ICU

Question 1

What is the difference between inotropy and chronotropy?

Answer 1

Inotropy refers to contractility while chronotropy refers to HR. Therefore, inotropes increase contractility and chronotropes increase HR.

Question 2

Give one example of an inoconstrictor

Answer 2

Adrenaline (predominantly an inotrope, has pressor effects as well)

Question 3

On which receptors does adrenaline act, and what are the effects of adrenaline on these receptors?

Answer 3

Acts on both alpha and beta adrenergic receptors

Alpha 1: vasoconstriction (at high doses)
Beta 1: inotropy and chronotropy
Beta 2: vasodilation (at low doses)

Net effect: vasoconstriction, inotropy and chronotropy

Question 4

List three adverse affects of adrenaline

Answer 4

Tachyarrhythmias
Increased myocardial oxygen demand (risk of AMI in those with coronary heart disease)
Lactic acidosis

Question 5

What type of inotrope is dobutamine? Which receptors are mainly targeted and what the net result?

Answer 5

Inodilator. Predominantly B1 followed by b2 and a1 stimulation - net outcome being cardiac stimulation and some vasodilation

Meaning! increased inotropy and cardiac output with decreased afterload secondary to the vasodilator effects

Question 6

What are the main effects of PDE3 phosphodiesterase inhibitors? (e.g. milrinone, inamrinone)

Answer 6

Inotropy and chronotropy and vasodilation (decreased SVR)

Question 7

What drug class does levosimendan belong to and what are its net effects?

Answer 7

A relatively new inotropic agent, it is a calcium sensitiser (binds to troponin and augments actin-myosin coupling) leading to inotropy and vasodilatation

Question 8

What drug class does levosimendan belong to and what are its net effects?

Answer 8

A relatively new inotropic agent, it is a calcium sensitiser (binds to troponin and augments actin-myosin coupling) leading to inotropy and vasodilatation

Question 9

Which receptors does noradrenaline bind to and what are its net effects?

Answer 9

B1 = a1 > b2 = a2

Net effect: vasoconstriction and weak inotropic and chronotropic effect

Question 10

When is noradrenaline used in the crit care setting? (2)

Answer 10

Used in severe hypotension and septic shock

Often used to counteract the vasodilatory effects of inotropes such as dobutamine and milrinone`

Question 11

When is dopamine used in the crit care setting?

Answer 11

Acute HF, cardiogenic shock and acute RF

Question 12

Generalised effects of various varopressors/inotropes

Answer 12

Phenylephrine –> vasopressin –> noradrenaline –> adrenaline –> dopamine –> dobutamine

From increased SVR to decreased SVR
From decreased CO to increased CO

Question 13

Define shock

Answer 13

When there is an insufficient tissue perfusion to meet the metabolic requirements of the body

Question 14

Define cardiogenic shock

Answer 14

Defined as a sustained reduction in systolic pressure of less than 90mmHg caused by a cardiac index of less than 2.2L/min/mm2

Cardiac index = CO/SA of body (usually 2.6-4.2)

Question 15

What is isopreterenol used for in the crit care setting?

Answer 15

Bradycardia and atroventricular block

Question 16

Define SIRS

Answer 16

Systemic inflammatory response syndrome

At least two or more of the following:

1. T greater than 38 C or less than 36 C
2. P >90/min
3. RR >20/min or PaCO2 less than 32 mmHg
4. WCC >12 or >10% immature band forms

Question 17

Define sepsis

Answer 17

SIRS + confirmed or presumed infection

SIRS (2 or more of the following)

1. T greater than 38 C or less than 36 C
2. P >90/min
3. RR >20/min or PaCO2 less than 32 mmHg
4. WCC >12 or >10% immature band forms

Question 18

Define severe sepsis

Answer 18

Sepsis + evidence of organ dysfunction

• hypotension
• altered mental state
• hyperglycaemia in the absence of diabetes
• hypoxaemia: sats less than 93%
• Acute oligurea: UO

Question 19

Define septic shock

Answer 19

Sepsis + hypotension despite adequate fluid resuscitation or use of vasopressors/inotropes

Question 20

What are the initial vasopressors of choice in septic shock?

