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4th Year ACC > Critical Care > Flashcards

Critical Care Flashcards

1
Q

What are the levels of care?

A

0 = needs can be met through normal ward

1 = at risk of condition deteriorating - advice and support from critical care

2 (HDU) = More detailed observation (hourly) or intervention - single organ support (more than 50% O2, NIV, vasoactive drug infusions, post-op care.

3 (ICU) = advanced respiratory support alone or multiple organ failure. Haemodialysis = level 3 due to intensity involved in maintaining it.

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2
Q

Components of NEWS?

A 
RR
O2 sats
Supplmenetal oxygen
Temp
Systolic BP
HR
Level of consciousness
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3
Q

What are low, medium and high NEWS scores and what do they mean?

A

0 = 12 hourly monitoring minimum

1-4 = low = minimum 4 hourly obs

5 (or 3 in one parameter) = medium = minimum 2 hourly obs

7+ = high = minimum 1 hourly obs

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4
Q

Causes of hypovolaemic shock?

A

Blood loss - trauma, GI bleed, ruptured AAA/ectopic

Fluid loss/redistribution - burns, GI losses, pancreatitis, sepsis

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5
Q

Presentation and physiological response to hypovolamic shock?

A

Cool and pale

Reuduced CO –> increased SVR

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6
Q

Causes of distributive shock?

A

Sepsis, anaphylaxis, neurogenic, liver failure, adrenal insufficiency, drugs and toxic exposures

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7
Q

Presentation and physiological response to distributive shock?

A

Warm and vasodilated

Low SVR –> Increased CO

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8
Q

Causes of cardiogenic shock?

A

Primary = MI, arrhythmias, valve dysfunction, myocarditis

Secondary = tamponade, massive PE, tension pneumothorax

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9
Q

Presentation and physiological response to cardiogenic shock?

A

Cool and pale

Low CO –> increased SVR

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10
Q

What are clinical signs of shock?

A

General = systolic BP <90, lactate >3, increased CRT, increased BE

Brain = lethargy, somnolence

Kidneys = oliguria/anuria (only directly measurable indicator of organ function)

Attempted compensation = tachycardia, tachypnoea

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11
Q

What are haemodynamic goals in cardiovacular failure?

A

MAP >65 mmHg (or higher if usually hypertensive)

Urine output > 0.5 ml/kg/hr

CVP 8-12 mmHg

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12
Q

How to calculate the MAP?

A

Diastolic pressure + one third of the pulse pressure

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13
Q

Systemic goals in cardiovascular failure?

A

Optimise oxygen delivery to tissues…

Central venous oxygen saturation >70%
Normalise lactate
Ensure adequate ventilation/breathing

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14
Q

Receptors that inotropes work on?

A 
Adrenaline = b > a
Noradrenaline = a > b
Dopamine = DA > b > a
Dobutamine = b1 and b2
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15
Q

Clinical features of hypoxia?

A

Dyspnoea; restlessness; agitation; confusion; central cyanosis.

If long-standing hypoxia: polycythaemia; pulmonary hypertension; cor pulmonale.

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16
Q

Clinical features of hypercapnia?

A

Headache; peripheral vasodilatation; tachycardia; bounding pulse; tremor/flap; papilledema; confusion; drowsiness; coma.

Bounding pulse because CO2 causes reduced SVR –> increased HR

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17
Q

Investigations in respiratory failure?

A

Aimed at identifying underlying cause.

Bloods – FBC; U&E; CRP; ABG.
CXR
Microbiology; sputum and blood cultures (if febrile)
Spirometry (COPD, neuromuscular disease, Guillain-Barré syndrome).

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18
Q

Definition of type 1 respiratory failure?

A

Hypoxaemia without hypercapnia

pO2 < 8 kPa ON AIR
pCO2 < 6.0 kPa
Able to blow off the CO2

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19
Q

Causes of type 1 respiratory failure?

A

V/Q mismatch (Pneumonia, pulmonary oedema, PE, asthma, emphysema, pulmonary fibrosis, ARDS)

Upper airway obstruction

Low oxygen in inspired air

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20
Q

Management of type 1 respiratory failure?

A

Treatment of the underlying cause

Treatment of the hypoxia
• Start high and reduce later when proven patient does not need it.

If still PaO2 < 8kPa despite maximal oxygen therapy (60%) –> HDU/ICU and CPAP.

21
Q

Definition of type 2 respiratory failure?

A

Hypoxaemia with hypercapnia

pO2 < 8 kPa ON AIR
pCO2 > 6.0 kPa
Not able to blow off the CO2

22
Q

Causes of type 2 respiratory failure?

A

Hypoventilation or Increased dead space

Pulmonary disease
• Asthma, COPD, pneumonia, end-stage pulmonary fibrosis, obstructive sleep apnoea.

Reduced respiratory drive
• Sedative drugs, CNS tumour or trauma.

Neuromuscular disease
• Cervical cord lesion, diaphragmatic paralysis, poliomyelitis, myasthenia gravis, Guillain-Barré syndrome.

Thoracic wall disease
• Flail chest, kyphoscoliosis

23
Q

Management of type 2 respiratory failure?

A

Treat underlying cause

Controlled oxygen therapy – start at 24% - recheck ABG after 20 mins –> if PaCO2 is steady or lower, increase O2 concentration to 28%. If PaCO2 has risen or patient still hypoxic, consider NIV.

Last resort, intubation and ventilation if appropriate.

