Flashcards in Critical Care Kanani III Deck (37):
What is CVP and how may it be determined?
This is the pressure in the right atrium (right atrial filling pressure).
It may be estimated clinically by examining the jugular venous pulse at the root of the neck, or measured directly by central venous cannulation.
What is the normal value for the CVP?
0–10 mmHg or 0–8 cmH2O.
How useful is it as a measure of the circulating volume?
The absolute value of the CVP in determining filling is not as useful as its response to a 200–300 ml fluid challenge over 1–3 min (see below).
In some critically ill (mainly cardiac and pulmonary diseases) where the myocardial compliance is affected, or in cases of valvular heart disease, the CVP reading provides an inaccur- ate estimate of the volume state. Thus, the reading has to be interpreted in the light of other physiological parameters.
What are the uses of the central venous cannula?
Central venous lines have both short- and long-term uses:
Pulmonary artery catheterisation providing various
direct and derived measures of cardiovascular function
Drug administration: for toxic or irritant drugs, such as
amiodarone, potassium or inotropes
Transvenous cardiac pacing
What are the uses of the central venous cannula?
Venous blood sampling in the long-term, e.g. Hickman
Drug administration: such as cytotoxics
Feeding by the use of total parenteral nutrition
To reduce infection risk, these lines may be tunneled beneath the skin for a distance before entering the vein. Also, patency is ensured by regular heparin-saline f lushes.
Which vessels may be used for central access?
Internal jugular vein (most common)
Less commonly, the axilliary, cephalic or external jugular
In which two ways may the information from a central line be presented?
As a continuous waveform using a transducer attached to an oscilloscope, or intermittently by the use of a manometer sys- tem at the bedside.
Why is the serum creatinine a better indicator of renal function than serum urea concentration?
Serum urea is a poorer indicator of the glomerular filtration rate (GFR) than creatinine, since 50% or so of the filtered urea undergoes reabsorption at the tubules, leading to an underestimation of the GFR. Also, the daily production of urea is more variable than creatinine.
Other than renal failure, what are the complications of polycystic kidneys?
The extra-renal manifestations are:
Cysts in other organs: liver, pancreas, spleen, ovaries
Berry aneurysms at the circle of Willis: increased risk of subarachnoid haemorrhage
Mitral valve prolapse
What do platelets do, and what is their origin?
Platelets have a number of functions during the haemostatic response
Vasoconstriction: during the platelet release reaction, vasoactive mediators such as serotonin, thromboxane A2 and ADP are released
Factor-binding: platelet membrane phospholipid, through a reaction involving calcium and vitamin K, binds to factors II,VII, IX, and X. This serves to concentrate and co-ordinate factors into the same area for maximum activation
Formation of the primary haemostatic plug: further stabilised by platelet granule enzymes
Platelets are formed in the bone marrow and released by megakaryocyte fragmentation.
What is von Willebrand’s factor?
von Willebrand factor is a molecule synthesised by megakaryocytes and endothelial cells. It facilitates the bind- ing of platelets to the sub-endothelial connective tissue, and binds to factorVIII.
What is the function of vitamin K?
Vitamin K, a fat-soluble vitamin, is involved in the pathway that leads to factors II,VII, IX and X binding to the surface of platelets. Specif ically, it is involved in the carboxylation of these factors which allows them to bind to calcium, and hence the surface of platelets.
What is the end result of the coagulation cascade?
The end product of the coagulation cascade is the formation of a stable meshwork of cross-linked fibrin around the pri- mary platelet plug. This therefore forms the stable haemo- static plug.
What is the basic pathophysiology of DIC?
There is pathological activation of the coagulation pathway by damaged tissues that release cytokines and tissue factors. This is followed by pathologic activation of the fibrinolytic pathway. This has a number of effects
Diffuse intravascular thrombosis leading to small and large vessel occlusion by fibrin
Vascular occlusion leads to shock and end organ failure
Bleeding tendency with consumption of clotting factors
This manifests itself as bleeding from mucosal surfaces and
a petechial rash
If presenting as shock, there is a low cardiac index and
hypotension despite tachycardia
Patients may therefore develop renal failure and acute
respiratory distress syndrome
Which blood products are used in the management of DIC?
