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Flashcards in Critical Care Kanani IV Deck (37):
1

Why should the ICP be controlled?
What techniques are available?

There are two main reasons why the ICP should be con- trolled
A high ICP can lead to cerebral herniation
A high ICP causes a reduction of the cerebral perfusion
pressure (since the cerebral perfusion pressure = mean
arterial pressure - ICP)
There are a number of techniques used to reduce the ICP
Controlled ventilation, keeping the PaCO2 between
4–4.5 kPa. This controls the degree of intracranial
vasodilatation
Fluid restriction, which prevents cerebral oedema
Diuretics, e.g. mannitol or furosemide. Mannitol is an
osmotic diuretic given at a dose of 0.5–1.0 g/kg over 20 min. It can be used to ‘buy time’ while preparing for surgery
Direct tapping off the CSF from a ventricular catheter
Tilting the end of the bed 20 degrees
Barbiturates, e.g. thiopentone if the ICP is resistant to the
above measures
Note that steroids are helpful in reducing the swelling
around cerebral tumours, but not in situations of trauma

2

What are the other complications of a severe head injury?

Shorter term:
Meningitis and brain abscess: where there has been an open communication

Longer term:
Epilepsy: especially common in the situation of a
depressed fracture, intracranial haematoma or
prolonged amnesia
Hydrocephalus: caused by obstruction from an
intraventricular haemorrhage

3

What are the effects of dopamine on the circulation?

In low doses (15 g/kg/min) it acts on beta receptors. At this high dose, and faster infusion rates, it also acts on alpha receptors. Thus at low doses it causes renal and mesenteric vasodilatation, causing diuresis and natriuresis. However, evidence suggests that some of the improved urine output is due to a direct inotropic effect. At higher doses causes vasoconstriction and tachyarrhythmias.

4

What are the indications for the use of norepinephrine?

Norepinephrine, having mainly alpha effects, is a potent vasoconstrictor that is useful in supporting the arterial pressure in cases of septic shock. The resulting vasoconstric- tion leads to reduced peripheral perfusion at higher doses despite improved arterial pressure. It can also be used with the phosphodiesterase inhibitors, so the patient benefits from increased ejection fraction, without excessive vasodi- latation.

5

What are the effects of epinephrine on the circulation?

At low doses, the beta effects predominate. At higher doses, the

6

What about dobutamine?

Having strong beta-1 effects, has both inotropic and chronotropic effects, increasing the cardiac output. Also reduces the systemic vascular resistance (

7

What are the general problems associated with the use of inotropes?

Some of the problems of inotropic agents are
Tachyarrhythmias
Bradycardia, e.g. norepinephrine
Hypertension, e.g. epinephrine
Hypotension, e.g. dobutamine, phosphodiesterase
inhibitors
Increased myocardial oxygen consumption and demand

8

How does an intra-aortic balloon pump work?

The basic principle involves mechanical assistance to the fail- ing heart through afterload reduction and an improvement of the coronary blood f low. The device sits in the descending aorta and is connected to an external console that pumps helium in and out of the balloon in phase with the ECG. The balloon expands in diastole, causing an increase in the coronary perfusion pressure. By def lating just before the onset of systole, it leads to afterload reduction, reducing impedance to left ventricular ejection and reduced myocardial workload.

9

How and where is intra-aortic balloon inserted?

It may be inserted at the time of cardiac surgery or in the ITU through the femoral artery at the groin, using the Seldinger technique.

10

How may the causes of lactic acidosis be classified?

The Cohen andWoods (1976) classification divides the causes thus
TypeA:
Results from poor tissue perfusion and cellular hypoxia with resulting anaerobic metabolism
Lactate is generated from pyruvate
Can be caused by any cause of shock – cardiogenic,
hypovolaemic, septic or obstructive

Type B:
As a complication of other diseases: liver disease, renal
failure, diabetic ketoacidosis, malignancy, short-bowel
syndrome
Also, inborn error of metabolism: e.g. pyruvate
dehydrogenase deficiency
May also be drug-induced: paracetamol/salicylate
overdose, metformin, epinephrine, alcohol intoxication

11

What is the minimum acceptable urine output in adults and children?

