Anaesthetics III Flashcards
Cerebral blood flow
Cerebral blood flow (CBF) is approximately 50 ml/100 g of brain tissue per minute and is maintained at this constant rate over a wide range of mean arterial pressures (not systolic blood pressures). This phenomenon is called autoregulation and occurs between mean arterial pressures (MAP) of 60-130 mmHg.
The autoregulation curve for cerebral blood flow is shifted to the right (not left) with hypertension and is lost around areas of diseased brains.
Hypothermia is defined as a core temperature below 35°C and is associated with a reduction in CBF.
Hypercapnoea causes cerebral vasodilatation which increases CBF. In hypocapnoea the CBF falls due to cerebral vasoconstriction, for example, a reduction in PaCO2 from 5 kPa-4 kPa (40-30 mmHg) results in a 30% fall in blood flow.
CBF increases when the PaO2 falls below 6.7 kPa (50 mmHg) and is doubled at a PaO2 of 4 kPa (30 mmHg).
Cervical plexus
The cervical plexus is formed by the anterior primary rami of C1 to C4 and divides into superficial and deep branches.
The superficial branches pierce the deep fascia at the middle of the posterior border (not anterior) of the sternocleidomastoid, and provide sensation from the lower border of the mandible (not maxilla) to the level of the second rib.
The deep branches supply motor fibres to the neck muscles and diaphragm and are located in the sulci of the transverse processes.
Complications of a cervical plexus block include
• Injection of local anaesthetic into the vertebral artery, subarachnoid and epidural spaces
• Blockade of the phrenic nerve, recurrent laryngeal nerve and cervical sympathetic plexus.
Thrombosis risk
Patients with deep venous thrombosis usually present with physical signs that are unreliable or non-specific, and frequently require investigation to confirm the diagnosis. Some calf vein thromboses can be asymptomatic. Risk factors associated with DVT and pulmonary embolism (PE) include hypercoagulable states, such as deficiencies of • Protein C • Protein S • Antithrombin III • Plasminogen. Other risk factors are • Malignancy • Prolonged immobility • The oral contraceptive pill • Pregnancy • Obesity • Previous DVT • Varicose veins • Polycythaemia • Myocardial infarction • Cardiac failure • Connective tissue diseases.
Lumbar (not thoracic) epidurals and spinals have been associated with a reduced incidence of DVT. This has been attributed to the increased blood flow to the lower limbs, reduced venous stasis and reduced blood viscosity (from intravenous fluid loading).
Pulmonary embolism
A pulmonary embolus can present with
• Dyspnoea
• Pleuritic chest pain (with an audible pleural rub)
• Haemoptysis
• Cyanosis
• Pulmonary hypertension
• Right ventricular failure
• Cardiac arrest.
They can also be asymptomatic.
A pleural rub may be found on auscultation in pneumonia, so it cannot be used to confirm a PE.
A positive V/Q scan will show persistent ventilation in a region with absent perfusion (not ventilation). The presence of co-existing pulmonary pathology reduces the sensitivity of this investigation.
The associated ECG changes in a PE are not diagnostic, but include signs of right (not left) ventricular strain with right axis deviation, right bundle branch block and the S1, Q3, T3 pattern (S wave in lead I, Q wave and inverted T wave in lead III).
The classical findings on arterial blood gas analysis show
• Hypoxia
• Hypocarbia (not hypercarbia)
• An increased alveolar-arterial oxygen gradient.
Treatment of a PE requires systemic anticoagulation (heparin followed by warfarin), and in selected cases only (central PE) surgical embolectomy may be performed.
helps to prevent the development of multiple organ dysfunction syndrome (MODS) in trauma patients? Early nasogastric feeding
Multiple organ dysfunction syndrome (MODS) is defined as ‘the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention’ (1992 American College of Chest Physicians/Society of Critical Care Medicine consensus panel). It is a frequent complication of the systemic inflammatory response syndrome (SIRS) and sepsis.
Enteral feeding via a gastric tube should be started as soon as possible in all trauma patients. In the absence of enteral nutrition, the gut mucosa atrophies and bacteria may ‘translocate’, which is thought to be the cause of sepsis and MODS.
Selective decontamination of the digestive tract (SDD) may reduce the incidence of nosocomial infection, but there is little evidence to suggest it reduces the incidence of MODS. The use of broad spectrum antibiotics will merely encourage the development of resistant bacteria.
Fractures should be stabilised as soon as possible. Using propofol for long term sedation on the ICU is no longer popular; however this is not associated with the development of MODS.
