Indications A-Z

Pathophysiology

ACS is a spectrum of conditions resulting from acute myocardial ischemia (inadequate blood flow to the heart muscle). It is most commonly caused by the rupture of an atherosclerotic plaque in a coronary artery. This rupture triggers platelet aggregation and thrombus (clot) formation, which partially or completely occludes the artery, leading to unstable angina, NSTEMI (non-ST-elevation myocardial infarction), or STEMI (ST-elevation myocardial infarction).

Pathophysiology

A life-threatening emergency caused by an acute, severe deficiency of cortisol (a glucocorticoid) and often aldosterone (a mineralocorticoid). This occurs in patients with known adrenal insufficiency (Addison's disease) or those on long-term steroid therapy who are exposed to a physiological stressor (e.g., infection, trauma) without an increase in their steroid dose. The lack of cortisol leads to an inability to maintain blood glucose and mount a stress response, while the lack of aldosterone causes sodium wasting and potassium retention, leading to severe hypovolemia, hypoglycemia, and shock.

Pathophysiology

A hypersensitivity reaction of the immune system to an allergen (e.g., pollen, food, insect sting). On exposure, IgE antibodies trigger mast cells and basophils to release inflammatory mediators, most notably histamine. This causes localized vasodilation (redness), increased vascular permeability (swelling, urticaria), and sensory nerve stimulation (itching).

Pathophysiology

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is transmitted via nociceptors (pain-sensing nerves) from the periphery, through the spinal cord, to the brain. The experience of pain is subjective and can be modulated by inflammatory mediators (peripheral sensitization) and central nervous system pathways (central sensitization).

Pathophysiology

A severe, life-threatening, systemic hypersensitivity reaction. Following re-exposure to an allergen, IgE antibodies trigger a massive, body-wide degranulation of mast cells and basophils. This releases a flood of mediators (histamine, leukotrienes) that cause systemic vasodilation (leading to profound hypotension and shock), increased capillary permeability (leading to angioedema), and bronchospasm (leading to respiratory distress and airway compromise).

Pathophysiology

A chronic inflammatory disease of the airways. During an exacerbation (triggered by allergens, infection, etc.), three key events occur: 1) Bronchospasm (acute contraction of bronchial smooth muscle), 2) Airway inflammation and edema (swelling), and 3) Increased mucus production. This combination leads to widespread, reversible airway obstruction, air trapping, and increased work of breathing.

Pathophysiology

A life-threatening syndrome in patients with a spinal cord injury at or above T6. A noxious stimulus (e.g., full bladder, bowel impaction) below the injury level triggers a massive, uncontrolled sympathetic reflex discharge. This causes widespread vasoconstriction below the injury, leading to severe, acute hypertension. The brain detects this hypertension and tries to compensate by sending inhibitory signals (which are blocked by the spinal injury) and by stimulating the vagus nerve, causing bradycardia and vasodilation above the injury level.

Pathophysiology

Acute behavioural disturbance is a presentation of severe agitation, aggression, or psychosis that poses an immediate risk of harm to the patient or others. It is a symptom, not a diagnosis. Causes are broad and include psychiatric illness (e.g., schizophrenia, mania), drug intoxication (e.g., stimulants, hallucinogens), drug withdrawal, delirium (due to infection, hypoxia, metabolic issues), or dementia.

Pathophysiology

A heart rate below the normal range (e.g., <60 bpm in adults) that is insufficient to maintain adequate cardiac output, leading to symptoms of hypoperfusion (e.g., ALOC, hypotension, chest pain, syncope). This can be caused by sinus node dysfunction (e.g., sinus bradycardia) or a failure of conduction through the AV node (e.g., heart blocks).

Pathophysiology

CPO is a form of acute heart failure where the left ventricle fails to pump blood effectively (e.g., due to an AMI or chronic heart failure). This failure causes blood to back up into the left atrium and pulmonary veins. The resulting increase in pulmonary capillary hydrostatic pressure forces fluid to leak from the capillaries into the lung's interstitial spaces and alveoli, impairing gas exchange and causing severe dyspnoea.

Pathophysiology

An acute worsening of respiratory symptoms in a patient with Chronic Obstructive Pulmonary Disease (COPD). It is typically triggered by a respiratory infection or environmental irritant. This trigger causes a rapid increase in airway inflammation, bronchospasm, and mucus production, superimposed on the patient's baseline chronic bronchitis and/or emphysema. This leads to severe airflow limitation, air trapping, and potential respiratory failure (hypoxia and/or hypercarbia).

Pathophysiology

A phenomenon where high-quality CPR generates enough cerebral perfusion to cause a patient in cardiac arrest to exhibit signs of consciousness (e.g., purposeful movement, eye-opening, fighting the ventilator, groaning). This creates a distressing and dangerous situation, as the patient's "CPR-induced interference" (fighting the resuscitation) can compromise the quality of compressions and ventilation, thereby worsening outcomes.

Pathophysiology

A dangerously high serum potassium level. High extracellular potassium reduces the resting membrane potential of cardiac myocytes (makes it less negative), decreasing excitability. This slows conduction, and at severe levels, can lead to life-threatening arrhythmias (e.g., bradycardia, heart blocks, ventricular fibrillation) and asystole. Classic ECG changes include tall, peaked T-waves, widened QRS, and loss of P-waves.

