SAAS Clinical Manual - Notes PDF

**MEDICAL** Medical Index ============= Acute cardiogenic pulmonary oedema Anaphylaxis Bronchospasm and asthma Chronic obstructive airways disease Cardiac arrest Diabetes mellitus Ischaemic chest pain ECGs Narcotic overdose Obstetrics Paediatric croup Pain Seizures Sepsis Shock ACUTE CARDIOGENIC PULMONARY OEDEMA ================================== Definition ---------- An accumulation of fluid in the tissue of the lung and alveoli, forming a barrier to gas exchange. Acute pulmonary oedema occurs in a relatively short space of time and causes a rapid onset of profound hypoxia. Causes ------ 2 main causes: haemodynamic disturbance increased capillary permeability - **Cardiac causes:** ---------------------------- ---------------------------------------------- o hypoxia o CCF o MI o LVF o IHD o cardiomyopathy o pericardial disease ---------------------------- ---------------------------------------------- - valvular incompetence -- not all the blood is ejected from the ventricle in the right direction o chronic HT → hypertrophy -- cardiac muscle thickens and reduces the size of the chamber, less blood can be injected - cardiac tamponade -- large amounts of blood in the pericardial sack impeding stretch of the myocardium - dysrhythmias - **Other Causes:** ----------------------------------------------------------------------------------------------------------------------------- --------------------------------------------------------------------------------------------------------------------------------- o overdose o CVA o near drowning o irritant gas inhalation o rapid IV infusion o blood disorders o intracranial haemorrhage o lymphangitis carcinomatosis o PE o shock/sepsis o eclampsia o pancreatitis o lymphatic disorder o capillary epithelial damage ----------------------------------------------------------------------------------------------------------------------------- --------------------------------------------------------------------------------------------------------------------------------- - hypoalbuminaemia - ARDS (diffuse alveolar damage leads to increased capillary permeability) Pathophysiology --------------- - APO is a result of left ventricular dysfunction with pulmonary venous hypertension & alveolar flooding - left ventricular failure occurs due to a primary cardiac/hypoxic event, meaning it becomes unable to effectively receive blood from the right side of the heart and pump blood into the systemic circulation - the left vertical stiffens due to hypoxia (the muscle needs ATP in order to relax, however due to hypoxia, anaerobic metabolism is required to produce ATP) and cannot stretch to accept the volume of blood being pumped into it - the reduced elasticity of the left ventricle leads to diminished cardiac output (Frank-Starling's Law) - left ventricular pressure increases and is transmitted back into the atria and then into the pulmonary venous circulation and pulmonary capillaries - when the hydrostatic pressure (pushes fluid out of capillaries) exceeds the oncotic pressure (pulls fluid into capillaries) of plasma proteins, the serum portion of blood is forced out, into the interstitial space and eventually alveoli - when the hydrostatic pressure exceeds the oncotic pressure, there is a net movement of fluid into the interstitial and alveoli and the lymphatic system cannot cope - under normal conditions lymphatic drainage would remove excess fluid in the interstitial of the lungs - in APO the lymphatic drainage does increase to an extent, however is overwhelmed and unable to increase enough - due to the fluid in the interstitial space and alveoli, the amount of oxygen crossing the membrane & fluid barrier decreases (V/Q mismatch) - significant fluid accumulation in the alveoli can dilute alveolar surfactant (decreases surface tension in normal alveoli), making reinflation of alveoli difficult therefore ↑WOB - a sympathetic response is stimulated due to the hypoxic state, therefore HR increases, and blood vessels constrict to increase oxygen supply to the heart - this stimulation only increases the left ventricles inability to eject blood, by further increased the speed and pressure blood enters into the right side of the heart, further increasing the pressure in the left ventricle, and further transmitting pressure back into the pulmonary venous circulation and pulmonary capillaries - this function further potentiates hypoxia and left ventricle stiffening - if pressure is maintained or increase, eventually RBCs will be forced across the membrane, further attracting fluid, causing irritation & coughing, as well as decreasing the available haemoglobin for oxygen transport - RBCs in the alveoli, with diluted surfactant, will eventually produce pink frothy sputum - deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, decreasing systemic arterial oxygenation and causing significant dyspnoea - the ventricular stiffening due to hypoxia and the sympathetic response, as well as the inability to eject blood, with the increasing left ventricular pressure and pulmonary hypertension is a spiralling effect which self-perpetuates, until the patient is in acute respiratory distress and respiratory failure Patient Presentation -------------------- - acute dyspnoea - pale or cyanosed - crackles, gurgles and wet breathing sounds - tachycardia, elevated BP, diaphoretic -- sympathetic response to compensate for cardiac failure - decreased SpO~2~ - shallow, rapid respirations - agitation and confusion as hypoxia develops - chest pain- from cardiac cause, may be masked by respiratory distress - coughing and pink, frothy sputum (late stage) - wheeze/bronchospasm (protective reflex, body interprets fluid in lungs and tries to stop more entering, not realising the origin of the fluid) - altered GCS - peripheral oedema - jugular vein distention ANAPHYLAXIS =========== Definition ---------- The severe form of life threatening allergic reaction after repeated exposure to antigen -- usually a protein. Anaphylactic reactions can differ in severity. Severe anaphylaxis often has hypotension, bronchospasm and oedema components. Causes ------ Almost any substance can bring about an anaphylactic reaction, including: - drugs (antibiotics, penicillin, aspirin, NSAIDs) - bites, stings & venom - foods (peanuts, shell fish) - preservatives - unknown Pathophysiology --------------- - in some individuals, an exposure to an allergen (usually a protein), causes a primary IgE production - an allergen is introduced into the circulation, where Helper T cells help stimulate specific B cell production of IgE antibodies, specific to the allergen - this is a local response to the allergen which activates the immune system to provide large amounts of IgE - large amounts of allergen-specific IgE antibodies bind to receptors on the surface of mast cell membranes which remain inactive until a repeat exposure to the antigen (i.e. the person is now 'sensitised' or 'primed') - mast cells are normally distributed throughout connective tissue, especially in mucus membranes of the respiratory, GI and genitourinary tracts, and adjacent to blood and lymph vessels - when an allergen binds and cross-links to an IgE-sensitised mast cells (in tissue) & basophils (mast cell equivalent in the blood stream), histamine is released from their intracellular granules, along with other chemical mediators such as bradykinins, acetylcholine, adenosine and chemotactic mediators - mast cell exocytosis also causes the release of arachidonic acid from the cell membrane, which - the immediate histamine release causes the following: - respiratory system: - bronchospasm - mucus plugging - inflammation and airway swelling o cardiovascular system: - peripheral vasodilation (causing erythema) - increased capillary permeability → leakage/loss of plasma from circulation (circulatory shock) o gastrointestinal system: - increased GI activity (smooth muscle constriction) - increased mucus secretion/ fluid in gut → nausea and vomiting, diarrhoea, cramps and increased saliva production - central nervous system: - impaired gas exchange and shock causing nervous system response - deterioration of neurological function (confusion, weakness, headache, seizures, coma) o skin: - signs secondary to vasodilation - erythema and urticaria - itching - there are two defined phases of anaphylaxis -- a primary or early-stage, characterised by vasodilation and vascular leakage and smooth muscle contraction and a secondary or late-phase response, which is a more intense infiltration of tissues with acute and chronic inflammatory cells (such as eosinophils) in addition to epithelial cell damage - primary phase usually occurs within 5-30 minutes post exposure, and usually subsides within 60 minutes - late phase can occur 2-8 hours later and last up to several days - anaphylactoid reactions are clinically indistinguishable from anaphylaxis, however they are not IgE mediated, and do not require prior sensitization - the LIFE THREAT in the case of anaphylaxis is airway constriction and oedema and circulatory collapse Patient Presentation -------------------- - SOB, dyspnoea - angioedema - use of accessory muscles - wheeze - stridor/hoarse voice - altered GCS - urticaria - anxiety - nausea and vomiting - tachycardia - hypotension - abdominal cramps and chest tightness - flushed skin - itching and hives - cyanosis BRONCHOSPASM AND ASTHMA ======================= Definition ---------- Bronchospasm: an abnormal contraction of smooth muscle resulting in narrowing of the lumen and obstruction of the airways. This is a main characteristic of asthma. Asthma: a reversible respiratory condition characterized by episodes of SOB, wheeze and cough, which is caused by spastic contraction of the smooth muscle in the bronchioles (bronchospasm), mucosal oedema and mucus production, which is often triggered by hypersensitivity of the bronchioles in response to a foreign substance in the air. Causes ------ - extrinsic (allergy) o allergens o pollen o animal dander and dust mites - intrinsic (non-allergic) o exercise o cold air o smoke o laughter o aspirin/NSAIDs/other medications o emotional stress o infection Pathophysiology --------------- - there is a two-phase reaction upon exposure to a trigger (an early/immediate and a late stage) the key features of asthma are bronchospasm, airway oedema and excessive mucus production - the early stage has an onset of 10-20 minutes and presents with: - bronchoconstriction and bronchiolar oedema resulting from the introduction of an allergen into the airways - when an allergen enters the airway and cross-links onto IgE mediated mast cells, it causes exocytosis and the release of inflammatory mediators (histamine, leukotrienes, prostaglandins, thromboxane, serotonin, platelet activating factor and bradykinin) - bronchoconstriction is precipitated by histamines, leukotrienes and cholinergic receptors (such as acetylcholine) - stimulation of the H1 receptor (histamine) on bronchial smooth muscle triggers bronchoconstriction - afferent nerve endings originate under the inner lining of the bronchus, and when stimulated by a pathogen, release acetylcholine from efferent nerve endings in the bronchial small airways through vagal pathways - acetylcholine effect on bronchial smooth muscle results in further bronchoconstriction o the inflammatory mediators also cause increased bronchiolar capillary permeability, resulting in leakage of fluid and therefore bronchiolar oedema and mucus production, as well as increased mucus viscosity - these factors greatly reduce expiratory airflow - the late phase occurs 4-8 hours after the exposure and presents with: - further bronchoconstriction, oedema and mucous plugging o cytokines that were activated in the immediate stage have been working for 4-8 hours to recruit further inflammatory mediators (basophils, eosinophils & neutrophils) - these mediators cause damage to the epithelium of the airway, resulting in further exocytosis of mast cells and basophils and producing acute airway hyper responsiveness - damage to the epithelium exposes bronchial nerves which become hypersensitive and produce a cough, overdrive in mucous production (to try to protect and cover the exposed nerves) and oedema - this further impairs mucociliary function (clearance of mucous) and reduces clearance of the respiratory tract - this results in widespread mucous plugging in small bronchi and bronchioles, as the production of mucous is increased, and the clearance is reduced - these functions further compromise the airway and reduce expiratory airflow - untreated/unresponsive asthma: - in either the early phase, or late stage of asthma, if the exacerbation is not corrected, bronchospasm, airway oedema and excessive mucous production can lead to respiratory acidosis - as intrathoracic pressure increases from gas trapping, venous return decreases due to compression of the vena cava - this drops blood pressure, preload and cardiac output, thereby cerebral perfusion is impaired and respiratory acidosis occurs, leading to loss of consciousness and respiratory arrest Patient Presentation -------------------- Presentation varies from patients with mild to severe asthma. ### Mild Symptoms - dyspnoea - cough (especially in children) - expiratory wheeze - increased HR, RR and BP - decreased SpO~2~ - use of accessory muscles - able to speak in short or broken sentences ### Severe Symptoms - altered GCS - speaking in single words - decreased SpO~2~++ - cyanosed, pale, sweaty - expiratory and inspiratory wheeze or no breathing sounds CHRONIC OBSTRUCTIVE AIRWAYS DISEASE =================================== Definition ---------- Chronic airways disease can be described as the chronic obstruction of expiratory air flow combined with symptoms of chronic bronchitis along with emphysema and usually asthma. **COAD triad:** - chronic bronchitis - emphysema - asthma Causes ------ - smoking - passive smoking - air pollution and fumes - workplace exposure to dust, smoke, fumes or chemicals - genes -- about 3% of people with COAD have DNA containing a defect called alpha-1 antitrypsin deficiency where the tissue of their airways has a deficiency in a protein needed to provide protection from damage, which can lead to severe COAD - asthma -- although not common, asthma left untreated can lead to COAD due to a lifetime of damage Pathophysiology --------------- COAD has two main pathophysiological mechanisms coupled together: - chronic bronchitis -- chronic, productive cough for 3 months over 2 years. - emphysema -- abnormal and permanent enlargement of the air spaces distal to the terminal bronchioles and destruction of their walls. Patients may have a predominance of one or the other mechanism. ### Chronic Bronchitis - continual exposure of the airway tissue to irritants such as cigarette smoke causes chronic inflammation with swelling and excess mucus production, altering the cells lining the airways, narrowing the large and small airways - inflammation's purpose is to destroy a foreign organism, clear debris and promote healing and repair - there are two components: vascular and cellular - with the initial exposure/injury, there are chemical mediators released by the damaged tissue resulting in a series of events - the vascular response is an initial vasoconstriction followed by vasodilation, promoting blood flow to the area and increasing the hydrostatic pressure (the pressure exerted by a fluid) and a resultant increase in capillary permeability - the irritant binds to the antibodies adhering to the outer membrane of the mast cells (leukocytes) and trigger degranulation (EXOCYTOSIS) and the release of chemical mediators such as histamine and serotonin - these chemical mediators signal vasodilation and disrupt the tight junctions between the cells in the vessel walls, resulting in leaky capillaries - other chemical mediators include cytokines which help activate nearby immune system cells, trypase which stimulates B and T cell lymphocytes, thromboxane which aids in blood clot formation and prostaglandin - one of the cytokines produced by mast cells in Tumour Necrosis Factor (TFN) is released primarily in response to bacterial products - they regulate immune cells, act as a chemoattractant to bring neutrophils to the area and also signal the response of more TFN release - the increase in hydrostatic pressure exerted by the increase in blood flow and the opposing slight oncotic pressure of the surrounding tissues causes the movement of plasma out of the capillaries along with large amounts of protein (EXCUDATE) - the site of inflammation becomes thick with cells and debris, such as serous fluid, red blood cells and fibrinogen, also known as PURULENT or pus - phagocytes such as neutrophils and monocytes, being attracted to the chemical mediators, move towards the areas and adhere to the vessel wall (MARGINATION) - the phagocytes then slip out through the junctions (EMIGRATION), recognize the pathogen/irritant, attaches to it and engulf it, causing degranulation and destruction of the pathogen/irritant - the inflammatory cells also produce large amount of Platelet Aggregating Factor (PAF) and coagulation proteins cascade commences - constant exposure to an irritant such as smoking eventually damages the ciliated cells found in the airways, from the continual inflammation of the airways - via their finger-like projections, these cells move particles and fluid (mucus) to keep the airways - the function of these cilia is reduced and eventually destroyed with continue irritant exposure and often these cells are replaced by goblet cells (mucus-producing), thus a more warm, moist environment in which bacteria can breed is created - thus, with the inflammatory process, the increase in mucus production and the decrease in cilia available to clear away this mucus, a chronic cough can develop - all these processes over a period of time cause scarring and remodelling, which narrow the airways and limit airflow and can also decrease the production of regulatory products such as AngiotensinConverting Enzyme ### Emphysema - emphysema is a lung disease characterized by abnormal enlargement of the airways of the lung, beyond the level of the terminal bronchioles and is due to the destruction of the septa of the alveoli - the septa contain elastic connective tissue that drives lung recoil after inhalation - normal lung is stretched with the intake of air and then air is expelled due to the lungs elasticity when relaxing - with the loss of septa there is a loss in the integrity of the shape and hence when air is exhaled, parts of the alveoli collapse - this has several consequences such as a reduced amount of surface area available for gas exchange - the lack of elasticity of the tissue decreases the ability of the air to flow passively out through the airways, thus over inflation of the alveoli occurs and gas trapping - many of these sufferers use accessory muscles during exhalation and appear "barrel chested" - their work of breathing increases and coupled with a decrease in gas exchange, they can easily become markedly dyspnoeic - exposure to irritants such as cigarette smoke also damages the vasculature surrounding the alveoli further decreasing gas exchange - pathogenesis in emphysema is based on the over destruction of alveolar septa, which occurs with a chronic exposure to irritants such a cigarette smoke but only normal plasma levels of alpha-1 antitrypsin (α1-AT) - α1-AT antagonises the action of the serine elastase enzyme, which is released by macrophages responding to injury and does cause some damage in the process - by antagonizing this enzyme, damage is reduced and more CT can be replaced, thus fewer septa are lost - however, in most smokers there is no increase in α1-AT plasma levels and thus the loss of septa mounts ### Cor Pulmonale - cor pulmonale is the decreased function of the right ventricle due to increased resistance in pulmonary circulation, when the mean pulmonary arterial pressure is \>20mmHg - complete right sided failure occurs when the pressure exceeds 40mmHg - there are several causes for this increase in arterial pressure, one being that chronic hypoxia leads to pulmonary arteriolar constriction through over increased involvement of the physiological mechanism to maintain the balance of ventilation and perfusion in the lungs - also, chronic hypercapnia and respiratory acidosis which also causes pulmonary vasoconstriction and the anatomical disruption of the vasculature bed of the lungs due to the disease process peripheral oedema may be seen in patients with cor pulmonale Patient presentation -------------------- The degree to which chronic bronchitis or emphysema is present in a patient determines the emergence of particular signs and symptoms. Clinical presentation for emphysema predominance: - rapid breathing and increased work of breathing - pursed lips due to the increase work of expiration against collapsed airways - thin and gaunt and "barrel chested" Clinical presentation for chronic bronchitis predominance: - productive cough - systemic oedema reflecting right sided heart failure - hypoventilation and heart failure produces characteristic cyanosis - little hyperventilation despite the increase in PCO~2~ Other signs and symptoms: - febrile - wheeze - dyspnoea at rest and on exertion - fatigue - peripheral oedema - chest tightness, often not relieved with nitrates - haemoptysis due to pulmonary arteriolar rupture or leakage - hepatic congestion (late stage) -- anorexia, jaundice, right upper quadrant pain - frequent respiratory infections - prolonged expiratory phase CARDIAC ARREST ============== Definition ---------- Sudden cessation of cardiac output and effective circulation. The prime aim of arrest management is oxygen delivery to the heart and brain via continuous compressions, with defibrillation when appropriate. Compressions deliver oxygen, ventilation replaces oxygen on the haemoglobin and adrenaline confines oxygenated blood to the core and thus coronary/cerebral circulation. Causes ------ - CAD/IHD - VT/VF - cardiac tamponade - hyper/hypokalaemia and other electrolyte disturbances - drug toxicity - electrocution - trauma i.e. head injury, direct cardiac injury - burns, asphyxia - hypovolaemia - pulmonary embolism - tension pneumothorax Pathophysiology --------------- - blood flow and oxygen supply to the coronary arteries ceases due to one of many possible causes - oxygen supply and waste removal stops due to cessation of blood flow - hypoxia leads to anoxia (total depletion of oxygen) and dysrhythmias arise due to the hearts inherent demand for oxygen for cardiac muscle contraction and relaxation, and electrical conduction through the use of ATP to power ion channel pumps - depletion of oxygen and glucose to the brain causes a loss of consciousness which leads to inadequate or absent breathing - global ischemia occurs with consequences at the cellular level that adversely affect organ function after resuscitation - the main consequences involve direct cellular damage and oedema formation, this is