Treating pain in trauma patients
Decreases muscle spasm, does not increase identification of clinical signs
Appropriate analgesia should be given to all trauma patients. Pain will usually cause immobilisation of the patient and thus increases the risk of developing venous thrombosis and venous thromboembolism.
When in pain, patients have shallow respirations and usually are reluctant to cough or sigh. This causes atelectasis and increases the risk of pulmonary infections. When adequate analgesia is provided, tidal volumes are greater with less atelectasis and a reduced incidence of pulmonary complications is seen.
Pain causes adrenergic stimulation and this increases metabolic responses, for example,
• Gluconeogenesis
• Glycolysis
• Lipolysis
• Production of free fatty acids.
Treatment of pain will decrease this response.
Pain associated with fractures can cause skeletal muscle spasm, which if left untreated not only helps to maintain the pain but can also make the reduction of fractures very difficult.
Although analgesia improves patient co-operation during examination and radiological investigation, some important clinical signs and symptoms can be masked. The interpretation of an abdominal examination may be more difficult and some cervical spine fractures have also been missed following the administration of analgesia.
Traumatic rupture of aorta
Widened mediastinum
The thoracic aorta is at risk in any patient sustaining a significant decelerating force, for example, fall from a height or high speed road traffic accident (not penetrating injuries).
Widening of the mediastinum may have been overlooked on the original AP radiograph. This is a sensitive sign of aortic rupture, though not very specific: 90% of widened mediastina are due to venous bleeding.
Other features frequently associated with aortic rupture are:
• Fractures of the upper three ribs
• Deviation of the trachea to the right
• Depression of the left mainstem bronchus
• Deviation of the nasogastric tube to the right
• Loss of the aortic knob
• Pleural capping.
Interscalene block Can cause ipsilateral horners syndrome
An interscalene block anaesthetises the brachial plexus at the level of the roots, and reliably blocks the shoulder and radial aspect of the forearm. It is often associated with sparing in the ulnar nerve territory (not radial).
The key landmark for performing this block is the interscalene groove which is located between the anterior and middle scalenus muscles. At least half of patients having an interscalene block develop Horner’s syndrome on the same side (ipsilateral).
One of the main advantages of the interscalene block is that pneumothorax is avoided, and the supraclavicular block is associated with the highest risk of pneumothorax.
Nerves to be blocked in an ankle block
In order to perform an ankle block, five nerves need to be anaesthetised.
They are the saphenous nerve (the terminal branch of the femoral nerve) and four nerves derived from the sciatic nerve:
• Tibial nerve
• Sural nerve
• Superficial peroneal nerve
• Deep peroneal nerve (not common peroneal nerve).
Muscle of inspiration
Scalenus anterior
The internal intercostals are muscles of expiration.
Latissimus dorsi has no role in either inspiration or expiration.
The rectus abdominus aids expiration by pushing the relaxing diaphragm upwards and pulling the ribs down and in.
In deep forced inspiration, every muscle that can raise the ribs is brought into action, including the scalenus anterior and medius and the sternocleidomastoid muscle.
Femoral nerve
Supplies part of foot but not in femoral sheath, and doesn’t share origin with sciatic nerve
The femoral sheath contains the femoral artery and vein as well as lymphatics, but not the nerve. The femoral nerve lies behind and lateral to the sheath.
The femoral nerve gives off three cutaneous branches
• Two from its anterior division (medial and intermediate cutaneous nerves of thigh which supply the skin of the medial and anterior surfaces of the thigh)
• One from its posterior division (saphenous nerve).
It has no branches to the scrotum.
The saphenous nerve runs down the medial side of the leg and supplies the medial side of the calf as far as the medial malleolus. It terminates in the region of the ball of the big toe and may supply the medial side of the dorsum of the foot.
The femoral nerve is the largest branch of the lumbar plexus and comes from the same lumbar nerves as the obturator nerve, L2, L3 and L4.
Hyperkalaemia treatment
When electrocardiogram abnormalities are present, treatment of hyperkalaemia is an emergency. The treatment includes
• Calcium chloride
• Sodium bicarbonate
• Dextrose/insulin
• Beta agonists
• Loop diuretics
• Drugs to bind potassium in the gastro-intestinal tract
• Dialysis.
The underlying condition must also be sought and treated.
Amiloride, atenolol, magnesium and phosphate have no role in the management of hyperkalaemia.
Causes of hypokalaemia
Causes of hypokalaemia can be divided into the following: • Transcellular shifts o Alkalosis o Insulin o Beta-agonists • Renal losses o Diuresis o Diabetic ketoacidosis after therapy o Conn's disease • Extrarenal losses o Diarrhoea o Nasogastric suction • Decreased intake o Malnutrition o Alcoholism. Angiotensin converting enzyme inhibitors and rhabdomyolysis tend to cause hyperkalaemia.
