Applied Bioscience for Health Complexity: Comprehensive Notes on Respiratory, Trauma, Burn, and Cardiac Disorders
Assessment Details for GMED3009
Case Study: Due 31/07.
Invigilated E-test: Scheduled for 10/08 and 04/09.
Exam: Scheduled for early November.
Overview of Respiratory Failure
Definition: A syndrome where the respiratory system fails in one or both of its primary gas exchange functions, resulting in insufficient oxygenation and carbon dioxide () elimination.
Hypoxemic Respiratory Failure (Type I):
Characteristic: PaO_2 < 60\,mmHg with a normal or low .
Prevalence: This is the most common form of respiratory failure.
Pathophysiology: Associated with almost all acute lung diseases, generally involving fluid filling or the collapse of alveolar units.
Specific Examples: Cardiogenic or noncardiogenic pulmonary oedema, pneumonia, and pulmonary hemorrhage.
Common Causes: COPD, pneumonia, pulmonary oedema, pulmonary fibrosis, asthma, pneumothorax, pulmonary embolism (PE), and pulmonary arterial hypertension.
Hypercapnic Respiratory Failure (Type II):
Characteristic: PaCO_2 > 50\,mmHg. Normal range for is .
Clinical Presentation: Hypoxemia is common in patients breathing room air. The pH is dependent on bicarbonate levels, which vary based on the duration of hypercapnia.
Common Causes: COPD, severe asthma, drug overdose, poisonings, myasthenia gravis, primary muscle disorders, cervical cordotomy, head and cervical cord injury, pulmonary oedema, and ARDS.
Key Parameters:
: Partial pressure of carbon dioxide in the blood. If it exceeds , the lungs are not removing enough carbon dioxide, leading to dangerous systemic levels.
Hypoventilation: In these cases, , , and the alveolar-arterial gradient are normal.
Mechanisms of Improved Gas Exchange and Pathological Impairment
Alveolar-Arterial (A-a) Gradient: Measures the efficiency of gas exchange by finding the difference between the calculated oxygen pressure available in the alveolus and the arterial oxygen tension.
CNS Depression: Can be caused by drugs such as opioids.
Ventilation/Perfusion (V/Q) Mismatch:
The most common cause of hypoxemia.
Occurs when air (ventilation) and blood flow (perfusion) are not properly matched.
The V/Q Ratio: Describes the balance between air reaching the alveoli and blood flow through the lung capillaries. Disruption leads to impaired gas exchange and low oxygen levels.
Correction: Administering usually corrects hypoxemia caused by a V/Q mismatch.
Shunt:
A pathological mechanism where alveoli are perfused but not ventilated.
Effect: Deoxygenated blood bypasses ventilated areas and remains unoxygenated even with inhalation, resulting in persistent hypoxemia.
Associated Conditions: Pulmonary oedema, pneumonia, and atelectasis.
General Treatment Options for Respiratory Failure:
Correction of hypoxemia.
Ventilatory support.
Positioning.
Pharmacological therapy.
Pulmonary Oedema: Cardiogenic vs. Non-cardiogenic
Cardiogenic Pulmonary Oedema:
Mechanism: Caused by increased hydrostatic pressure in the pulmonary capillaries, usually due to left ventricular failure.
Membrane Status: The alveolar-capillary membrane remains intact.
Result: Fluid is forced into the interstitial space and alveoli, impairing gas exchange and causing hypoxaemia.
Underlying Causes: Heart failure, coronary artery disease with left ventricular failure, cardiac arrhythmias, fluid overload, cardiomyopathy, obstructing valvular lesions, myocarditis, and infectious endocarditis.
Non-cardiogenic Pulmonary Oedema:
Mechanism: Caused by increased permeability of the alveolar-capillary membrane due to inflammation or lung injury.
Membrane Status: Damage allows protein-rich fluid to leak into the alveoli.
Result: Impaired gas exchange, alveolar collapse, and severe hypoxaemia.
Underlying Causes: ARDS, smoke inhalation, head trauma, overwhelming sepsis, hypovolaemic shock, acute lung re-expansion, near-drowning, and overwhelming aspiration.
Acute Respiratory Distress Syndrome (ARDS)
Synonyms: Shock lung, adult hyaline membrane disease.
