ICP shock

Anaphylactic shock: - Management - Talk to administration of steroids by healthcare personnel - Talk to adrenaline adminsitration - Back up - Transport

- Comfortable positioning - patient's in anaphylaxis can deteriorate if made to sit/stand up due to the risk of a postural drop in BP - Call for RSI back-up early, particularly if there are signs of upper airway oedema (airway compromise), severe respiratory distress (breathing compromise), GCS ≤10, rapid deterioration despite IM adrenaline - O2 if indicated - Large bore IV access - Adrenaline: • If the patient has angioedema, stridor or bronchospasm in association with anaphylaxis, or if patient is not improving following adrenaline IM, these are an indication for adrenaline IM (or IV in the latter case), not nebulised adrenaline • IM: adults (0.5mg IM). Paediatrics (0.01mg/kg). Repeat adrenaline IM every 10mins if the patient is not improving, or earlier if the patient is deteriorating • If the patient is deteriorating despite adrenaline IM, administer adrenaline IV: adult (infusion pump: start at 0.5mg/hr, and adjust as required. Infusion: 1mg/1L (1:1,000,000 solution - 0.001mg/ml) start at 2 drops/sec and adjust rate as required. Bolus: 10ml (0.01mg) of a 1:1,000,000 solution (0.001mg/ml) every 1-2mins as required). Paediatrics 5-14yo (infusion pump: start at 0.25mg/hr, and adjust as required. Infusion: 1mg/1L (1:1,000,000 solution - 0.001mg/ml) start at 1 drop/sec and adjust rate as required. Bolus: 0.0002mg/kg of a 1:1,000,000 solution (0.001mg/ml) every 1-2mins as required). Paediatrics <5yo (bolus: 0.0002mg/kg of a 1:1,000,000 solution (0.001mg/ml) every 1-2mins as required). - IV fluids if patient has signs of hypovolaemia or poor perfusion: • Adults: 1L • Paediatrics: 20ml/kg. • Administer further doses as required. - Anti-histamines and steroids have no role during the acute treatment of anaphylaxis. However, following treatment, if all signs of systemic anaphylaxis have disappeared and the patient has a prominent itch (rare for this to occur), administer: • Loratadine: >40kg (10mg PO). Paediatrics >5kg (aged 1) to 30kg (5mg PO) • Prednisone/prednisolone: adults (40mg PO). Paediatrics (syrup 1mg/kg PO). Additional treatment: There is no use for anti-histamines or steroids in the acute treatment of anaphylaxis. It is rare for a patient to meet the criteria for administration of anti-histamines or steroids following anaphylaxis. Promethazine (Phenergan) administration by other healthcare providers should be strongly discouraged because it does not treat anaphylaxis and it causes sedation and hypotension. Adrenaline: Have a low threshold to administer adrenaline if anaphylaxis is suspected, even if it is not immediately life-threatening. The risk of death is increased in patients whose need for adrenaline (or repeat adrenaline) is under-recognised. Have a low threshold for repeat adrenaline. A dose of 0.5mg IM is appropriate for the majority of adults, but ILS/ICP may make the decision to reduce the dose, particularly if the patient is small, frail, or has IHD. IV adrenaline infusion is preferred over IV boluses as this decreases the risk of sudden surges of adrenaline. Back-up: Consider RSI, particularly if there are: - Signs of airway or breathing compromise - GCS ≤10 - Rapid deterioration despite IM adrenaline. Transport All patients' receiving tx for anaphylaxis should be given a firm recommendation to be transported to a medical facility via ambulance. Transport should be to ED, unless all the following are met: - Has previously had anaphylaxis - Has rapidly improved with a single dose of IM adrenaline - Is being taken to a primary care facility with the capacity to observe them for several hours.

Presentation of cardiogenic shock

- Cool, pale, clammy skin (hypoperfusion and vasoconstriction) - Weak/absent radial pulses - Tachycardia - Tachypnoea - PO with crackles/rales heard on auscultation - Hypotension (late) with decreased MAP - Narrow PP - JVD - Cyanosis (due to stagnation of blood flow through capillaries and increased extraction of O2 from haemoglobin as it passes through the capillary bed) - Altered LOC - Dysrhythmias and signs of myocardial ischaemia.

Sepsis to septic shock pathophysiology

A localised infection is provoked by a microorganism (usually a bacteria, but may be a virus, fungus, or parasite) invading a normally sterile part of the body. When this localised infection becomes widespread, dysregulated, and uncontrolled, sepsis ensues. Sepsis describes a widespread immunological host response to a presumed or confirmed site of infection, wherein the body's immune response begins to involve healthy tissue remote to the initial site of infection, resulting in a malignant, dysregulated, uncontrolled systemic intravascular inflammatory process (i.e. SIRS). Sepsis does not occur secondary to the inflammatory process posed by trauma or burns, however if infection spreads into wounds or burns, then sepsis may ensue. This emphasises that sepsis is an immunologically induced inflammatory process. Left untreated, sepsis can develop into septic shock and MODS. Septic shock is a subset of sepsis, in which underlying circulatory, and cellular and metabolic abnormalities, are profound enough to substantially increase mortality. When sepsis with hypotension persists, requiring vasopressors to maintain a MAP over 65mmHg and serum lactate over 2mmol/L despite adequate volume resuscitation, septic shock has developed. If septic shock is left untreated, then end-stage organ dysfunction can ensue, and the risk of mortality increases to over 40%. Septic shock is described as a type of distributive shock because it is associated with vasodilation, increased permeability of blood vessels (with loss of intravascular volume), and impaired cardiac function. All of the below highlights a normal immune response to eradicate infections, however, in overabundance, these mechanisms constitute SIRS and can result in shock due to profound peripheral vasodilation, peripheral pooling of blood, and decreased intravascular volume. This causes anaerobic metabolism, organ hypoperfusion, ischaemia, hypoxaemia, metabolic acidosis and inadequate organ function. Consequently, MODS in addition to signs of shock constitutes septic shock. The predominant components integral to the immune systems reaction to infection are cytokines, activated complement, and activated coagulation factors. This ultimately causes aberrant leukocyte activation and their recruitment into host tissue, with subsequent breakdown of the vascular endothelium. This causes a widespread, malignant intravascular immunological inflammatory response, that exceeds the borders of the initial local infection site. Cytokines: When bacteria or their breakdown products (i.e. endotoxins) are present in the circulation, they become engulfed by leukocytes, tissue macrophages, and by huge granular lymphocytes. When these bacterial products are digested as past of the immune response, this stimulates dendritic cells, macrophages, mast cells, helper T lymphocytes, and endothelial cells to release cytokines. Cytokines are signalling molecules that predominantly act locally, either on the producing cell itself or on neighbouring cells. Cytokines integral to the inflammatory process triggered by sepsis include: - Interleukin 1 (IL-1) - Interleukin 6 (IL-6) - Tumor necrosis factor alpha (TNFα) - Interferons (which inhibit replication of viruses, and are thus known as an antiviral). Cytokines, in addition to endotoxins, recruit, activate, and proliferate inflammatory leukocytes to amplify the pro-inflammatory response to infection. When cytokines are manufactured in large quantities (i.e. during sepsis), they are swept into the circulation and cause a systemic reaction, causing collateral damage and death of host cells and tissues. TNFa and IL-1: TNFα (produced from activated macrophages) and IL-1 (produced from activated macrophages, neutrophils, endothelial cells, and epithelial cells) are the two major cytokines that mediate inflammation. They: - Increase the plasma concentration of hepatic acute phase reactant proteins (procalcitonin and C reactive protein (CRP), which are produced by the liver). This ultimately results in some of the hallmark symptoms of infection, including fever, anorexia, malaise, and lethargy by: • Playing a role in blood coagulation, defence against infection, the transportation of metabolites, nutrients, and hormones, and the maintenance of homeostasis • Contributes to skeletal muscle catabolism (to provide amino acids that can be used during the immune response and for tissue repair) • Elevates erythrocyte sedimentation rate (ESR), and increased numbers of erythrocytes - As TNFα and IL-1 levels increase during sepsis, so too do the levels of plasminogen activator inhibitor-1 (PAI-1), which is synthesised by vascular endothelial cells and hepatocytes. PAI-1 plays an important role in the regulation of fibrinolysis because it inhibits plasminogen activator, which is a key enzyme involved in the breakdown of plasminogen to plasmin (which dissolves the fibrin of blood clots). This in turn: • Inhibits fibrinolysis (the enzymatic breakdown of the fibrin in blood clots). The build up of fibrin clots causes direct endothelial injury, resulting in the release of tissue factor (from monocytes, macrophages and the vascular endothelium), which triggers marked activation of the coagulation cascade • Elevated PAI-1 levels are a risk factor for thrombosis, including DIC, stroke, MI, and PE, because dissolution of multiple end-organ microthrombi becomes more difficult. This may be detrimental, because it contributes to microcirculatory impairment, which causes local perfusion defects, resulting in tissue hypoxia, and eventually MODS. Complement cascade: Cytokines also activate the complement system, which is a sequential set (i.e. a cascade) of protein activations that enhances (i.e. complements) the ability of antibodies and phagocytic cells to immobilise (thus preventing spread of infection), break down, and clear microbes/damaged cells from an organism. The compliment system first activates the C3 protein, which then activates all the other C proteins (C5 to C9). This causes: - C3a: attracts neutrophils via chemotaxis into the tissue to enhance the inflammatory response. - C3b: "coats" the bacteria, allowing them to be phagocytized - C3a, C4a and C5a: multiplies the effects of the local immune reaction by stimulating the release of more cytokines (e.g. mast cells and basophils). This causes these cytokines to release histamine, heparin and other substances. These mediators of the inflammatory response cause: • Vasodilation for increased tissue blood flow • An increase in localised capillary permeability of endothelial cells, which allows increased leakage of fluid, plasma and WBC's to the site of inflammation • Neutrophils, macrophages and monocytes recruited via chemotaxis to initiate an inflammatory reaction at the site. Activation of the compliment system eventually increases the susceptibility of the invading pathogen to phagocytosis and initiates a localised inflammatory reaction, with the ultimate result being lysis of the pathogens. Neutrophils: released from their storage site in the bone marrow. Neutrophils then migrate into the blood stream, and: - Display a high affinity to the activated endothelial cells and adhesion molecules in the blood, stimulating them to up-regulate their production of pro-inflammatory cytokines. This contributes to antimicrobial activity - Neutrophils display high affinity adhesion to endothelium, causing capillary bed sequestration of neutrophils, which contributes to microvascular occlusion. This promotes tissue ischaemia and organ dysfunction, particularly in the pulmonary and hepatic tissues which are capillary rich - Neutrophils secrete nitric oxide (NO), which is involved with migration, proliferation, and apoptosis, but is also a potent vasodilator that increases circulation to the site of infection. However, this may contribute to the development of hypotension and septic shock. Coagulation factors: Tissue factor: cytokines (TNFα and IL-1) inhibit fibrinolysis, which causes a build up of fibrin clots. This causes direct endothelial injury, resulting in the release of tissue factor from monocytes, macrophages and the vascular endothelium. Tissue factor causes systemic activation of the coagulation cascade, resulting in production of thrombin, activation of platelets, and formation of platelet-fibrin clots through the deposition of fibrin. This forms a sticky mesh that helps to fence in and restrict the spread of microbes from the vicinity. Bradykinin and histamine: another consequence of the coagulation reactions is the activation of pro-inflammatory bradykinin, which contributes to: - Leukocyte chemotaxis (particularly neutrophils and macrophages) - Pain sensation - Vascular leakage - Augments the actions of histamine (released from mast cells and basophils in response to the activation of complement proteins) and prostaglandins (released by activated neutrophils, mast cells, and endothelial cells). Histamine and prostaglandins further promote vasodilation and increased capillary permeability due to disruption of the endothelial tight junctions, which augments vascular leakage. This causes local tissues to become oedematous with protein-rich fluid. - Abundant production of bradykinin may induce hypotension, with the development of septic shock and MODS.