In adults, the minimum acceptable urine output is 0.5 ml/kg/h. In children, 1 ml/kg/h.

12

What is the normal serum level of magnesium?

0.7–1.0 mmol/L.

13

What is the distribution of magnesium in the body?

Magnesium is the second most abundant intracellular cation after potassium. The total body magnesium is ~25 g, with 65% being located in the bone. Only 1% of the body mag- nesium is found in the serum, so that the serum level is a poor ref lection of the total body store.

14

What purpose does magnesium serve?

Magnesium is an essential co-factor in a number of enzymes, notably in the transfer of phosphate groups, and protein syn- thesis. It is most conspicuously important for the normal function of the central nervous, neuromuscular and cardio- vascular systems.

15

What is the relationship between magnesium and serum calcium?

High magnesium levels prevent calcium cellular uptake, and for this reason, hypermagnesaemia can lead to bradycardia and sluggish deep tendon reflexes.

16

What drug is used to reverse the effects of severe hypermagnesaemia?

Calcium gluconate.

17

Which organ is largely responsible for magnesium homeostasis?

The kidney is the major site for magnesium balance. It is freely filtered at the glomerulus, and reabsorbed mainly at the prox- imal convoluted tubule and thick ascending limb of Henle.

18

What are the main causes of hypomagnesaemia?

Renal losses: any state of excess diuresis, e.g. diuretic use, diuretic phase of acute renal failure, hypercalcemia
Alcoholism
Gut losses/malabsorption: diarrhoea, inflammatory bowel disease, malnutrition, intestinal resection and bypasses
Endocrine disturbance: diabetes mellitus, hyperparathyroidism, hyperthyroidism

19

How can hypomagnesaemia be recognised?

It may be difficult to recognise hypomagnesaemia due to its varied presentations. Recognised features include:
Cardiac arrhythmias such as atrial fibrillation and torsade
de pointes (rapid ventricular arrhythmia with a
characteristically twisting wave front)
ECG changes: prolonged P-R interval (

20

Give some examples of the therapeutic role of magnesium-containing compounds.

Anti-arrhythmic: can be used to achieve chemical
cardioversion for acute atrial fibrillation, or in torsade de pointes
Acute myocardial infarction: some studies suggest a survival benefit from early administration
Antacid: e.g. magnesium trisilicate, or hydroxide
Laxative: e.g. magnesium sulphate
Eclampsia: for the prevention of recurrent seizures in this condition

21

What are the basic modes of ventilation?

Pressure control: either a pre-set inspiratory pressure is delivered, or the cycle changes from inspiration to expiration when a certain pressure is reached
Volume control: a f ixed tidal volume is delivered, and is generally used by older and simpler circuits
Assisted modes: the ventilator augments each inspiratory effort initiated by the patient – either by pressure or volume support, e.g. PSV (pressure support ventilation), SIMV (synchronised intermittent mandatory ventilation)

22

What is PEEP (positive end-expiratory pressure), and what physiological changes occur with it?

PEEP is used in conjunction with IPPV, and involves deliv-
ery of additional pressure (5–20cmH2O) at the end of the respirator cycle to prevent alveolar collapse at the end of expiration. Thus, oxygenation is improved when additional alveoli are recruited. Other than alveolar recruitment, some of the other physiological effects are
Increased compliance
Increased functional residual capacity (leading to the above)
Reduced physiological shunting with increasedV/Q ratio

23

Give some examples of the physiological effects and complications of intermittent positive pressure ventilation (IPPV).

Cardiovascular: by making the intrathoracic pressure ‘less
negative,’ it reduces the venous return to the heart. Lung expansion also distorts the alveolar capillaries, increasing the pulmonary vascular resistance. These have the effect of reducing the cardiac output and arterial pressure. Therefore, tissue oxygen delivery may be impaired

Respiratory: overdistension of the lungs produces barotrauma in the form of alveolar rupture. This manifests predominantly as pneumothorax or pneumomediastinum. Also increases the risk of nosocomial pneumonia

Renal: leads to a reduction of the renal perfusion pressure, and hence the urine output

Paralytic ileus: caused by uncertain mechanisms

24

What is renal tubular acidosis?