Regarding burns
Full thickness are painless
Chemical burns should be brushed off (if dry substance) and irrigated. Using an alkaline substance to neutralise the acid may result in an exothermic reaction (generating heat), which could exacerbate the injury.
Superficial partial thickness burns are painful and erythematous, deep partial thickness burns are blistered and very painful, and full thickness burns are white, leathery and painless.
The anterior trunk is 13% of body surface area (Lund and Browder chart). The ‘rule of nines’ is just a simple approximation.
The half-life of carboxyhaemoglobin in 100% oxygen is approximately 30 minutes; in air it is four hours.
Principles of traumatic head injury
Principles in the management of a head injury include
• Nursing the patient in a head up tilt of 30 degrees (not down)
• Avoiding hypoglycaemia and hyperglycaemia
• Using normal saline (0.9%) as the primary maintenance fluid
• Maintaining normocapnoea (not hyperventilation to a pCO2 of 3.0 kPa)
• Active treatment of fever and seizures.
The prophylactic treatment of seizures has not shown to be of benefit.
Severe traumatic brain injury Loss of autoregulation
Primary brain injury is usually irreversible and occurs at the time of injury.
Causes of secondary brain injury include
• Hypoperfusion
• Hypoxia
• Reperfusion injury.
The factors that determine the cerebral perfusion pressure (CPP) include the mean arterial blood pressure (not systolic blood pressure) and the intracranial pressure (ICP) as shown in the following equation:
Cerebral perfusion pressure = mean arterial pressure - intracranial pressure.
The cerebral perfusion pressure is usually maintained above 70 mmHg.
In severe traumatic brain injury, the autoregulation of cerebral blood flow is lost.
Cerebral oxygen consumption should be minimised following head injury (not maximised).
GCS
The Glasgow coma score (GCS) provides a score from 3 to 15, depending on the best response observed in three different parameters. The minimum score is 1 in each of these.
• Eye opening
• Verbal response
• Motor response.
The pupil response to light is not included.
The GCS was originally developed for use in brain trauma but is now used when evaluating other cerebral insults.
A modified version is used in young children.
Hypovolaemic shock
CVP pressure is reduced
False:
Hypovolaemic shock occurs when the intravascular volume is depleted as a consequence of blood or fluid loss.
The commonly encountered haemodynamic findings include
• A decrease in stroke volume, cardiac output and filling pressures (that is, central venous pressure and pulmonary capillary wedge pressure)
• An increase in heart rate and systemic vascular resistance.
Invasive arterial measurement complication
False aneurysms Complications of arterial cannulation include • Haematoma formation • Distal ischaemia • Infection • Embolisation • False aneurysm • Arteriovenous fistula • Blood loss. Flush volumes must be limited in children, otherwise fluid overload may occur. Replacing the pressure bag with a syringe pump may provide some protection against such an occurrence.
Inappropriate cannulation site
Brachial artery
Commonly used sites for the insertion of arterial cannulae include the radial, femoral, axillary and dorsalis pedis arteries.
Short catheters should be used for the radial and dorsalis pedis arteries.
Longer, softer and more flexible cannulae should be used for the femoral and axillary arteries (to minimise injury).
The brachial artery should be avoided because the collateral circulation is limited.
ARDS
ARDS is diagnosed when all the following are present
• Acute onset of impaired oxygenation
• Severe hypoxia where the paO2:FiO2 ratio is
Life threatening asthma features
Asthma may be classified as 1. Moderate exacerbation 2. Acute severe 3. Life-threatening 4. Near fatal. The features of life-threatening asthma are • A peak expiratory flow rate (PEFR)
Metabolic acidosis causes
The causes of a metabolic acidosis include
• Renal failure
• Gastrointestinal bicarbonate loss
• Drug poisoning (for example, salicylates, diabetes mellitus, starvation and lactic acidosis).
The other options all cause a metabolic alkalosis (hyponatraemia/kalaemia, calcium antacids, hypochloraemia)
Increased pulmonary capillary wedge pressure
Fluid overload and left ventricular failure (LVF) cause an increase in pulmonary capillary wedge pressure (PCWP).
The PCWP may misrepresent the left ventricular end-diastolic pressure (LVEDP) in
• Pulmonary venous obstruction (pulmonary fibrosis, vasculitis, atrial myxoma)
• Valvular heart disease (mitral stenosis, mitral regurgitation and aortic regurgitation).