Med viva/revision for Anaes M.Med Part 2

2. Diagnosis?

3. Define QT interval

4. Define QT interval
Time from the start of the Q wave to the end of theT wave.

5. What does the QT interval
represent?

6. What does the QT interval
represent?
It represents the time taken for ventricular depolarisation and repolarisation.

7. How does QT relate to the
heart rate?

8. How does QT relate to the
heart rate?
QT interval is inversely proportional to heart rate

9. Why does QT needs to be
corrected?

10. Why does QT needs to be
corrected?
This allows comparison of QT values at different heart rates and improves
detection of patients at increased risk of arrhythmias.

11. So what is it corrected to?

12. So what is it corrected to?
Corrected QT interval (QTc) estimates the QT interval at a heart rate of 60 bpm.

13. What is the problem with
prolonged QTc?

14. What is the problem with
prolonged QTc?
An abnormally prolonged QT is associated with an increased risk of ventricular
arrhythmias, especiallyTorsades de Pointes.

15. What is normal QTc?

16. What is normal QTc?
< 440ms in men
< 460ms in women

17. Name me a formula for
calculation.

18. Name me a formula for
calculation.
QTC = QT / √ RR

19. What is the formula
called?

20. What is the formula
called?
Bazett’s formula

21. What is the limitation of
Bazett’s formula?

22. What is the limitation of
Bazett’s formula?
It over-corrects at heart rates > 100 bpm
under-corrects at heart rates < 60 bpm,
(but provides an adequate correction for heart rates ranging from 60 – 100 bpm).

23. Name some causes of
prolonged QTc

24. Name some causes of
prolonged QTc
Hypo-MCT
MI
High ICP
Drugs

25. Does hypokalemia cause
prolonged QTc?

26. Does hypokalemia cause
prolonged QTc?
Technically no.
U wave may cause apparent prolonedQTc.
But risk ofTdP not there.
Severe hypokalemia = asystole, remember?

27. Name some drugs which
cause prolonged QTc.

28. Name some drugs which
cause prolonged QTc.
Ondansetron
Droperidol
Diphenhydramine
Erythromycin
Amiodarone

29. What is shortened QTc?

30. What is shortened QTc?
< 350ms

31. Names some causes

32. Name some causes
Hypercalcaemia
Digoxin
Congential short QT syndrome

33. Any problems with short
QT?

34. Any problems with short
QT?
increased risk of paroxysmal atrial and ventricular fibrillation
sudden cardiac death.

35. BREAK

36. Diagnosis?
70 year old male. Hypertension.Otherwise asymptomatic.

37. Brugada

38. Problem with Brugada?

39. Problem with Brugada?
Sudden cardiac death

40. Brugada Sign
 Coved ST segment elevation >2mm in >1 ofV1-V3
 followed by a negativeT wave

41. How many types of
Brugada?

42. How many types of
Brugada?
3 types:
Type 1: Brugada Sign + Clinical criteria
(DocumentedVT orVF. Family history of sudden cardiac death at <45 years old
.Coved-type ECGs in family members. Inducibility ofVT with programmed electrical
stimulation. Syncope. Nocturnal agonal respiration.)
Type 2:Type 2 has >2mm of saddleback shaped ST elevation
Type 3: morphology of either type 1 or type 2, but with <2mm of ST segment
elevation

43. Pathophysiology of
Brugada?

44. Pathophysiology of
Brugada?
Mutation in the cardiac sodium channel gene.

45. Treatment of Brugada?

46. Treatment of Brugada?
AICD implantation

47. What anaesthetic drug to
use with caution in
Brugada?

48. What anaesthetic drug to
use with caution in
Brugada?
Propofol!

49. BREAK

50. Diagnosis

51. Inferior infarct + posterior
infarct

52. What else should you look
out for?

53. What else should you look
out for?
RV infarct and heart block
Inferior infarct: must look for posterior infarct (V1-3)
Inferior infarct: must look for RV infarct

54. How to diagnose RV
infarct with ECG?

55. How to diagnose RV
infarct with ECG?
rV4

56. Describe the position of
rV4

57. Describe the position of
rV4
V4 position on right side

58. What is significant change
in rV4 to be called an RV
STEMI?

59. What is significant change
in rV4 to be called an RV
STEMI?
0.5 mm or half a square.
Why?

60. How does the
management of RV infarct
differ from LV infarct?

61. How does the
management of RV infarct
differ from LV infarct?
Fluid responsive therefore fluid loading may help BP.
Avoid nitrates.