Platelets and FFP are used to replenish the consumed factors.
Packed red cells may also be required if the haemolytic anaemia is severe enough.
What will haematologic investigations show in cases of DIC?
D-dimer: this is a fibrin-degradation product, elevation of
which indicates activation of the fibrinolytic pathway
Platelet count below 15
What are the indications for enteral nutrition?
Enteral feeding should be provided for those patients with a functionally intact gastro-intestinal system that cannot meet their daily nutritional requirements.
What is the difference between a polymeric and elemental diet?
A polymeric diet is given to those with well functioning GI tracts, unlike elemental diets which are reserved for those with malabsorption, e.g. short bowel syndrome.
With polymeric diets, whole protein is used as the source of nitrogen, but for elemental, free amino acids or oligopeptides are used. Glucose polymers and long-chain triglycerides are the source of carbohydrate and fat respectively for elemental diets.
By which routes may enteral nutrition be administered?
- Oral nutritional supplementation: these are taken between
meals, being mainly milk or soya protein-based
- Nasoenteric feeding: either into the stomach (nasogastric, NG) or jejunum (nasojejunal, NJ) using a f ine bore feeding tube to minimise oesophageal irritation.
NJ feeding bypasses the stomach for those with impaired gastric motility and reduces pancreatic stimulation in those with pancreatitis. Therefore it has reduced the risk of pulmonary aspiration
- Gastrostomy: this may be placed during surgery or percutaneously by endoscopic or f luoroscopic techniques. It is suitable for prolonged feeding, particularly in those with head injuries or other neurological deficits affecting co-ordinated swallowing
- Jejunostomy: this is usually placed at laparotomy in those in whom prolonged feeding is anticipated. The tube is sutured to the antimesenteric side of the jejunum. Note that this bypasses the pancreas and biliary tree and reduces the risk of aspiration
What other enteral diets are available?
Modular diets: this diet has been enriched in a particular nutrient for the requirement of specific patients
Special formulation diets: these are arranged for specific diseases, e.g. ventilated patients are given a diet rich in fat as the main energy source as opposed to glucose, in order to reduce CO2 generation during metabolism
What happens to the bowel in those who are not fed enterally?
It is known that absence of enteral feeding leads to atrophic changes in the intestinal mucosa. This is because local hormonal release in response to food stimulates the release of enzymes necessary for mucosal integrity.
Why is it necessary to give gastrically fed patients a break from feeding at some point during a 24-hour period?
There are two main reasons why gastric feeding is not continuous:
Feeding without a break encourages bacterial colonisation of the stomach. This increases the risk of a nosocomial pneumonia if there is aspiration
Continuous intragastric feeding causes a secretory response from the ascending colon leading to diarrhoea. This may be due to the loss of the normal cephalic phase of secretion
Give some complications associated with enteral feeding.
Displacement of the tube: jejunal migration can lead to
Infection around a gastrostomy or jejunostomy wound
Refeeding syndrome: leads to hypophosphataemia in the
malnourished, with thrombocytopenia and confusion
Hyperkalaemia in those with renal impairment
Hyperglycaemia in those with the reduced glucose
tolerance of the critically ill
Briefly mention some of the ventilation strategies used to wean from mechanical ventilation.
T-piece ventilation: added to the end of the circuit, and can
be used just prior to extubation. When used on its own, it is more successful in those who have been intubated for a short period of time only (a couple of days at the maximum)
T piece and CPAP: one of the problems of intubation is that it abolishes the small amount of natural PEEP provided by the laryngeal complex. The use of CPAP adds to the PEEP, permitting the T-piece to be used for longer periods in those who require it. Thus, during weaning, the T-piece is left on during parts of the day, while mechanical ventilation is continued at night
Intermittent mandatory ventilation (IMV): the ventilator provides a certain tidal volume at a specified rate. Between these mechanical breaths, the patient supplements with their own, spontaneous breaths. The mandatory rate is progressively reduced, while increasing the spontaneous breaths
Pressure support ventilation: the patient breathes spontaneously, but each breath is augmented with a positive inspiratory pressure. This is progressively reduced until full extubation, or CPAP
What are the precautions with using colloids?
