on 13-Dec-2021 (Mon)

Shock is a systemic state of low tissue perfusion that is inade- quate for normal cellular respiration. With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion, cell death ensues.

Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non-haemor- rhagic causes. Non-haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diar- rhoea, urinary loss (e.g. diabetes), evaporation, or ‘third-spacing’ where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction or pancreatitis. Hypovolaemia is probably the most common form of shock, and to some degree is a component of all other forms of shock. Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of cause.

Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues. Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy. Cardiac insufficiency may also be due to myocardial depression caused by endogenous factors (e.g. bacterial and humoral agents released in sepsis) or exogenous factors, such as pharmaceutical agents or drug abuse. Evidence of venous hypertension with pulmonary or systemic oedema may coexist with the classical signs of shock.

In obstructive shock there is a reduction in preload due to mechanical obstruction of cardiac filling. Common causes of obstructive shock include cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. In each case, there is reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in cardiac output.

Distributive shock describes the pattern of cardiovascular responses characterising a variety of conditions, including septic shock, anaphylaxis and spinal cord injury. Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord injury there is failure of sympathetic outflow and adequate vascular tone (neurogenic shock). The cause in sepsis is less clear but is related to the release of bacterial products (endotoxin) and the activation of cellu- lar and humoral components of the immune system. There is maldistribution of blood flow at a microvascular level with arteriovenous shunting and dysfunction of cellular utilization of oxygen. In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spaces and there may be con- comitant myocardial depression, complicating the clinical picture

Endocrine shock may present as a combination of hypovolae- mic, cardiogenic or distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insuf- ficiency. Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls due to low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to circulating and exogenous catecho- lamines. Adrenal insufficiency may be due to pre-existing Addison’s disease or be a relative insufficiency due to a patho- logical disease state, such as systemic sepsis.

Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of cause.

Endocrine shock may present as a combination of hypovolae- mic, cardiogenic or distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insuf- ficiency.

. In com- pensated shock, there is adequate compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of hypovolaemia.

Blood transfusions should be avoided if possible, and many previous uses of blood and blood products are now no longer considered appropriate. The indications for blood transfusion are as follows: ● Acute blood loss, to replace circulating volume and main- tain oxygen delivery; ● Perioperative anaemia, to ensure adequate oxygen deliv- ery during the perioperative phase; ● Symptomatic chronic anaemia, without haemorrhage or impending surgery.

If antibodies present in the recipient’s serum are incompatible with the donor’s cells, a transfusion reaction will result. This usually takes the form of an acute haemolytic reaction. Severe immune-related transfusion reactions due to ABO incompat- ibility result in potentially fatal complement-mediated intra- vascular haemolysis and multiple organ failure. Transfusion reactions from other antigen systems are usually milder and self-limiting. Febrile transfusion reactions are non-haemolytic and are usually caused by a graft-versus-host response from leukocytes in transfused components. Such reactions are associated with fever, chills or rigors. The blood transfusion should be stopped immediately. This form of transfusion reaction is rare with leu- kodepleted blood.

Complications from blood transfusion can be categorised as those arising from a single transfusion and those related to massive transfusion. Complications from a single transfusion Complications from a single transfusion include: ● incompatibility haemolytic transfusion reaction; ● febrile transfusion reaction; ● allergic reaction; ● infection: ● bacterial infection (usually due to faulty storage); ● hepatitis; ● HIV; ● malaria; ● air embolism; ● thrombophlebitis; ● transfusion-related acute lung injury (usually from FFP). Complications from massive transfusion Complications from massive transfusion include: ● coagulopathy; ● hypocalcaemia; ● hyperkalaemia; ● hypokalaemia; ● hypothermia. In addition, patients who receive repeated transfusions over long periods of time (e.g. patients with thalassaemia) may develop iron overload. (Each transfused unit of red blood cells contains approximately 250 mg of elemental iron.)