General Profile: A common condition with complex pathophysiology, frequently occurring in critically ill patients or those in septic shock. It has a global mortality rate between .
Definition: An acute, diffuse, inflammatory form of lung injury characterized by noncardiogenic pulmonary oedema and severe refractory hypoxaemia.
Triggers: Risks include pneumonia, nonpulmonary infection, trauma, transfusion, burn, aspiration, and shock.
Consequences: Increased pulmonary vascular and epithelial permeability, lung oedema, and gravity-dependent atelectasis leading to loss of aerated lung tissue.
Clinical Hallmarks:
Arterial hypoxia.
Diffuse radiographic opacities.
Increased shunting.
Increased alveolar dead space.
Decreased lung compliance.
Diagnostic Criteria:
Acute onset.
Bilateral infiltrates on Chest X-Ray (CXR).
No evidence of left ventricular heart failure.
Clinical Symptoms:
Tachypnoea, tachycardia, and respiratory alkalosis within first hours.
Breath sounds may be clear initially, but crackles and rhonchi develop later.
Cyanosis.
Progresses to respiratory failure within hours of symptom onset.
Chest CT may show widespread patchy or coalescent airspace opacities, usually more apparent in dependent lung zones.
Pathophysiology (Unregulated Response):
Increased pro-inflammatory cytokines occur due to direct lung injury or systemic insult.
Activated neutrophils secrete cytokines, increasing inflammation.
Released cytokines include tumour necrosis factor-alpha () and interleukins.
Neutrophils produce oxygen radicals and proteases that injure capillary endothelium and alveolar epithelium.
Injury causes increased permeability and an influx of protein-rich fluid into the alveolar space.
Impaired fibrinolysis lead to capillary thrombosis and microinfarction.
Phases of ARDS:
Exudative Phase ( days): Increased permeability of the alveolar-capillary barrier leading to fluid influx. Intrapulmonary shunts develop; blood passing through cannot be oxygenated. Alveoli collapse (atelectasis).
Proliferative Phase ( weeks): Influx of neutrophils, monocytes, fibroblasts, and lymphocytes destroys pulmonary vasculature. Connective tissue and fibroblasts proliferate. Lung tissue appears densely cellular ("stiff lung"). Fibrotic tissue and enlarged air spaces appear by weeks . Impaired fibrinolysis occurs mostly here.
Fibrotic Phase ( weeks): Lung reorganizes and recovers. Inflammation and fibrosis settle. Oxygenation improves, potentially allowing removal of mechanical ventilation. Resolve may take up to months.
Treatment:
Aggressive early treatment of the underlying cause.
Fluid management: Avoid fluid overload (controversial but critical).
Surfactant: Improves survival in neonates with infant respiratory distress syndrome but has not shown improvement in adults.
Steroids: Controversial/considered in late fibrotic phase.
Ventilation: Lower tidal volumes and limited ventilation pressure reduces mortality.
Prone positioning: Can improve oxygenation by reducing oedema and atelectasis in posterior dependent lung zones.
Anatomy and Mechanisms of Burn Injury
Skin Layers: Epidermis, Dermis, Subcutaneous.
Underlying Structures: Fascia, nerves, tendons, ligaments, muscles, and organs.
Mechanisms of Injury:
Heat: Related to flames, hot liquids, solids, or steam. Injury depth depends on temperature, contact duration, and skin thickness.
Electrical: Energy transforms into heat through body tissue resistance. Injury magnitude depends on current pathway, resistance, strength, and duration.
Friction: Combination of mechanical disruption and heat generation.
Chemical: Acids cause coagulation necrosis; alkaline agents cause liquefaction necrosis.
Radiation: Ionizing or radio frequency energy damage (e.g., sunburn, therapeutic/diagnostic radiation).
Inhalation Injuries:
Toxic Inhalation: From synthetic resin combustion, cyanide, or hydrogen sulphide. Systemic poisoning is more frequent than thermal inhalation burns.
Carbon Monoxide (CO): Colourless/odourless byproduct of incomplete carbon combustion. Has greater affinity for haemoglobin than oxygen, leading to hypoxaemia and hypercarbia.