62. Describe other lead
positions you can place

63. Describe other lead
positions you can place
V7,8,9

64. Where areV7,8 and 9
placed?

65. Where areV7,8 and 9
placed?
Posterior, below scapula along 6th IC space

66. What isV7,8,9 good for?

67. What isV7,8,9 good for?
Diagnosis of posterior infarct.

68. What is the recommended
door to balloon time?

69. What is the recommended
door to balloon time?
60 min

70. What is the difference
between BMS and DES?

71. What is the difference
between BMS and DES?
Bare metal – more thrombogenic but epithelization more rapid.
Earlier thrombosis
Dual anti-platelet shorter.
DES – less thrombogenic but epithelization slower
Less thrombosis
Dual anti-platelet longer.

72. Recommended BMS DAP
duration

73. Recommended BMS DAP
duration
4 weeks

74. BREAK

75. Diagnosis?

76. Patient’s asymptomatic.
Management?

77. Patient’s asymptomatic.
Management?
Refer EPS

78. ECG repeated: BP 120/80.Tx?

79. Stable
Vagal maneuvers
Amiodarone
Fleclanide
Procainamide

80. ECG repeated: BP 70/40.Tx?

81. Unstable
Synchronized cardioversion

82. Data Intepretation
 34 yo female intubated and ventilated following a
prolonged generalized tonic-clonic seizure. Initial non-
contrast CT brain shows bilateral
intracerebralhaemorrhages. ABG and GBC post
intubation:

83. Data Intepretation
 List the abnormalities on the ABG and give the most likely
cause in each case.

84. Data Intepretation
 Metabolic acidosis – lactic acidosis induced by prolonged
seizure
 Respiratory acidosis / inadequate compensation –
inappropriate mechanical ventilation
 Increased A-a gradient – aspiration pneumonitis or
neurogenic pulmonary oedema

85. Data Intepretation
 Give three possible diagnoses for her presentation based on
the history and investigations.

86. Data Intepretation
 TTP / HUS
 Eclampsia
 Vasculitis

87. Difference betweenTTP
and HUS?

88. Difference betweenTTP
and HUS?
TTP : more brain, adult female
HUS: more kidneys, kids, related to E. coli

89. BREAK

90. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What is the likely diagnosis?

91. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What is the likely diagnosis?
 Supratherapeuticwarfarinisation

92. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What are possible causes of
supratherapeuticwarfarinisation?

93. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What are possible causes of
supratherapeuticwarfarinisation?
 Overdose
 Drug interaction
 Change in diet

94. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What are possible drug interactions causing high INR in
this patient?

95. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What are possible drug interactions causing high INR in
this patient?
 Antibiotics
 Omeprazole
 Amiodarone

96. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What is the likeliest mechanism for antibiotics to cause
high INR in this patient?

97. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What is the likeliest mechanism for antibiotics to cause
high INR in this patient?
 Vitamin K metabolism altered due to change in gut flora.

98. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What is the likeliest mechanism for omeprazole to cause
high INR in this patient?

99. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 What is the likeliest mechanism for omeprazole to cause
high INR in this patient?
 Liver enzyme inhibition

100. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 Outline your management of this patient if not bleeding.

101. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 Outline your management of this patient if not bleeding.
 Stop warfarin
 Vitamin K in as low a dose as possible
 Consider FFP or factor concentrate if high risk of bleeding

102. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 How much FFP should be given?

103. Data Intepretation
 68-year-old male with chronicAF is noted to have the
following coagulation profile:
 How much FFP should be given?
 At least 10-15ml/kg.

104. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 What anomaly do you notice in the blood gas report?

105. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 What anomaly do you notice in the blood gas report?
 Hypercapnia / resp acidosis.
 Metabolic acidosis

106. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 Anything about the P50?

107. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 Anything about the P50?
 A left shifted curve despite a high PCO2 and a low pH.

108. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 List 2 other investigations you would perform to elucidate
the cause of the anomaly.

109. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 List 2 other investigations you would perform to elucidate
the cause of the anomaly.
 CoHb
 Measure temperature
 Measure 2,3 DPG

110. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 How can you treat carbon monoxide poisoning?