The clinical manifestations of heatstroke reflect a total loss of ther- moregulatory function. Typical vital-sign abnormalities include tac- hypnea, various tachycardias, hypotension, and a widened pulse pressure. Although there is no single specific diagnostic test, the historical and physical triad of exposure to a heat stress, CNS dysfunc- tion, and a core temperature >40.5°C helps establish the preliminary diagnosis. Some patients with impending heat stroke will initially appear lucid. The definitive diagnosis should be reserved until the other potential causes of hyperthermia are excluded. Many of the usual laboratory abnormalities seen with heatstroke overlap with other con- ditions. If the patient’s mental status does not improve with cooling, toxicologic screening may be indicated, and cranial CT and spinal fluid analysis can be considered. The premonitory clinical characteristics may be nonspecific and include weakness, dizziness, disorientation, ataxia, and gastrointestinal or psychiatric symptoms. These prodromal symptoms often resemble heat exhaustion. The sudden onset of heatstroke occurs when the main- tenance of adequate perfusion requires peripheral vasoconstriction to stabilize the mean arterial blood pressure. As a result, the cutaneous radiation of heat ceases. At this juncture, the core temperature rises dramatically. Since many patients with heatstroke also meet the crite- ria for systemic inflammatory response syndrome and have a broad differential diagnosis, rapid cooling is essential during the extensive diagnostic evaluation (Table 455-1). There are two forms of heatstroke with significantly different man- ifestations (Table 455-2). Classic (epidemic) heatstroke (CHS) usually occurs during long periods of high ambient temperature and humidity, as during summer heat waves. Patients with CHS commonly have chronic diseases that predispose to heat-related illness, and they may have limited access to oral fluids. Heat dissipation mechanisms are overwhelmed by both endogenous heat production and exogenous heat stress. Patients with CHS are often compliant with prescribed medica- tions that can impair tolerance to a heat stress. In many of these dehy- drated CHS patients, sweating has ceased and the skin is hot and dry. If cooling is delayed, severe hepatic dysfunction, renal failure, dis- seminated intravascular coagulation, and fulminant multisystem organ failure may occur. Hepatocytes are very heat sensitive. On presenta- tion, the serum level of aspartate aminotransferase (AST) is routinely elevated. Eventually, levels of both AST and alanine aminotransferase (ALT) often increase to >100 times the normal values. Coagulation studies commonly demonstrate decreased platelets, fibrinogen, and prothrombin. Most patients with CHS require cautious crystalloid resuscitation, electrolyte monitoring, and—in certain refractory cases— consideration of central venous pressure (CVP) measurements. Hyper- natremia is secondary to dehydration in CHS. Many patients exhibit significant stress leukocytosis, even in the absence of infection. Patients with exertional heatstroke (EHS), in contrast to those with CHS, are often young and previously healthy, and their diagnosis is usually more obvious from the history. Athletes, laborers, and mili- tary recruits are common victims. Unlike those with CHS, many EHS patients present profusely diaphoretic despite significant dehydration. As a result of muscular exertion, rhabdomyolysis and acute renal fail- ure are more common in EHS. Studies to detect rhabdomyolysis and its complications, including hypocalcemia and hyperphosphatemia, should be considered. Hyponatremia, hypoglycemia, and coagu- lopathies are frequent findings. Elevated creatine kinase and lactate dehydrogenase levels also suggest EHS. Oliguria is a common finding. Renal failure can result from direct thermal injury, untreated rhabdo- myolysis, or volume depletion. Common urinalysis findings include microscopic hematuria, myoglobinuria, and granular or red cell casts. With both CHS and EHS, heat-related reve...

Dipeptides are formed when two amino acids are joined together by a condensation reaction, forming a peptide bond.

atty acids can be: ◦ Saturated – there are no double C=C bonds and the molecule has as many hydrogen atoms as possible

Monomers are individual molecules that make up a polymer.

Polymers are long chains that are composed of many individual monomers that have been bonded together in a repeating pattern.