Airway Thermal Burn: Supraglottic structures usually absorb heat to protect the lower airway. Common from steam.
Clinical Indicators: Stridor (crowing sounds), singed facial/nasal hair, black sputum, progressive respiratory obstruction due to swelling.
Burn Classification, Assessment, and Management
Depth Classification:
Superficial (Epidermal): Minor (<50\% Total Body Surface Area - TBSA), Moderate (>50\% TBSA).
Partial-thickness: Epidermis and portions of dermis. Minor (<15\% TBSA), Moderate ( TBSA), Critical (>30\% TBSA).
Full-thickness: Destroys all layers of dermis. Minor (<2\% TBSA), Moderate ( TBSA), Critical (>10\% TBSA).
Deeper (Fourth Degree): Extends into fascia, muscle, or bone.
Clinical Manifestations: Pain, chest pain, blisters, skin sloughing, burnt hair, oedema, hoarseness, dysphagia, dysphasia, hemorrhage, and dyspnoea.
Estimation of Burn Size:
Lund-Browder Chart: Most accurate method for adults and children; accounts for body surface changes during growth.
Wallace Rule of Nines: Expeditious adult assessment. Head (), specific arm ( each), specific leg ( each), anterior trunk (), posterior trunk ().
Note: Superficial (1st degree) burns are excluded from TBSA assessment.
Complications: Hypothermia (), hypovolaemia (), eschar (leathery dead skin), infection (greatest risk), organ failure (), hypermetabolism, scarring/keloids, and contractures.
Emergency Management:
Minor: Cool water immersion for minutes, remove clothing, analgesics, clean with aqueous chlorhexidine or Normal Saline (NS), remove loose/non-viable tissue.
Moderate/Serious: Dry sterile dressings, prevent hypothermia, fluid therapy. If needed, IVs can be placed in partial-thickness burn sites.
Inhalation: High-flow via non-rebreather mask, intubation if swelling, hyperbaric oxygen therapy.
Parkland Burn Formula: Used for fluid resuscitation over hours.
Administration Schedule: Half the total amount in the first hours; the remaining half over the next hours.
Jackson’s Theory of Thermal Wounds:
Zone of Coagulation: Center of the burn with most damage (clotted/thrombosed vessels).
Zone of Stasis: Surrounding area with decreased blood flow.
Zone of Hyperaemia: Peripheral area with increased blood flow.
Systemic Phases of Burn Response:
Emergent Phase: Pain, catecholamine release, tachycardia, tachypnoea, mild hypertension, anxiety.
Fluid Shift Phase ( hours): Massive oedema as fluids shift from intravascular to extravascular space; peaks in hours.
Hypermetabolic Phase: Lasts days to weeks; high nutrient demand for repair.
Resolution Phase: Scar formation and rehab.
Spinal Cord Injury (SCI)
Definitions:
SCI: Damage to the spinal cord that causes loss of function (mobility/feeling). The cord does not need to be severed; compression or bruising is sufficient.
Quadriplegia: Cervical region injury affecting arms, legs, bowel, and bladder.
Paraplegia: Thoracic, lumbar, or sacral injury affecting lower body, bowel, and bladder.
Shock States:
Spinal Shock: Temporary () areflexic state with loss of autonomic control. Occurs in cervical and upper thoracic injuries.
Neurogenic Shock: Haemodynamic triad of hypotension, bradycardia, and peripheral vasodilation from severe autonomic dysfunction. Hypothermia may occur.
Forces of Injury: Hyperflexion, hyperextension, axial loading (compression), and flexion-rotation.
Classification:
Complete SCI: Total loss of function below level of injury.
Incomplete SCI: Partial interruption; variable function/sensation remaining.
Levels and Symptoms:
Cervical: Affects arms, legs, and middle body. High cervical leads to breathing difficulties.
Thoracic: Affects legs. May cause blood pressure and temperature control issues.
Lumbar Sacral: Affects legs, bowel, and bladder.
Clinical Presentation & Complications:
Vital Signs: Bradycardia and hypotension ().
Autonomic Dysreflexia: Level or above. Excessive response to noxious stimuli (e.g., full bladder/bowel). Results in sudden severe hypertension, bradycardia, pounding headache, and flushing. Treated by removing stimuli and administering antihypertensives.