111. Data Intepretation
 ABG obtained from a patient admitted to the ICU after a
suicide attempt.
 How can you treat carbon monoxide poisoning?
 Supportive
 100% oxygen

112. BREAK

113. Diagnosis?
 55 year old man presents with chest pain and shortness of
breath following vomiting four hours earlier.

114. 

115. Pneumothorax and pleural
effusion on right side.

116. This CXR and history:
diagnosis?

117. This CXR and history:
diagnosis?
Boerhaave’s syndrome

118. Management?

119. Management?
supplementary oxygen,
IV fluid resuscitation,
appropriate IV antibiotics,
an appropriate size chest drain,
urgent surgical referral

120. BREAK

121. Diagnosis?

122. What is the classical
description of the patient?

123. What is the classical
description of the patient?
Lucid interval

124. Management?

125. BREAK

126. Case Scenerio
 68 year-old man who had cardiac surgery 4 days
previously.
 He is intubated and ventilated and developed an
increasing FiO2 requirement over the course of the day.

127. Xray yesterday

128. Xray today
Diagnosis?

129. Left consolidation
But did you see the right pneumothorax?

130. BREAK

131. For Fun:

132. Situsinversus

133. BREAK

134. Case
 19 year old male admitted after a severeTBI.
 Due to refractory intracranial hypertension he has been
intubated, sedated and paralysed
 You are called to the bedside because he has desaturated
to 85% on 100% oxygen.

135. Describe?
Diagnosis?

136. Left upper, Right lower
collapse

137. Why is the patient hypoxic
despite administration of
100% oxygen?

138. Why is the patient hypoxic
despite administration of
100% oxygen?
Shunt

139. How to manage?

140. How to manage?
Bronchoscopy Recruitment manoeuvres

141. Describe how you recruit?

142. What are the
complications of
recruitment maneuvers?

143. What are the
complications of
recruitment maneuvers?
Pneumothorax
Hypotension
Hypoxia
Raised intracranial pressure

144. Long Case

145. Story
 30 year old male.
 ASA 2 smoker. History of childhood respiratory disorder
but well since.
 Admitted for right ankle fracture following mountain bike
accident.
 Underwent ORIF of right ankle fracture.
 POD1: informs nurse of acute breathlessness and you are
contacted for an assessment.

146. Story
 Parameters
 BP 115 / 75 mmHg
 HR 95 / min
 SpO2 97% on room air
 Temperature 37.5 C
 Medication chart
 PO Paracetamol 1g qdsprn
 PO Synflex 550 mg bdprn
 PO Oxycodone 5 mg q2h prn
 IV Ondansetron 4 mg tdsprn

147. What are your
differentials?

148. Describe your approach

149. Describe your approach
My primary approach is to treat the underlying pathophysiology by first
elucidating the cause.
I will d0 so by reassessing the History, performing a directed Physical
Examination and ordering targeted Investigations.

150. What would you like to
know about the history?

151. What will you be looking
for in the your physical
examination?

152. What will you be looking
for in the your physical
examination?
Starting from the Head, I will look for …

153. How would you
investigate this patient?

154. Data Intepretation
 ABG (room air)
 pH 7.47
 pCO2 31
 pO2 85
 BE -2
 HCO3 23
 SpO2 97%
 Interpret the ABG

155. Data Intepretation
 FBC
 TWC 12k
 Hb 12g/dL
 Platelets 151K
 UE
 Cr 65
 K 4.3
 Lactate 1

156. Data Intepretation

157. Story changes
 Patient is progressively breathless. Unable to speak.
 Wheezing worsens.

158. What treatments will you
start?

159. What treatments will you
start?
Beta agonist
Anticholinergics
Magnesium
Aminophylline
Ketamine
Volatile agents
Steriods

160. Data Intepretation
 ABG repeated:
 pH 7.25
 pCO2 52
 pO2 65
 BE-8
 HCO3 23
 SpO2 92%

161. Story continues
 Patient worsens and consciousness drops.
 You decide to intubate the patient.
 Describe your intubation technique and choice of drugs.

162. Story continues
 After intubation, describe you would ventilate this
patient?

163. Data Interpretation
 FBC
 TWC 15 k
 Hb11.9 g/dL
 Platelets 255 K
 UE
 Cr 65
 K 3.2
 Lactate 8

164. END