Anaphylactic shock: - Pathophysiology

Anaphylactic shock is described as a type of distributive shock because it is associated with vasodilation, increased permeability of blood vessels (with a subsequent loss of intravascular volume), and impaired heart function. Anaphylaxis is rapid in onset, generalised, and effects multiple organs. Anaphylaxis represents the most severe systemic type 1 hypersensitivity reaction that is mediated by IgE. It most commonly occurs in response to: - Venom (especially wasps and bees) - Food (especially eggs, nuts, soy, wheat and shellfish) - Medications (e.g. antibiotics). Dendritic cells (i.e. an antigen presenting cell) are part of the innate immune system, and when they encounter an antigen they present this antigen to naïve T cells, which then differentiate into TH1 and TH2. TH1 cells direct the activity of macrophages and cytotoxic T cells to kill invading microbes, and produce IL-2 and IFN-a. This is critical in cellular defence mechanisms in response to infection. In comparison, TH2 cells respond to allergens by activating B lymphocytes to differentiate into IgE-producing antibodies and produces growth factors for mast cells. IgE attaches to mast cells and basophils and sensitises them to the presence of the specific antigen for which the IgE was made. Thus, the first time that the allergen is introduced to the body, the inflammatory response will not be initiated, because sensitised mast cells/basophils are required for a hypersensitivity reaction to occur (exception: anaphylactoid reactions). If a sensitised mast cell/basophil encounters its antigen (or a closely similar molecule), degranulation is triggered with the release of inflammatory mediators: - Histamine (most widely recognised) causes: • Bronchoconstriction with subsequent bronchospasm • Epithelial barrier dysfunction, resulting in increased capillary permeability, with leakage of fluid into the interstitial space, resulting in oedema (e.g. laryngeal oedema) • Cutaneous vasodilation • Enhanced mucous production • Pruritus - Tryptase is a major protease released from mast cells. It causes the following: • Potentiates histamine release • Increases HR • Bronchoconstriction - Cytokines: • IL-4 and IL-13: Maintains TH2 cell differentiation and proliferationSwitches B cells to IgE synthesis • TNFa: proinflammatory cytokine that promotes histamine release - Prostaglandin D2 causes: • Bronchoconstriction • Peripheral vasodilation • Coronary artery vasoconstriction. This is potentiated by decreased vascular tone and capillary leakage. May contribute to dysrhythmias • Pulmonary artery vasoconstriction • Enhances histamine release from basophils - Leukotrienes cause: • Augment vascular permeability, causing interstitial oedema • Bronchoconstriction - Platelet-activating factors - Macrophage inflammatory proteins. Anaphylactic shock and/or death can ensue within minutes without appropriate medical intervention.

Management of cardiogenic shock: - Talk to metaraminol - Talk to adrenaline - Transport

Cardiogenic shock has a high mortality rate unless the underlying problem is corrected in a timely manner. The only 2 prehospital interventions that significantly alter outcome include: - Initiating fibrinolytic therapy for STEMI when indicated - Transporting the patient to a hospital with a cardiac catheter room/lab. The following is for management of cardiogenic shock in adults. Seek clinical advice if the patient is a paediatric. - 12-lead ECG - Large bore IV access ACF - Fluid IV if there are signs of poor perfusion provided that there are no signs or symptoms of PO and the primary problem is not dysrhythmia: • 250-500ml • Repeat as required if the patient continues to show signs of poor perfusion, but to a maximum of 1L • Stop the fluid if the patient becomes SOB or develops PO • Inferior MI more likely to respond well to IV fluid. Anterior or anterolateral MI generally does not respond well to fluid, and fluid administration may make PO worse - Metaraminol if SBP <100mmHg: • Infusion pump: initial bolus: 0.5-1mg. IV Infusion pump set to 2mg/hr and adjust the rate as required • Bolus: 0.5-1mg IV, repeated every 5-10mins as required - Adrenaline: if the BP is unresponsive to metaraminol, or if the patient is hypotensive and bradycardic: • Infusion pump: 0.5mg/hr, adjust the rate as required • Infusion: 1:1,000,000 solution. Start at 2 drops/sec, and adjust the rate as required (this will administer 0.4mg/hr) • Bolus: 1:1,000,000 solution, administer 10ml (0.01mg) every 1-2mins as required - Treat as per the appropriate section if dysrhythmia, myocardial ischaemia, or PO is present: • STEMI: check fibrinolytic checklist, call the STEMI coordinator • Aspirin (if myocardial ischaemia is present) 300mg • Do not administer GTN • Be cautious with opiates, amiodarone, CPAP or PEEP. Metaraminol: preferred vasopressor over adrenaline because it doesn't increase myocardial O2 consumption and demand, and it is less likely to cause tachycardia and/or tachyarrythmias when compared to adrenaline. Adrenaline: the decision to administer adrenaline must weigh up the potential benefit in improving CO, against the potential risks of increasing myocardial O2 consumption and demand, and the risks of causing tachycardia and/or tachyarrythmias. This is why adrenaline is reserved for if the patient is hypotensive and bradycardic. Transport: To a hospital with a cardiac catheter room/lab whenever feasible and safe.

