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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
What does this CXR show?
Upper lobe diversion
26
What does this cxr show?
Kerley b lines
27
Name causes of pulmonary oedema
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
28
Name symptoms of pulmonary oedema
SOB Orthopnoea Coughing up frothy pink sputum PND Ankle oedema
29
Name signs of pulnoary oedema
B/l creps Raised JVP Gallop rhythm (3 heart sounds due to rapid ventricular filling)
30
How would you manage pulmonary oedema
High flow o2, CPAP if required Stop IVI ECG Furosemide IV morphine Metoclopromide Monitor urine output Treat underlying cause
31
What is the JVP?
JVP provides indirect measure of CVP -Internal JV connects right atrium without any intervening valves: thus acting as column of blood from right atrium
32
JVP wave form
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
Name causes aortic stenosis
Calcific degeneration Bicuspid valve Rheumatic disease
34
What are symptoms of aortic stenosis
Angina Syncope SOB
35
What are signs of aortic stenosis
Slow rising low volume pulse Heaving apex beat Ejection systolic murmur loudest in aortic area radiating to carotids
36
Describe pathology of Aortic stenosis
-Left ventricle generates higher pressure with each contraction to effectively pump blood out of heart into aorta -Over time LV dilatation occurs
37
What investigations would you request for pt at pre-op clinic with ejection systolic murmur?
ECG CXR Echo CPEX test Anaesthetic assessment Referral to cardiology for optimisation of medical therapy
38
What are indications for aortic valve surgery?
-Symptomatic severe aortic stenosis -Asymptomatic severe aortic stenosis with abnormal CPEX test
39
What are the types of aortic valve replacement?
Tissue (porcine) valves Mechanical valves e.g. monoleaflet/tilting disk, bi-leaflet, ball and cage (eg starr edwards)
40
Advantages and disadvantages of tissue valve
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
Advantages and disadvantages mechanical valve
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
INR targets for types of metallic valve
-AVR: higher flow, 2-3 -MVR: lower flow, 2.5-3.5 -TVR: lower flow, 3-3.5
43
Describe action potential of cardiac myocyte
-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
What is the difference between inotropes and vasopressors?
Inotropes increase cardiac contractility Vasopressors increase systemic vascular resistance and therefore MAP Both work via autonomic nervous system
45
Describe action of alpha 1 adrenergic receptor and location
Located in vascular walls and the heart. Activation leads to longer duration of contraction and vasoconstriction
46
Describe Location and action of beta 1 adrenergic receptor
Located in heart. Activation increases inotropy and chronotropy with minimal vasoconstriction
47
Describe action of Beta 2 adrenergic receptor, and location
Located in vascular walls. Activation induces vasodilatation
48
Describe action of Dopamine 1/2 receptor
Located in kidneys. Activation induces diuresis.
49
What are the main categories of receptor relevant to vasopressor and intotrope activity?
-Alpha 1 adrenergic receptor -Beta 1 adrenergic receptor -Beta 2 adrenergic receptor -Dopamine 1/2 receptor
50
In what situations would you consider inotrope/vasopressor therapy?
-Hypotension refractory to fluid therapy -Low cardiac output states -Peripheral vasodilatation
51
Which agent is useful in cardiogenic shock and why?
-Dobutamine -Acts on beta 1 and beta 2 receptors, increasing cardiac output and reducing afterload -1--> increased inotropy -2--> increased vasodilatation
52
What agent would you use in septic shock?
-Noradrenaline -Alpha 1 receptor agonist that induces vasoconstriction -less likely to cause tachycardia than adrenaline
53
How would you monitor response of patient in septic shock on inotropes?
-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
What is MAP?
-Average pressure in arteries during one cardiac cycle -Considered better measure of organ perfusion than systolic BP -MAP = (CO x SVR) + CVP
55
What is preload?
The amount the myocardium has been stretched by the end of filling in diastole
56
What is afterload?
The amount of pressure that the heart needs to exert to eject the blood during ventricular contraction
57
How would you define an aneurysm?
-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
What type of AAA is most common and why?
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
What is laplace's law?
Circumferential wall tension is product of the pressure times the vessel radius: -Tension = pressure x radius
60
What is significance of laplace's law in AAA?
At any given diameter, the higher the pressure, the higher the intraluminal tension and the greater the likelihood of rapid expansion
61
Define cardiac output
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
Define blood pressure
Cardiac output X SVR
63
What is stroke volume? How is it determined?
-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
Describe Frank-Starling's law of the heart
-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
Describe effect of baroreceptors on blood pressure
-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
Describe effect of RAAS system on BP
-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
Describe reflex mechanisms that occur with changes in BP
Low BP: Baroreceptors stretched less --> increase in HR and vasoconstriction. RAAS activated High BP: More baroreceptor stretch, less vaso and venoconstriction. Less RAAS
68
Where is arterial BP monitored and where are they found?
Baroreceptors found in aortic arch and carotid sinuses
69
Which nerves transmit changes in arterial BP to brainstem?
Carotid baroreceptors: glossopharyngeal Aortic baroreceptors: Vagus nerve
70
What is cardiogenic shock?
Inadequate tissue perfusion as a direct consequence of cardiac dysfunction
71
Why is cardiac ischaemia more likely if pt is tachycardic for prolonged period?
-Perfusion to the heart via coronary arteries only occurs during diastole -Diastole rather than systole is shortened during tachycardia
72
Why are beta blockers used in MI?
-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
Why are ACE inhibitors used in MI?
Reduces work of myocardium by reducing afterload (antihypertensive)
74
How does frank starling law explain post operative postural hypotension?
Blood pools in dependent areas, reducing preload
75
What is mechanism of action of warfarin? What part of coagulation cascade does it act on?
Extrinsic pathway Inhibits vitamin K Therefore inhibits vitamin K dependent clotting factors (2, 7, 9, 10)
76
How would you manage pt on warfarin requiring emergency surgery?
Discuss with haematologist and inform anaesthetic team Give vitamin K (will take several hours) Give prothrombin complex concentrate: contains 2, 7, 9, 10
77
How would you manage pt on warfarin with metallic heart valve needing elective surgery?
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
Describe actions of adrenoreceptors
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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