misc Flashcards

1
Q

when to discontinue renal replacement therapy

A

urine output more than 450 ml per day

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2
Q

are trauma or burn patients sufferring from alcohol intoxication more likely to hav worse prognosis?

A

although intoxicated trauma patients do not hav worse prognosis intoxicated burn patients hav a 6 times worse prognosis

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3
Q

normal lactate pyruvate ratio

A

10:1

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4
Q

daily lactate production

A

1500 moles

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5
Q

sites of lctate production

A

skeletal musc
skin
rbc brain
itestine

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6
Q

sites of lactate clearance

A

liver
kidneys
heart

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7
Q

energy generated by anaerobic glycolysis

A

32

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8
Q

energy generated from lactate metabolism

A

each glucose molecule generates 2 moolecules lactate which yields 326 kcal each

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9
Q

some uncommon causes of hyperlactataemia in the icu

A

hepatic insuffiency
acute asthma
haematological malignancy

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10
Q

what is alkalosis elated hyperlactataemia

A

alkalosis leads to upregulation of the glycolytic enzymes which will lead to upregulation of lactate production

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11
Q

what is carbicarb

A

bicarbonate is an ineffective buffer at the physiological ph.also it has a co2n content of almost 200 mm hg.carbicarb is a comerciallly available buffer that is a 1;1 ixture of sodi bicarb and disodium carbonate.it has much less co2 content

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12
Q

what is the source of ketones in the body

A

in the absence of carbs lipolysis leads to the formation of fatty acids which are broken down into ketones in the liver

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13
Q

what is the predominant ketoacid in blood

A

beta hydroxy butyrate

acatoacetate reacts with NADH to form betahydroxybutyrate which is the pre doinant ketone body in blood
the ratio of beta hydroxy is upto 3 times in diabetic keto acidosis and 8 tyms in alcoholic ketoacidosis

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14
Q

short comung of the nitro prusside reaction

A

it detects only acetoacetate and not beta hydroxy butyrate which is the pre dominant ketne.hence it is poorly sensitive

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15
Q

cut off for positive nitroprusside reaxn

A

acetoacettefor 3 mmol/l

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16
Q

regarding stress ulcer prophylaxis..vap is caused more by h2ra or PPI ?

A

no difference in vap rates betweeen the two

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17
Q

ain is assosciated with

A

ppi

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18
Q

regarding pericardiocentesis,what are the indications

A
  1. any effusion causing haemodynamic compromise
  2. large effusions (> 20 mm measured in diastole by echocardiography) without compromise, or for diagnostic reasons.

(Page 241).

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19
Q

what are the aqpproaches? what is the most common approach ?

A

The safest and most common approach is subxiphoid, which avoids the pleural space and the coronary and internal mammary arteries. Other possible approaches include parasternal and apical.

(Page 241).

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20
Q

should pericardiocentesis always be image guarded

A

Fluoroscopic guidance requires the transfer of the patient to the cardiac catheterisation laboratory but has the highest success rate, particularly for small or posterior effusions.

(Page 241).

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21
Q

what are the monitoring required during pericardiocentesis

A

haemodynamic monitoring, ecg to rule out cardiac puncture

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22
Q

common inflammatory mediators implicated in septic shock

A

Pro-inflammatory cytokines commonly implicated in septic shock are IL-1, IL-6 and TNF-.

(Page 136).

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23
Q

can intraosseous access be used for giagnostic purposes

A

it can be used to draw sampples for electrolytes as well as haemoglobin estimation

24
Q

role of amiodarone during cpr in a patient with vf

A

Amiodarone alone will not cardiovert VF. Its membrane-stabilizing effects will increase the efficacy of subsequent defibrillation.

(Page 19).

25
Q

dose of adrenaline delivered by epipen

A

.3 mg of 1:1000

26
Q

is the ventricular fibrillation waveform entirely random ?

A

The VF waveform is not entirely random, having a degree of predictability.

(Page 20).