Pathophysiology

A blood glucose level (BGL) < 4.0 mmol/L in a symptomatic patient. The brain relies almost exclusively on glucose for energy. A lack of glucose (neuroglycopenia) impairs CNS function, leading to confusion, ALOC, seizures, and coma. The body's counter-regulatory response also triggers adrenergic symptoms (sweating, tachycardia, anxiety) as it tries to raise BGL.

Pathophysiology

An invasive infection caused by the bacterium *Neisseria meningitidis*. It most commonly presents as meningitis (inflammation of the meninges) or meningococcal septicaemia (sepsis). In septicaemia, the bacteria release endotoxins that trigger a massive inflammatory cascade, leading to widespread vascular damage, disseminated intravascular coagulation (DIC), and a characteristic non-blanching purpuric rash. This progresses rapidly to multi-organ failure and shock.

Pathophysiology

Nausea and vomiting are protective reflexes controlled by the vomiting center in the brainstem. This center receives inputs from several sources, including the chemoreceptor trigger zone (CTZ) (which detects toxins/drugs in the blood), the vestibular system (motion sickness), the GI tract (irritation), and higher cortical centers (anxiety, pain). Mediators like dopamine, serotonin, and histamine play key roles in signaling.

Pathophysiology

Nerve agents are a class of organophosphates that irreversibly inhibit the enzyme acetylcholinesterase. This enzyme is responsible for breaking down the neurotransmitter acetylcholine (ACh) in the synapse. With the enzyme inhibited, ACh accumulates and continuously stimulates all muscarinic and nicotinic receptors in the parasympathetic, sympathetic, and central nervous systems, leading to a cholinergic crisis (SLUDGEM: Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis, Miosis) and ultimately death from respiratory muscle paralysis.

Pathophysiology

Identical to nerve agent poisoning. Organophosphates are commonly found in insecticides. They irreversibly inhibit the acetylcholinesterase enzyme, leading to a cholinergic crisis (SLUDGEM) due to the accumulation and overstimulation of acetylcholine at muscarinic and nicotinic receptors. This causes respiratory failure from excessive bronchial secretions, bronchospasm, and skeletal muscle paralysis.

Pathophysiology

Opioids (e.g., heroin, fentanyl, oxycodone) cause an overdose by binding to mu-opioid receptors in the brainstem. This stimulation directly suppresses the respiratory drive, leading to respiratory depression (slow, shallow breathing) which progresses to apnea, anoxia, and death. It also causes miosis (pinpoint pupils) and CNS depression (coma).

Pathophysiology

A traumatic breach of the globe (eyeball) by a foreign object. This is a sight-threatening emergency. Any pressure on the globe (e.g., from the object, rubbing, or vomiting) can cause the extrusion of intraocular contents (vitreous humor, iris), leading to permanent blindness. Vomiting significantly increases intraocular pressure.

Pathophysiology

After Return of Spontaneous Circulation (ROSC) from cardiac arrest, many patients remain comatose. Those who regain consciousness are often agitated, confused, or combative due to post-anoxic brain injury. This agitation can lead to "patient-ventilator dyssynchrony" (fighting the advanced airway), increased metabolic demand, and hemodynamic instability, all of which worsen neurological outcomes. Sedation is required to facilitate ongoing ventilation, cooling, and transport.

Pathophysiology

Intraosseous (IO) access involves placing a needle into the medullary cavity of a long bone. While a life-saving procedure, the infusion of fluid or medication into this non-collapsible space can be extremely painful for a conscious or semi-conscious patient, as it rapidly increases intra-medullary pressure and stimulates nociceptors within the bone.

Pathophysiology

Post-Partum Hemorrhage (PPH) is excessive bleeding after childbirth. The most common cause is uterine atony, where the uterus fails to contract adequately after the placenta is delivered. The "living ligatures" (interwoven muscle fibers of the uterus) do not clamp down on the blood vessels that supplied the placenta, leading to catastrophic, rapid blood loss.

Pathophysiology

In an ST-Elevation Myocardial Infarction (STEMI), a coronary artery is typically 100% occluded by a thrombus (blood clot). This starves the downstream myocardium of oxygen, leading to transmural ischemia and irreversible cell death (infarction). "Time is muscle," and the goal of therapy is to restore blood flow (reperfuse) as quickly as possible.

Pathophysiology

A seizure is a transient disturbance of cerebral function caused by abnormal, excessive, and hypersynchronous neuronal activity in the brain. Status Epilepticus is a state of continuous seizure activity (≥5 minutes) or recurrent seizures without recovery. This is a neurological emergency, as prolonged seizure activity can cause neuronal death, hypoxia, acidosis, and rhabdomyolysis.

Pathophysiology

Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF) are life-threatening arrhythmias originating from the ventricles. In cardiac arrest, these rhythms may be "refractory," meaning they persist despite defibrillation attempts. This is often due to underlying ischemia, electrolyte abnormalities, or structural heart disease creating an unstable electrical environment.

Pathophysiology

A specific form of polymorphic ventricular tachycardia (pVT) characterized by a "twisting" of the QRS complex around the isoelectric line on an ECG. It is almost always associated with a prolonged QT interval (either congenital or acquired, e.g., from drugs or electrolyte imbalance). This prolonged repolarization phase allows for early afterdepolarizations, which can trigger the arrhythmia. It can degenerate into VF.

Indications for Fluid Therapy