Pathophysiology

Pathophysiology

Loss of contractility and increased preload cause the inability of blood to leave the left ventricle, causing backflow into the left atria, through pulmonary veins and into the lungs, increasing hydrostatic pressure within pulmonary capillaries, resulting in transudation of fluid, causing pulmonary odema.

Signs and symptoms

• Respiratory - SOB, bubbling on auscultation, cough, cyanosis
• Other - Oedema in ankles, legs and/or abdomen

Treatment

• Oxygen
• 400-800 micrograms of GTN - every 5-10 minutes - maximum dose 2.4 milligrams
• 40 milligrams of IV Furosemide

Pharmacology

Oxygen
Increases perfusion and cell metabolism 

GTN
Vasodilator which reduces pre load and after and improves perfusion
Smooth muscle relaxant 
Reduces cardiac output causing less strain on the muscle

Furosemide
Loop diuretic that promotes reabsorption of Chlorine (Cl), Potassium (K) and Sodium (Na) in ascending Loop of Henle
Promotes formation of urine reducing preload and blood volume

Pathophysiology

Plague build-up in coronary arteries causes lumen narrowing, reducing blood flow, which in turn increases blood pressure. This build-up of pressure causes plaque to break away and get lodged, causing a thrombus and leading to cardiac cell necrosis. 

Signs and symptoms

• Cardiac - ECG changes, chest pain radiating to teeth, neck, arm, jaw, shoulder and/or back
• Respiratory - SOB
• Appearance - Perspiration, pallour, grey in colour
• Mental - Sense of impending doom
• GI - Nausea, vomiting

Treatment

• Apply defib pads
• If confirmed STEMI contact PPCI
• 300 milligrams of Asprin
• 400-800 micrograms of GTN - every 5-10 minutes (unless inferior right-sided infarct)
• Gain access
• 10 milligrams of Morphine (titrate) - every minutes - maximum dose 20 milligrams 
• Time-critical transport to PPCI 
• Consider additional drug interventions (Clopidogrel, Heparin and Tenecteplase)

Pharmacology 

Aspirin
COX1 and CO2 inhibitor, providing analgesic effects and anti-platelet actions 

Clopidogrel
A selective antagonist for ADP which prevents binding to platelet receptors and inhibits platelet activation/aggregation

GTN
Vasodilator which reduces pre-load and after and improves perfusion
Smooth muscle relaxant
Reduces cardiac output causing less strain on the muscle

Morphine
Inhibits nociceptor impulse transmission at synapses
Triggers histamine release, causing vasodilation, bronchoconstriction and urticaria
Reduces the effect of the respiratory control centre's response to CO2 and electrical stimulation. 

Pathophysiology

Aortic Stenosis is a heart valve disease in which the aortic valves start to narrow and become stiff, reducing their ability to fully open and close, which results in reduced blood flow around the body,

Signs and symptoms

• Cardiac - chest pain*, heart flutter on auscultation (sometimes heard as a whooshing sound or an extra heart beat)
• Respiratory - SOB*
• General - dizziness*, fatigue, blackouts*, weight loss
• GI - bleeding

*present on exertion

Pathophysiology 

Occurs when the foramen ovale does not close properly after birth, leaving a hole between the left and right atrium.

Signs and symptoms

• Cardiac - Arrhythmias, heart murmur (whooshing sound audible through auscultation), palpitations
• Respiratory - SOB*
• General - Fatigue, oedema

*present on exertion

Pathophysiology

Systolic dysfunction of the left or both ventricles, increasing ventricular volume and causing enlargement of the heart (cardiomegaly), as it attempts to work harder to maintain cardiac output.

Signs and symptoms

• Cardiac - Chest pain, arrhythmias, palpitations
• Respiratory - SOB (worse when laying flat)
• General - Oedema, fainting, fatigue

Pathophysiology 

Overview term for any disease causing damage to the heart muscle, reducing cardiac output and causing the heart chambers to stretch, thicken or become stiff.