27
Q

whyich is more likely to be cardioverted coarse or fine vf ?

A

A coarse rhythm is more likely to be cardioverted successfully.

(Page 20).

28
Q

what is the primary determinant of successful defibrillation of vf ?

A

duratiuon of vf

29
Q

most common cause of pea

A

respiratory arrest

30
Q

when does pulmonary embolism lead to pea

A

when more thgan 50 % opf the pulmonary vascular tyree

31
Q

dose for paediatric defibrilklation

A

In children, the current AHA guidelines recommend an initial dose of 2 J/kg, and escalating to 4 J/kg if the first one to two shocks are unsuccessful, while the ERC does not recommend escalation beyond the initial dose of 4 J/kg

32
Q

pad size for defibrillation

A

The AHA currently recommends the largest paddle or pad size that can be placed on a child’s chest that should be used.[46] In small children, care must be taken to ensure that the pads do not overlap.

33
Q

while using paddles in the apical position should they be aligned horizontally or vertically

A

if using a paddle in the apical position, there was a lower transthoracic impedance when the paddle was positioned longitudinally rather than horizontally.

34
Q

DEFIBRILLATION GUIDELINES IN INFANTS

A

For infants, a manual defibrillator is preferred
to an AED for defibrillation. If a manual defibrillator is not
available, an AED equipped with a pediatric dose attenuator
is preferred. If neither is available, an AED without a pediatric
dose attenuator may be used.

35
Q

how does therapeutic hypothermia affect potassium

A

hypokalaemia

36
Q

Question 20
During external chest compression:
a. myocardial blood flow only occurs during the
relaxation phase (diastole)
b. defibrillation is likely to be more successful if
delivered during the relaxation phase (diastole)
c. a heart that is still beating is unlikely to be harmed
d. it is recommended that in pregnant women at
term, hand position should be slightly higher on
the sternum
e. tracheal intubation should not be performed
because of risk of trauma to the airway

A

a. False. Unlike the beating heart, myocardial blood flow occurs during both systole and diastole.
b. True.
c. True. Although some studies have suggested a greater risk of inducing VF.
d. True. e. False. When possible, tracheal intubation should be performed without interruption to external chest compression.

(Page 21).

37
Q

defibrillatrion considerations for aicd

A

Defibrillation pads or paddles should be placed at least 8 cm away from this device to avoid escape current damaging the device or being transmitted down the defibrillation electrode to damage the myocardium.

(Page 22).

38
Q

preferred paddle position for pacing

A

The preferred paddle position is right pectoral–apical, but anterior–posterior placement is also effective. The current should be gradually increased until there is electrical and mechanical capture.

(Page 148).

39
Q

current rtequired for trans cutaneous pacing

A

50 to 100 mohm

40
Q

initial cardiovascular response to hypothermia

A

Initially peripheral vasoconstriction and tachycardia is seen.

(Page 150).

41
Q

what are the other cardiovascular changes seen inhypothermia

A

As the temperature falls, a progressive bradycardia occurs, due to reduced spontaneous depolarisation of the pacemaker cells. Increased systemic vascular resistance may maintain the blood pressure. Repolarisation abnormalities are also seen, and this is the cause of Osborn waves (also known as J waves), usually best observed in the lateral leads on the ECG. Progressive changes include broadening of the QRS complex, ST changes, T-wave inversion, increased PR interval, second- or third-degree heart block and prolonged QT interval. At temperatures below 24 °C there is a high risk of asystole.

(Page 150).

42
Q

what is dcd ?

A

DCD should be considered for all patients who have no hope of recovery, for whom withdrawal of life-sustaining therapy is under consideration, but who do not meet the criteria for DBD. The decision to withdraw life-sustaining treatment must be entirely divorced from the consideration of DCD.

(Page 194).

43
Q

what is controlled and uncontrolled DCD

A

controlled dcd : withdrawal of treatment should occur at a time when the organ-retrieval team is available.