Cardiogenic shock: - Pathophysiology - Causes - Talk to inadequate LV function - Talk to inadequate RV function - Talk to compensatory mechanisms during cardiogenic shock

Cardiogenic shock is defined as failure of the heart to pump adequately to meet the systemic demands, causing hypoperfusion, indications of tissue hypoxia and potentially hypotension, despite adequate intravascular volume. Cardiogenic shock may occur in: - AMI (most common cause): - Poor LV function: most common cause is acute anterior, anteroseptal, or anterolateral STEMI - Poor LV function: uncommon cause of cardiogenic shock, but may be caused by inadequate RV function (i.e. inferior STEMI with RV involvement) - Acute valve or papillary muscle rupture - PE - Dysrhythmia (particularly VT) - Cardiac tamponade - Myocarditis. - Ventricular aneurysm - Ventricular septal rupture - Cardiac surgery - Other types of shock causing inadequate coronary blood flow. Regardless of the cause of cardiogenic shock, there is a decrease in myocardial contractility, increased afterload (due to peripheral systemic pooling of blood and pulmonary congestion of blood) and increased/excessive preload (due to compensatory mechanisms stimulating vasoconstriction), which exacerbate decreased SV and CO. Decreased CO causes insufficient perfusion to meet the cellular metabolic demands of O2, causing systemic hypoxia and hypoperfusion. Eventually, the increased afterload and excessive preload causes volume overload and increased ventricular wall tension during systole and diastole. Excessive preload and afterload decreases coronary artery perfusion during diastole, and increased ventricular wall tension decreases coronary artery perfusion during systole. As a result, impaired coronary artery perfusion further reduces myocardial O2 supply, which subsequently causes decreased cardiac function. Inadequate LV function: most commonly cardiogenic shock is caused by inadequate LV function, with the most common cause being anterior, anteroseptal or anterolateral MI. This is most commonly associated with the development of PO. Shock is unlikely to respond to fluid, and if administered it must be with caution as it may make the PO worse. Inadequate RV function: occasionally cardiogenic shock is caused by inadequate RV function, with the most common cause being an inferior MI with RV involvement. In this setting, there is a combination of impaired RV function, and peripheral pooling of blood in the pulmonary and systemic circulation. This decreases LV preload, and impairs LV filling (as the RV is unable to pump a sufficient amount of blood to the pulmonary circulation, therefore a minimal amount of blood is returning to the LV and also LV filling (i.e preload) is dependent on the passive flow of blood down a venous pressure gradient between the inferor vena cava, the superior vena cava, and the left atrium). This is why shock secondary to inadequate RV function is likely to respond well to IV NaCl. GTN is not contraindicated in this setting, however there must be a strong indication for its use. It must be used with caution, because LV filling is dependent on RV preload. GTN causes a reduction in RV preload due to venous dilation, which may significantly reduce CO.

Compensatory shock: - Define - Compensatory mechanisms - Presentation

Compensatory shock is defined as when the compensatory/homeostatic mechanisms (e.g. RAAS, activation of neural humoral mechanisms/SNS, shunting of blood to essential organs such as the heart, brain, liver, and kidneys) are maintaining an adequate/normal CO and BP in an attempt to restore tissue perfusion and oxygenation in the early stages of shock. However, a normal BP does not ensure adequate perfusion and oxygenation of vital organs at a cellular level. Compensated shock is also known as class 1 and 2 shock, where the patient has lost approximately <750-1500ml of blood, or 15-30% of their BV. This stage of shock will continue until the problem is solved, or until the compensatory mechanisms fail, in which there will be a drop in BP and decompensatory shock will begin. Presentation: Some medications, such as beta blockers, will hide the signs and symptoms of compensatory shock. - Tachycardia - Tachypnoea (to compensate for lactic/metabolic acidosis and to increase O2 supply to hypoxic tissues) - Normal BP or HTN - Decreased skin perfusion (e.g. prolonged CRT, cool, clammy, pale skin, cyanosis) - Altered LOC - Dilated pupils (due to sympathetic tone stimulating the contraction of the smooth cells of the radial muscle, therefore leading to mydriasis) - Narrow PP due to peripheral vasoconstriction: • Hypovolaemic shock • Cardiogenic shock • Anaphylactic shock • Warm septic shock • Severe HF • Cardiac tamponade - Wide PP: • Anaemia • Pregnancy • Cold septic shock (as compensatory mechanisms begin to fail). Compensatory mechanisms: Neural mechanisms: Located in the reticular formation of the medulla and lower third of the pons. This area of the brain stem contains the vasomotor and cardiac control centres, and is often collectively termed the cardiovascular centre. Includes sympathetic responses. Sympathetic responses: transmitted to the heart and blood vessels via the spinal cord and peripheral SNS nerves. Sympathetic stimulation of the adrenal medulla causes release of catecholamines adrenaline and noradrenaline, which circulate to the heart. At the heart, these hormones simulate adrenergic B1 receptors, producing positive inotropic, chronotropic and dromotropic effects on the heart, which helps to increase SV, HR and subsequently CO (CO = HR x SV). They also bind to the adrenergic a1 receptors in the peripheral smooth muscle, causing vasoconstriction, which increases SVR and increases BP. Baroreceptors: pressure sensitive receptors that are located in the the carotid bodies and the aortic arch. Baroreceptors quickly sense a decrease in BP, and transmit this signal to the cardiovascular centres in the brainstem medulla. This sends appropriate responses to alter inotropy, chronotropy, dromotropy and vascular smooth muscle tone. Arterial chemoreceptors: located in the carotid bodies, thus the arterial chemoreceptors are always in close contact with arterial blood. Arterial chemoreceptors are chemosensitive cells that monitor O2, CO2 and hydrogen ion concentration in the blood, therefore their main function is to regulate ventilation (e.g. hypercarbia = increased RR). Also, arterial chemoreceptors communicate with the cardiovascular centre in the brain stem to induce widespread vasoconstriction. RAAS: granular cells (in the afferent arteriole of the JGA) contain mechanoreceptors, which detect a change in pressure and stretch (i.e. BP). It is important for the BP to be maintained at 60mmHg in the nephron, to help with filtration of urea and creatinine out of the glomerular capsule and into the proximal convoluted tubules. The granular cells synthesise, store and release renin. When the mechanoreceptors detect a decreased BP in the afferent arteriole, the granular cells are stimulated to release renin. Additionally, the macula densa cells (located in the distal convoluted tubules of the JGA at the point where they contact the granular cells) detect changes in filtrate concentration and flow rate of the fluid within the lumen of the distal convoluted tubules. When the macula densa cells detect an increase in the filtrate concentration, then they signal the granular cells to release renin. Renin: initiates an enzymatic chemical reaction by converting angiotensinogen (an inactive hormone) into angiotensin I. Angiotensin I is then converted to angiotensin II by ACE, which is found in high concentrations in the pulmonary capillary endothelium, so most angiotensin and ACE contact is maximised, thus most conversion occurs in the lungs. Angiotensin II: stimulates: - acts on arteriolar smooth muscle, causing blood vessels to contract, resulting in widespread potent vasoconstriction, which increases PVR and helps to elevate BP. - the thirst centre, which helps to increase the BV and BP - the adrenal cortex to release aldosterone. Aldosterone: angiotensin II triggers the adrenal cortex to release aldosterone. Aldosterone opens the Na channels in the proximal convoluted tubules and collecting ducts, and promotes the reabsorption of Na from the filtrate and into the peritubular capillaries. H20 follows Na into the peritubular capillaries, which helps to increase BV and BP. ADH: osmoreceptors in the hypothalamus constantly monitor blood solute concentration and osmolality. When blood solute concentrations and blood osmolality increases, angiotensin II stimulates the posterior pituitary gland to release ADH. ADH acts on the principle cells, which insert aquaporins into their plasma membrane. H2O moves via osmosis from the higher concentration in the collecting ducts, and back into the peritubular capillaries. This causes increased BV and BP. Shunting of blood: - Spleen: can expel up to 200ml of blood into the venous circulation when required. - Fluid shifts: there are passive fluid shifts that occur in the body. Decreased fluid volume causes an increase in blood osmotic pressure, which causes fluid to shift from the interstitial space and into the intravascular space. This helps to increase BV and BP. - Skin and GI tract: due to potent peripheral vasoconstriction and increased SVR, blood is shunted away from the skin and GI tract and towards major organs. As a result, this causes the skin to look cool, clammy and pale, decreases gastric activity, and helps to maintain major organ perfusion.

