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MRCS Critical care > Critical care cardiology > Flashcards

Critical care cardiology Flashcards

1
Q

What does this ECG show? What are the features of this condition?

A

-First degree AV block

Features first degree heart block
-Prolonged PR (>0.2s/200ms/5 small squares)
-Constant heart rate
-PR always followed by QRS

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2
Q

What does this ECG show? What are the features of this condition?

A

Mobitz 1 (wenckebach)

-Progressive lengthening of PR interval until wave fails to be conducted
-Then cycle repeats itself

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3
Q

Describe mobitz type 2

A

-PR intervals are normal in length and constant in timing
-Occasionally P wave not conducted

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4
Q

Describe 3rd degree heart block

A

No recognisable relationship between p waves and qrs complexes

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5
Q

Where would you place ECG leads?

A

-Bipolar (limb leads are attached to right arm, left arm and left leg.
-Neutral lead is attached to right leg

Unipolar (chest) leads are attached to chest:
-V1: 4th intercostal space 2cm to right of sternum
-V2: 4th intercostal space 2cm to left of sternum
-V3: Midway between V2 and V4
-V4: Left 5th intercostal space, midclavicular line (usually corresponds to left nipple)
-V5: Anterior axillary line, level of V4
-V6: mid axillary line at level of V4

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6
Q

What is the QTc interval and how is it calculated?

A

-QT interval corrected for variation in heart rate
-Standardises ‘QT’ interval to HR 60bpm
-At Hr 60, QT = Qtc.
-Normal range 0.35-0.43

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7
Q

What signs would pt with 3rd degree heart block present with?

A

-Cannon ‘a’ waves (atrial waves-atrium and ventricle contracting together, atrium contracts against closed tricuspid valve)
-Variable first heart sound

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8
Q

How would you manage a pt with complete heart block?

A

Initially temporary pacing until permanent pacing can be established

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9
Q

What is pre,-peri and post operative mx of a patient with pacemaker in situ?

A

Preop:
-Theatre staff, anaesthetists and operating surgeon should be informed
-Pacemaker should be checked in pre and post op stage

Peri-operatively:
-resus trolley with temporary external/transvenous pacing + cardiac defibrillator should be present nearby
-Bipolar diathermy should be used

Post op:
-Pacemaker should be checked in pre and post op stage

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10
Q

Name two types of diathermy used in theatre

A

-Monopolar: electric current travels from diathermy instrument through pt and diathermy pad
-Bipolar: electric current travels between forceps

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11
Q

What type of diathermy is preferred in pt with pacemaker and why?

A

Bipolar: pacemaker not affected by electric current

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12
Q

Where should diathermy pad be placed on pt with pacemaker?

A

-As far away from pacemaker as possible
-Should never be on back of pt directly behind pacemaker

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13
Q

Name some causes of bradycardia

A

-Drugs: (beta blockers)
-MI
-Arrhythmia
-Hypothermia
-Hypoxia
-Raised ICP

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14
Q

What is the immediate management of symptomatic or unstable bradycardia and how does it work?

A

-Atropine
-Competitive muscarinic acetylcholine receptor inhibitor
-inhibits parasympathetic activity from vagus nerve, causing hr to increase

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15
Q

Systematically interpreting ecg:

A

Rate, rhythm, wave form (PR interval, P waves, QRS)

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16
Q

What are the treatment goals for new onset AF

A

-Treat cause of AF (eg electrolyte imbalance, hypovolaemia)
-Rhythm control if acute onset/reversible cause
-If rhythm control not desirable, then rate control
-Would need to be combined with anticoagulation

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17
Q

When would it be safe to target rhythm control in AF without starting anticoagulation?

A

If acute presentation within 48 hours

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18
Q

What are the different approaches to managing rhythm control and when would this be applicable?

A

-Rhythm control can be achieved pharmacologically or with electrical cardioversion
-Electrical cardioversion is indicated in acute setting with haemodynamic compromise/in elective setting beyond 48 hrs

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19
Q

What scores are used to assess risk of stroke from AF and risk of bleeding from anticoagulation?