Neurogenic Bladder/Bowel: Incontinence, infections, and constipation/impaction.
Secondary Injury Pathophysiology: Occurs over hours to days. Inflammatory processes, vascular changes, and calcium changes lead to oedema, ischaemia, and eventually necrosis of grey and white matter. Function loss occurs within hours. Macrophages remove neurons within days.
Interventions:
Decompression laminectomy to remove fluid/tissue pressing on the cord.
Vasopressors (e.g., dopamine/noradrenaline) to maintain BP.
Lower molecular weight heparin for VTE prevention.
Baclofen or Botox for muscle spasticity.
Trauma Assessment and Management
Types of Injury: Blunt trauma (compression, shear, overpressure) and penetrating trauma.
Preparation/Triage: Team assembly, equipment checks, and sorting patients by acuity.
Primary Survey (ABCDE):
A - Airway & C-Spine: Loss of airway can cause death in <3 minutes. Use chin lift/jaw thrust, suction, or definitive airway (intubation). Immobilize C-spine with rigid collars.
B - Breathing & Ventilation:
Tension Pneumothorax: Air trapped in pleural space. Signs: absent breath sounds, tracheal shift, distended neck veins. Treatment: Needle decompression.
Haemothorax: Blood in pleural space. Signs: dullness to percussion. Treatment: Chest tube.
Flail Chest: Two or more fractures on two or more ribs. Signs: Paradoxical chest movement. Treatment: Improve gas exchange, avoid fluid overload.
Open Pneumothorax: Sucking chest wound. Treatment: Three-sided occlusive dressing.
C - Circulation:
Shock: Assume haemorrhagic in trauma until proven otherwise.
Pericardial Tamponade: Heart compressed by blood in pericardium. Beck's Triad: Muffled heart sounds, hypotension, distended jugular veins. Treatment: Pericardiocentesis.
D - Disability: GCS, pupils, AVPU scale, extremity movement, and spinal clearance.
E - Exposure/Environment: Remove all clothing, logroll to check back, maintain warmth to avoid coagulopathy.
Special Populations: In pregnancy after weeks, enlarged uterus causes Supine Hypotensive Syndrome by compressing the inferior vena cava. Patients must be kept in the left lateral decubitus position.
Cardiac Conduction and Arrhythmias
Inherent Pacemaker Rates:
SA Node: .
AV Node: .
Ventricles: .
Components of ECG Strip:
P Wave: Atrial depolarisation.
PR Interval: Atrial and nodal activity (atrial depolarisation + AV node delay).
QRS Complex: Ventricular depolarisation (corresponds to pulse).
T Wave: Ventricular repolarisation.
Atrial Arrhythmias:
Atrial Fibrillation (AF): Chaotic signals cause atria to quiver. High stroke risk due to pooling blood. Categories: Paroxysmal (<7 days), Persistent (>7 days), Permanent (>1 year).
Atrial Tachycardia (AT): Rate >100, narrow QRS. Often due to COPD, hypoxia, or acidosis.
Ventricular Arrhythmias:
Ventricular Tachycardia (VT): Rate >100. Monomorphic (regular) or Polymorphic (life-threatening if sustained).
Ventricular Fibrillation (VF): Fine or coarse quivering. No waveforms.
R on T Phenomenon: PVC occurring on the downslope of T wave (refractory period) can cause VF.
Conduction Blocks:
1st Degree: Prolonged PR.
2nd Degree Type I (Wenckebach): Irregular PR and R-R.
2nd Degree Type II (Mobitz II): Regular PR, dangerous.
3rd Degree: Complete heart block; PR irregular, R-R regular.
Treatment for Acute Myocardial Infarction (AMI):
Oxygen: Limit ischaemia (target <95\%).
Aspirin: PO; blocks platelet aggregation.
Nitroglycerin: SL every minutes; dilates vessels. Avoid if recent Viagra use.
Morphine: slow IVP every minutes if nitroglycerin fails.
Congestive Cardiac Failure (CCF)
Definition: Impaired ability of the ventricles to fill or eject blood. If the Ejection Fraction (EF) is <40\%, the heart cannot meet metabolic demands.