Decompensatory shock: - Define - Presentation

Decompensated shock begins when the compensatory mechanisms begin to fail, resulting in a decrease in CO and BP (BP = SVR x CO). The compensatory mechanisms can no longer sustain adequate perfusion to tissues, which causes: - Significant hypoxic injury - Free radical damage Stimulation of the inflammatory response. - Lactic acidosis may occur due to the accumulation of anaerobic metabolism by-products (e.g. lactic acid, because after the cell breaks down glucose for energy, it cannot enter Krebs/citric acid cycle, which means pyruvic acid degenerates into lactic acid) or a decreased clearance due to poor liver and kidney perfusion. Lactic acidosis alters the acid-base balance of the blood, which may lead to metabolic acidosis. - Metabolic acidosis places a greater burden on the respiratory and renal systems, and can effect electrolyte balance, which may contribute to cardiac dysrhythmias and further dysfunction on the pulmonary, renal and cardiac systems. Decompensated shock is also known as class 3 shock, when there has been a 1500-2000ml loss of blood, or 30-40% of BV. Presentation: - Severe tachycardia - Weak/absent radial pulse - Tachypnoea (to compensate for lactic/metabolic acidosis and to increase O2 supply to hypoxic tissues) - Severely prolonged CRT - Cool, clammy, pale skin - Hypotension - Altered LOC: agitation (common, and late), restlessness, confusion, or falling LOC, usually with preservation of the motor score (common, and late) - Dilated pupils (due to sympathetic tone stimulating the contraction of the smooth cells of the radial muscle, therefore leading to mydriasis).

Complications from shock: - DIC - ARDS - MODS

Disseminated intravascular coagulation: DIC is a paradox in the homeostatic mechanisms, that may be caused by: - Sepsis (most common cause) - Obstetric disorders (e.g. placental abruption or amniotic fluid embolism) - Vascular disorders (e.g. large aortic aneurysms) - Trauma - Burns - Shock - Acidosis - Severe toxic or immunological reactions (e.g. snake bites, drugs, transplant rejection, haemolytic transfusion reactions). DIC is characterised by massive systemic intravascular activation of coagulation, leading to deposition of fibrin in the circulation, with generation of microthrombi. This causes vascular occlusion, with microcirculatory impairment, which may leads to tissue hypoperfusion and ischaemia. In specific relation to septicaemia, DIC is mediated by cell membrane components of microorganisms (e.g. endotoxins, lipopolysaccharides), or bacterial exotoxins, which causes a generalised inflammatory response through activation of pro-inflammatory cytokines, with subsequent activation of the coagulation cascade. This coagulation process also consumes all available anticoagulants (e.g. platelets, coagulation proteins and clotting factors V/VII), which increases the risk of bleeding. The bleeding that occurs may manifest as petechiae, purpura, severe haemorrhage or oozing from the puncture site. Petechiae and purpura: the inflammatory mediators that are stimulated by tissue ischaemia, hypoxia or necrosis cause the precapillary sphincters to relax and open. More blood surges into the capillary bed, however it is important to note that perfusion does not increase, because during shock there is minimal O2 in the blood. Despite an increase in the volume of blood in the capillary bed, the postcapillary sphincter remains contracted and closed. Therefore, this blood begins to stagnate and the pressure increases in the capillary beds, causing capillary beds to rupture. This manifests and petechiae and purpura. D-dimer: measurements of D-dimer may be ordered, along with other tests, to help diagnose DIC. When haemorrhage occurs, haemostasis is initiated to create a blood clot. This process produces fibrin (threads of a protein), which crosslink together to form a fibrin net. That net, together with platelets, helps hold the forming blood clot in place at the site of the injury until it heals. Once the area has had time to heal and the clot is no longer needed, the body uses plasmin (an enzyme) to disintegrate the clot (thrombus) into small pieces (fibrin degradation products (FDP), which consist of variously sized pieces of crosslinked fibrin) so that it can be removed. One of the final fibrin degradation products produced is D-dimer, which can be measured in a blood sample when present. D-dimer is normally undetectable or detectable at a very low level unless the body is forming and breaking down blood clots. However, the level of D-dimer in the blood can significantly rise when there is significant formation and breakdown of fibrin clots in the body, therefore the D-dimer level will typically be very elevated in DIC. A negative D-dimer test (D-dimer level is below a predetermined cut-off threshold) indicates that it is highly unlikely that a thrombus is present. However, a positive D-dimer test cannot predict whether or not a clot is present, but only indicates that further diagnostic procedures are required (e.g., ultrasound, CT angiography) to rule out PE or DVT. Acute respiratory distress syndrome: ARDS describes non-cardiogenic PO that is characterised by bilateral pulmonary infiltrates and severe hypoxaemia (due to pulmonary vasoconstriction and a marked increase in intrapulmonary shunting) in the absence of evidence for CPO. ARDS is caused by pathologies that cause diffuse injury to epithelial cells in the pulmonary capillaries. This injury increases the permeability of the alveolar-capillary membrane, allowing fluid to move from the vascular compartment and into the interstitium and alveoli. This damages the alveolar cells, which results in accumulation of protein-rich fluid in the alveoli, degradation and decreased production of surfactant (given that the alveolar epithelial cells produce surfactant) with subsequent decreased alveolar compliance, alveolar collapse (i.e. contributing to atelectasis), and compromised gas exchange (low V/Q ratio, low V but high Q). All combined make the lungs stiffer and harder to ventilate. As the condition progresses, PO may ensue, in addition to a systemic response that can result in multiple organ failure. Presentation: - Auscultation reveals wet crackles or rhonchi - Rapid onset of profound dyspnoea that usually occurs 12-48 hours after the initiating event - Accessory muscle use - Haemoptysis, pink frothy sputum (severe), or white/yellow sputum - Hypoxaemia - Cyanosis (late) - Cold, clammy extremities - HTN (may evolve into hypotension as the fluid originates from the circulation, which may then lead to cardiogenic shock) - JVD - Sitting upright or leaning forwards. Management: the aim of non-cardiogenic treatment of PO is to decrease preload and afterload, and increase O2 intake to meet the physiological demands. - Sit the patient upright - 12-lead ECG to distinguish between PO/APO or CPO - O2 if indicated - Severe PO: PEEP set to 10cmH20 - There is no role for treatment of non-cardiogenic PO with GTN. Multiple organ dysfunction syndrome: MODs is a life-threatening complication of an uncontrolled and marked SIRS response to severe illness or injury, particularly septic shock, severe trauma, prolonged periods of hypotension and advanced age. MODS represents the presence of altered organ function with progressive dysfunction of ≥2 organ systems (e.g. kidneys, lungs, liver, heart, brain) in an acutely ill patient, where homeostatic mechanisms cannot be maintained without intervention.

Hypovolaemia from fluid loss: - Indications - Management - Transport

For hypovolaemia from fluid loss that does not clearly fit into another section e.g: - Fluid loss (e.g. hyperglycaemia, D&V) - Other (e.g. diving incidents) - Hyperthermia. Management: - Gain IV access - Fluid if the patient has signs of hypovolaemia or poor perfusion: • Adults: 1L IV • Paediatrics: 20ml/kg • Repeat as required. Hyperglycaemia: rapid IV fluid boluses cause a rapid fall in glucose concentration via dilution, which causes a rapid fall in osmolality. This causes fluid to shift from the intracellular space and into the interstitial space in the brain, which contributes to cerebral oedema. Children and young adults are at a high risk of cerebral oedema. Therefore, fluid administration should occur over 1 hour to limit the possibility of cerebral oedema. If severe shock is present, fluid administration can occur more rapidly than one hour. Transport: - If IV NaCl is administered, the patient should be clearly recommended to be transported to ED via ambulance - If shock is severe, transport to a hospital with intensive care facilities.

Hypoadrenal shock: - Pathophysiology - Management - Transport

Hypoadrenal shock (i.e. adrenal crisis) is caused by inadequate levels of circulating cortisol. Under normal conditions, the adrenal glands produce additional cortisol during times of increased physiological stress, and this is important for a normal cardiovascular response to occur. However, some clinical conditions may result in abnormal adrenal function. Patients at a higher risk of abnormal adrenal function include patients with: - Congenital adrenal hypoplasia (reduced development of the adrenal gland from birth) - Addison's disease (a long-term hypofunctional endocrine disorder causing the body to produce insufficient amounts of cortisol, and aldosterone) - Previous pituitary surgery - Those taking high daily doses of steroids. These patients with inadequate adrenal function are at a risk of hypoadrenal shock if they have injury or illness, even if minor, particularly if they have been unable to increase their dose of oral steroid. Management Hypovolaemia from fluid loss: - Patients with inadequate adrenal function may have their own hydrocortisone for injection in the event of illness or injury. In this setting, personnel should follow any instructions (including verbal) regarding IM or IV administration of hydrocortisone, and should seek clinical advice if uncertain - O2 administration - Gain large bore IV access - Fluid administration if signs of poor perfusion. Aiming for a SBP of 120mmHg: • Adults: 1L NaCl • Children: 20ml/kg NaCl • Repeat as required - Pain relief if required - Keep the patient warm. Hypothermia worsens bleeding by contributing to coagulopathy - Trauma management: • Compress any external bleeding • Splint and immobilise any fractures • Firmly wrap pelvis and secure legs together, if fractured pelvis. Transport - All patients at risk of inadequate adrenal function require urgent medical assessment if they have an illness or injury that is more than minor. All patients receiving hydrocortisone should be assessed in ED. - If the patient has trauma and hypovolemic shock, transport to major trauma hospital whenever feasible