Restrictive - walls cannot relax after contracting
Hypertrophic - ventricle walls thicken
Dilated - ventricle walls become stretched and thinner
Acute stress (broken heart) - left ventricle changes shape and gets larger, but is temporary and reversible.

Signs and symptoms

• Cardiac - Chest pain*, heart murmur, palpitations
• Respiratory - SOB*, unable to lay flat
• General - Fatigue, fainting*

*Present on exertion

Pathophysiology 

Inflammation of the myocardium owing to infection, reducing contractility. 

Signs and symptoms

• Cardiac - Chest pain, arrhythmias 
• Respiratory - SOB
• General - Fatigue, oedema, light-headedness, flu-like symptoms

Pathophysiology 

Bronchitis is a persistent inflammation of the bronchi, thought to be caused by overproduction and hypersecretion of mucus by goblet cells in response to toxic, infectious stimuli, resulting in the release of inflammatory mediators, such as pro-inflammatory cytokines. 

Signs and symptoms

• Respiratory - Cough, wheeze, expectoration (coughing up mucus), SOB, cyanosis
• Other - Oedema, fatigue

Treatment

• 5 milligrams of Salbutamol - every 5-10 minutes
• 500 micrograms of Ipratropium Bromide 
• 100 milligrams of Hydrocortisone 
• Oxygen to maintain 88-92%

Pharmacology

Salbutamol
Selective Beta-2 adrenoreceptor agonist which relaxes smooth muscles, reducing bronchoconstriction and bronchospasm. 

Ipratropium Bromide
Non-selective anti-muscarinic antagonist which produces bronchodilation and holds anti-cholinergic properties, reducing bronchospasm and mucus production. 

Hydrocortisone
Glucocorticoid steroid which helps to restore blood pressure, cardiac synchronicity and volume.
Additionally displays an antihistamine effect by stabilising mast cell membranes and inhibiting mast cell degranulation.

Oxygen
Increases perfusion and cell metabolism.

Pathophysiology 

Defined as a loss of elasticity within the alveoli. In emphysema, the inner walls of the alveoli weaken and rupture, creating larger air spaces instead of many smaller ones, thus reducing the surface area of the lungs and the resulting amount of oxygen available in the bloodstream.

Signs and symptoms

• Respiratory - Productive cough, wheeze, SOB, audible whistling on expiration, cyanosis
• Other - fatigue

Treatment

• 5 milligrams of Salbutamol - every 5-10 minutes
• 500 micrograms of Ipratropium Bromide 
• 100 milligrams of Hydrocortisone 
• Oxygen to maintain 88-92%

Pharmacology

Salbutamol
Selective Beta-2 adrenoreceptor agonist which relaxes smooth muscles, reducing bronchoconstriction and bronchospasm. 

Ipratropium Bromide
Non-selective anti-muscarinic antagonist which produces bronchodilation and holds anti-cholinergic properties, reducing bronchospasm and mucus production. 

Hydrocortisone
Glucocorticoid steroid which helps to restore blood pressure, cardiac synchronicity and volume.
Additionally displays an antihistamine effect by stabilising mast cell membranes and inhibiting mast cell degranulation.

Oxygen
Increases perfusion and cell metabolism.

Pathophysiology

Mast cell degranulation occurs after exposure to an allergen, causing the release of primary and secondary inflammatory mediators, such as histamine, kinins and heparin, which results in bronchoconstriction, airway inflammation and mucus impaction.

Signs and symptoms

• Respiratory - Wheeze (inspiratory and expiratory), productive cough, SOB, tachypnoea, cyanosis
• Cardiac - Tachycardia, hypotension
• Other - Exhaustion, anxiety, collapse

Treatment

• (Life-threatening only) 500 micrograms of Adrenaline - every 5-10 minutes
• 5 milligrams of Salbutamol - every 5-10 minutes
• 500 micrograms of Ipratropium Bromide
• 100 milligrams of Hydrocortisone

Pharmacology

Adrenaline
A non-selective sympathomimetic adrenic drug, which stimulates alpha- and beta-adrenoreceptors in the sympathetic nervous system.
Alpha 1 - improves vascular resistance, causing vasoconstriction 
Beta 1 - increases the contractility of the heart muscle, increasing cardiac output
Beta 2 - relaxes smooth muscles, causing bronchodilation 

Salbutamol
Selective Beta-2 adrenoreceptor agonist which relaxes smooth muscles, reducing bronchoconstriction and bronchospasm.