Left-Sided Failure:
Systolic: EF <40\%. Failure to contract adequately. Starling's Law initially increases contraction force but eventually fails.
Diastolic: EF >40\%. Failure to relax/fill. Leads to pulmonary crackles, orthopnoea, and paroxysmal nocturnal dyspnoea.
Right-Sided Failure: Failure to pump to pulmonary circulation. Leads to systemic congestion: peripheral oedema, jugular venous distension, and hepatomegaly.
Compensatory Mechanisms:
RAAS: Renin release leads to sodium/water retention to increase preload and BP.
SNS: Catecholamine release increases heart rate to maintain CO but increases oxygen demand.
ADH Activation: Water retention via renal collecting ducts.
Pharmacological Management:
ACE Inhibitors/ARBs: Decrease fluid volume and promote reverse remodelling.
Beta Blockers: Decrease afterload and promote remodelling.
Digoxin: Increases stroke volume and cardiac output.
Loop Diuretics: Volume management (watch for electrolyte imbalance).
Calculations:
Congestive Cardiac Failure (CCF)
Complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood
Cardiac output becomes insufficient to meet the metabolic needs of the body
Stroke volume determined by preload, afterload and myocardial contractility
If the ejection fraction is less than 40%, the heart will not supply enough blood and oxygen to the cells to meet metabolic needs
Ejection fraction (EF) → amount of blood pumped from the ventricle in one heartbeat
Aetiology
Acute:
AMI
Arrhythmias
Pulmonary emboli
Thyrotoxicosis
Hypertensive crisis
Papillary muscle rupture
Ventricular septal defect
Chronic:
Anaemia
Bacteria endocarditis
Valvular disorder
Coronary artery disease
Congenital heart disease
Cardiomyopathy
Pulmonary diseases
Hypertension
HIV infection
Diagnostic evaluation
Pt history
Physical exam
ECG, ECHO, CT
Radionuclide
FBC, U&Es, LFTs, ABGs, blood glucose
Magnetic resonance
Cardiac catheterisation with angiography
biopsy
Management of CCF
Lifestyle changes → salt restriction, exercise, stop smoking and alcohol, body weight, supportive stockings
Pharmacological
Angiotensin-converting enzyme (ACE) inhibitors → decrease fluid volume, improve renal blood flow
Angiotensin II receptor blockers → promotes reverse remodelling
Beta blockers → promote reverse remodelling, decrease afterload
Other vasodilators → reduced cardiac afterload, leading to increased CO
E.g. nitroglycerin
Cardiac glycosides → increase SV and CO
E.g. digoxin
Aldosterone receptor blockers → decrease fluid volume, improve renal blood flow
E.g. spironolactone
Loop diuretics
Potassium-sparing diuretics
Thiazide and thiazide-like diuretics
Anticoagulants
E.g. heparin
Opioids to relieve anxiety and pain
E.g. morphine
Positive inotropic drugs → drugs that make muscle contract more forcefully
E.g. dopamine
Oxygen for pulmonary edema is required
Non-pharmacological
Coronary artery bypass grafting → revascularisation
Surgical procedure used to treat coronary heart disease
It diverts blood around narrowed or clogged parts of the major arteries to improve blood flow and oxygen supply to the heart
Percutaneous coronary intervention → Angioplasty
Non-surgical procedure that uses a catheter to place a stent to open up blood vessels in the heart that have been narrowed by plaque buildup (atherosclerosis)
Valve replacement
Biventricular pacemaker
Heart transplantation
Left ventricular assist device (LVAD
Nursing management
Maintain the patient in high Fowler's position
Elevate extremities
Frequently monitor vital signs
Change position frequently
Monitor intake and output and daily weight
Restrict fluids as ordered
Teach the patient and family and provide emotional support (lifestyle change)
Explain the side effects of diuretic medications; additional actions/side effects of diuretics include electrolyte imbalance and symptomatic hypotension
Use aseptic procedures when caring for invasive lines
Help patient to conserve energy
Pathophysiology of CCF
Left-sided failure
Occurs when the left ventricle of the heart is affected
Common causes include CHD and hypertension
Cardiac output is reduced due to loss of ventricular functioning
Divided into 2 categories:
Systolic dysfunction → impaired ventricular contraction and ejection
EF <40%
Diastolic dysfunction → impaired relaxation and ventricular filling
EF > 40%