24
Q

What is ARDS?

A

May be caused by direct lung injury or occur secondary to systemic illness. Lung damage and release of inflammatory mediators cause increased capillary permeability and pulmonary oedema, often accompanied by muti-organ failure.

25
Q

Causes of ARDS?

A

PULMONARY
Pneumonia; gastric aspiration; inhalation; injury; vasculitis; contusion.

OTHER
Shock; septicaemia; haemorrhage; multiple transfusions; DIC; pancreatitis; acute liver failure; trauma; head injury; malaria; fat embolism; burns; obstetric events; drugs/toxins.

26
Q

Clinical features of ARDS?

A

Cyanosis; tachypnoea; peripheral vasodilatation; bilateral fine inspiratory crackles.

27
Q

What is CPAP?

A

Oxygen delivered with a positive pressure of between 4 and 25 cmH2O.

Delivered via face mask/hood.

Improves V/Q mismatch and decreases the work of breathing.

28
Q

How does CPAP improve V/Q mismatch and decrease the work of breathing?

A

i. Decreases atelectasis – splints open the alveoli.
ii. Decreases leakage of fluid into lungs.
iii. Splints airways open

29
Q

When is CPAP indicated?

A

type 1 respiratory failure

30
Q

Problems with CPAP?

A

i. Can expand pneumothoaces
ii. Can cause hypotension (↑intrathoracic pressure –> ↓venous return to heart (preload) – careful in pulmonary oedema.
iii. Difficult to apply if there are facial injuries
iv. Patient intolerance

31
Q

What is BIPAP?

A

CPAP but with additional pressure to support inspiration – gives respiratory support with each breath to increase the tidal volume.

i. EPAP – expiratory positive airway pressure (or PEEP) – analogous to CPAP.
ii. IPAP – inspiratory positive airway pressure – pressure given to support inspiration.

32
Q

When is BIPAP indicated?

A

Indicated in type 2 respiratory failure. Extra tidal volume will clear the CO2.

33
Q

Problems with BIPAP?

A

Similar to CPAP – greater need for patient co-operation as ventilator synchrony with the patient is more difficult to achieve.

34
Q

Contraindications to NIV?

A

Haemodynamic instability

Severe hypoxia/hypercapnia

Poor pt co-operation

Lack of trained staff

Relative = need for urgent ETT, reduced consciousness

35
Q

Indications for invasive ventilatory support?

A

Respiratory failure that is refractory to other treatment

Respiratory failure with low conscious level

Tiring on other treatment

Airway compromise

36
Q

Complications of invasive ventilation

A

Sedation (Hypotension, gastroparesis, immoblility, vascular access)

Risk of pneumonia

Limited to specialist areas (ICU)

Invasive ventilation can also fail and some patients can develop refractory hypoxia or hypercapnia

37
Q

Causes of pre-renal renal failure?

A 
Hypovolaemia
Sepsis
Renal artery stenosis +/- ACEi
Burns
Cardiac failure
38
Q

Causes of renal renal failure

A

Tubular – ATN - as a result of pre-renal damage or nephrotoxins such as drugs, radiological contrast, and myoglobulinuria in rhabdomyolysis.

Glomerular

Interstitial

Vascular

39
Q

Causes of post-renal renal failure?

A

Luminal – stones, clots, sloughed papillae.

Mural – malignancy (ureteric, bladder, prostate), BPH, strictures.

Extrinsiccompression – malignancy (pelvic), retroperitoneal fibrosis.

40
Q

Nephrotoxic drugs?

A 
ACEi
Diuretics
Gentamicin
Radiocontrast
NSAIDs
Vancomycin
41
Q

Complications of AKI?

A

TOSHO

Toxicity
Obstruction
Shock
Hyperkalaemia
Oedema
42
Q

Indications for RRT?

A

Really really really unhappy dialysis (patients)

Refractory hyperkalaemia
Refractory fluid overload
Refractory metabolic acidosis
Uraemia
Drug intoxication (salicylates, theophylline)
43
Q

What is continuous RRT (CRRT)?

A

Gentler than dialysis

IV access with vascath
Extrcorporeal blood circuit
Peristaltic pumps drive blood to semipermeable membrane

44
Q

What is the best vaso active agent for low BP and low HR?

A

Ephedrine (a + b)

45
Q

What is the best vaso active agent for low BP and high HR?

A

Phenylephrine or metaraminol (mainly a-receptors

46
Q

Agents for bradycardia

A

Atropine

Glycopyrrolate

47
Q

How to confirm death?

A

5 minutes observation

Absence of central pulse or heart sounds
Asystole on ECG
Absence of pulsatile flow on arterial pressure monitoring
Absence of contractile activity on echo

Absence of: pupillary light reflexes, corneal reflex, motor response to supraorbital pressure

48
Q

Criteria for diagnosing brainstem death?

A

No doubt that condition is due to irreversible brain damage of known aetiolgy

Exclude potetntially reversible causes of coma (depressant drugs, hypothermia, metabolic/endocrine disturbance)

Exclude alternative causes of apnoea (neuromuscular, high cervical spine injury)

Absence of brainstem reflexes

49
Q

What are the brainstem reflexes?

A

Pupils fixed and don’t respond to light (II, III)

No corneal reflex (III, V)

Oculo vestibular reflexes are absent (icy water into ear, no nystagmus - V, VIII)

No motor response (V, VII)

No gag reflex (IX, X)

4th Year ACC (9 decks)

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