Hypovolaemia from controlled bleeding: - What do you need to exclude - Indications and why - Management - Transport

Hypovolaemic shock is usually caused by blood loss, but it is very important to exclude: - Tension pneumothorax, which may cause hypovolaemia by obstructing venous return from the vena cava and causing obstructive shock - Blunt trauma causing SCI, resulting in loss of sympathetic tone to peripheral blood vessels and/or the heart and thus neurogenic shock. The following follow a pattern of bleeding that is relatively controlled in nature (e.g. bleeding from a solid organ: liver, liver, spleen, kidney): - GI bleeding - APH - Peripheral trauma controlled - PPH - Blunt trauma - Bleeding from another cause. Management: - Request blood early if shock is severe - Compress any external bleeding: • Direct, sustained, firm external pressure • No benefit in raising a bleeding limb unless the bleeding is clearly venous and coming from near the hand or foot • Tourniquet: apply a tourniquet to peripheral bleeding if it cannot be controlled with direct pressure. Apply over a dressing tight enough to assist with direct pressure, but not tight enough to stop arterial flow. Re-evaluate the need for a tourniquet after bleeding is controlled. Consider releasing the tourniquet if there is a focal bleeding point that can be controlled with direct pressure and transport time to ED is >30mins • Topical adrenaline: if a clinically significant bleed continues despite direct pressure, and the wound is unsuitable for tourniquet application, then consider topical adrenaline: 1:10,000 solution. Either flood the wound with this solution and continue to provide direct pressure, or if there is a significant wound cavity, then pack the wound with adrenaline soaked gauze - O2 administration if indicated - Gain large bore IV access - Fluid administration for signs of hypovolaemia or poor perfusion: • Adults: 500ml IV • Paediatrics: 10ml/kg IV • Repeat as required if the patient continues to show signs of poor perfusion • Request blood - TXA: if fluid is being administered for signs of hypovolaemia or poor perfusion: • Adults: 1g IV over 1-2mins • Paediatrics: 20mg/kg IV - Keep the patient warm. Hypothermia worsens bleeding by contributing to coagulopathy - Splint and immobilise any fractures. If shock is associated with a possible pelvic fracture then firmly wrap pelvis and secure legs together, if fractured pelvis is present - Pain relief if required. Transport: - Clear recommendation to be transported to ED via ambulance if there are signs of hypovolaemia or poor perfusion - Transport patients with trauma and shock directly to a major trauma hospital.

Hypovolaemic shock: - Define - Causes - Blood loss severity - Presentation

Hypovolemic shock is defined as inadequate intravascular volume as a result of loss of whole blood, plasma or extracellular fluid. Due to decreased RBC concentration and/or decreased volume in the intravascular space, O2 delivery to the tissues is impaired, which results in cellular hypoxia and ischaemia. Approximately 10% of the total BV can be removed from the body without changing CO or BP. Therefore, hypovolemic shock occurs when there is an acute loss of 15-20% of the total BV. Causes: - Loss of whole blood: e.g. external haemorrhage, internal haemorrhage (e.g. AAA, peptic ulcers, blunt trauma, TB (haemoptysis)) - Loss of plasma: e.g. burns (loss of semi-permeable integrity of the cellular membrane causes leakage of plasma and proteins from the intravascular space and into the interstitial space) - Loss of extracellular fluid (whether that be due to a decreased intake of fluid, into the environment, or movement of fluid into the interstitial space) e.g. severe dehydration, loss of GI fluids (D&V), ascites, bowel obstruction, peritonitis, pancreatitis, environmental factors. Blood loss severity: Calculating blood loss if often variable and unreliable, because it includes a calculation of internal and external blood loss and several patient characteristics, such as: - Area of trauma: • Humerus: 500-750ml • Tibia/fibula: 500-750ml • Femur <1500ml • Pelvis >2000L - Age and weight: • A child has 80ml/kg • An adult has 70ml/kg • Youth: if a young persons' BP is falling, it usually reflects a significant loss of intravascular volume that requires immediate treatment • Elderly: in an elderly patient with a reduced ability to compensate, a small loss of intravascular volume may result in a fall in BP, even though shock is not severe • The bigger you are, the more blood you have, hence why blood loss in a child is relatively life-threatening, whereas that same volume may be fine for an adult - Pre-existing medical conditions: • Pregnancy: 40% increase in BV when you are pregnant, thus you can lose more blood before you display signs of hypovolaemia • Heart disease • Anaemic patients will lose more blood and become sicker faster, because they have thinner blood. - Blood pressure is a very poor indicator of blood loss severity. Some patients may not present with hypotension when they are in shock because: • Young adults and children have the capacity for profound vasoconstriction, which may help to maintain a normal BP, despite very low CO • Exercise tolerance • Medications (e.g. beta blockers) • Keep in mind that a normally hypertensive patient (e.g. geriatrics) may have a significant fall in their "normal" BP rendering them "hypotensive" for them, but their BP may be within the "normal" ranges. • Base it off MAP instead (MAP = 1/3PP + DBP). >65mmHg maintains optimal end organ perfusion, and >85mmHg maintains optimal CPP - Tachycardia may not be present despite significant hypovolaemia because: • Beta blockers • End stage hypovolaemic shock with a falling HR • Ectopic pregnancy (dilatation of the fallopian tube may cause vagal stimulation) • Miscarriage (dilatation of the cervix may cause vagal stimulation)

Septic shock: - Management - Talk to blood cultures - Transport and referral

If the patient is <12 years, provide supportive treatment and seek clinical advice regarding antibiotic administration if the child is very unwell, and transport time to hospital is prolonged. - Assess: • RR • SpO2 • HR • BP • Temperature • CRT • BGL • LOC and GCS • Presence of risk factors (above) - Gain IV access if there are: • Signs of hypovolaemia • Signs of poor perfusion • ≥1 high risk factors - Administer antibiotics only if there ≥1 high risk factors present, the patient is aged ≥12 years, and the time to hospital is >30mins: • Augmentin if the site of infection is the soft tissues, a joint, or the chest: 1.2g IV over 1-2mins, preferably through a running line • Gentamicin if the site of infection is the abdomen, urinary tract, or unknown: <60kg (240mg), 60-80kg (320mg), >80kg (400mg), IV over 1-2mins, preferably through a running line, after augmentin - NaCl: if there are signs of hypovolaemia or poor perfusion: • Adult: 1L • Paediatrics: 20ml/kg • Repeat as required - Metaraminol: administer if, despite 2x doses of NaCl, the SBP is <100mmHg in an adult, or significantly less than the normal predicted SBP in a paediatric: • Adult: infusion pump (administer an initial bolus of 0.5-1mg, then start at a rate of 2mg/hr (most adults are likely to require ~2-3mg/hr). Adjust the rate as required), bolus dosing (0.5-1mg IV every 5-10mins as required). • Paediatric: 0.01-0.02mg/kg IV every 5-10mins as required. - Adrenaline: if the BP is unresponsive to metaraminol, or the patient is hypotensive and bradycardic, then administer adrenaline: • Adult: infusion pump (start at a rate of 0.5mg/hr and adjust the rate as required). Infusion (1:1,000,000 solution. Start at 2drops/sec and adjust the rate as required). Bolus (1:1,000,000 solution (0.01mg/ml) Administer 0.01mg (10ml) of adrenaline every 1-2mins as required) • 5-14 years: infusion pump (start at a rate of 0.25mg/hr and adjust the rate as required). Infusion (1:1,000,000 solution. Start at 1drop/sec and adjust the rate as required). Bolus (1:1,000,000 solution (0.01mg/ml). 0.0002mg/kg every 1-2mins as required) • <5 years: do not administer an infusion. 0.0002mg/kg bolus doses of a 1:1,000,000 solution (0.01mg/ml) every 1-2mins as required. Administration of metaraminol: in an adult, administer IV, undiluted, and preferably through a running line. In a paediatric: Take a 100ml bag of 5% glucose Remove and discard 10ml Add 10mg/1ml of metaraminol in the bag (solution contains 0.1mg/ml) Shake well and label Draw up the doses from the bag of 5% glucose. Blood cultures. These are not carried in an ambulance because they have a very short shelf life, and some hospital personnel ill not process blood culture bottles that have been filled by ambulance personnel. Administering antibiotics without taking blood cultures is a balance of risk, because not taking blood for culture increases the risk of not making a microbiological diagnosis, and this alters the choice and duration of subsequent antibiotic treatment. Conversely, delaying antibiotic administration increases the risk for deterioration, which increases morbidity and mortality, particularly if the transport time to hospital is prolonged. For these reasons, antibiotics are only administered if the patient is ≥12 years, has a provisional diagnosis of sepsis, has ≥1 high risk factors, and if the time to hospital is >30 mins (this is defined as the time from inserting an IV to handover in ED). Referral and transport - Patients with ≥1 high risk factor, or ≥2 moderate risk factors, must be given a clear recommendation to be: • Transported to ED via ambulance (particularly if the patient is living independently) or • Seen within 2h in primary care (preferably their own GP). This may be the best option for patients living in an aged residential care facility, or is frail. Contact primary care staff to confirm an appointment before leaving the scene. Safe transport for the patient (if required) must be available or organised. - Primary care: • Patients with no high risk factors and only 1 moderate risk factor, are usually suitable to be given a clear recommendation to be seen in primary care (preferably their own GP) within 6h. Contact primary care staff to confirm an appointment before leaving the scene. Safe transport for the patient (if required) must be available or organised. • Patients with no high or moderate risk factors, and only low risk factors, are usually suitable to be given a clear recommendation to be seen in primary care (preferably by their own GP) within 24h.