Potential risk of disease transmission: with blood and blood products
Coagulopathy: Dextran 70, gelatins, and high molecular weight starches interfere with platelet adhesion and von Willebrand factor
Interaction with blood transfusion: the calcium content of Haemaccel can cause blood to clot if infused into the same cannula
Immunological reactions: other than blood, Dextran 70, and gelatins may cause pruritis or anaphylaxis. May also occur with starches, but much more rarely
Risk of worsening oedema: if loss of capillary integrity causes the colloid to leak into the interstitial compartment
What is the result of mucosal atrophy?
Loss of cellular adhesion and development of cellular channels
Translocation of bacteria across the bowel wall into the systemic circulation is encouraged. This can lead to sepsis, or perpetuation of the systemic inf lammatory response in the critically ill
Where is CSF produced, and at what rate?
70% of CSF is produced by the choroid plexus of the lateral, third and fourth ventricles. 30% comes directly from the vessels lining the ventricular walls. It is produced at a rate of 0.35 ml/min, or ~500 ml/day.
Where is the CSF finally absorbed?
80% of CSF is absorbed at the arachnoid villi, and 20% is absorbed at the spinal nerve roots.
What are the arachnoid villi composed of?
The arachnoid villi are formed from a fusion of arachnoid membrane and the endothelium of the dural venous sinus that it has bulged into.
What is the Cushing reflex?
This is mixed vagal and sympathetic stimulation that occurs in response to an elevated intracranial pressure. It leads to hypertension, which ensures an adequate cerebral perfusion pressure. There is also a resultant bradycardia.
What substances can pass through the BBB?
The BBB is permeable to lipids, lipid soluble molecules (such as opiates and general anaesthetics), respiratory gases and glucose. Chronically, it is also permeable to protons (H+)
Which parts of the brain lie outside of the BBB?
Three main areas lie outside of the BBB
The posterior lobe of the pituitary gland
(neurohypophysis): which produces vasopressin and
Circumventricular organs around the 3rd and
4th ventricles: such as the supraoptic crest, the area
postrema and tuber cinerium
The median eminence of the hypothalamus
What are the signs and symptoms of a raised ICP?
The four cardinal signs and symptoms of a raised ICP are
Headache: often worse in the morning
Nausea and vomiting: worse in the morning
Reduced level of consciousness: may manifest as simple drowsiness. This is an important sign, since its signif icance may be missed
Papilloedema: a def initive sign of raised ICP, as the pressure is transmitted along the subarachnoid space of the optic nerve
In the infant (below 18 months) there may be a tense anterior fontanelle
What varieties of brain herniation are there, and how may they manifest themselves?
There are three types of brain herniation
Subfalcine: where the cingulate gyrus herniates beneath
the falx cerebri
Foramen magnum herniation: leading to displacement of the medulla and the cerebellar tonsils. Compression of the respiratory centre leads to respiratory depression
Transtentorial: the uncus of the temporal lobe passes through the tentorial hiatus
With transtentorial herniation, can lead to ipsilateral
compression of the oculomotor nerve (CN III) and pyramidal tract running in the midbrain. This is clinically manifest as an ipsilateral dilated pupil and a contralateral hemiparesis
Displacement of the posterior cerebral artery may produce visual field defects with transtentorial herniation
Pressure on the brainstem stimulates Cheyne–Stokes respiration and the Cushing ref lex
Exponential rise in the ICP as f low of the CSF is suddenly occluded by the herniated brain
Name a ‘false localising sign’ – why does this occur?
The classical false localising sign is an abducent (CN VI) nerve palsy, with an inability to abduct the eye. This falsely points to the abducent motor nucleus as being the site of the lesion. In reality it results from herniation producing kinking of the sixth nerve as it runs a long intracranial course.