(Page 194).

uncontrolled DCD Uncontrolled DCD is a term describing organ retrieval organised after the death 194 of a patient, following unsuccessful resuscitation in the community or in hospital.

(Page 194).

44
Q

what is warm ischaemia time ?

A

WIT is the period of time for which organs are at body temperature with inadequate oxygen delivery, defined as systolic BP < 50 mmHg, SpO2 < 70%, or both. WITs are organ-specific, as follows:

liver: 30 minutes
pancreas: 30 minutes
lung: 60 minutes
kidneys: 2 hours

( LIP LocK )
(Page 195).

45
Q

define SIRS

A

HEART RATE > 90
respiratory rate > 20/minute or PaCO2 < 32 mmHg (4.3 kPa)
temp < 36 and > 38
WBC < 4000 and > 12000 or greater than 10 % immature band form

46
Q

what are primary and secondary spontaneous pneumothorax

A

primary spontaneous pneumothorax are those which hav no underlying lung disorder vand secondary are those with underlying lung disorder
Any pneumothorax in a patient over 50 with significant smoking history should be treated as an SSP.

(Page 31).

47
Q

radiologically what is a large pneumothorax

A

A large pneumothorax is diagnosed by a finding of a rim of air exceeding 2 cm at the level of the hilum on a PA chest radiograph.

(Page 31).

48
Q

role of suction inchesty drains

A

Chest drains should not be placed under suction in the first instance, because of the risk of re-expansion pulmonary oedema, but suction may be appropriate in patients with a persistent air leak after 48 hours or so. Such cases should be discussed with respiratory physicians or thoracic surgeons.

(Page 31).

49
Q

management of primaryt spontaneous pneumothorax

A

Management of a PSP should be conservative (discharge with follow-up in respiratory clinic) if it is small and the patient is not breathless. Large PSPs should be aspirated with a 16G cannula, as should smaller PSPs in breathless patients. If the pneumothorax resolves, the patient may be discharged and followed up in clinic. If the pneumothorax fails to resolve, a chest drain should be placed and the patient admitted to hospital. Bilateral or tension pneumothoraces should always be treated with chest drains and hospital admission.

(Page 31).

50
Q

management of secondary pneumothorax

A

Patients with SSP should always be admitted to hospital. If the pneumothorax is small and the patient is not breathless, aspiration with a 16G cannula may be suffi- cient treatment, but the patient should be admitted for 24 hours of oxygen therapy and observation. Larger or non-resolving pneumothoraces should be treated with a chest drain and admission, as should breathless patients with small SSPs.

(Page 31).

(Page 31).

51
Q

what are the contraundications of a chest drain

A
  1. any coagulopathy should be corrected prior to chest drain insertion.however routine coagulation screening is not warranred.
  2. Lung densely adherent to the chest wall throughout the hemithorax is an absolute contraindication to chest drain insertion.

(Page 1).

52
Q

how to decide the site of insertio n

A

A chest tube should not be inserted without further image guidance if free air or fluid cannot be aspirated with a needle at the time of anaesthesia. [C] • Imaging should be used to select the appropriate site for chest tube placement.

(Page 3).

53
Q

what is the triangle of safety

A

the triangle oif safety is bound below by the fifth ics and anteriorly by the anterior axdillary fold andd posteriorly by the anterior borfer of lattisim us dorsi

54
Q

which should be preferred large or small bore tubes

A

small bore tubes should be preferred as they are more comfortable to the partient
large botre tubrs are preferred in case of ghaemothoraces.

55
Q

type of xray film reqwuired for diagnosis of pneumothorax

A

traditionally standing expoiratopry films have been recommended but recent guidelines state that they predovide no additional information

56
Q

should chest dsrains be clamped during transfer

A

A bubbling chest drain should never be clamped, but post-pneumonectomy patients or cases of large pleural effusions may need intermittent clamping to prevent mediastinal shifts and re-expansion pulmonary oedema,

(Page 202).