Cardiogenic shock compensatory mechanisms

In cardiogenic shock, the compensatory mechanisms include: - RAAS - SNS stimulation - Frank Starling mechanism These compensatory mechanisms ultimately stimulate positive inotropic, chronotropic and dromotropic effects, as well as stimulating potent vasoconstriction, which increases SVR, preload and afterload. However, through an increase in preload and afterload, these compensatory mechanisms may increase myocardial workload and O2 demand on an already failing heart, which may actually worsen cardiogenic shock. RAAS: The JGA of the nephron consists of the granula cells (located in the afferent arteriole. Contain mechanoreceptors which detect a change in pressure and stretch (i.e. BP). They synthesise, store, and release renin in response to a decreased BP), and the macula densa cells (detect changes in filtrate concentration and flow rate of the fluid within the lumen of the distal convoluted tubules. When the macula densa cells detect an increase in the filtrate concentration, then they signal the granular cells to release renin). Renin initiates an enzymatic chemical reaction by converting angiotensinogen (an inactive hormone) into angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE), which is found in high concentrations in the pulmonary capillary endothelium, so most angiotensin and ACE contact is maximised, thus most conversion occurs in the lungs. Angiotensin II acts on arteriolar smooth muscle. It causes blood vessels to contract, causing widespread potent vasoconstriction, which increases PVR and helps to elevate BP. Secondly, angiotensin II stimulates the thirst centre, which helps to increase the BV and BP. Lastly, angiotensin II triggers the adrenal cortex to release aldosterone. Aldosterone opens the Na channels in the proximal convoluted tubules and collecting ducts, and promotes the reabsorption of sodium from the filtrate and into the peritubular capillaries. Water follows sodium into the peritubular capillaries, which helps to increase intravascular volume and increase venous return to the heart. This subsequently increases preload (ventricular end-diastolic volume), which activates the Frank Starling mechanism, resulting in an increase in force of contraction and subsequently SV, CO and BP. However, in the setting of HF, although this may preserve CO, the chronic elevation of ventricular preload (due to increased intravascular volume) causes systemic and pulmonary congestion, which worsens symptoms associated with HF, and worsens cardiac function unless treated. Additionally, it is important to add that in HF, inotropy is already compromised by an abnormality in cardiac function. Therefore, despite an increase in preload causing an increase in CO, the SV will never be as high as the SV in a normal heart. ADH: osmoreceptors in the hypothalamus constantly monitor blood solute concentration and osmolality. When blood solute concentrations and blood osmolality increases, angiotensin II stimulates the posterior pituitary gland to release ADH. ADH acts on the principle cells, which insert aquaporins into their plasma membrane. H2O moves via osmosis from the higher concentration in the collecting ducts, and back into the peritubular capillaries. This causes increased BV and BP. SNS stimulation: When CO reduces, baroreceptors in the carotid bodies and aorta sense a decrease in BP, they signal the cardiovascular centres in the medulla. This causes an increase circulating catecholamines. This increases inotropy and chronotropy in an attempt to maintain SV and CO. Furthermore, sympathetic stimulation increases SVR, which is often why HF patients are hypertensive, unless they have cardiogenic shock. Although this is initially helpful, the increase in catecholamines and systemic vascular resistance may actually be excessive. Frank Starling mechanism: The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return. When there is increased venous return to the heart, this causes increased ventricular filling pressure (i.e. LV end-diastolic pressure, which therefore causes increased preload (defined as initial stretching of the cardiac myocytes prior to contraction) which stretches the ventricles prior to contraction. Myocyte stretching increases sarcomere length, which causes an increase in force generation and thus ventricular contraction, thereby enabling the heart to eject the additional venous return. This subsequently increases SV. However, with an increase in muscle stretch that occurs during the Frank Starling mechanism, there is also an increase in ventricular wall tension and an increase in myocardial O2 consumption and demand. Because of this, ischaemia can ensue, which further impairs myocardial function. Therefore, in this situation, the increase in preload as seen in HF is no longer contributing to compensation, but rather causing HF to worsen.

Irreversible shock: - Define - Presentation

Irreversible shock is also known as class 4 shock, where >2000ml of blood is lost, or >40% of BV. Compensatory mechanisms have failed, and the vascular system subsequently fails. Arterioles become unresponsive to catecholamines, and previously constricted capillary vascular beds begin to dilate. Widespread vasodilation and low CO contribute to severe hypotension, which is insufficient for adequate organ perfusion. Consequently, tissue damage worsens, which activates the clotting cascade, and leads to: - Sludging of blood across the capillary bed - Vascular thrombosis which may cause vascular occlusions - Severe tissue ischaemia - Release of inflammatory mediators And ultimately: - Renal failure - Hepatic failure - DIC - ARDS - MODS - Death. Presentation - Falling HR - A falling or unrecordable BP - Severe tachypnoea (to compensate for lactic/metabolic acidosis and to increase O2 supply to hypoxic tissues) - Cool, clammy, pale, mottled, cyanotic skin - Hypoxia causing decreased saturations - Hypoxaemia - Altered LOC or coma.

Neurogenic shock: - Management - Transport

Management: Hypovolaemia from fluid loss: - Assess for the presence of other major injuries: • Compress any external bleeding • Splint and immobilise any fractures • If pelvic fracture is suspected, firmly wrap pelvis and secure legs together - Stabilise the C spine and immobilise the body. Protect from pressure injury - Keep the patient warm (the pt may feel hot to touch, but actually c/o feeling cold). Hypothermia worsens bleeding by contributing to coagulopathy. Also these patients have a loss of thermoregulatory control - O2 administration - Gain large bore IV access - Fluid administration if signs of hypovolaemia or poor perfusion, or if the SBP is <120mmHg in an adult: • Adults: 1L NaCl • Children: 20ml/kg NaCl • Administer one further bolus if required, and refrain from administering more because excess fluid may cause circulatory overload - Metaraminol: in addition to NaCl, if SBP is <120mmHg in an adult: • Adults: infusion pump (loading dose of 0.5-1mg IV. Set the infusion pump up to administer 2mg/hr and adjust the rate as required). Bolus (0.5-1mg IV every 5-10mins as required) • Paediatrics: 0.001-0.002mg/kg - Adrenaline: if the BP is unresponsive to metaraminol and NaCl, or if the patient is hypotensive and bradycardic - Pain relief if required. Fluid: spinal cord circulation is dependent on the spinal cord perfusion pressure following SCI (same way that cerebral circulation is dependent on CPP following TBI). A reduction in spinal cord perfusion pressure leads to spinal cord ischaemia, and this worsens outcome. The pressure around the spinal cord is commonly raised in patients with SCI, hence why maintenance of an adequate SBP is important. Circulatory overload may occur if you administer too much fluid. Presentation: - Tachycardia - Signs of respiratory distress (e.g. wheezing, crackles, dyspnoea) - Elevated BP - Altered LOC: anxiety, restlessness - Headache - CP - JVD - Diaphoresis Referral and transport - Transport directly to an SCI centre whenever feasible and safe (e.g. MMH, Starship) even if they have major trauma - If the patient has major trauma and is deteriorating with an immediately life-threatening problem and it is possible that hypovolaemic shock is present, then transport to the most appropriate major trauma hospital if transport to an SCI centre is significantly longer than transport to a major trauma hospital - Early R40.