Answer 20

Noradrenaline or dopamine

Vasopressin can be subsequently added

Question 21

Define SVT

Answer 21

The term supraventricular tachycardia (SVT), whilst often used synonymously with AV nodal re-entry tachycardia (AVNRT), can be used to refer to any tachydysrhythmia arising from above the level of the Bundle of His.

Question 22

How are SVTs classified?

Answer 22

SVTs can be classified based on site of origin (atria or AV node) or regularity (regular or irregular)

Question 23

How is SVT in the ICU setting managed? (5)

Answer 23

1. May respond to vagal maneuvers with reversion to sinus rhythm.
2. The mainstay of treatment is adenosine.
3. Other agents which may be used include calcium-channel blockers, beta-blockers and amiodarone.
4. DC cardioversion is rarely required.
5. Catheter ablation may be considered in recurrent episodes not amenable to medical treatment.

Question 24

What are the recommended doses of adenosine in adults?

Answer 24

6mg, 12 mg, 12 mg

Question 25

What is the half-life of adenosine?

Answer 25

Less than 10 seconds

Question 26

What is the mechanism of action of adenosine?

Answer 26

Adenosine slows conduction time through the A-V node, can interrupt the reentry pathways through the AV node, and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff- Parkinson-White Syndrome.

Question 27

What needs to be considered before administering adenosine?

Answer 27

Warn patients of feeling of 'impending doom!'. Facial flushing. Can give IV midazolam beforehand?

Question 28

How is respiratory failure defined?

Answer 28

Syndrome in which respiratory system fails in one of both of its gas exchange functions: oxygenation and carbon dioxide elimination (LOSS OF OXYGENATION OR VENTILATION)