particularly damaging to the brain - systemically, the body is forced into anaerobic metabolism, increasing levels of lactic acid, thereby reduced blood pH and causing metabolic acidosis - ATP becomes depleted, especially quickly in rhythms such as VF/VT - decreased ATP production leads to loss of membrane integrity and ionic redistribution (sodium/potassium pumps fail) - there is an efflux of potassium and influx of sodium and calcium into the cell - excess sodium in the cell causes cellular oedema as water follows sodium into the cells. - cells swell and burst/lyse - excess calcium damages mitochondria (thereby further depressing ATP production), as well as increases nitric oxide production, forming damaging free radicals - abnormal ion flux also results in unwanted depolarization of neurons, releasing potentially harmful neurotransmitters - inflammatory and chemical mediators are released which may cause loss of vascular integrity and further oedema **Circulatory Obstruction** i.e. pericardial tamponade, tension pneumothorax, large PE - decreased coronary artery perfusion pressure (CAPP): o ↓CAPP: ↑pressure on vena cava → ↓venous return → ↓preload → ↓afterload  ↓CAPP - generally initial tachycardia and hypotension, which eventually progresses to bradycardia and then PEA due to a lack of cardiac output - occasionally VF or asystole are seen - DVT → PE -- saddles in the branch of the pulmonary arteries ### Metabolic causes - hyperkalaemia (excess potassium) leads to widening of the QRS and peaked T waves, that may deteriorate into VT, VF, asystole or PEA - an ionic distribution problem ### Drug Toxicity - specific characteristics depend on the drug - antidote to the drug may be immediately available - worthwhile prolonging CPR until it is - cyanide- mitochondria unable to convert ADP back to ATP (stops oxidative phosphorylation) ### Electrocution - causes dysrhythmia via electricity has a direct effect on electrical conducting system of the heart - apnoea - electrical damage to respiratory centre ### Trauma - direct injury to the heart or brain (respiratory, vasomotor or cardiovascular centre) - secondary to other causes (burns → airway swelling → asphyxia) - hypovolaemia ### Three Phases of Cardiac Arrest - a study presented a three-phase model of cardiac arrest to reflect the time-sensitive progression of cardiac arrest and resuscitation. - phase one shows that the most important and effective intervention during the first 4 minutes is defibrillation - the second phase suggests that the generation of adequate cerebral and coronary perfusion pressure is critical during this time to achieve neurological normal survival, this is achieved through effective compressions - the third phase occurs between 8-10 minutes and greater. During the metabolic stage, defibrillation and CPR become significantly less effective, due to the diffuse cellular damage which has occurred to internal organs, chance of survival is poor DIABETES MELLITUS ================= Definition ---------- Diabetes mellitus is an endocrine disorder characterized by inadequate insulin production resulting in high blood sugar levels, with low blood sugar a complication of medication. The control of blood glucose is about energy supply. A failure to supply the cells with glucose leaves those cells without an effective energy supply forcing the body to use other strategies to meet energy needs. Insulin from the beta cells in the islets of Langerhans in the pancreas promotes glucose and potassium entry into cells. Glucagon from the alpha cells in the islets of Langerhans promote the breakdown of glycogen to glucose in liver cells using the second messenger cyclic AMP. Type 1 diabetes is about a failure of insulin production, while type 2 diabetes is about a failure of insulin receptors. Type 1 or juvenile diabetes tends to occur early in life and is thought to be associated with an autoimmune response to an infection; it is treated with insulin. Type 1 diabetes is the main type of diabetes that emergency medical services will encounter. The type 2 diabetic is usually an older presentation of the disease and is managed with diet and oral medication. The type 2 diabetic is much less likely to encounter the emergency medical services. Endocrine Function in Blood Glucose Homeostasis ----------------------------------------------- - endocrine function secrets hormones into the blood that maintain homeostasis of blood sugar these hormones are secreted from islets of Langerhans in the pancreas - each islet cell contains: - blood glucose homeostasis is maintained by the secretion of insulin and glucagon ### Insulin - produced by beta cells - stimulates the uptake of glucose from the blood into the cell - triggered by an increase in BGL, thus facilitating cellular uptake of glucose, thereby reducing BGL - promotes glycogenesis (conversion of glucose to glycogen for storage) in the liver and skeletal muscle - inhibits gluconeogenesis (generation of glucose from non-carbohydrate source) - prevents glycogenolysis (breakdown of glycogen back to glucose) - inhibits lipolysis (fat breakdown) ### Glucagon - produces by alpha cells - travels from pancreas to liver via the portal vein where it stimulates glycogenolysis - maintains BGL between meals and when fasting - stimulates gluconeogenesis - stimulates lipolysis - inhibited by a high BGL ### Adrenal Cortex - catecholamine release, such as adrenaline, is released from the adrenal medulla during periods of hypoglycaemia - adrenaline acts similarly to glucagon- stimulates glycogenolysis - increases lipolysis - adrenal cortex also releases growth hormone and cortisol in response to prolonged hypoglycaemia and stimulate gluconeogenesis in the absence of glucose ### Blood Glucose Homeostasis Type 1 Diabetes: IDDM --------------------- Absolute Insulin Deficiency - initially a million beta cells -- immune response triggered that kills them (immune mediated diabetes) - characterised by high BGLs, weight loss, polyuria, polydipsia, and polyphagia. - requires exogenous insulin - juvenile onset - breakdown of proteins and body fats develops ketosis in the absence of insulin ### Causes - genetic: predisposition, destruction of beta cells - immune: HLA Markers (human leukocyte antibodies) - viral: Mumps or chemical toxins shut down beta cells ### Pathophysiology - despite high blood sugar levels the cells are depleted of glucose (cellular starvation), leading to gluconeogenesis - increases in ketones (by product of lypolysis) leads to ketoacidosis - metabolic acidosis leads to glycosuria (osmotic diuresis) and dehydration Type 2 Diabetes --------------- Decrease in insulin production or receptor abnormalities -- relative insulin deficiency - more common than type 1, previously known as mature onset - slow onset associated with obesity - decrease in insulin production and/or less functioning or poor functioning receptors (insulin resistance) - enough insulin to prevent lypolysis and therefore ketoacidosis - patients are prescribed oral medication -- some may also require exogenous insulin, so therefore type 2 diabetics can be NIDDM or IDDM. ### Causes - initially insulin resistance results in increased secretion form pancreatic beta cells - over time secretion declines due to exhaustion - this results in heightened blood sugar levels ### Pathophysiology - weight increase results in a decrease in available insulin receptors - insulin receptors become defective or less sensitive to insulin -- require more insulin - initially more endogenous insulin is secreted to maintain a normal BGL (hyperinsulinemia) in presence of excess glucose, but over time the beta cells becomes exhausted and secretion declines - this results in increases blood sugar levels - NIDDM may eventually lead to IDDM Hyperglycaemia -------------- An increased blood sugar level due to relative or absolute lack of insulin production or uptake. ### Pathophysiology - osmotic diuresis -- polyuria and polydipsia o excess glucose in the blood spills into urine to be excreted o filtration becomes hyperosmolar -- increased H~2~O loss as water follows the glucose o therefore excess urination to remove excess glucose from the blood - cellular dehydration -- polydipsia due to polyuria o increased osmotic pressure in extracellular fluid due to decrease in diffusion of glucose into the cell - no water, or glucose in the cell → cellular dehydration → increased thirst → polydipsia o additionally, excess water being excreted through polyuria - weight loss -- polyphagia o uninhibited lypolysis occurs due to unavailability of glucose o appetite increases due to cellular starvation - ketoacidosis o decreased glucose availability means fat is broken down for energy production o fatty acid portion travels to liver and converted to ketones o acidosis decrease blood pH = metabolic acidosis - electrolyte Imbalance o ketoacidosis may induce vomiting increasing dehydration o loss of electrolytes Na^+^, K^+^ and H~2~O ### Signs and Symptoms - hot, flushed skin - confusion and agitation - vomiting, nausea - sweat, ketone smelling breath - dehydration - increased thirst, hunger and urination - deep, rapid respirations -- compensation of acidosis - tachycardia - weakness - the three P's: polyuria, polyphagia, polydipsia - can lead to coma Hypoglycaemia ------------- Decreased blood glucose due to too much insulin or lack of glucose. ### Pathophysiology - depletion of blood glucose o due to accidental or purposeful insulin overdose o lack of education in diabetes management (i.e. must eat prior to taking insulin, effects of fever and illness/infection on BGL etc.) - lack of blood glucose o infection causing increased energy requirements o starvation o exercise increasing energy consumption o excessive alcohol consumption - interference of cellular respiration - alcohol is metabolised preferentially to carbohydrates - competition for NAD+ - inhibits gluconeogenesis ### Signs and Symptoms - altered GCS (glucose required for brain function) - cool, pale and diaphoretic (adrenaline release to stimulate glycogenolysis) - hunger (cellular starvation) - anxiety - tachycardia - seizures, unconsciousness, coma Ketoacidosis ------------ - usually occurs in type 1 diabetics - slow onset - no insulin = inability to inhibit lipolysis - fatty acid released from fat cells → converted to ketones in the liver - fatty acid metabolism → ketone production → leads to ketoacidosis - this is a form of metabolic acidosis - acidotic state due to increased ketones leads to: o increased respirations to correct acidosis o ongoing dehydration leads to circulatory shock o cardiac dysrhythmia, fatal arrhythmias ISCHAEMIC CHEST PAIN ==================== Definition ---------- The result of anaerobic metabolism/ischemia and lactic acid production due to cardiac oxygen supply/demand mismatch. Causes ------ - atherosclerosis - angina - myocardial infarction - thrombus - hypoxia - shock - rate related pain Pathophysiology --------------- - afferent pain fibres are divided into somatic and visceral: o somatic: the skin and deep tissue (i.e. parietal pleura) are innervated by somatic pain fibres, which tend to stimulate more intense pain that is easier to pinpoint and locate - visceral: internal organs and blood vessels are innervated by visceral pain fibres, and tend to be dull/vague pain which is harder to localise and pinpoint, often described as "discomfort, heaviness or aching" - nociceptors detect both somatic and visceral pain fibres o patients frequently misinterpret the origin of visceral pain as it is often