Neurogenic shock: - Who does it occur in - Pathophysiology - Presentation

Neurogenic shock occurs in patients with a primary (occurs within minutes of injury) or secondary (occurs within hours to days after injury) SCI above T6 (most common). Any injury between T1-T4 (this is the area in which the SNS supply to the heart leaves the spinal cord) may interrupt impulses to the vasomotor in the brain stem, or impair sympathetic outflow to the blood vessels. This leads to: - Vasodilation, peripheral pooling of blood and distribution of blood volume away from the heart and central circulation. This decreases venous return and decreases CO. - The vagus nerve (CN X) is unaffected in SCI, thus it exerts a continuous inhibitory effect on the HR, leading to PNS control. This causes slowing of the HR and vasodilation. This explains why patients with SCI may not be tachycardic despite hypovolaemia - Vasodilation is also caused by the inability of the adrenal glands to release adrenaline and noradrenaline, because SNS stimulation is decreased. Consequently, these catecholamines are unable to exert their compensatory effects. - Due to maldistribution of BV, decreased CO and BP, there is decreased cellular O2 supply and tissue perfusion, which impairs cellular metabolism. Presentation: - Loss of SNS outflow/sympathetic tone to the peripheral blood vessels and/or the heart, causing: • Warm, dry, pink skin (due to loss of cutaneous control of sweat glands, causing an inability to sweat, and peripheral pooling of blood with vasodilation) • Bradycardia • Hypotension • Widened PP (due to vasodilation) • The patient may complain of feeling very cold, despite being warm to touch (because they have a loss of thermoregulatory control) - Loss of motor, sensory function below the level of the injury, causing: • Flaccidity • Paralysis • Loss of reflexes. - Diminished respiratory effort: • C1-3 injury (risks injury to the section of the brain stem containing the RAS, which controls ventilatory drive. May result in a lack of respiratory effort requiring assisted ventilation) • C3-5 injury (this segment of the spine contains the phrenic nerve, which innervates the diaphragm and intercostal muscles. May cause shallow breaths and decreased TV, A weak cough due to respiratory muscle weakness and diaphragmatic paralysis/dysfunction, with diaphragmatic breathing)

Spinal shock: - Define - Presentation - Manegement - Transport

Not to be confused with neurogenic shock. Spinal shock and cervical spinal cord neuropraxia are used interchangeably, wherein there is a temporary loss of motor and/or sensory function, with flaccidity of muscles and loss of reflexes, followed by recovery over a few minutes to hours. This occurs due to bruising and/or stretching of the cervical spinal cord, and is often associated with hyperflexion or hyperextension of the neck. Furthermore, there is a high association between cervical cord neuropraxia and pre-existing cervical stenosis (narrowing of the cervical canal through which the spinal cord runs). If cervical stenosis is present this often requires urgent surgery. Commonly, the patient does not have a cervical fracture and may be completely symptom free following recovery from their symptoms. Presentation: Immediate symptoms with any combination of the following: - Burning pain - Numbness - Tingling - Weakness - Paralysis All four limbs are usually involved, but the patient may experience symptoms in only some limbs. Management: - The symptoms may have resolved by the time ambulance gets to scene. In this setting: • The history must be recorded and passed on to medical staff as it is likely to change the subsequent investigation of the patient • The patients C spine should not be cleared clinically, even if the patient does not have symptoms. Transport: - Provided that the signs and symptoms of cervical spinal cord neuropraxia have completely resolved, then the patient does not need to be transported to an SCI centre - The patient should instead be transported by ambulance to an ED that has CT scanning facilities, whenever feasible and safe.

Obstructive shock: - Pathophysiology - Management

Obstructive shock is a type of circulatory shock that results from mechanical obstruction of blood flow into or out of the heart. It can be caused by: - Inadequate ventricular filling: • Cardiac tamponade (affects the filling of both ventricles) • Tension pneumothorax increases intrathoracic pressure, which compresses the vena cava and subsequently impedes venous return to the RV, thus resulting in inadequate RV filling - Obstruction of outflow from the heart: • PE causes increased pressures within the pulmonary circulation, which increases RV afterload, causing inadequate RV function • Cardiac myxoma/neoplasm • Dissecting aortic aneurysm - Evisceration of the abdominal contents into the thoracic cavity, which compresses the heart and major blood vessels, and directly effects ventricular function e.g. ruptured hemidiaphragm. Management: Hypovolaemia from controlled bleeding: - LATER - Keep the patient warm. Hypothermia worsens bleeding by contributing to coagulopathy - Gain large bore IV access - Fluid administration if signs of poor perfusion. Aiming for a SBP of 120mmHg: • Adults: 500ml NaCl • Children: 10ml/kg NaCl • Repeat as required. - O2 administration - Trauma: • Tension pneumothorax: NT or FT • Compress any external bleeding • Splint and immobilise any fractures • Firmly wrap pelvis and secure legs together, if fractured pelvis - Pain relief if required.

Talk to deranged metabolism: - Oxygen - Glucose

Oxygen: Under normal conditions, aerobic metabolism occurs (O2 + glucose = CO2 + H2O + ATP). In the presence of O2, glucose is broken down into pyruvic acid via glycolysis. This creates 2 ATP (step one). Pyruvic acid is oxidized to form acetyl-coA, which is further oxidized in the Krebs/citric acid cycle, producing CO2, H20 and 38 moles of ATP (step two). Severe shock: anaerobic metabolism is the predominant cellular metabolic process. Glucose breaks down into pyruvic acid, but there is not enough O2 present to enter the Krebs' citric acid cycle for aerobic metabolism. Therefore, the cell cannot enter the second step, thus only uses glycogen and fat stores for energy. As a result, minimal ATP is produced, and the cell loses ATP faster than it is produced. Pyruvic acid accumulates in the cell, and then degrades into lactic acid. Excess lactic acid accumulates in the cellular and extracellular compartments causing a decrease in blood pH, which shifts the oxyhaemoglobin disassociation curve to the right. This means that haemoglobin has a decreased affinity for O2, therefore O2 is "let off" easier, but O2 becomes harder to "pick up". This causes increased cell permeability and decreased enzyme disassociation, which concordantly decreases cell function/repair/division. Without sufficient energy production, normal cell function and the electrochemical gradient across the membrane cannot be maintained. The Na/K pump is impaired, resulting in excess Na inside the cell and K loss from the cell. The increase in intracellular Na causes cellular oedema (where Na goes H20 follows) and increased cell membrane permeability. This increases the loss of fluid from the intravascular compartment, which decreases BV. Mitochondrial activity becomes severely depressed and lysosomal membranes may rupture. This results in the release of digestive enzymes that cause further intracellular destruction. This is followed by cell death and the release of intracellular contents into the extracellular space. The destruction of the cell membrane activates the arachidonic acid cascade, the release of inflammatory mediators and the production of O2 free radicals that extend cellular damage. Myocardial and neuronal cells are profoundly and immediately affected. Glucose: Deranged glucose metabolism may be caused by either impaired cellular glucose uptake or impaired glucose delivery. Firstly, during septic and anaphylactic shock, glucose uptake is prevented by vasoactive toxins, endotoxins, histamine and kinins. Secondly, the body's compensatory mechanisms are activated by shock, causing a high level of cortisol, growth hormone and catecholamines in the blood. These factors cause hyperglycaemia and insulin resistance, among other effects. Due to impaired glucose use, cells shift to glycogenolysis, gluconeogenesis and lipolysis. This increases the energy requirements, which can result in cellular failure.

Shock: - Define - Presentation - Populations at high risk

Shock is defined as global organ, tissue, and cellular hypoperfusion, due to an imbalance between O2 supply and demand. This may be caused by reduced O2 delivery, increased O2 consumption, inadequate O2 utilisation, or a combination of these processes. It most commonly occurs when there is circulatory failure (manifested as hypotension). Adequate perfusion of the cells is dependent on the three components of the circulatory system: heart (pump), blood vessels (pipes) and blood. Therefore, compromise in any one of these three components results in: - Global hypoperfusion causing cellular hypoxia - Diffusion across the capillary bed is slow, which causes sludging. This causes decreased diffusion of nutrients and wastes into and out of the cell, which causes electrolytes imbalances and activates the clotting cascade, resulting in DIC and/or ARDS. - Anaerobic metabolism and sludging of blood in the capillary bed cause cellular and organ dysfunction due to the accumulation of products from metabolism within tissues, triggering an inflammatory response that causes cellular/organ dysfunction (i.e. DIC, ARDS, and/or MODS) - Signs of shock. Presentation: To have shock, a patient must have either hypotension or signs of significantly impaired perfusion, including: - Cool, pale, clammy, cyanotic skin - Dry mucous membranes - Skin tenting - Prolonged CRT - Hypoxia - Tachycardia - Tachypnoea (to compensate for lactic/metabolic acidosis and to increase O2 supply to hypoxic tissues) - Altered LOC - Hypotension - Narrowed PP (due to potent vasoconstriction increasing DBP) Severe shock: - Severe tachycardia - A falling HR (very late i.e. decompensation) - Absent/weak radial pulses - Very prolonged CRT (check central, because some patients may have PVD which decreases the reliability of peripheral CRT) - Falling or unrecordable BP - Severe tachypnoea (to compensate for lactic/metabolic acidosis and to increase O2 supply to hypoxic tissues) - Altered LOC: agitation, confusion, falling LOC, often with preservation of motor score. Populations at high risk: - Infants: have a high risk of shock because they have a small vascular volume, immature immune system and a greater BSA. - Geriatrics: are increasingly susceptible to shock due to polypharmacy, blunted compensatory mechanisms and comorbidities.