A

CHA2DS2-VASc score: 2 or greater should be offered anticoagulation

Orbit score assesses bleeding risk

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20
Q

What is first line management for AF, and which people would not be suitable?

A

Rate control first line, except if:
-AF has reversible cause
-Rhythm control deemed to be better based on clinical judgement
-AF induced heart failure
-Atrial flutter which is deemed suitable for ablation
-New onset af

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21
Q

Acute mesenteric ischaemia features and management

A

Often caused by AF

Mx
-Thrombolysis/endovascular intervention
-Resection of ischaemic bowel

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22
Q

Ischaemic colitis features and pathogenesis

A

Cause: Global hypoperfusion to large bowel e.g. low bp
Symptoms: Abdo pain, PR bleeding, diarrhoea

Pathogenesis: Global hypoperfusion to large bowel causing ischaemia in watershed areas eg splenic flexure

Mx:
-Usually non operative
-NBM, IVI, analgesia

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23
Q

Describe CXR features pulmonary oedema

A

-Bilateral hazy/fluffy shadowing with ‘bat wing’ appearance
-Upper lobe diversion
-Loss of costo-phrenic angle
-Kerley ‘B’ lines
-Cardiomegaly
-Fluid in horizontal fissure

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24
Q

What does this cxr show?

A

Bat wing shadowing

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25
Q

What does this CXR show?

A

Upper lobe diversion

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26
Q

What does this cxr show?

A

Kerley b lines

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27
Q

Name causes of pulmonary oedema

A

Cardiac causes:
-MI
-Fast AF (and other tachyarrythmias)
-Valve disease: mitral or aortic regurg

Non cardiac causes:
-Acute renal failure
-Severe hypertension
-Iatrogenic fluid overload

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28
Q

Name symptoms of pulmonary oedema

A

SOB
Orthopnoea
Coughing up frothy pink sputum
PND
Ankle oedema

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29
Q

Name signs of pulnoary oedema

A

B/l creps
Raised JVP
Gallop rhythm (3 heart sounds due to rapid ventricular filling)

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30
Q

How would you manage pulmonary oedema

A

High flow o2, CPAP if required
Stop IVI
ECG
Furosemide
IV morphine
Metoclopromide
Monitor urine output
Treat underlying cause

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31
Q

What is the JVP?

A

JVP provides indirect measure of CVP
-Internal JV connects right atrium without any intervening valves: thus acting as column of blood from right atrium

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32
Q

JVP wave form

A

A wave: right Atrial contraction
C wave: right ventricular Contraction causing triCuspid valve to bulge towards right atrium
X descent: atrial relaXation and rapid atrial filling
V wave: Venous filling when tricuspid valve closed and venous pressure increases
Y descent: rapid emptYing of atrium into ventricle following opening of tricuspid valve

33
Q

Name causes aortic stenosis

A

Calcific degeneration
Bicuspid valve
Rheumatic disease

34
Q

What are symptoms of aortic stenosis

A

Angina
Syncope
SOB

35
Q

What are signs of aortic stenosis

A

Slow rising low volume pulse
Heaving apex beat
Ejection systolic murmur loudest in aortic area radiating to carotids

36
Q

Describe pathology of Aortic stenosis

A

-Left ventricle generates higher pressure with each contraction to effectively pump blood out of heart into aorta
-Over time LV dilatation occurs

37
Q

What investigations would you request for pt at pre-op clinic with ejection systolic murmur?

A

ECG
CXR
Echo
CPEX test
Anaesthetic assessment
Referral to cardiology for optimisation of medical therapy

38
Q

What are indications for aortic valve surgery?

A

-Symptomatic severe aortic stenosis
-Asymptomatic severe aortic stenosis with abnormal CPEX test

39
Q

What are the types of aortic valve replacement?

