SHOCK

Question 1

Definition of shock

Answer 1

State of inadequate cellular energy production.

Question 2

Most common cause of shock? (Broad)

Answer 2

Shock is most commonly seen when delivery of oxygen to tissues (DO2) does not meet their oxygen requirement.

VO2 > DO2

where VO2 represents oxygen consumption and DO2 represents oxygen delivery.

Question 3

what does oxygen delivery depend on? (include equation)

Answer 3

Tissue perfusion and oxygen content of blood.

Expressed as DO2 = Q x CaO2

(Q represents flow and CaO2 represents blood oxygen content).

Under normal circumstances, the body has a physiological reserve that allows DO2 to fall without causing a decrease in VO2 and vice versa. This means that in times of increased oxygen requirement (e.g. increased metabolic rate) or decreased oxygen delivery (e.g. mild anaemia); the tissues still receive adequate oxygen for aerobic metabolism. This holds true up to a critical point known as DcO2 (critical DO2), when the cell can no longer compensate and anaerobic glycolysis must occur to support cellular energy requirements. Anaerobic glycolysis results in the production of far fewer ATP (adenosine triphosphate) moles than aerobic metabolism. Anaerobic metabolism also results in the production of excess hydrogen ions thus results in a metabolic acidosis. Eventually ATPase pumps fail; there is disruption to the structure and function of the cell with release of intracellular calcium and free radical production.

Question 4

What is blood oxygen content (include equation)

Answer 4

(CaO2) is the total amount of oxygen carried by the blood i.e. the sum of haemoglobin carried oxygen and dissolved oxygen (PaO2). It is calculated by the following equation: CaO2 = ([Hb] x SaO2 x 1.34) + (0.003 x PaO2)

Question 5

Describe blood oxygen content equation

Answer 5

CaO2 = ([Hb] x SaO2 x 1.34) + (0.003 x PaO2) where CaO2 is measured in mL/dL SaO2 is the percentage saturation of haemoglobin with oxygen [Hb] is the blood concentration of haemoglobin 1.34 is the approximate mL of oxygen that each gram of haemoglobin carries 0.003 is the mL of oxygen dissolved in each dL of blood for each mm Hg PO2.

Question 6

How is shock classified?

Answer 6

Many different types of classifications system exist . In addition, a critical patient may have more than one type of shock going on within the body.

Patients with septic shock may be suffering hypovolaemic shock, distributive shock, metabolic shock, and cardiogenic shock concurrently.

Regardless of the classification, various types of shock may share many characteristics.

Question 7

D hypovolaemic shock?

Causes of?

Pathophys?

Answer 7

Hypovolaemic shock occurs secondary to a decrease in circulating blood volume.

Causes of hypovolaemic shock

• haemorrhage (often termed haemorrhagic shock)
• severe dehydration
• loss of fluid into third spaces and loss of plasma secondary to severe burns.

A fall in intravascular volume stimulates the aortic and carotid body baroreceptors.

They transmit neural signals to the vasomotor centre of the medulla oblongata, which acts to inhibit the parasympathetic nervous system and stimulates the sympathetic nervous system.

This causes vasoconstriction and an increase in heart rate and contractility.

Preferential shunting of blood occurs to the vital organs such as the brain and heart and away from the gastrointestinal tract, muscles and skin.

Sympathetic catecholamines and decreased renal blood flow cause release of renin from the juxtaglomerular apparatus in the kidney.

This stimulates the renin-angiotensin-aldosterone system. Angiotensin II causes vasoconstriction, stimulates the release of aldosterone from the adrenal glands and stimulates noradrenaline release from the adrenal gland and sympathetic neurons.

Hypovolaemia also leads to the release of vasopressin (ADH) from the posterior pituitary. Vasopressin also acts on V1 receptors located on the endothelial cells causing vasoconstriction.

Vasopressin also acts on V2 receptors in the kidney ensuring reabsorption of water. These compensatory mechanisms, which aim to restore effective circulating volume and to maintain blood flow to vital organs, may be sufficient to prevent progression of shock.