referred to a different area of the body which corresponds with adjacent somatic nerves (i.e. arm pain is the complaint, when in fact the patient is having a myocardial infarction) - cardiac chest pain is caused by a lack of oxygen supply to the heart; more specifically a mismatch between oxygen supply and the oxygen required (demand) - during periods of low oxygen myocardial demand (e.g. during rest), blood supply through vessels may be adequate to meet the demand of the heart - however during times of increased oxygen demand, blood flow through vessels is limited and the region of the heart supplied by the affected vessel may potentially become ischemic - cardiac myocytes compensate to oxygen deprivation by switching to anaerobic metabolism, in which insufficient ATP is produced - lactic acid is a by-product of anaerobic metabolism, and reduces the pH level in the blood - as anaerobic metabolism continues, lactic acid builds up in the tissue - visceral afferent nerves are stimulated by the lactic acid in the coronary vessels which are detected by nociceptors and interpreted as pain by the cerebral cortex - heart rate, contractility, preload and after load determine cardiac oxygen demand o preload: pressure/volume ratio -- condition of the ventricle when contraction begins, preload is the stretch of the LV at end-diastole (Frank-Starling Law) - afterload: the tension of stress developed in the left ventricle during ejection, i.e. it is the end load in which the heart contracts to eject blood - cardiac output is determined by heart rate and stroke volume (CO = HR x SV) - as mean arterial pressure is deduced from BP, a reduction in BP subsequently reduces MAP - determinants of coronary artery blood flow o perfusion pressure (diastolic pressure; coronary arteries are perfused during diastole) o pressure gradient o heart rate o resistance to flow (wall stress/atherosclerosis) - coronary artery perfusion pressure (CAPP) = MAP- LVED pressure (preload) ### Coronary Artery Disease - also known as ischemic heart disease - group of diseases including: - common symptom is chest pain. - underlying cause is the slow build-up of atherosclerotic plaques in the coronary arteries ### Atherosclerosis - a progressive narrowing of the lumen of medium and large sized arteries (coronary, cerebral, carotid, iliac, popliteal) - thick, hard plaques called atheroma, develop in the blood vessels as a result of circulating low density lipoproteins depositing behind the lumen - these harden and calcify behind the lumen, narrowing the artery, reducing blood flow - this restriction of blood flow translates to a reduction in oxygen delivery ### Angina - angina is a symptom of coronary artery disease (CAD) resulting in demand/supply mismatch of oxygen delivery and waste removal - angina can be caused by atherosclerosis or vasospasm o stable angina - occurs during exertion - during rest, blood flow is sufficient to meet demand, however on exertion, oxygen demand is increased beyond the supply restrictions imposed by a partially occluded coronary artery - lasts for 3-5 minutes - resolved with rest, reassurance, oxygen and nitrates o unstable angina - atherosclerotic plaque has ruptured (fibrous cap covering atheroma ruptures), platelet-rich thrombus develops at the site of rupture - severe CAD complicated by vasospasm, platelet aggregation, transient thrombi & emboli due to inflammatory mediates released at the site of rupture - recurrent transient reduction in coronary blood supply because of vasoconstriction & thrombus formation at the site of plaque rupture - critical narrowing of vascular lumen - can occur at rest - increased severity and duration to that of stable angina ▪ not easily relieved - caused by coronary artery spasm restricting myocardial blood flow - pain can occur at any time, including during sleep - management as per angina ### Myocardial Infarction - death of cardiac muscle due to prolonged hypoxia - the death of tissue is surrounded by a ring of injured tissue and a ring of ischemic tissue - normally occurs in the presence of CAD and caused by coronary thrombosis or coronary artery spasm - when atherosclerotic plaque ruptures, it releases toxins and attracts factors that causes platelet coagulation and promote clot formation leading to partial or full occlusion - anaerobic metabolism in oxygen deprivation produces lactic acid and causes pain - further ischemia leads to sodium/potassium pump failure (reduction in O~2~ and therefore lack of ATP), thus ionic redistribution around the membrane causes dysrhythmia - sodium floods into the cell, water follows and cells swell and burst - cell death occurs in 1-6 hours - classified as a STEMI (ST elevation Myocardial Infarct) or non-STEMI (presence of infarct based on elevation of troponin) ### Acute Coronary Syndromes (ACS) - an umbrella term used to cover any group of clinical symptoms and covers the spectrum of cardiac clinical conditions - two categories o unstable angina high/low risk o MI -- STEMI or non-STEMI ### Rate Related Chest Pain #### [Tachycardia] - chest pain potentially may be experienced if a patient is in a prolonged state of tachycardia, or has a very rapid tachycardia (i.e. SVT, conscious VT) - again this is a supply/demand mismatch as the heart is pumping too quickly, and there is decreased filling time of the coronary arteries in diastole - the coronary arteries are poorly perfused - cardiac muscle is forced into anaerobic metabolism due to the reduced blood supply and therefore reduced oxygen supply, and lactic acid is produced, stimulating nociceptors and causing pain [Bradycardia] - chest pain potentially may be experienced if a patient is in a prolonged state of bradycardia, or has a very slow bradycardia - as the heart rate is reduced, diastole occurs less frequently, therefore the coronary arteries are perfused less frequently - supply/demand mismatch is present, as the supply is reduced - cardiac muscle is forced into anaerobic metabolism, lactic acid is produced, nociceptors are stimulated, and interpreted as pain Patient Presentation -------------------- ### Stable Angina - pain in chest- tightness, squeezing, lightness - pain radiates to shoulder, back, jaw, arm and neck - anxiety, fear of impending doom - SOB, diaphoresis - pale - dysrhythmia - ECG changes ### Unstable Angina - same as stable angina - more intense pain and a longer duration - pain occurs at rest ### Acute Myocardial Infarction - severe, constant, retrosternal pain - pain across the chest lasting more than 20 minutes - pain radiates to throat, jaw and arms (typically the left arm, but can be either) - nausea and vomiting - diaphoretic and pale - SOB, weak, dyspnoea - ECG changes/dysrhythmia - feeling of impending doom ECGs ==== Action Potential ---------------- - cardiac myocyte AP -- require depolarization of pacemaker cells to depolarize themselves - pacemaker cell AP -- automaticity; fire off on their own, to set off myocyte to generate muscle contraction ### Cardiac Myocyte - resting membrane potential is approx -90mV - membrane threshold is approx -70mV - cell is stimulated to depolarize by an adjacent cell through a gap junction - Phase 0 (depolarisation phase): o within the cardiac myocyte there are many fast sodium channels, when they open they increased membrane potential from negative to positive very quickly as sodium floods into the cell - fast Na^+^ channels are signalled to open when the cell is slightly depolarized via an influx of cations through gap junction, from an adjacent cell - Phase 1: o fast Na^+^ channels close and rapid Na^+^ influx terminates o K^+^ exits the cell via K^+^ vaulted gated ion channels o net result of a decrease in positive electrical charges within the cell o membrane potential drops a little bit, back down to about 0mV - Phase 2: o prolonged phase of slow repolarization (plateau) o allows finish of contraction and beginning of relaxation of muscle o membrane potential stays at about 0mV o Ca^2+^ slowly enters the cell through slow Ca^2+^ channels o K^+^ continues to slowly leave the cell o Ca^2+^ and K^+^ balance each other out, resulting in no change in membrane potential = plateau - Phase 3: o Ca^2+^ channels quickly snap shut -- influx terminates o K^+^ efflux continues o as K^+^ leaves the cell, the inside of the cell becomes markedly more negative - membrane potential returns to -90mV o repolarization is complete by the end of phase 3 - Phase 4: o period between action potentials o membrane is at -90mV o still excess of Na^+^ in the cell and K^+^ outside, therefore Na^+^/K^+^ pump is activated, removing Na^+^ from the cell and replacing K^+^ into the cell ### Pacemaker Cells - found in SA node, AV node, Junction and Ventricles - primary pacemaker is SA node - no fast Na+ channels - presence of funny channels - funny channels = automaticity - funny channels constantly leaking Na^+^ and Ca^2+^ and therefore fire off at their own rate - only three phases of action potential in pacemaker cell - no phase 2 because the pacemaker cell is not about contraction, but about generation of action potential to stimulate myocytes - resting membrane potential approximately -70-60mV -- higher than myocytes as they're more easily stimulated to depolarize - membrane threshold approximately -40-30mV - Phase 4: - - Phase 0 (Depolarisation): - - Phase 3 (Repolarisation): o K^+^ channels open → K^+^ efflux o Ca^2+^ channels close o membrane potential comes back down to -60mV - SA node affected by sympathetic and parasympathetic innervation o sympathetic (adrenaline) ↑ rate of depolarization o parasympathetic (vagus nerve stimulation -acetylcholine) ↓ rate of depolarization **Refractory Periods** - absolute and relative refractory period - absolute (ARP) - another action potential absolutely CAN NOT be stimulated to depolarize; begins with the onset of phase 0 and ends midway through phase 3 - relative (RRP) - repolarisation is not complete, however has repolarised to threshold potential, and can be stimulated to depolarize if stimulus is strong enough - the relative refractory period corresponds with the T wave on the ECG - this is important for paramedics as R on T phenomenon can be the cause of sudden cardiac arrest - R on T phenomenon (aka commotio cordis) occurs when an action potential is stimulated before the previous one has fully repolarised - the cause may be blunt force trauma (i.e. a cricket ball to the chest) at exactly the right time (during the RRP), resulting in ventricular fibrillation - very unlucky, and unlikely, however another cause for R on T phenomenon is the generation of a PVC during the RRP, also potentially resulting in ventricular fibrillation - for this reason, during electrical cardioversion a clinician will 'sync' the cardioversion to line up with the 'R' wave to avoid R on T ### Classes of Cardiac Drugs - Class I: sodium channel blockers (fast Na^+^ channels) o works on phase 0 of myocytes - Class II: beta blockers o effects firing rate of pacemaker cells - Class III: potassium channel blockers o slows conduction through AV node o extends the absolute refractory period so irritable cells cannot fire off - Class IV: calcium channel blockers o shortens phase 2 of myocytes → decreases contraction of myocytes o affects phase 0 of pacemaker cells → decreases firing rate → decreases speed - Class V: adenosine & digoxin o adenosine stops conduction through AV node for approx 7 seconds o digoxin slows conduction through AV node to allow for ventricular filling; poisons ATP at Na^+^/K^+^ pump, Na^+^ and Ca^2+^ stays