A

Tissue (porcine) valves
Mechanical valves e.g. monoleaflet/tilting disk, bi-leaflet, ball and cage (eg starr edwards)

40
Q

Advantages and disadvantages of tissue valve

A

Advantages:
-No warfarin required
-No clicking

Disadvantages
-Valve degeneration
–> 0-15 yrs for aortic valve
–> 6-10 yrs for mitral valve
–> degeneration increases with age <70 yrs old

41
Q

Advantages and disadvantages mechanical valve

A

Advantages:
-Lasts longer

Disadvantages:
-Metallic click
-Thromboembolic risks
-Warfarinisation required post op
-Warfarin may be contraindicated in patients with bleeding diathesis, women of child-bearing age, professional sports players

42
Q

INR targets for types of metallic valve

A

-AVR: higher flow, 2-3
-MVR: lower flow, 2.5-3.5
-TVR: lower flow, 3-3.5

43
Q

Describe action potential of cardiac myocyte

A

-Depolarisation of neighbouring cells causes opening of Na channels
-Phase 0: influx of na, membrane becomes transiently positive
-Phase 1: K channels open causing efflux of potassium
-Phase 2: Balancing of potassium efflux opens ca channels. Influx of ca initiates excitation-contraction coupling
-Phase 3: Closure of ca channels cause more efflux of k leading to repolarisation and membrane potential returns to -90mV
-Phase 4: resting period, cell prepares for next depolarisation

44
Q

What is the difference between inotropes and vasopressors?

A

Inotropes increase cardiac contractility
Vasopressors increase systemic vascular resistance and therefore MAP
Both work via autonomic nervous system

45
Q

Describe action of alpha 1 adrenergic receptor and location

A

Located in vascular walls and the heart. Activation leads to longer duration of contraction and vasoconstriction

46
Q

Describe Location and action of beta 1 adrenergic receptor

A

Located in heart. Activation increases inotropy and chronotropy with minimal vasoconstriction

47
Q

Describe action of Beta 2 adrenergic receptor, and location

A

Located in vascular walls. Activation induces vasodilatation

48
Q

Describe action of Dopamine 1/2 receptor

A

Located in kidneys. Activation induces diuresis.

49
Q

What are the main categories of receptor relevant to vasopressor and intotrope activity?

A

-Alpha 1 adrenergic receptor
-Beta 1 adrenergic receptor
-Beta 2 adrenergic receptor
-Dopamine 1/2 receptor

50
Q

In what situations would you consider inotrope/vasopressor therapy?

A

-Hypotension refractory to fluid therapy
-Low cardiac output states
-Peripheral vasodilatation

51
Q

Which agent is useful in cardiogenic shock and why?

A

-Dobutamine
-Acts on beta 1 and beta 2 receptors, increasing cardiac output and reducing afterload
-1–> increased inotropy
-2–> increased vasodilatation

52
Q

What agent would you use in septic shock?

A

-Noradrenaline
-Alpha 1 receptor agonist that induces vasoconstriction
-less likely to cause tachycardia than adrenaline

53
Q

How would you monitor response of patient in septic shock on inotropes?

A

-By monitoring MAP
-Current recommendation for patients in septic shock is 65mmhg
-Can also be titrated to achieve adequate end organ perfusion (e.g monitoring urine output)
-Also monitor HR and BP

54
Q

What is MAP?

A

-Average pressure in arteries during one cardiac cycle
-Considered better measure of organ perfusion than systolic BP
-MAP = (CO x SVR) + CVP

55
Q

What is preload?

A

The amount the myocardium has been stretched by the end of filling in diastole

56
Q

What is afterload?

A

The amount of pressure that the heart needs to exert to eject the blood during ventricular contraction

57
Q

How would you define an aneurysm?

A

-Localised dilatation of the walls of a blood vessel

True aneurysm
-Involves all 3 layers of arterial wall (Tunica intima, media, adventitia)

False aneurysm/pseudo-aneurysm
-Occurs with breach in vessel wall resulting in leakage of blood through wall but contained within adventitia or surrounding soft tissue

58
Q

What type of AAA is most common and why?

A

Infra-renal AAA (90%)
-Diameter of aorta decreases from root to bifurcation
-Wall of abdo aorta contains less elastin
-Mechanical tension of abdominal aorta is therefore higher than thoracic aorta
-Laminar flow of infra-renal aorta is disrupted by junction with renal arteries

59
Q

What is laplace’s law?

A

Circumferential wall tension is product of the pressure times the vessel radius:
-Tension = pressure x radius

60
Q

What is significance of laplace’s law in AAA?