However if ongoing volume loss occurs hypovolaemic shock ensues and can progress into decompensated or terminal shock. Note: Baroreceptor activation leads secretion of high concentrations of vasopressin/ADH – these high concentrations activate V1 receptors causing powerful vasoconstriction. A lower amount of vasopressin/ADH is secreted when osmoreceptors are activated – these low concentrations activate the V2 receptors without activating the V1 receptors.

Question 8

3 phases of hypovolaemic shock?

Answer 8

Traditionally, hypovolaemic shock has been broken up into three phases. Categorisation in this way can help with clinical recognition and understanding of the body’s response to hypovolaemic shock. In reality, these phases are not distinct at all but represent parts of a continuum.

1. Early/compensated/hyperdynamic shock
2. Early decompensated
3. Decompensated/terminal shock

Question 9

Desc early compensatory shock

Answer 9

Early/compensated/hyperdynamic shock

Clinical signs in this stage may be subtle.

Cardiac output and tissue oxygen consumption are higher as increased catecholamines cause a hypermetabolic state. Heart rate is increased, membranes are red, CRT is < 1 sec, blood pressure can be normal or increased and pulses may be taller and narrower than normal.

The hyperdynamic stage of shock may be mistaken for nervousness or excitement upon entering the veterinary clinic however; patients in this stage of shock have a quiet demeanor and may have a look of anxiety on their faces.

Question 10

Desc decompensatory shock

Answer 10

In this phase DcO2 has been reached and so anaerobic metabolism is occurring. Sympathetic output has reached its maximum. Heart rate is increased, mucous membranes are pale (due to maximum peripheral vasoconstriction), CRT is prolonged (> 2 sec), pulses have become short and narrow, extremities and skin are cool to touch and rectal temperature is low. The patient becomes increasing dull and weak. Blood pressure measurements are low. Arterial hypotension is systolic arterial pressure of less than 90 mm Hg or mean arterial pressure of less than 70 mm Hg.

Question 11

desc decompensatory/terminal shock

Answer 11

This is the final, and usually irreversible, stage of shock. The brain and heart are experiencing hypoxia and cell death. Cerebral hypoxia causes depression of central respiratory and neural centres. Myocardial hypoxia and poor sympathetic tone cause decreased contractility. Blood pooling occurs at the peripheries resulting in decreased preload. Mucous membranes are pale, CRT is non-existent, pulses are absent or extremely weak. Patients are stuporous or comatose, bradycardic, hypotensive and hypothermic. Patients may be oliguric or anuric and may develop pulmonary oedema.

Question 12

Define distributive shock

Answer 12

Distributive shock results from a maldistribution of blood volume.

Question 13

Causes of distributive shock

Answer 13

Causes of distributive shock include sepsis, anaphylaxis, gastric-dilation volvulus (GDV), obstruction (saddle thrombus, heartworm disease), trauma and pneumothorax. This encompasses a large cohort of differing diseases capable of causing shock. While the pathophysiology of the underlying disease may vary, all cause a maldistribution of blood within the vascular system that leads to tissue hypoperfusion.

Question 14

Pathophysiology of septic shock?

Answer 14

In septic shock this is generally caused by a lack of vasomotor tone and pooling of blood within the vasculature. Gastric dilation results in compression of the inferior vena cava thus reducing venous return to the heart (this is sometimes called obstructive shock). This is the same mechanism by which pneumothorax can cause distributive shock. Pericardial effusions prevent right atrial filling thereby reducing preload. This condition falls into the two categories of shock: distributive shock and cardiogenic shock. Anaphylaxis results in widespread vasodilation and increased vascular permeability resulting in profound hypotension and thus distributive shock.

Question 15

Define septic shock and clinical findings

Answer 15

Septic shock is defined as acute circulatory failure and persistent arterial hypotension despite fluid resuscitation. Septic shock is complex and involves dysregulation of vasomotor tone, increased vascular permeability, dysfunctional microcirculation and impaired cellular oxygen utilisation. This is propagated by inflammatory cytokines released secondary to an infectious insult. The initial hyperdynamic phase is characterised by red or injected mucous membranes, a fast CRT (< 1 sec), bounding pulses (tall and narrow pulses), tachycardia and fever. If left untreated, hyperdynamic septic shock can progress to hypodynamic septic shock with reduced cardiac output and signs of hypoperfusion. Clinically, patients have pale or icteric mucous membranes, increased heart rate, prolonged CRT, poor pulse quality, hypothermia and dull mentation.