in the cell, K^+^ stays out of the cell ### Muscle Contraction - excitation-contraction coupling refers to the series of events that link the action potential to muscle contraction - the contractile apparatus of myocytes are myofibril which consist of myosin (thick filament) and actin (thin filament) - muscle contraction is the shortening of myofibril by actin and myosin sliding past each other as seen below - Ca^2+^ comes in and binds to troponin resulting in tropomyosin winding off of actin, exposing binding sites for myosin heads - myosin head wiggles along actin onto binding sites, shortening the myofibril and causing muscle contraction - ATP is required to remove the myosin head from actin, which is muscle relaxation - rigor mortis occurs due to the lack of ATP, which is required to remove myosin heads from actin, causing muscle relaxation, therefore, muscles stay in a contracted state Normal ECG ---------- ### P wave -- atrial depolarisation - depolarization of atria begins near SA node and progresses across the atria from right to left and then downwards - first half represents depolarization of right atrium, second half is left atrium - duration: \0.12 seconds - there must be a P wave - BBBs are distinguished in V1 - if the second half of the QRS complex is UP (positive) = RIGHT BBB - if the second half of the QRS is DOWN (negative) = LEFT BBB **Left Bundle Branch Block: Right Bundle Branch Block:** - LBBBs tend to cause ST segment elevation, making it difficult to diagnose ST segment elevation in acute myocardial infarction (AMI) - "Sgarbossa criteria" *suggests* if the elevation is greater than 5 squares, is it indicative of AMI; however ALWAYS treat the patient not the ECG, if they look like they're having an MI, they probably are #### 12 Lead ECGs - 6 x chest leads (V1 -- V6) - 3 x unipolar leads (I, II, III) - 3 x augmented leads (aVF, aVR, aVL) - augmented leads are the same electrodes used for leads I, II & III, however the machine switches the electrode designation - the leads of the 12 lead ECG show different areas of the heart: - the right and posterior sides of the heart are not visible from a normal 12 lead ECG - additional leads can be placed on the patient's back to view the posterior region (V7, V8, V9) - similarly, by removing V4, and placing it in exactly the same spot, on the right side of the chest, it becomes V4R and views the right side of the heart -- this needs to be written on the ECG print out if it is attempted **Contiguous Leads:** - ST elevation is indicative of myocardial infarction (STEMI) - elevation must be present in two or more contiguous leads (leads looking at the same area of the heart) - for example if there is an inferior infarct, there must be elevation in two or more of the leads that look at the inferior portion of the heart (Leads II, III, aVF), to be clinically significant - in the unipolar (limb leads) and augmented leads, only ONE square of elevation in two or more contiguous leads is required to be clinically significant - in chest leads, TWO or more squares are required in two or more contiguous leads to be clinically significant - this is due to the position of the electrodes, the chest leads are closer to the heart, thus more elevation is required for it to be clinically significant **Reciprocal changes:** - during an acute STEMI, when STE is present in the leads that face the acute injury, ST depression is often present in the leads that face the "injury boundary" - if there is posterior elevation, there will be depression in the anterior leads - inferior elevation will have reciprocal changes in the lateral leads - this is easy to remember through the acronym "PAIL" (posterior, anterior; inferior, lateral) **Acute Myocardial Infarct Diagnosis Criteria:** - clinical history - serial ECGs - serial blood tests (troponin, CK-MB) o below is a 12-lead ECG with clinically significant elevation is inferior leads as seen in red o the blue lines show reciprocal changes (ST depression) in lateral leads o this STEMI shows an inferior infarct ### AMI ECG Transition - hyper-acute T waves -- first minutes of injury - ST elevation -- hours to days - Q wave -- hours to days ### Benign Early Repolarization - benign ST elevation - common in young males - "swooping" pattern of ST elevation rather than "tomb stone" - treat the patient -- if the patient is pale, sweaty and complaining of chest pain, it is probably an infarct - no chest pain, sweat or pallor, and you have been called for a primarily non-cardiac cause, but there is ST elevation, it may be early repolarization - ST elevation can be caused by many things, not just MI, therefore it's important to treat your patient, not the ECG, as well as get a thorough clinical history - ST elevation is indicative of poor coronary perfusion, thereby in theory can be cause by low diastolic pressure, or a head injury ### Pericarditis - global ST elevation - may present as PR depression making the ST segment appear elevated - history -- chest pain is usually sharp pain, not crushing or tightness - often associated with a viral or bacterial infection -- may be febrile ### Accessory Pathways -- Re-entry Tachycardia - the AV node should be the only conduction pathway between the atria and ventricles - in some people there can be an accessory pathway where conduction can pass through to the ventricles - supraventricular tachycardia is a re-entry tachycardia, which occurs from an accessory pathway - Wolff-Parkinson-White Syndrome is also cause by an accessory pathway ![](media/image25.jpg) - the AV node has a minor physiological conduction delay to allow time for ventricular filling, however an accessory pathway will not have a conduction delay and therefore will depolarise faster - in normal conditions the fast pathway depolarises quicker than the slow pathway (AV node) however they meet up, and in this situation they cancel each other out, and the cells depolarise as normal and normal ventricular contraction follows - re-entry tachycardia requires a premature atrial contraction (PAC) to happen at the correct time in order to occur - if a PAC occurs down the slow to depolarise AV node, by the time the premature depolarisation has occurred, and already quickly repolarised, the abnormal conduction comes through from the accessory pathway, and instead of meeting up and cancelling each other out, the conduction continues through the accessory pathway and begins a re-entry tachycardia (such as SVT) as it goes around and around ### Wolff-Parkinson-White Syndrome - due to the normal physiological delay of conduction through the AV node, conduction through the atrium reaches the ventricle faster through the accessory pathway which normally has no conduction delay - because of this, part of the ventricle begins to depolarise before the normal conduction pathway can catch up - this causes the upwards slurring of the QRS at the initiation of the QRS complex, known as the delta wave - delta waves will only be visible in normal rhythms, it will not be seen in a re-entry tachycardia ### SVT vs VT - VT with aberrancy (wide QRS) can look suspiciously like VT - the best way to tell the difference is the haemodynamic stability of the patient; a patient in SVT will usually have a better BP and HR than someone in conscious VT - SVT often occurs in younger patients, thus if the patient is \>35 years of age, there is an 80% chance it is VT - previous history of MI also significantly increases the chance that is it VT - roughly, VT tends to be 140-160bpm - SVT roughly sits between 180-240bpm, however rate alone should NOT be a diagnostic tool - VT is likely if either of the following are present in a 3-lead: - Capture Beats -- occurs when the SA node transiently 'captures' the ventricles to make a normal - VT is likely if any of the following are present in a 12-lead ECG: o concordance in V~1~-V~6~, either all positive (as seen below), or all negative - left rabbit ear in V~1~ is taller - north-west axis (lead I -- negative; aVF -- negative; aVR -- positive) VT is the only rhythm where a north-west axis is seen NARCOTIC OVERDOSE ================= Definition ---------- Poisoning from a pharmacological agent, which may be legal or illegal. Opiates are often heroin, but can include medical morphine, pethidine or fentanyl. Codeine is sometimes used and methadone has been used intravenously. Opiates cause respiratory depression which in turn causes hypoxia and hypercarbia. The aim of Naloxone dosage is to use the minimum dose to achieve a gag reflex and self-ventilation. Doses over this level will only produce symptoms of opiate withdrawal which will be translated into distress and possible aggression. Ideally patients should be allowed to metabolise the drug over time in a safe observed environment. Causes ------ - intentional overdose - accidental -- dose miscalculation, polypharmacy, drug strength variability - recreational drug use **[Pathophysiology]** ### Narcotics - Pharmacology - definition: a drug that relieves pain and also induces stupor and insensibility and depressed brain function - routes: IM, IV, oral o enteral -- via GI tract o parental -- by injection - classifications: pure agonists o act on opioid receptors -- Mu, Kappa, Delta, Epsilon o produce analgesia, euphoria, sedation, respiratory depression, constipation - receptors o Mu analgesia, respiratory depression, euphoria, miosis (pupil constriction) o Kappa analgesia, respiratory depression, sedation, miosis - Delta analgesia - Sigma psychotomimetic (hallucinations) - opioid receptors are found throughout the CNS but particularly in areas associated with pain perception (i.e. brain/brainstem and dorsal horn of spinal cord) - receptors are also located in some sensory nerves, on mast cells and in some of the GI tract - opioid receptors are stimulated by endogenous endorphins and enkephalins - these endogenous opiates modulate nociception and produce analgesia - exogenous opioids are produced (naturally or synthetically) and mimic endogenous opioid action - opiates bind to receptor sites to: - decrease the release of neurotransmitters or: - open potassium channels -- hyperpolarization of presynaptic neurons leads to reduced neuronal excitability and inhibition of release of excitatory transmitters - acts similarly to inhibitory neurotransmitters → CNS depression → respiratory depression - respiratory depression causes indirect elevation of intracranial pressure by increasing CO~2~ levels (hypoxia), which in turn dilates cerebral vasculature - orthostatic hypotension can occur as a result of drug induced histamine release - nausea and vomiting can occur from direct action on opioid receptors on the chemoreceptor trigger zone (CTZ) in the medulla Patient Presentation -------------------- - pin point pupils - altered conscious state/GCS - sympathetic nervous system -- tachycardia, pale, diaphoresis (compensatory mechanism due to respiratory depression → as O~2~ is reduced, heart tries to pump O~2~ that is available around quicker) - can also be bradycardic and hypotensive - respiratory depression, slow RR or apnoeic OBSTETRICS ========== Trimester periods ----------------- 1^st^ trimester: 1 -- 12 weeks - the growing uterus is protected by the bony pelvis 2^nd^ trimester: 13 -- 28 weeks - the fundus (top of the uterus) is at the height of the umbilicus 3^rd^ trimester: 29 -- 40 weeks - the fundus is at the height of the xiphoid process Fundal height progression ------------------------- Physiological changes in pregnancy ---------------------------------- ### Cardiovascular - haemodynamics are altered to protect both the mother and foetus and to provide increased O~2~ and nutrient delivery to the foetus o the heart rate increases 10-20 beats/min over pre-pregnant rates by the 3^rd^ trimester because of increased blood volume and oxygen demand -- pulses of 80-95 are considered normal in both awake and sleeping states, sustained HR greater than 100 may indicate hypovolemia - cardiac output increases (due to increased HR and SV) by approximately 1.5L/min (20-30%) during the first trimester and peaks at 6-7 L/minute (40%-50% increase) at end of the 2nd trimester due to catecholamine release and remains increased until full term - blood pressure o 1^st^ trimester - little change in blood pressure o 2^nd^ trimester - the body becomes relatively resistant to the vasopressor effects of renin and angiotensin II and vessels dilate - relaxation of venous walls increases the capacity of veins to provide space for the increased plasma volume - due to vessel dilation, systolic BP decreases by 5-15 mmHg and diastolic BP by 5-10 mmHg o 3^rd^ trimester - BP rebounds and increases to normal levels due to increased blood volume - BP should never be higher than pre-pregnant levels - a hypercoagulable state is induced during pregnancy -- causes increased risk of DVT or PE ### Respiratory - as pregnancy progresses, the diaphragm is pushed upward by as much as 4cm causing the lungs to shorten and decreasing O~2~ reserve - this predisposes patients to hypoxia and shortness of breath -- dyspnoea occurs in 60% of women - thoracic breathing replaces abdominal breathing -- as the diaphragm elevates, lower lobes of the lungs become more difficult to expand - O~2~ requirements can increase by 10-20% above the non-pregnant state in response to increased metabolism in the maternal body - tidal volume increases to 600 mL and RR may increase -- increasing the minute volume ### Renal and GIT - by 28 weeks, glomerular filtration rate (GFR) increases 50% from 100-125 mL/min to 140-170 mL/minute - urinary frequency during the 1^st^ and 3^rd^ trimesters is due to increased renal filtration and compression of the bladder - more susceptible to UTI's - the bladder is especially vulnerable to rupture with direct trauma to the suprapubic area - the liver and spleen become mildly distended, compressed, or displaced making them more vulnerable to injury or rupture in trauma - growing uterus causing displaces abdominal organs su[c]h as the small bowel and other organs laterally (e.g. the appendix is in the RUQ at full term) - peristalsis is slower during pregnancy, so food stays in the stomach for longer -- patient is therefore at higher risk of vomiting/regurgitation and subsequent aspiration Obstetric emergencies --------------------- ### Ante-partum haemorrhage - Defined as bleeding of 15mL of more from the birth canal after the 20th week - 2 main causes dealt with pre-hospital o placental abruption o placenta praevia ### Placental abruption - this is defined as the separation of the placenta from the uterine wall - vaginal bleeding in the second half of pregnancy should raise high suspicion of placental abruption and be treated accordingly - placental abruption can be classified into 4 categories, depending on degree of separation o asymptomatic - mild -- no/mild vaginal bleeding, slightly tender uterus, no change in observations, no foetal distress - moderate -- mild to moderate vaginal bleeding (if present), moderate to severe uterine tenderness, possible contractions, maternal tachycardia and orthostatic changes in BP, foetal distress - severe -- heavy vaginal bleeding (if present), very painful uterus, maternal shock, foetal death is highly probable. ### Placenta praevia - occurs where the placenta is partly or wholly in the lower part of the uterus o minor - placenta is in the lower uterus but the lower edge does not cover the internal os o major - placenta is in the lower uterus and the lower edge does partially or completely cover the internal os - aetiology o the ovum implants lower in the uterus though the reason for this is not usually apparent o higher parity is one cause as is multiple pregnancy o bleeding occurs as the placenta shears away from the uterine wall during stretching/contraction/other movement of the uterine wall - clinical features o bleeding without significant pain or tenderness is most common o blood loss is invariably bright red and occurs most commonly between 34 and 38 weeks and can recur - onset is usually spontaneous but can be precipitated by such things as trauma, coitus, coughing or straining - blood loss may not occur until dilation of the cervix during labour o may be associated/complicated by malpresentation of the foetus o foetal-placental function can be compromised resulting in intra-uterine hypoxia o foetal movements may cease ### Uterine rupture - uterine rupture occurs when a full thickness disruption/rupture of the uterine wall occurs - this occurs more commonly in women with a previously scarred uterus from surgery or previous caesarean, however, blunt force and penetrating trauma can cause uterine rupture of an unscarred uterus - this results in significant haemorrhage and maternal/foetal distress as this also involves the overlying visceral peritoneum in comparison to a reopening of a previously scarred uterus which does not involve the viscera - signs and symptoms: o abnormal pain o vaginal bleeding o sympathetic response -- this may not present initially due to maternal compensation, if maternal tachycardia and hypotension is present, it is reasonable to assume significant foetal distress - significant haemorrhage and maternal shock will result in maternal/foetal distress and possible death, depending on the time between onset and definitive care - foetal consequences may include foetal hypoxia/anoxia, foetal acidosis and possible death due to maternal shock -- foetal death will be highly probable if maternal decompensation is evident - maternal consequences may include hypovolaemic shock, surgery, possible hysterectomy and possible death. ### Premature rupture of membranes - at term, programmed cell death and activation of catabolic enzymes cause the membranes to rupture - premature rupture of membranes (PROM) may occur anywhere from 37 weeks gestations, until term and is common - preterm premature rupture of membranes (PPROM) occurs prior to 37 weeks gestation, is unexpected and may be the result of infection or blunt force trauma - aetiology o multiple pregnancy o polyhydraminos o coitus o trauma o incompetent cervix o malpresentation of the foetus o placenta praevia o infection - management/treatment o transport o confirm no cord prolapse o sterile pad over vaginal opening to reduce likelihood of infection o monitor for signs of labour/imminent delivery ### Cord prolapse - umbilical cord of foetus prolapses outside of the cervix - the cord may spasm or be damaged in the change of environment or be caught between the foetus' presenting part and the pelvis therefore decreasing the blood supply to the foetus - an obstetric emergency and complication which can have dire consequences for the foetus - we will usually only diagnose it when a mother presents to us following ROM and upon inspection (external) the cord is seen on view - it may be occult -- out of the cervix but within the vagina, or obvious -- outside the vagina only see cord prolapsed when membranes have ruptured - causes: - poorly fitting presenting part (i.e. breech, premature) prevents occlusion of the inlet and with - placenta praevia o polyhydraminos -- excessive amniotic fluid - signs and symptoms o ruptured membranes o cord visible at vagina o painless o no signs of shock o mother may notice decreased foetal movements - treatment o inspect -- especially following ROM o primary survey o posture -- left lateral with hips elevated o if urge to push/imminent delivery, continue to deliver o 2° survey -- warm saline soaked pad over vulva and cord -- keep cord warm and moist -- do not touch cord unless absolutely necessary - high flow O~2~ o IV cannulation o analgesia o urgent smooth transport ### Primary postpartum haemorrhage - vaginal bleeding \>500mL in the 1^st^ 24 hours post-delivery of the foetus - 4 major causes o tone (uterus is not well contracted) o tissue (retained products from conception) o trauma (tearing) o thrombin (coagulation abnormalities) - treatment o whether or not placenta is in situ massage the fundus to ensure uterus is contracted, once contracted, hand off - if signs of separation of placenta and descent appear, allow natural delivery of the placenta o empty bladder (if safe to do so) o elevate feet - O~2~ - check for and apply pressure to any bleeding lacerations - put neonate to breast to suckle o IV cannulation and fluid bolus o observations o rapid transport ### Secondary postpartum haemorrhage - excessive blood loss 24 hours to 6 weeks post delivery - usually due to: o retained products of contraception o dissolution of a thrombus at the placental site o infection - treatment o massage uterus if still palpable o if laceration site breakdown -- consider pressure o consider O~2~ o consider IV cannulation and fluid bolus o pad vagina o take blood stained material with you o symptomatic care of the mother o rapid transport ### Pre-eclampsia - disorder during pregnancy characterised by high blood pressure and significant amounts of protein in the urine - thought to result from an abnormal placenta, or by substances produced by the placenta, particularly progesterone and oestrogen - this results in a vasospastic condition which manifests as an elevation in maternal blood pressure - progesterone dilates veins in the lower half of the body leading to a decrease in BP which results in baroreceptor mediated release of ADH and vasopressin - oestrogen causes retention of sodium and water and release of aldosterone from the adrenal cortex which can lead to increase capillary hydrostatic pressure and decreased colloid osmotic pressure which in turn results in oedema to extravascular tissue - there can also be vasospasm, most likely related to sodium and fluid shifts and an increase in the body's response to the RAAS - the greatest risk of pre-eclampsia is intra-uterine hypoxia due to vasospasm of uterine arteries which may lead to foetal distress - presentation: o oedema -- particularly evident in hands, feet and face o proteinuria o hypertension -- defined as \>15mmHg over normally expected values for the mother, or ### Eclampsia - onset of seizures in a woman with pre-eclampsia - follows on from pre-eclampsia, where cerebral hypoxia results from vasospasm and oedema life-threatening to both mother and foetus - presentation: - tonic-clonic seizures o respiratory arrest o cyanosis o persistent LOC - management: - treat as per seizure management i.e. DRABC, O~2~, posture, midazolam if required o rapid transport with early notification Obstetric trauma ---------------- ### Predisposing factors to trauma in pregnancy - larger abdomen causes gait unsteadiness and a change to the centre of gravity - loosening of pelvic ligaments and joints causing gait instability - pelvic pressure which causes pain and neuromuscular dysfunction of the lower extremities ### Clinical difference in trauma in pregnancy - hypervolemia during pregnancy can mask a 30% (1500 mL) gradual loss of maternal blood volume or a 25% acute blood loss before measurable changes in vital signs appear - the average pregnant patient can tolerate a 1500 mL (30-35%) volume loss before becoming extremely hypotensive - when blood loss occurs, the mother compensates and maintains vital signs at the expense of perfusion to the uterus placing the foetus at early risk for hypoxia  if maternal shock is present, there is an 80% chance of foetal mortality - women with pre-eclampsia have lost the resistance to angiotensin II and have become hyper-reactive to renin and angiotensin when in a supine position to counter-regulate the perceived decrease in blood return - the increase in renal vascular supply may lead to augmented blood loss in trauma in comparison to similar injuries in non-pregnant women. ### Assessment and Management - a patient in the third trimester of their pregnancy, with a mechanism of injury/type of injury which may be indicative of abdominal trauma, produces a high suspicion of haemorrhage and maternal/foetal trauma - as explained, when blood loss occurs, the mother compensates and maintains vital signs at the expense of perfusion to the uterus placing the foetus at early risk for hypoxia - signs of foetal distress will not be present during the early stages of shock and early intervention must be initiated to ensure adequate foetal perfusion - in the absence of changes in the mothers vital signs, abdominal pain, PV bleeding, abdominal rigidity and subtle changes such as skin colour may provide important clues and increase suspicion of trauma - positioning: - the large abdomen may produce pressure on the inferior vena cava when a pregnant patient is supine during the later stages of pregnancy - this may cause compression of the vena cava and reduce venous return; potentially causing obstructive shock - to avoid this, padding should be placed under the patients right hip to displace the uterus to the left side (left lateral position) and reduce compression of the vena cava - if spinal precautions are indicated, spinal immobilisation is also necessary, however padding under the right side of the vac mat is acceptable to sustain adequate circulation. - airway and oxygenation o during the third trimester, the patient's diaphragm is elevated and dyspnoea can become an issue, especially if supine - oxygen therapy may be necessary to maintain oxygen saturations and oxygen delivery to foetal circulation and assisted ventilations may be required during late stages of pregnancy - due to reduced peristalsis of the GI tract, there is an increased risk of vomiting/regurgitation and subsequent aspiration -- therefore maintain a patent airway and consider suctioning - IV fluid therapy o as outlined in our guideline, a fluid challenge is indicated to ensure adequate foetal perfusion o as stated, the mother will compensate by shunting blood away from foetal circulation o therefore even if a radial pulse is present, foetal circulation may still be compromised and fluid therapy is still indicated - the presence of an increase in maternal blood pressure or decrease in heart rate accompanied by normotension during the fluid challenge shows that foetal circulation is being maintained - when there are signs of adequate foetal perfusion, reduced flow rate is indicated as in normal fluid therapy to avoid dislodging clots in trauma - resuscitation o adequate resuscitation of the mother is key to survival of both the mother and foetus -- however if resuscitation of the mother is required post trauma, there is poor prognosis of the foetus. - transport options o In the metropolitan area, all significant pregnant trauma must be transported to Flinders Medical PAEDIATRIC CROUP ================ Definition ---------- The term croup refers to the clinical syndrome of a hoarse voice, harsh barking cough and inspiratory stridor. Cause ----- The commonest cause of this symptom complex is viral laryngotracheobronhitis (LTB). Other causes of upper-airway obstruction must be considered in the differential diagnosis. Pathophysiology --------------- - croup is a common cause of airway obstruction in young children - mainly affects children between 6-36 months of age - peak incidents 12-24 months of age - usually mild and self-limiting, however can occasionally cause severe respiratory obstruction - viral infection in the upper airway results in inflammation of the pharynx, larynx, trachea and bronchi due to infiltration of white blood cells - typically, viral croup develops over several days along with a concurrent coryzal illness (common cold) - it is specifically subglottic inflammation and swelling that compromises the airway - inflammation and swelling leads to airway obstruction which increases work of breathing - the narrowed subglottic region is the cause of stridor, due to the turbulent airflow moving through the small airway - during inspiration, areas of the airway that are easily collapsible are suctioned closed due to intraluminal pressure, these same areas are forced open during expiration - inspiratory stridor is the hallmark for croup, however stridor can be inspiratory or expiratory or both - the barking 'seal-like' cough associated with croup is caused by the swelling in the subglottic region, particularly around the larynx - symptoms usually last for 3-5 days - if airway obstruction is severe enough, respiratory failure may result, causing hypoxia and hypercarbia Patient Presentation -------------------- - determining the degree of airway obstruction is the most important consideration when assessing children with croup, they can worsen rapidly and repeated clinical assessment is essential **Mild Airway Obstruction** - child appears happy - prepared to eat, drink, play and take interest in surroundings - may be mild chest-wall retractions and mild tachycardia - nil stridor at rest ### Moderate Airway Obstruction - persistent stridor at rest - chest-wall retractions - use of accessory respiratory muscles - tachycardia - child is still interactive with people and surroundings ### Severe Airway Obstruction - child appears increasingly worried - fatigued - marked tachycardia persists - restlessness, agitation and irrational behaviour - decreased level of consciousness - hypotonia (poor muscle tone) - cyanosis and marked pallor are late signs of life-threatening airway obstruction PAIN ==== Definition ---------- Pain is an unpleasant sensory or emotional experience associated with actual or potential tissue damage. Pain is a subjective phenomenon. Physiology of Acute Pain ------------------------ Pain has two components, the sensation of the pain and the emotional response to the pain. The neural pathways of perception and how we respond to pain. There are two theories of the perception of pain: - specific theory o evoked by specific receptors -- nociceptors o information is transmitter to the brain for interpretation - pattern theory o different patterns of activity of neurons can signal both painful and non-painful responses o for example, a light touch is interpreted as touch, whereas a hit is interpreted as pain - sensory nerve fibres (nociceptors) are distributed throughout somatic (skin, sub-cut tissue, fascia/connective tissue, smooth muscle, mucous membranes) and visceral surfaces - noxious stimuli may be mechanical (i.e. pressure, swelling), thermal or chemical - tissue damage/injury from noxious stimuli leads to localised inflammation caused by the release of chemical mediators (i.e. prostaglandins, bradykinins, histamine) - the release of chemical mediators activates nociceptors → ion exchange occurs at the cell membrane resulting in stimulation and depolarisation of an action potential and the generation of a nerve impulse - myelinated A-delta fibres transmit fast, localised pain - unmyelinated C-fibres transmit slow, burning/aching, poorly localised pain - as a response to cellular damage and inflammatory mediators release, oedema occurs, which leads to compression of local blood vessels, causing hypoxia - this causes anaerobic metabolism and further increase to pain due to the release of lactic acid and the stimulation of nociceptors - glutamate is the neurotransmitter involved in the impulse transmission from A-delta fibres - substance P is the neurotransmitter involved in the impulse transmission from C-fibres Four processes of nociception (process of pain) ----------------------------------------------- - transduction o the process of free nerve endings (nociceptors) of A-delta and C fibres responding to noxious stimuli - nociceptors are exposed to noxious stimuli when tissue damage and inflammation occur - transmission o the pain impulse is transmitted from the site of transduction along the nociceptor fibre to the dorsal horn of the spinal cord where the impulses synapse - from here, A-delta fibres cross over to the other side of the spinal cord and follow up the spinothalamic tract into the brain stem - C-fibres do not cross over with A-delta fibres, but go up the anterolateral tract and cross over further up the spinal cord. - modulation o process of dampening or amplifying pain within the brain o the pain signal is modulated in both ascending and descending pathways by neurochemical mediators that act on Mu, Delta, Kappa and Sigma receptors - if these receptors are stimulated by endorphins or monoamines, these neurons inhibit further pain transmission - these mediators also have effect on sedation, respiratory drive and feeling of well being - perception o result of transduction, transmission, modulation as well as psychological aspects Chronic pain is presumably caused by persistent activation of nociceptors and psychological factors commonly contribute Reflex Arc ---------- - a nerve pathway within the body that connects muscle groups together, without input from the brain - primarily controls involuntary movements in response to stimulus - allows reaction to occur quickly - noxious stimulus occurs → nociceptor (afferent neuron) transmits signal to dorsal horn of spinal cord → spinal motor neurons activated → efferent neuron transmits new impulse back→ effector organ responds (pull hand away from pin) Gate Control Theory of Pain --------------------------- - proposed there are thin (pain) and large diameter (touch, pressure, vibration) nerve fibres that transmit pain from the site of injury to the dorsal horn in the spinal cord, and then up the spinothalamic tract - thin fibre transmission impedes inhibitory interneurons that would usually stop pain transmission, thus pain is felt when thin fibres are stimulated, whereas large diameter activity tend to stimulate inhibitory interneurons, impeding the transmission of pain. - for example, rubbing a site after an injection may reduce the pain of the needle sting as more large diameter fibres (touch, pressure) are stimulated than thin fibres (pain), reducing the sensation of pain SEIZURES ======== **[Definition]** A temporary alteration to behaviour and consciousness due to abnormal electrical discharges in the brain. Causes ------ Any process that interrupts the balance between neuronal excitation and inhibition can produce a seizure, these include: - head injury -- trauma both old and new (changes in cerebral blood flow auto regulation, or changes in intracranial pressure, also changes in blood brain barrier) - stroke -- occlusion of a vessel → reduced blood supply to effected area → hypoxia → alteration in membrane integrity - hypoxia -- ↓ ATP production → Na^+^/K^+^ pump failure → Na^+^ leaks into the cells→ rise in resting membrane potential - hypoglycaemia **--** ↓ ATP production → Na^+^/K^+^ pump failure → Na^+^ leaks into the cells→ rise in resting membrane potential - infection -- CNS or systemic infections as well as fever - toxins/substance