Pressures in the left ventricle and atrium increase as the amount of blood remaining in the ventricle after systole increases
These pressures impair filling, causing congestion and increased pressures in the pulmonary vascular system
results in fluid movement from the blood vessels into interstitial tissues and alveoli
Systolic failure
Aka heart failure with a reduced ejection fraction
Occurs when the ventricle fails to contract adequately to eject a sufficient blood volume into the arterial system
Affected by loss of myocardial cells due to ischaemia and infarction, cardiomyopathy or inflammation
Result is that heart may fill well during diastole, the failing myocardium is unable to eject sufficient blood during systole
Leads to dilation of the heart and stretching of the muscle fibres
Starling’s law → theres an initial increase in the force of contraction that helps to restore cardiac output
eventually, the compensatory mechanism starts to fail, and CO falls
Decreased CO, weakness, fatigue, decreased exercise tolerance
Diastolic failure
Occurs when heart cannot completely relax in a diastole, disrupting normal filling
Passive diastolic filling decreases, increasing the importance of atrial contraction to preload
Results from decreased ventricular compliance due to hypertrophic and cellular changes and impaired relaxation of the heart
Manifestations result from increased pressure and congestion behind the ventricle: SOB, tachypnoea, respiratory crackles if left-sided
signs/symptoms → SOB, tachypnoea, orthopnoea, paroxysmal nocturnal dyspnoea, resp crackles, S3 gallop, Cheyne-Stokes respiration, general fatigue, abnormal heart sounds, symptoms related to lack of oxygen
Right-sided failure
Right ventricle is impaired
Increased pressure in the pulmonary vasculature or right ventricular muscle damage impairs the right ventricle's ability to pump blood into the pulmonary circulation
Ventricle and atrium become distended, and blood accumulates in the systemic venous system
Increased venous pressures cause abdominal organs to become congested and peripheral tissue oedema to develop
Manifestations: ascites, peripheral oedema, enlarged liver
signs/symptoms → peripheral oedema, jugular venous distension, hepatomegaly, abdominal pain, nausea, anorexia, bloating
Compensatory mechanisms
MAP is closely regulated and is the product of CO and total peripheral resistance
Pt with HF has decreased CO, which leads to a decreased MAP and decreased tissue perfusion
The body tries to maintain adequate tissue perfusion and compensates to bring MAP back to normal using several mechanisms, including the Frank-Starling mechanisms, neurohormonal activation and ventricular remodelling
While initially beneficial, long-term effects will worsen HF
Stroke (CVA)
Anatomy and physiology of the brain
4 main regions
Cerebrum → interprets sensory input, controls skeletal muscle activity, intellectual, emotions and memory
2 hemispheres = 60% of brain weight
Hemispheres divided into frontal, parietal, temporal and occipital lobes
Diencephalon → regulates the autonomic nervous and endocrine systems
Brain stem → conduction pathway and regulates skeletal muscles
Cerebellum → processes information related to balance, posture, and coordinated muscle movement
Major arteries serving the brain and circle of Willis
Anterior part of brain supplied by 2 internal carotid arteries
Posterior part supplied with blood by vertebral arteries
These main arteries are connected by branches of smaller anterior and posterior communicating arteries to form a circle of connected blood vessels
The circle of Willis
Stroke
Aka cerebral vascular accident (CVA)
Condition in which neurological deficits result from sudden decrease in blood flow to a localised area of the brain
Risk factors
Modifiable risks → hypertension, heart disease, DM, blood cholesterol levels, smoking, substance abuse
Non-modifiable risks → age, race, sex, ethnicity, heredity
Types of stroke
Haemorrhagic
Bleed in or around the brain
Approx 15% of strokes
Occurs when a vessel in the brain ruptures/blood begins to leak directly into tissue
Cause → hypertension
Can originate from a weak spot in a vessel wall, or other blood vessel malformations
Appears as bright white on CT scan
Intracerebral haemorrhage (ICH) → leaking blood results in sudden increase in pressure that damages surrounding brain cells.