Question 16

How do cats differ from dogs in presentation of septic shock?

Answer 16

Cats differ from dogs in their presentation of septic shock and rarely present in hyperdynamic shock. Their heart rate is often decreased, membranes are generally pale or icteric, CRT is prolonged, and pulses tend to be weak and hard to feel. Cats generally tend to be hypothermic and often present weak and collapsed. Septic cats may appear clinically similarly to neuromuscular paralysis because of their extreme weakness.

Question 17

Define cardiogenic shock Common causes?

Answer 17

Cardiogenic shock is due to a decrease in forward flow from the heart. Causes of cardiogenic shock include congestive heart failure (valvular disease, dilated cardiomyopathy, restrictive or hypertrophic cardiomyopathy), severe brady or tachyarrhythmias and cardiac tamponade.

Question 18

Pathophysiology of cardiogenic shock?

Answer 18

Cardiogenic shock is shock secondary to cardiac dysfunction. This usually occurs with adequate or increased intravascular volume. Systolic dysfunction (dilated cardiomyopathy), diastolic dysfunction (hypertrophic cardiomyopathy) and severe arrhythmias such as third degree AV block, supraventricular tachyarrhythmias (SVT) or ventricular tachyarrhythmias (VT) can all cause reduced stroke volume, reduced cardiac output and thus cardiogenic shock.

Question 19

Clinical findings of cardiogenic shock?

Answer 19

Patients with cardiogenic shock have signs consistent with tissue hypoperfusion (low blood pressure, increased lactate, low temperature and pale mucous membranes) and may also present dyspnoeic due to increased pulmonary venous pressure resulting in pulmonary oedema. Treatment of cardiogenic shock is dependent on the underlying disease with the aim being to improve cardiac function and normalise cardiac output.

Question 20

Define metabolic shock Causes of?

Answer 20

Metabolic shock results from deranged cellular metabolism. Causes of metabolic shock include cytopathic hypoxia of sepsis, mitochondrial dysfunction, hypoglycaemia and cyanide toxicity.

Question 21

pathophys of metabolic shock?

Answer 21

This is a unique form of shock in that both tissue perfusion and arterial oxygen content of blood are adequate yet the cell is unable to meet energy requirements. Metabolic shock is generally secondary to intracellular or mitochondrial dysfunction which causes interruption of normal cellular metabolism. This is suspected to be a major contributing factor to septic shock. The brain is an obligate user of glucose for adequate energy production. It follows that hypoglycaemia leads to inadequate neuronal energy production. Neuronal dysfunction in the face of hypoglycaemia leads to a form of metabolic shock.

Question 22

Pathophysiology of cyanide toxicity?

Answer 22

Cyanide toxicity causes metabolic shock by disrupting normal mitochondrial oxidative phosphorylation. This means that anaerobic glycolysis will take place despite adequate DO2.

Question 23

Diagnosis of metabolic shock?

Answer 23

Aside from cyanide toxicity and hypoglycaemia it can be very difficult to diagnose or test for metabolic shock. Diagnosis is based on clinical suspicion and treatment is aimed at treating the underlying disease while optimising tissue perfusion and oxygen content.

Question 24

Define hypoxaemic shock

Answer 24

Hypoxaemic shock occurs secondary to decreased oxygen content of arterial blood. Any mechanism reducing blood oxygenation or the oxygen carrying capacity of blood can thus result in hypoxaemic shock.

Question 25

Causes of hyperaemic shock?