Ipratropium Bromide
Non-selective anti-muscarinic antagonist which produces bronchodilation and holds anti-cholinergic properties, reducing bronchospasm and mucus production. 

Hydrocortisone
Glucocorticoid steroid which helps to restore blood pressure, cardiac synchronicity and volume. Additionally displays an antihistamine effect by stabilising mast cell membranes and inhibiting mast cell degranulation.

Pathophysiology 

A PE occurs when one or more emboli, usually arising from a thrombus formed in the veins, become lodged in and obstruct the pulmonary arteries. 

When a PE is present, the lung tissue is ventilated by not perfused, resulting in intra-pulmonary dead space and V/Q mismatch.

Signs and symptoms

• Respiratory - SOB, cyanosis, cough, tachypnoea 
• Cardiac - Pinpoint pain in the chest or back, hypotension
• Other - Anxiety, collapse, hypoxic seizure, calf tenderness, unilateral lower limb swelling

Treatment

• Oxygen
• Urgent transport to definitive care

Pharmacology

Oxygen
Increases perfusion and cell metabolism 

Pathophysiology

CF is a genetic condition affecting the cystic fibrosis transmembrane regulator, which plays a role in the regulation of salt and water transport across cells lining the airway and gut. The result of this abnormality is a build-up of mucus in airways, reducing efficiency in removing bacteria and other potentially harmful products.

Signs and symptoms

• Respiratory - Recurring chest infections, wheeze, cough, SOB
• Other - Weight loss
• GI - Diarrhoea, constipation 

Pathophysiology

A bacterial infection that spreads through coughing and sneezing. Can be found in the lungs, bones, lymph nodes and menigies. 

Signs and symptoms

• Respiratory - Cough
• Other - Weight loss, pyrexia, night sweats, loss of appetite 

Pathophysiology 

Ischaemic: caused by large artery atherosclerosis. small artery occlusion or cardio-aortic embolism.  
Hemorrhagic: caused by an intracerebral hemorrhage or subarachnoid hemorrhage. 

Signs and symptoms

• FAST (face, arms, speech)
• AVVV (ataxia (coordination and balance), vertigo, vomiting and visual changes)
• Cranial nerve assessment

Treatment

•  Rapid transfer to the most appropriate receiving setting

Pathophysiology 

Paroxysmal manifestations of the electrical properties of the cerebral cortex. A seizure results when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons in favour of a sudden-onset net excitation. 

Signs and symptoms

• Consider tonic-clonic and absence.

Treatment

• Follow ABCDE approach, considering patient positioning if still convulsing. Assisted ventilation may be required.
• Consider and treat causes
• <5 minutes: protect from harm
• >5 minutes (or more than 3 seizures in one hour): 10mg Buccal Midazolam or 20mg PR Diazepam (10mg if >70 years old) 
• If still convulsing after ten minutes 10mg IV/IO Diazepam 

Pharmacology 

Midazolam
Benzodiazepine receptor agonist 

Diazepam
Benzodiazepine
CNS depressant 

Pathophysiology 

The release of inflammatory mediators and cytokines causes degranulation of mast cells and basophils in response to LgE secretion from B-Cells, following re-exposure to an antigen. Histamine is the main inflammatory mediator that causes ABC problems, causing blood vessel dilation, increased vascular permeability and bronchoconstriction.

Signs and symptoms

• Defined by rapid onset of ABC problems
• Skin and/or mucosal changes (urticaria, flushing, angioedema)
• Other: hypotension, abdominal pain, diarrhoea and vomiting

Treatment

• Remove trigger
• 15 litres of Oxygen
• 500 micrograms of IM 1:1000 Adrenaline, repeated every 5 minutes
• Sodium Chloride if hemodynamically unstable
• 10 milligrams (IV) or 4 milligrams (oral) of Chlorphenamine 
• 5 milligrams of Salbutamol, repeated every 5 minutes.