Hypovolaemia from uncontrolled bleeding: - Indications and why - Management - Talk to permissive hypotension - Transport

The following follow a pattern of bleeding that is relatively uncontrolled in nature: - Peripheral penetrating trauma uncontrolled - Penetrating truncal trauma - Leaking AAA - Ectopic pregnancy. Management: - LATER - Request blood early - Compress any external bleeding: • Direct, sustained, firm external pressure • No benefit in raising a bleeding limb unless the bleeding is clearly venous and coming from near the hand or foot • Tourniquet: apply a tourniquet to peripheral bleeding if it cannot be controlled with direct pressure. Apply over a dressing tight enough to assist with direct pressure, but not tight enough to stop arterial flow. Re-evaluate the need for a tourniquet after bleeding is controlled. Consider releasing the tourniquet if there is a focal bleeding point that can be controlled with direct pressure and transport time to ED is >30mins • Topical adrenaline: if a clinically significant bleed continues despite direct pressure, and the wound is unsuitable for tourniquet application, then consider topical adrenaline: 1:10,000 solution. Either flood the wound with this solution and continue to provide direct pressure, or if there is a significant wound cavity, then pack the wound with adrenaline soaked gauze - Penetrating objects: • Do not remove penetrating objects from the head or truncal area (i.e. neck, axillae, chest, abdomen, pelvis, or groin), because severe bleeding may occur that cannot be compressed. Instead, immobilise the penetrating object • Apply direct pressure around the object if severe bleeding is present and it is not removed • There is no role for spinal immobilisation if the patient has penetrating trauma to the neck or torso - Sucking chest wounds: cover with a standard dressing or colostomy bag - Eviscerated abdominal contents: cover with cling film - Splint and immobilise any fractures. If shock is associated with a possible pelvic fracture then firmly wrap pelvis and secure legs together - Keep the patient warm. Hypothermia worsens bleeding by contributing to coagulopathy - High flow O2 - Gain large bore IV access - Fluid administration if the patient is showing signs of severe shock: • Adults: 500ml NaCl • Children: 10ml/kg NaCl • Administer further fluid if the patient remains severely shocked. If the time to surgical intervention is going to be >1hr, then it is appropriate to lower the threshold at which fluid is administered. In this setting, continue to focus on permissive hypotension, but administer more fluid than the above and arrange for blood to be administered if possible • Arrange for blood to be administered if this protocol is available - TXA: • Not a priority, but should occur if IV access is obtained • Adults: 1g IV over 1-2mins • Paediatrics: 20mg/kg IV - Pain relief if required - R40 as early as possible. Permissive hypotension (i.e. low volume resuscitation): Mortality rates appear to be reduced when a patient with uncontrolled bleeding is kept permissively hypotensive prior to surgical control of the bleeding, hence the higher threshold for fluid administration compared to hypovolaemia from controlled bleeding (the former is indicated for severe shock, rather than signs of poor perfusion). Uncontrolled bleeding is usually from an artery rather than a vein, and clotting with haemostasis may occur when the BP is relatively low. If aggressive fluid resuscitation occurs, then this will increase BV and BP, and dilute clotting factors, both of which reduce the chance of clot formation and exacerbate blood loss. Therefore, when administering fluid to a patient with hypovolaemia from uncontrolled bleeding, clinical judgement is required to balance the risk of death from hypovolaemic shock, against the risk of exacerbating haemorrhage. Keep the patient permissively hypotensive, aiming for MAP of 65-85mmHg (optimal end organ perfusion and CPP, respectively. MAP = 1/3PP + DBP). Transport: - Clear recommendation to be transported to ED via ambulance - A patient with trauma and shock should be transported directly to a major trauma hospital.

Presentation of septic shock

The patient must have hypotension or signs of poor perfusion to be diagnosed with septic shock. However, some patients do not have hypotension, in which case they must have clear signs of very poor perfusion. Warm shock: the early phase of septic shock that is characterised by a hyper-dynamic (abnormally increased circulatory volume due to increased PVR causing increased BP) response, which is mediated by compensatory mechanisms in an attempt to increase perfusion (however, just because BP increases doesn't mean that perfusion is optimal). This usually begins within hours to days of the onset of inflammation of infection, and lasts for 6-72 hours. - Pink, warm, flushed skin (massive vasodilation) - Tachycardia - Full, bounding pulse - Tachypnoea (lactic and metabolic acidosis) - Auscultation may reveal crackles due to fluid shifts (increased capillary permeability causing fluid to move from the intravascular space to the interstitial fluid) - Pyrexia - Altered LOC: confusion Cold-shock presentation: the late or decompensated phase, which is characterised by a hypo-dynamic response. Cold shock begins approximately 6-72 hours after the beginning of warm shock. - Cool, clammy, pale, mottled, cyanotic skin (vasoconstriction shunts the blood remaining in the general circulation towards the crucial organs (e.g. heart and brain)) - Significant tachycardia - Weak or absent radial pulse - Hypotension despite fluid resuscitation (also known as refractory hypotension, where the patient may require >40ml/kg of NaCl IV) - Widened PP - Severe tachypnoea - Hypoxia (decrease in the number of functional capillaries and thus an inability to extract O2 for tissue and organs) - Severe pyrexia or temperature <36 - Altered LOC: confusion, agitation, restlessness, unconsciousness Subtle signs of septic shock: - Confusion - Diarrhoea - Nausea - Vomiting - Decreased urinary output - Aching muscles and joints - Rigors - Hyperglycaemia - EtCO2 <25mmHg.

Talk to: - Tourniquet application - Pelvic fracture assessment and splinting

Tourniquet application: A balance of risk. Tourniquets help control severe bleeding, but can cause significant tissue ischaemia and damage (i.e. to nerves and muscles). Therefore, a tourniquet should only be applied when direct pressure is insufficient to control severe bleeding, and it is preferable for bleeding to be controlled with direct pressure. Only use tourniquets issued by St John because self-made tourniquets cannot be tightened sufficiently to stop arterial blood flow. When applying a tourniquet: - Remove clothing from the limb if possible - Location: • 2 bones: if the tourniquet is applied to a forearm or lower leg, the presence of 2 bones may limit the pressure that can be applied to vessels. If bleeding continues despite the tourniquet being tightened maximally, then place the tourniquet on the upper arm or thigh • Femur: the tourniquet needs to be very tight, particularly if the thigh is large. Occasionally, you may need to apply 2 tourniquets over the thigh, with the second tourniquet applied proximally - Apply as distally to the wound as possible - Do not apply over a joint - Feel the distal pulse, and tighten the tourniquet until you can no longer feel the distal pulse, and until the bleeding at the wound has stopped. - Record the time of application - Leave the wound exposed so you can observe for bleeding - Re-check the tourniquet following treatment, because it may need to be tightened more if the BP improves - Provide pain relief: ketamine is likely to be required. If the patient is conscious and not in significant pain, it is likely that the tourniquet is not tight enough - Re-evaluate the need for a tourniquet after bleeding is controlled, IV access has been obtained, and appropriate fluid resuscitation has been commenced. Consider releasing the tourniquet if there is a focal bleeding point that can be controlled with direct pressure and transport time to ED is >30mins. If the bleeding cannot be controlled with direct pressure, then reapply the tourniquet. - A tourniquet may also be used to provide direct pressure over a dressing (e.g. a lacerated brachial artery). In this setting, the tourniquet needs to be tight enough to control bleeding, but not tight enough to stop arterial flow. Pelvic fracture: It is difficult to determine that the pelvis is fractured by clinical examination alone. Do not spring the pelvis for instability, but rather assume the pelvis is fractured if the patient has pelvic pain (occasionally radiating to lumbar), or is unable to report pain but has an MOI suggestive of pelvic fracture. Method: - Remove clothing whenever possible - Firmly splint the pelvis using a transfer/lifting belt, sagar strap/band, or a specific pelvic splint - Centre the pelvic splint over the pubic bone and apply firmly. It should feel like a firmly fitting belt - Do not use a sheet as this can rarely be applied firmly enough - Apply prior to extrication if this is feasible and the patient appears severely injured. If not feasible prior to extrication, then consider tying the legs together and placing the splint on the stretcher so that it can be applied immediately after extrication.