Answer 25

Causes of hypoxemic shock include severe anaemia, severe pulmonary disease, carbon monoxide toxicity and methaemoglobinaemia. States of hypoxaemic shock are characterised by normal tissue perfusion but abnormal oxygen content or oxygen unloading to the tissues and cells. Anaemia results in a fall in oxygen carrying capacity of blood due to reduction in haemoglobin. Severe pulmonary disease causes decreased oxygenation of arterial blood. Carbon monoxide competitively binds to haemoglobin at the same sites as oxygen but with an affinity that is 230-270 times that of oxygen and is thus capable of causing a marked hypoxaemic shock. Methaemoglobin is haemoglobin which contains iron that has been oxidised to its ferric state (Fe+3). Methaemoglobin is incapable of carrying oxygen and levels greater than 20% can lead to cellular hypoxia. The most common cause of methaemoglobinaemia in small animal practice is paracetamol toxicity.

Question 26

Pathophys of hyperaemic shock?

Answer 26

States of hypoxaemic shock are characterised by normal tissue perfusion but abnormal oxygen content or oxygen unloading to the tissues and cells. Anaemia results in a fall in oxygen carrying capacity of blood due to reduction in haemoglobin. Severe pulmonary disease causes decreased oxygenation of arterial blood. Carbon monoxide competitively binds to haemoglobin at the same sites as oxygen but with an affinity that is 230-270 times that of oxygen and is thus capable of causing a marked hypoxaemic shock. Methaemoglobin is haemoglobin which contains iron that has been oxidised to its ferric state (Fe+3). Methaemoglobin is incapable of carrying oxygen and levels greater than 20% can lead to cellular hypoxia. The most common cause of methaemoglobinaemia in small animal practice is paracetamol toxicity.

Question 27

Treatment of hyperaemic shock?

Answer 27

Treatment aimed at increasing oxygen content of blood and is dependent on the underlying cause of the hypoxaemia. Treatment would be red cell transfusion in the case of hypoxaemic shock secondary to anaemia, acetylcysteine administration in the case of paracetamol toxicity or oxygen in the case of carbon monoxide toxicity.

Question 28

Fluffy the collapsing Maltese with IMHA has a PCV/TS = 11%/75 g/L How can we categorise Fluffy’s shock?

Answer 28

Fluffy has hypoxaemic shock due to his severe anaemia. Fluffy has no reason to be hypovolaemic, most IMHA patients will be euvolaemic unless their medication is making them vomit. He is not likely to be in distributive shock unless he has developed systemic inflammatory response syndrome or sepsis.