These are a group of conditions that exhibit renal tubular dysfunction in the presence of a normal glomerular filtration rate and creatinine clearance. It leads to abnormalities in the renal handling of H+ and HCO

25

What is an ‘essential’ amino acid? Give examples

The essential amino acids are those ones that cannot be synthesised in the body and have to be ingested in the diet. These include: leucine, isoleucine, lysine, methionine, phenyl- alanine, threonine, tryptophan and valine.

26

Give some examples of essential minerals.

Zinc, magnesium, manganese, selenium, copper, chromium and molybdenum.

27

What are the fat-soluble vitamins, and what are they used for?

Vitamin A: important for cell membrane stabilisation and
retinal function
Vitamin D: for calcium homeostasis and bone mineralisation
Vitamin E (mainly

28

What are the names of the vitamin B group?
Which diseases occur when there is a deficiency?

The B group of vitamins, which are all water-soluble are composed of

Vitamin B1 (thiamine): deficiency leads to beri-beri or
Weinicke’s encephalopathy

Vitamin B2 (riboflavin): deficiency leads to a syndrome of
glossitis, angular stomatitis and cheilosis

Vitamin B3 (niacin): deficiency leads to pellegra

Biotin: def iciency rarely occurs in isolation, but can lead to reduced immune function

29

What are the functions of vitamin C?

Vitamin C is another of the water-soluble vitamins
Hydroxylation of proline and lysine residues during
collagen synthesis
Iron absorption at the gut
Synthesis of epinephrine from tyrosine
Antioxidant functions

30

How may oxygen be delivered to the patient?

Variable performance devices: the FiO2 delivered depends on the f low rate.
Nasal cannulae: a convenient way for the patient
Face mask (e.g. Hudson mask): at 2 l/min, the FiO2
achieved is 0.25–0.30. At 6–10 l/min: FiO2 = 0.30–0.40
If the f low is not high enough, then re-breathing of air exhaled into the mask occurs, leading to hypercarbia.
Fixed performance devices: there is a constant FiO2 delivered so the desired amount can be administered accurately.
Venturi mask: oxygen f lows through a device that entrains
air from side holes at a certain rate. The degree of air
mixing within the device produces the desired FiO2
Reservoir bag: this is attached onto the end of a face
mask. During tachypnoea, the patient inhales directly from the oxygen in the bag, so that the FiO2 is close to 1.0. This is used in the trauma setting to deliver as much oxygen as possible
Oxygen tent
Continuous positive pressure ventilation: this ensures that
the small airways do not collapse at the end of expiration by providing a positive pressure through the respiratory cycle
Invasive respiratory support with intubation and intermittent positive pressure ventilation

31

What are the indications for TPN?

General critical illness:
Severe malnourishment with

32

Which is the absolute indication for TPN?

The most important indication is the presence of an entero- cutaneous fistula.

33

How is TPN administered?

The high osmolality of the mixture causes irritation to small vessels, so that it is generally given through a central vein, e.g. tunnelled subclavian line. If it is to be given through a peripheral vein, it must be given as a solution of osmolality of

34

What are the basic components of a TPN regimen?

The basic components are water, carbohydrate, protein, lipid, vitamin and trace elements. Various drugs may also be added, such as ranitidine and insulin.

35

Why does liver function need to be monitored?

TPN can cause a derangement of the liver function tests sec- ondary to enzyme induction caused by amino acid imbal- ances. Also, it can cause fatty change of the liver.

36

What are the metabolic complications?

Hyper/hypoglycaemia
Hyperlipidaemia
Essential fatty acid deficiency
Hyperchloraemic metabolic acidosis: if there is an excess
of chloride
Hyperammoniaemia: if there is liver disease, or a
deficiency of L-glutamine and arginine
Ventilatory problems: with excess production of CO2 if
too much glucose is used in the mixture. In the ventilated critically ill patient, the amount of glucose given in 24 h may have to be restricted to 5 g/kg

37

What ECG changes may be found in hyper- and hypokalaemia?

In hyperkalaemia:
Tall, tented T-waves
Small P-waves
Wide QRS-complexes

In hypokalaemia:
Small/inverted T-waves
U-waves (seen after the T-waves)
Prolonged P-R interval
S-T segment depression