A

At any given diameter, the higher the pressure, the higher the intraluminal tension and the greater the likelihood of rapid expansion

61
Q

Define cardiac output

A

Heart rate x stroke volume

the quantity of blood pumped by the heart in a given period of time, typically measured in litres per minute.

62
Q

Define blood pressure

A

Cardiac output X SVR

63
Q

What is stroke volume? How is it determined?

A

-Stroke volume is the amount of blood pumped by left ventricle in one contraction
-It is determined by contractility, pre-load and after-load

64
Q

Describe Frank-Starling’s law of the heart

A

-Force of myocardial contraction is directly proportional to fibre length
-Stroke volume increases in response to a greater volume of blood filling the heart
-With uncontrolled increase in end-diastolic volume, myocyte is overstretched leading to heart failure.

65
Q

Describe effect of baroreceptors on blood pressure

A

-Baroreceptors located in aortic arch and carotid sinus
–> Baroreceptors stretched by increased BP, causing reflex decrease in HR and vasoconstriction. Consequent decrease in SVR, CO and BP
–> When BP decreases, baroreceptors are less stretched. Causes vaso and veno-constriction and reflex increase in HR and BP

66
Q

Describe effect of RAAS system on BP

A

-Low BP–>juxtaglomerular cells secrete renin
-Renin cleaves angiotensinogen to angiotensin 1
-Angiotensin 1 converted to angiotensin 2
-Angiotensin 2 causes blood vessels to constrict and stimulates secretion of aldosterone from adrenal cortex
-Aldosterone causes kidney tubules to increase reabsorption of sodium and water into blood

67
Q

Describe reflex mechanisms that occur with changes in BP

A

Low BP: Baroreceptors stretched less –> increase in HR and vasoconstriction. RAAS activated

High BP: More baroreceptor stretch, less vaso and venoconstriction. Less RAAS

68
Q

Where is arterial BP monitored and where are they found?

A

Baroreceptors found in aortic arch and carotid sinuses

69
Q

Which nerves transmit changes in arterial BP to brainstem?

A

Carotid baroreceptors: glossopharyngeal
Aortic baroreceptors: Vagus nerve

70
Q

What is cardiogenic shock?

A

Inadequate tissue perfusion as a direct consequence of cardiac dysfunction

71
Q

Why is cardiac ischaemia more likely if pt is tachycardic for prolonged period?

A

-Perfusion to the heart via coronary arteries only occurs during diastole
-Diastole rather than systole is shortened during tachycardia

72
Q

Why are beta blockers used in MI?

A

-Acts on Beta 1 receptor to reduce activity of adrenaline and noradrenaline on heart
-Prevents tachycardia and increased oxygen demand, preventing further ischaemic injury

73
Q

Why are ACE inhibitors used in MI?

A

Reduces work of myocardium by reducing afterload (antihypertensive)

74
Q

How does frank starling law explain post operative postural hypotension?

A

Blood pools in dependent areas, reducing preload

75
Q

What is mechanism of action of warfarin? What part of coagulation cascade does it act on?

A

Extrinsic pathway
Inhibits vitamin K
Therefore inhibits vitamin K dependent clotting factors (2, 7, 9, 10)

76
Q

How would you manage pt on warfarin requiring emergency surgery?

A

Discuss with haematologist and inform anaesthetic team
Give vitamin K (will take several hours)
Give prothrombin complex concentrate: contains 2, 7, 9, 10

77
Q

How would you manage pt on warfarin with metallic heart valve needing elective surgery?

A

Stop warfarin 5 days pre-op
Check INR on day 3 and bridge with LMWH
Post operatively stop LMWH once target inr achieved
Discuss plan with consultant haematologis, consult local guidelines and inform anaesthetics team

78
Q

Describe actions of adrenoreceptors

A

Describe action of alpha 1 receptor
Located in vascular walls and the heart. Activation leads to longer duration of contraction and vasoconstriction

Describe Location and action of beta 1 adrenergic receptor
Located in heart. Activation increases inotropy and chronotropy with minimal vasoconstriction

Describe action of Beta 2 adrenergic receptor, and location
Located in vascular walls. Activation induces vasodilatation

MRCS Critical care (11 decks)

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