Question 29

Desc treatment of a hypotensive shock patient

Answer 29

The effective treatment of a patient in advanced shock requires identification of immediate life-threatening issues followed by a coordinated team response that allows many treatment and monitoring steps to occur simultaneously. 1. Oxygen supplementation – treat hypoxaemia When an unstable patient first arrives oxygen supplementation, via flow-by or mask, should be administered while the patient is being further evaluated. Oxygen supplementation in this way will not harm the patient if it is not necessary. Only when it has been confirmed that the patient is oxygenating adequately, without excessive respiratory effort, is this oxygen support discontinued. Aside from provision of oxygen and correction of anaemia, all other forms of treatment for shock aim to improve perfusion to the tissues. Intravenous fluid therapy is used in order to ensure adequate preload and thus improve MAP. 2. Achieve vascular access Immediately place a wide bore venous catheter. The larger the radius of the catheter being used, the faster that fluid can be infused through it. For this reason, use the largest gauge catheter that can be inserted without damaging the vein. Very large dogs may require two IV catheters inserted in order to give the volume and rate of fluid required for treatment of shock. Establishing venous access also enables collection of blood for a minimum database. Full bloods can be drawn at this stage if appropriate; however, in severely compromised patients this may not be possible. It can be very hard to gain intravenous access in cats or very small dogs that are in shock. Cats in particular can be very hard to catheterise when they are in shock. Consider using either the jugular or medial saphenous veins, as they are much larger than the cephalic veins. If catheterising the jugular for the purpose of emergency venous access, use a large bore IV catheter and insert towards the heart. The catheter hub can then be rapidly secured to the skin with a fast drying glue such as Superglue. Another option for small or pediatric patients is to place an intraosseous catheter. In very small or pediatric patients, a regular hypodermic needle can be used; in other patients, a bone marrow needle or an intraosseous access device such as the EZ-IO can be used. Once the patient’s cardiovascular dynamics have improved, you can then place an IV catheter in the cephalic vein if necessary. Occasionally percutaneous intravenous catheterisation is unable to be achieved. A cut down procedure may be required in order to expose the vein prior to catheterisation. When a patient is in shock, this procedure is performed rapidly and without anaesthetic. Once the patient has adequate perfusion, any intraosseous catheters or intravenous catheters that were placed via a cut down should be replaced with percutaneous intravenous catheters if possible. 3. IVFT - treat hypovolaemia and improve preload Isotonic crystalloids are the fluids of choice for treatment of shock in the majority of cases. The shock dose of IV crystalloids is 60-90 mL/kg in the dog and 45-60 mL in the cat. [These doses reflect the approximate blood volumes of these species.] The shock dose is generally the maximum amount of fluid that will be required to be given in an hour. The effective volume required in order to stabilise a patient will depend on the degree of hypotension, the aetiology of shock and other comorbidities such as cardiac disease. With this in mind, the shock dose is administered in aliquots. Boluses of 10- 20 mL/kg over 15-20 minutes are used while perfusion parameters are continuously assessed in order to determine the need for ongoing fluid therapy. Fluid rates are slowed or discontinued if perfusion parameters normalise or if hypervolaemia is suspected. If a patient is receiving fluid boluses for shock but is failing to respond appropriately, early use of vasopressors such as noradrenalin may prevent fluid overloading. Hypovolaemia that persists after a full shock dose of fluid therapy warrants rapid investigation. For example, a trauma patient that is not responding to appropriate fluid resuscitation requires close assessment for ongoing haemorrhage. In such a patient further resuscitation with blood products and the use of damage-control surgery is required. 4. Transfusion therapy – treat anaemia Patients presenting in severe haemorrhagic shock may require immediate transfusion. If blood products are not immediately available, IV crystalloids should be initiated. Blood loss can be replaced with whole blood or component therapy i.e. packed red blood cells (PRBC) and plasma. Transfusions are ideally cross-matched and administered in a controlled manner. However when a haemorrhaging patient is unstable and at risk of life threatening anaemia, then the usual transfusion protocols may not be in the patient’s best interest. The emergency clinician has to judge what will be more life threatening to the patient: a transfusion reaction or the anaemia. When death due to haemorrhagic shock is imminent, administration of an unmatched transfusion may be required. Standard doses of PRBCs and/or plasma and of whole blood are 10-20 mL/kg and 20-30 mL/kg respectively. However, the final volume administered will depend on response to therapy with some patients requiring far greater volumes to in order to stabilise their shock. The aim should be to keep the haematocrit to a minimum of 20%, or 25% if patients are to undergo surgery. 5> Gradual warming Patients presenting hypothermic and in shock should NOT be warmed until they are cardiovascularly stable. Warming of a patient in shock will cause peripheral vasodilation and could precipitate further cardiovascular instability. Once a patient’s hypotension has been rectified, gradual warming to achieve a normal temperature is beneficial. The exception to this rule is the traumatic brain injury patient. All the same, these patients should not be left to shiver. Shivering increases a patient’s metabolic rate and thus oxygen consumption.

Question 30

Use of synthetic colloids in resuscitation?

Answer 30

The use of colloids in resuscitation is controversial. Multiple trials in human medicine have failed to find benefit in the use of colloids over crystalloids for resuscitation1. Along with the discovery of the the potential deleterious effects of synthetic colloids such as injury to the kidneys and detrimental effects on coagulation their use for fluid resuscitation is hard to justify.

Question 31

Use of HTS in resuscitation?

Answer 31

Hypertonic Saline If low volume resuscitation is required, the use of hypertonic saline (HTS) can be considered. Administration of 3-5 mL/kg of 7% hypertonic saline over 10-15 minutes can result in rapid rises in intravascular volume due to the increased osmotic draw of fluid from the interstitial into the intravascular compartment. The effect will be transient, as the sodium will equilibrate across the endothelium, however this temporary improvement in cardiovascular stability may prove lifesaving in the emergency setting. Along with causing rapid increases in intravascular volume, hypertonic saline is also thought to reduce endothelial cell swelling, modulate inflammation, increase cardiac contractility, cause mild peripheral vasodilation and decrease intracranial pressure. Hypertonic saline may be advantageous for those patients in shock with head trauma as it acts to reduced intracranial pressure. Even so, a randomised controlled trial in human patients that compared resuscitating severe brain injury patients with HTS or Hartman’s did not establish a survival benefit with the use of HTS2. Use of HTS should always be followed with use of crystalloids and serum sodium concentration should be monitored. Contraindications to HTS use include dehydrated patients and hypernatraemic or hyperosmolar patients.