Question 29

List the 'four' types of respiratory failure

Answer 29

``` Type 1 (Hypoxaemic): failure of oxygen exchange Type 2 (Hypercapnic/ventilatory): failure to exchange or remove carbon dioxide Type 3 (Peri-operative): increased atelectasis due to low FRC in setting of abnormal abdo wall mechanic; generally a subset of type 1 Type 4 (Shock): due to CV instability ```

Question 30

What are the two most common causes of hypoxaemic respiratory failure in ICU? How to clinically differentiate between the two?

Answer 30

V/Q mismatch e.g. COPD exacerbation Shunt i.e. perfusion without ventilation V/Q mismatch responds very readily to oxygen whereas shunt is oxygen insensitive

Question 31

List 4 examples of pulmonary shunting

Answer 31

Pulmonary Oedema, ARDS, pneumonia, atelectasis

Question 32

List 2 primary causes of type 2 respiratory failure

Answer 32

1. Increased Co2 production (secondary to increased metabolism e.g. sepsis, burns, fever, overfeeding) 2. Decreased alveolar ventilation (e.g. decreased CNS drive, neuromuscular disease, increased work of breathing leading to respiratory muscle fatigue and inadequate ventialtion, increased physiologic dead space e.g. PE)

Question 33

What is minute ventilation?

Answer 33

The amount of air moved in and out of lungs per min (RR x Vt); decreased in type 2 respiratory failure

Question 34

What is the most common cause of acute respiratory failure in the post-operative period?

Answer 34

Atelectasis (Type 3 resp failure)

Question 35

Define type 4 resp failure. How is it treated?

Answer 35

Hypoperfusion (shock) leading to resp failure Ventilator therapy often instituted in order to minimise steal of the limited CO by overworking respiratory muscles until the aetiology of the hypoperfusion state is identified and corrected

Question 36

What are the two legal definitions of death in Australia?

Answer 36

Cardiac death - irreversible cessation of circulation of blood in the body of a death Brain death - irreversible cessation of all function of the brain of a person

Question 37

What is the difference between brain death, coma and a vegetative state?

Answer 37

Brain death - cessation of intracranial blood flow causing irreversible apnoea and loss of consciousness that is always followed by cardiac a systole within days Coma - sleep like unresponsiveness from which a patient cannot be roused; May or may not breathe spontaneously Persistent vegetative state - loss of higher cortical function with functional brainstem; able to breathe spontaneously

Question 38

What is the Cushing's reflex? (2)

Answer 38

When the hypothalamus activates the sympathetic nervous system in response to increased ICP and ischaemia (the arterial pressure is less than ICP). Physiological response that leads to Cushing's triad (hypertension, bradycardia and irregular breathing pattern) Indication of imminent brainstem herniation

Question 39

How is brain death diagnosed? (3)

Answer 39

1. Diagnosed independently by 2 medical practitioners of at least 5 years experience 2. Neither practitioner should be: a member of the transplant group (looking after organ recipient, part of transplant team) or the designated officer of the hospital (person who authorises organ/tissue removal) 3. Diagnosis must be made by imaging or clinical brain death testing

Question 40

What are the 9 preconditions for clinical brain death testing?

Answer 40

1. Diagnosis of severe brain injury consistent with deterioration to brain death 2. Normotension (MAP above 60 mmHg) 3. Normothermia (T greater than 35) 4. Exclusion of coma caused by drugs or poisoning 5. Exclusion of metabolic or endocrine causes for coma 6. No paralysis - confirmation of intact neuromuscular conduction 7. Must be able to assess brainstem reflexes - must be possible to examine at least one ear or eye 8. Must be able to perform apnoea test (no assoc. lung injury or high cervical spine injury) 9. At least 4 hours of observation during which preconditions must be met

Question 41

What is the apnoea test?

Answer 41

Disconnect patient from ventilator and allow CO2 blood levels to rise (more than 60mmHg). If no spontaneous breathing to this stimulus, respiratory centres considered to be non-functional. Catheter placed on ETT and O2 passed down to prevent hypoxia during test. Blood gas performed before and after test.

Question 42

List the 6 tests involved in clinical brain death testing.

Answer 42

1. No pupillary response to light (II and III) 2. No corneal response (blinking to cotton wool test) - v and VII 3. Supra orbital pressure - no response (grimacing/limb movement) - V and VII 4. Vestibulo-ocular reflex - no eye movement in response to cold water test (50mL of cold water in each ear, observe for 60s) - III, IV and VIII 5. No gag response to stimulation of posterior pharynx - IX and X 6. No cough/tracheal response to bronchial suctioning - X ONLY IF ALL ABOVE REFLEXES ABSENT, PROCEED WITH APNOEA TEST

Question 43

When should imaging be performed in brain death testing?

Answer 43

When preconditions for clinical testing of brain death cannot be met

Question 44

What is the rationale behind the use of imaging in the testing of brain death?

Answer 44

Imaging used to demonstrate absent blood flow from both vertebro-basilar and supratentorial circulations.

Question 45

Which imaging modalities is used in brain death testing?(2)

Answer 45

1. 4 vessel angiography - vertebral and carotid arteries are filled from the arch of the aorta. Blood flow should not be demonstrated above the level of the carotid bifurcation 2. Radionuclide scanning - cerebral perfusion scanning demonstrates absence of brain perfusion; no uptake of radionuclide in brain parenchyma

Question 46

How is brain death in children tested? (2)

Answer 46

1. In those greater than 30 days, same criteria as adults 2. In first 30 days of life -minimum 48h of observation before 1st test and then 2nd test after 24h. Be cautious. Preservation of some intracranial blood flow in children and infants has been reported

Question 47

When is "time of death?"

Answer 47

Death is certified when two medical practitioners have both completed the process required for determination of brain death