exposure -- speed or fantasy hypopolarise the cell, nerves are more excitable and only sight sensory input can elicit a response (hypopolarised brings resting membrane potential to threshold) - metabolic changes -- electrolyte disturbances or endocrine dysfunction (thyroid, adrenal, pituitary) - lesion/tumour Pathophysiology --------------- **Normal electrolyte balance:** - normally more potassium inside cells, and sodium outside of cells - passive Na^+^ channels -- selectively let Na^+^ into the cell with concentration gradient - passive potassium (K^+^) channels -- selectively let K^+^ out of the cell with concentration gradient - active (requires energy from ATP) pump - K^+^ back into the cell, and Na^+^ out of the cell, against concentration gradient - in circumstances where ATP is not available (hypoxia, hypoglycaemia etc.), Na^+^/K ^+^pump fails, and more Na^+^ enters the cell, as more K^+^ leaves, causing an electrolyte imbalance, and hyperpolarising the cell, resulting in raising the resting membrane potential closer to threshold ### Seizure activity - changes in permeability of neuronal membrane secondary to structural or metabolic alteration - the neuronal membrane becomes more permeable to sodium and potassium, enhancing the neurons ability to depolarize - increased permeability to sodium allows sodium to leak into the cell - resting membrane potential is raised towards threshold potential - neurons are more excitable and more readily to depolarise - body actions and behavioural alterations are dependent on the area of the brain affected Types of Seizures ----------------- **Generalised seizures:** Affects both hemispheres of the brain, consciousness may be impaired - tonic-clonic seizure **--** stiffness followed by jerking movements of the whole body - absent seizure -- often mistaken for daydreaming, characterised by staring, loss of facial expression and unresponsiveness, usually last 2-10 seconds - myoclonic seizure -- brief but significant muscle jerks of a muscle, or group of muscles - clonic seizure **--** myoclonus that is regularly repeated jerking movements, typically 2-3 per second - tonic seizure **--** brief stiffening of the muscles of the whole body, causing the body to go rigid - atonic seizure **--** sudden loss of muscle tone of the whole body, also known as "drop attacks" **Partial seizures:** Affects one area of the brain, but may spread, retain consciousness - simple partial (focal seizure) -- numbness or tingling in one area of the body, of just one limb twitching, deja vu or hallucination - complex partial (focal dyscognitive) **--** awareness and responsiveness altered, may display strange, random, repetitive behaviour (often chewing or mumbling) ### Status epilepticus - defined as either continuous seizure activity lasting longer than 30 minutes, or 2 or more seizures in a row without gaining consciousness - may result in neurological damage, respiratory failure and death due to prolonged hypoxia SEPSIS ====== **[Definition]** infection: invasion of normally sterile tissue by organisms. cytokines: immune cell signalling molecules. bacteraemia: the presence of viable bacteria in the blood. sepsis: the clinical syndrome that results from an inflammatory response to an infection that is dysregulated, non-resolving and deleterious. There is a systemic presence and effect of the infection. septic shock: septic shock = sepsis + hypotension despite the administration of a fluid challenge MODS: Multi Organ Dysfunction Syndrome = Septic shock + organ failure Sepsis arises form an infection source that then travels via the vasculature throughout the body. It starts from microbes such as bacteria, fungi and viruses, the most common being Gram Positive bacteria and most commonly occurring in the lungs, abdomen and kidneys. Although for most patients these infections remain localised, are treated accordingly and resolve without progressing to sepsis, in some patients the same microbe and infection site may progress to sepsis. Although bacteria such as *Neisseria Meningitidis* and *Streptococcus Pyogenes* are less likely to progress to sepsis, others such as *Staphylococcus Aures* or *Enterococci* can be more likely. These bacteria are known as *commensal* bacteria and can be more likely to become systemic in those with weakened immune systems. Pathophysiology --------------- ### Invading microorganism → the body's immune response - cytokines: temporary and fast acting o macrophages migrate towards site of invasion and when they recognise the invading microbe they produce the pro-inflammatory cells, cytokines - neighbouring endothelial cells respond to the sudden surge of cytokines and produce adherence molecule, also neutrophils are drawn from the bloodstream and stick to the activated endothelial cells - these neutrophils then produce even more pro-inflammatory cytokines - activated complement system: mast cells release histamine o this cascade of protein activations help immobilize and break down pathogens and the complement proteins identify and label the foreign molecules, some also lyse the foreign cell membranes - this cascade also multiples the effects of the local immune reactions by sending in more cytokines - activated coagulation factors: o in this stage there is a local activation of the blood coagulation system resulting in a deposition of fibrin by the coagulation cascade → STICKY MESH o this fences in the microbes and helps prevent their spread - the coagulation reactions also activate bradykinin, a circulating peptide that dilates blood vessels and increases capillary leakage adding to the vasodilation already present → local tissue swells with protein-rich oedema fluid. - it is here that sepsis diverges as a result of the normal "winding down" that does not occur, hence, sepsis is known as malignant (uncontrolled, unregulated and self-sustaining), intravascular (blood-borne spread) and inflammatory (all features are exaggerations of normal inflammatory responses) - within cells are suppressor factors that decrease manufacturing and release of pro-inflammatory cytokines and outside the cell anti-inflammatory cytokines oppose the pro-inflammatory molecules - there is also a systemic increase of cortisol, epinephrine, prostaglandins and proteases which inhibit immune reaction throughout the body - all of these factors together with specific restorative compounds that are released, mean that the inflammatory process are regulated and remain localised - in sepsis there is an atypical inflammatory reaction of unending cytokine production and the spread through the vasculature of the infection to remote sites (the pro-inflammatory processes dominate) - one example of the abnormal control pathways in sepsis is activated protein C -- patients with sepsis usually have low levels of activated protein C, an anticoagulation pathway that controls the coagulation system, therefore fibrin is deposited widely and small clots form throughout the vasculature - activated protein C also promotes fibrinolysis and reduces endothelial cell sensitivity to the proinflammatory molecules and enhancing their normal function as barriers between blood and tissue - this reduced opposition of coagulation can lead the DIC (Disseminated Intravascular Coagulation) which is widespread clot formation, impaired tissue perfusion and thrombosis of small vessels which in turn increases the inflammatory response and thus the cycle continues ### Effects of the spreading inflammatory reaction - endothelial damage: o normally healthy endothelium forms the barrier between the bloodstream and the tissues, however this healthy barrier can change to dysfunctional due to abnormal vasomotor activity, the production of a pro-coagulant surface and an increase in the inflammatory response - organ damage: o sepsis → MODS (Multi Organ Dysfunction Syndrome) o widespread damaged vascular endothelium → oedema and collection of neutrophils and macrophages + decreased gas exchange + decreased nutrient exchange + decrease in the removal of waste →organ becomes poorly perfused and ischaemic → decrease in function and fails - sepsis continues and organ dysfunction spreads, as each organ fails, the risk of the patient of dying doubles - the lungs suffer early with the progression of sepsis as the surface area of the lungs is large and therefore the damage can be quite significant - the areas of the lungs that are affected fill with neutrophils and macrophages, fibrin deposited and decreased surfactant → poor compliance and decreased gas exchange - also in sepsis hypoxic pulmonary vasoconstriction (HPV) is counteracted thus the protective mechanism that normally redirects arterial blood away from any non-functioning parts in order to better ventilate areas - circulating inflammatory molecules decrease the ability of the arterioles to constrict and therefore blood will continue to flow through useless regions of the lungs and increase hypoxia - this eventually leads to lung dysfunction and lung failure and takes the form of ARDS (Acute - as sepsis continues the heart muscle can weaken due to the depressant effect of circulating inflammatory molecules - weakened ventricle stretch means stoke volume must increase to compensate o the kidneys are affected when sepsis occurs, as they are entirely dependent on maintaining a significant area of intact vascular endothelium - the septic reaction invades the kidneys as neutrophils and macrophages fill the interstitial tissue and the endothelial tissue is damaged - as with other organs, the perfusion of the kidneys is decrease and they become hypoxic → decrease in GFR + increase in serum creatinine levels → tubular necrosis and renal failure - another area of the body affected by sepsis is the gastrointestinal tract as the spreading hypoperfusion reduces the O~2~ supply to the intestines → aerobic metabolism is overcome by anaerobic → bacteria and toxins from the gut lumen move through the gut wall and into the bloodstream and lymphatics → small painless erosions in the mucosa of the upper GI tract → continue blood leakage - severe sepsis or septic shock can lead to paralytic ileus. - a key organ affected by sepsis is the liver, as it plays a major role in the first line of defence in the clearance of the infectious agents and their products - sepsis damages the hepatocytes of the liver and alters the haemodynamic balance o this damages causes an overflow of bacteria, toxins and debris into circulation, elevates liver enzymes and coagulation problems may occur therefore decreasing the amount of ammonia excretion which can result in encephalopathy - sepsis also affects the brain as circulating inflammatory molecules disrupt the endothelium of the BBB → leaky BBB →inflammatory molecules and white blood cells cross across into the neural tissue → oedema + collections of cells around the arterioles reduced the entry of O~2~ and Nutrients and reduce the excretion of waste products → neurons shut down and cerebral functions slows ### Progression to Shock - arterioles fail to constrict → septic shock (hypotension cannot be reversed with fluids) - unresponsive arteriole wall muscles due to 3 processes: - increase of lactic acid → hyperpolarizes the arterial muscle cells → unable to vasoconstrict when required - sepsis → suppression of ADH (pituitary hormone that maintains arterial wall muscle tone) o sepsis → increase in production of nitric oxide (potent vasodilator) from endothelial cells Signs and symptoms ------------------

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