Question 32

When would you consider vasopressor resuscitative therapy?

Answer 32

Vasopressors – treat maldistribution of blood flow and improve MAP If a patient remains hypotensive despite intravascular volume resuscitation, treatment with vasopressors is recommended. Vasopressor therapy aims to correct hypotension via vasoconstriction. Mean arterial pressure, which is an indicator of tissue perfusion, is a product of cardiac output and systemic vascular resistance. MAP = CO x SVR where MAP = mean arterial pressure, CO = cardiac output, SVR = systemic vascular resistance Vasopressor therapy is used to manipulate systemic vascular resistance when hypotension persists despite adequate volume resuscitation. • Noradrenaline, adrenaline, dopamine and vasopressin are the most commonly used vasopressors. Noradrenaline and adrenaline are catecholamines that act on adrenergic receptors to cause vasoconstriction. • Dopamine acts on dopaminergic and adrenergic receptors. There is individual variation in response to the vasoconstricting effects of dopamine so its effects may not be reliable. • Vasopressin is a potent vasoconstrictor acting on V1 receptors in the endothelium.

Question 33

Recommendations on the use of vasopressors in resuscitation - types, first, second, third line?

Answer 33

Current surviving sepsis guidelines3 advocate the use of noradrenaline as a first line vasopressor. Noradrenalin activates the alpha-1 adrenergic receptors. It is a rapid acting, powerful vasoconstrictor. It needs to be administered as a constant rate infusion (CRI). The dose for Noradrenalin is 0.1-2 μg/kg/min. Start at the lower end of the range and titrate up as required. Vasopressor therapy is used to manipulate systemic vascular resistance when hypotension persists despite adequate volume resuscitation. • Noradrenaline, adrenaline, dopamine and vasopressin are the most commonly used vasopressors. Noradrenaline and adrenaline are catecholamines that act on adrenergic receptors to cause vasoconstriction. • Dopamine acts on dopaminergic and adrenergic receptors. There is individual variation in response to the vasoconstricting effects of dopamine so its effects may not be reliable. • Vasopressin is a potent vasoconstrictor acting on V1 receptors in the endothelium.

Question 34

Role of +ve inotropes in resuscitative therapy? How do you determine if your patient needs positive inotropic therapy? What will you use? Why?

Answer 34

Positive Inotropes Treat Poor Cardiac Contractility Adequate cardiac output (and thus tissue perfusion) requires adequate stroke volume. CO = SV x HR where SV = stroke volume, HR = heart rate, CO = cardiac output Stroke volume is determined by preload, afterload and contractility. The use of positive inotropes aims to increase cardiac contractility and thus optimise cardiac output. Therapy of choice in cardiogenic shock secondary to systolic failure such as dilated cardiomyopathy. Systolic failure can occur secondary to sepsis induced myocardial dysfunction, severe acidosis or alkalosis, drug administration or toxin exposure. Ultrasound examination of the heart can allow evaluation of cardiac contractility (via measurements of fractional shortening) and therefore may provide guidance on the use of inotropic therapy. Dobutamine is the inotropic drug of choice. It is a beta-1 adrenergic agonist with some beta-2 and alpha-2 activity. Dobutamine must be used as a constant rate infusion as its effects are short acting. This can also allow a reasonably safe therapeutic trial. The dose for dobutamine is 2-20 μg/kg/minute in the dog and 2-10 μg/kg/minute in the cat. If there is uncertainty as to whether hypotension is secondary to myocardial systolic dysfunction or decreased systemic vascular resistance it would be appropriate to first trial dobutamine. An improvement in blood pressure can validate its use however if no improvement is seen, the patient should be reassessed and alternative therapies considered.

Question 35

Define cardiogenic shock and PE findings that may alert you to its possibility?

