 75% + IVF 25%)

Therefore, 660mls intracellular fluid.

340mls ECF = 255mls ISF, 85mls IVF.

This is such a small volume that the volureceptor threshold is probably not triggered to inhibit ADH, but the osmolality is probably reduced and so osmoreceptor threshold is likely exceeded.

56
Q

What effects does the Valsalva manoeuvre lead to on the CVS system?

A

Defining feature - increased intrathoracic pressure. Can be achieved by expiration against a closed glottis.

57
Q

What is Phase I of the valsalva manoeuvre?

A
  • BP slight rise, HR steady
  • squeezes intrapulmonary vessels
  • returns more blood to LA
  • increased preload results in increased SV
  • direct transmission of intra-thoracic pressure onto aorta
58
Q

What is Phase II of the valsalva manoeuvre?

A
  • BP falls, HR rises
  • impaired blood return to thorax
  • reduces CO and BP
  • baroreceptors sense reduced BP
  • sympathetic compensation increases HR and peripheral vasoconstriction
59
Q

What is Phase III of the valsalva manoeuvre?

A
  • slight fall in BP, HR still rising
  • release of strain leads to loss of squeeze on intrapulmonary vessels
  • calibre of intra pulmonary vessels increases
  • this temporarily reduces return of blood to heart, BP falls
    • too brief an interval for HR changes
60
Q

What is Phase IV of the valsalva manoevre?

A
  • BP overshoots, HR slows
  • venous return to LA normalises
  • CO now delivered to highly constricted peripheral circulation
  • overshoot of BP sensed by carotid baroreceptors
  • reflex vagal slowing of HR
61
Q

What is the valsalva ratio?

A

A ratio of > 1.5 indicates competent functioning of the autonomic cardiac control.

62
Q

What is the effect of age on the Valsalva ratio?

A

Blunts the baroreceptor response so reduced Valsalva ratio.

63
Q

Where are the baroreceptors located?

A
  • carotid sinus (an enlargement of the internal carotid just above the carotid bifurcation)
  • aorta
  • heart
64
Q

What is the afferent neuronal pathway from the carotid sinus baroreceptors to the vasomotor centre?

A

Via the Nerve of Nering, a branch of the glossopharyngeal nerve.

Baroreceptors from the aorta and heart project via the Vagus nerve.

65
Q

What are pre-ganglionic fibres in the sympathetic NS like?

A

Typically short and myelinated.

They’re B fibres (in the Erlanger and Gasser classification system). Other nerve fibre types in this classification are: Aα, Aβ, Aγ, Aδ, and C fibres.

66
Q

What neurotransmitter does synaptic transmission between pre- and post-ganglionic sympathetic fibres use?

A

Both the sympathetic and parasympathetic use ACh between pre and post ganglionic fibres which acts on nicotinic receptors.

67
Q

Where do the majority of pre-ganglionic sympathetic fibres synapse?

A

On post ganglionic fibres in the paravertebral chain.

This means pre-ganglionic sympathetic fibres are typically short, ganglia are located far away from the target organ and the post-ganglionic fibres are long structures.

The reverse is true in the parasympathetic system where pre-ganglionic fibres are long and the ganglia are found close to or within the walls of the target organ.

68
Q

What is the neurotransmitter used in the majority of blood vessels?

A

The majority of blood vessels receive noradrenergic stimulation from post-ganglionic sympathetic fibres.

But blood vessels in skeletal muscle have post-ganglionic sympathetic cholinergic transmission (onto muscarinic receptors) and some renal vessels have dopaminergic transmission (D1 receptors).

69
Q

How does alpha blockade affect the Valsalva manoeuvre?

A
  • alpha blockade prevents vasoconstriction during the body’s attempt to restore CO in phase II
  • therefore there is an exaggerated increase in HR
  • when strain is released and venous return restored, the elevated HR increases CO and overshoots the BP in phase IV
70
Q

Where are volureceptors located?

A

The right atrium and great veins

71
Q

Where are baroreceptors located?

A

The carotid sinus

72
Q

What is the volureceptor threshold for stimulation?

A

8-10% (400-500mls)

73
Q
A

Exam Prep Tutorials (Physiology) (10 decks)

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