Pharmacology

Oxygen
Increases perfusion and cell metabolism 

Adrenaline
A non-selective sympathomimetic adrenic drug, which stimulates alpha- and beta-adrenoreceptors in the sympathetic nervous system.
Alpha 1 - improves vascular resistance, causing vasoconstriction 
Beta 1 - increases the contractility of the heart muscle, increasing cardiac output
Beta 2 - relaxes smooth muscles, causing bronchodilation 

Chlorphenamine 
Competitive non-selective antagonist for central and peripheral H1 receptors, blocking the effects of histamine. 

Salbutamol
Selective Beta-2 adrenoreceptor agonist which relaxes smooth muscles, reducing bronchoconstriction and bronchospasm.

Pathophysiology 
Abnormal focal dilation of the aorta to at least 150% of its normal diameter, eventually leading to excessive dilation and rupture.

Signs and symptoms

• Abdominal: sudden, severe pain in the abdomen or lower back
• Cardiac: tachycardia
• Respiratory: tachypnoea 
• Other: dizziness, syncope, diaphoresis

Treatment

• Time critical transfer
• Patient positioning (legs raised)
• 250ml of Sodium Chloride if indicated (consider permissive hypotension)

Pharmacology

Sodium Chloride
Increases vascular fluid volume, which consequently raises cardiac output and perfusion.

Pathophysiology

Appendicitis likely originates from direct luminal obstruction, increasing bacteria and causing acute inflammation.

Signs and symptoms

• Abdominal: lower-right-sided pain, nausea, loss of appetite, constipation/diarrhoea 
• Other: fever

Positive Rovsings, Psoas and Obturator signs.

Treatment

No specific treatment. Consideration should be given to:

• Antiemetics (Ondanstron)
• Analgesia (not Entonox)
• Sepsis management if required

Pathophysiology

Reduced levels of available blood glucose within blood plasma, resulting in cells being unable to metabolise. 

Signs and symptoms

• Generalised: diaphoresis, fatigue, dizziness, hunger, tremors, palpitations, irritation, pallor
• Later stage: weakness, seizures, visual change, slurred speech, behaviour change, syncope

Treatment

• Exclude other causes for LOC or altered mental state
• Consider oral carbohydrate/glucose if viable. Glucose 40% gel, every 5 minutes, to a maximum of 30 grams.
• Consider IM Glucagon, 1 milligram. 
• IV Glucose 10%, every five minutes, to a maximum of 30 grams.

Pharmacology

Glucose 10% Gel
Rapid increase in blood glucose levels via buccal absorption

Glucagon
Synthetic polypeptide hormone which binds to glucagon receptors in the liver, stimulating the liver to convert glycogen stores into glucose to increase blood sugar. 

Glucose 40%
Increases intravascular blood glucose levels to combat hypoglycemia.

Pathophysiology 

Insulin deficiency and an increase in counterregulatory hormones (glucagon, catecholamines, cortisol) cause the body to metabolize triglycerides and amino acids instead of glucose for energy.

Signs and symptoms

• Respiratory: Kussmauls respiration, fruity breath
• Other: altered mental state, dehydration, polyuria, visual change, leg cramps, raised blood sugar levels 

Treatment

500ml of Sodium Chloride, to a maximum of 2 litres.

Pharmacology

Sodium Chloride
Increases vascular fluid volume, which consequently raises cardiac output and perfusion.

Pathophysiology

Damage to the adrenal glands results in the body not producing enough cortisol and aldosterone. A significant, rapid fall in cortisol is Addison's Crisis. 

Signs and symptoms

• Crisis: severe weakness, altered mental state, lower back and leg pain, severe abdominal pain, diarrhoea and vomiting.

Treatment 

• 100 milligrams of Hydrocortisone

Pharmacology

Hydrocortisone
Glucocorticoid steroid which restores blood pressure, blood sugar, cardiac synchronicity and volume.