Answer 35

Cardiogenic shock occurs secondary to diastolic or systolic failure of the heart. Early recognition of patients in cardiogenic shock is vital, as treatment is unique for this subset of patients compared to other forms of shock. Shock occurs in these patients due to failure of the cardiac pump and often these patients have increased intravascular volume despite being hypotensive. The following findings in addition to signs of shock should alert you to the possibility of cardiogenic shock: • respiratory distress without history of a trauma, choking, drowning or coagulopathy • a cardiac murmur • a cardiac arrhythmia • muffled heart • pulsus paradoxus

Question 36

Treatment considerations in cardiogenic shock?

Answer 36

Patients in cardiogenic shock are particularly fragile and great care should be exercised in handling to minimise stress. Oxygen should be administered immediately in the least stressful manner. Flow-by, mask, hood, nasal prongs and oxygen cages can all be used. Minimise movement and stress. Stabilisation must take precedence over diagnostic testing. If a patient’s anxiety is contributing to increased oxygen consumption, an anxiolytic is indicated. Low dose butorphanol (0.05 mg/kg IV/IM) is cardiovascularly sparing and the dose can be titrated up as required. Treatment of cardiogenic shock is aimed at increasing forward flow and reducing backward congestion.

Question 37

Desc treatment of systolic failure in cardiogenic shock

Answer 37

Systolic failure (e.g. secondary to dilated cardiomyopathy) requires treatment with inotropes such as dobutamine.

Question 38

Desc mainstay of treatment in CHF

Answer 38

• For patients in congestive failure diuretic therapy is the mainstay of treatment

Question 39

Disc rate control in cardiogenic shock

Answer 39

Reduce the heart rate of tachyarrhythmias by using anti-arrhythmic therapy such as lignocaine or diltiazem Increase the heart rate in bradyarrhythmias if possible with the use of atropine, glycopyrrolate or isoproterenol..

Question 40

D bacterial translocation

Answer 40

Bacterial translocation – the passage of viable bacteria from within the gastrointestinal tract to other sites in the body

Question 41

D Krebs cycle

Answer 41

Citric acid cycle/Krebs cycle – the series of biochemical reactions that take place in order to generate energy from acetyl-CoA. Acetyl Co-A is cleaved by pyruvate dehydrogenase from pyruvate (in the presence of oxygen). Pyruvate is a product of glycolysis.

Question 42

D cytopathic hypoxia

Answer 42

Cytopathic hypoxia – diminished oxidative phosphorylation despite adequate availability of oxygen

Question 43

What is a free radical?

Answer 43

Free radical – a molecule or atom that has an unpaired electron. Free radicals are highly reactive.

Question 44

What is the juxtaglomerular apparatus?

Answer 44

Juxtaglomerular apparatus – the juxtaglomerular cells of the glomerular afferent arteriole and the macula densa cells of the distal convoluted tubule combine to form the juxtaglomerular apparatus. Macula densa cells give the juxtaglomerular cells information about sodium concentration and flow rate in the distal tubule. Juxtaglomerular cells excrete renin in response to reduced sodium concentration and reduced flow rate as measured by the macula densa.

Question 45

Define plethysmogram and plethysmograph

Answer 45

Plethysmogram – the tracing made by a plethysmograph Plethysmograph - a machine that measures variation of volume (such as pulse waves) within the body

Question 46

Define pulsus paradoxus

Answer 46

Pulsus paradoxus - a variation in pulse pressure that occurs with breathing. Pulsus paradoxus commonly occurs with pericardial tamponade

Question 47

Define stuporous

Answer 47

Stuporous – affected by stupor and thus arousal only with vigorous stimulation

Question 48

Define septic shock

Answer 48

Septic shock – hypotension in a septic patient that is persistent despite resuscitation with fluids

Question 49

D Type A & Type B hyperlactataemia

Answer 49

Type A hyperlactataemia – an increased serum lactate concentration as the result of increase anaerobic glycolysis that has occurred due to a pathological deficiency in oxygen delivery to the cells Type B hyperlactataemia – an increased serum lactate concentration that has an aetiology that is not that of Type A hyperlactataemia