If volume of blood increases rapidly, extreme pressure buildup leads to unconsciousness or death
More insidious and have progression of deficits. Presents as fluctuating LOC
Subarachnoid haemorrhage (SAH) → bleeding in the subarachnoid space, ventricles and spine
Secondary to trauma, cerebral aneurysmal rupture or rupture of an arteriovenous malformation (AVM)
Present with sudden onset headache, N+V, signs of meningism; decreased LOC occurs in 60% of patients; seizures occur in 10%
Cerebral aneurysm → weak bulging spot on the wall of a brain artery, like a thin balloon or weak spot on an inner tube
Form from wear and tear on the arteries, sometimes from injury, infection or inherited tendency
Ischaemic
Blocked blood flow to the brain
Approx 85% of strokes
Obstruction of an artery leading to or into the brain, preventing oxygenated blood and nutrients from reaching parts of the brain
Either thrombotic or embolic
If a clot obstructs it's thrombotic; if it breaks free and travels it's embolic
Thrombotic ischaemic stroke → 2 types
Large vessel thrombosis → most common, occurs in the brain's larger arteries
Small vessel disease → occurs when blood flow is blocked to a very small arterial vessel, lacunar infarction (deep brain infarct)
Embolic ischaemic stroke → blood clot forms in one area of the body and travels through the bloodstream to lodge
Eventually an embolus will reach a blood vessel small enough to block passage
Emboli can be fat globules, air bubbles, bits of atherosclerotic plaque, or fragments of thrombus from a cardiac source
Transient ischemic attack (TIA) → transient obstruction to blood flow where no significant damage is detected on CT or MRI
Symptoms resolve within 24 hours, although there are suggestions to change to <1 hour
Direct warning that major stroke could occur
Medical attention urgent!
Herniation (coning)
Neurological injury or space-occupying mass within the skull; pressure in cranium may rise
Brain tissue may be displaced to an area of lower pressure
When pressure rises, brain tissue herniates downward
Causes alterations in the function of the neurons
Clinical symptoms: hemiplegia, dilated pupils, restlessness
If pressure persists, brain tissue may continue to be pushed down through the foramen magnum
Coning → squeezing of the brain and brainstem through the foramen magnum as a result of swelling. Leads to loss of basic cardiorespiratory function
Surgery - hemicraniotomy
Cerebral oedema
Common complication of large multi-lobe strokes
Usually peaks 3 to 5 days and is only a problem in the first 24 hours in young stroke patients or those with large cerebellar strokes
Young people have no cerebral atrophy and thus no room to accommodate a swelling brain
Clinical signs: raised intracranial pressure can include a change in level of consciousness, worsening neurological deficits, new pupillary changes, or changes in respiratory patterns
Changes in level of consciousness are an early sign, whereas pupillary changes are a late sign.
Midline shift
Shift of the brain past the midline
Commonly associated with a distortion of the brain stem, failure of the pupils to constrict in response to light
Often associated with high ICP
Manifestations according to cerebral vessel involved
Internal carotid artery
Contralateral paralysis of the face, arm and leg
Contralateral sensory deficit of the arm, face and leg
Aphasia, apraxia, agnosia, unilateral neglect
Middle cerebral artery
Drowsiness, stupor, coma
Contralateral hemiplegia of the arm and face
Global aphasia → affects language understanding
Homonymous hemianopia → vision loss in the same half of each eye
Anterior cerebral artery
Contralateral weakness or paralysis of the foot and leg
Contralateral sensory loss of the toes, foot and leg
Loss of ability to make decisions or act voluntarily
Urinary incontinence
Vertebral artery
Pain in face, nose and eye
Numbness and weakness of the face
Gait, Dysphagia
Warning signs of stroke
Face → looks uneven
Arms → one arm hanging down
Speech → slurred speech
Time → call 000
Treatment
Reperfusion
Remove clot by thrombolytic medication or clot retrieval device
Use of IV recombinant tissue plasminogen activator (rt-PA) to treat ischaemic stroke. Also associated with increased risk of haemorrhage
Post stroke
Antiplatelet therapy
Aspirin 100- 300 mg daily
Alternatives: dipyridamole and clopidogrel
Combination therapy: Dipyridamole 200 mg BD plus aspirin
Clopidogrel 75 mg daily → slightly more potent
Anticoagulation
Low-dose subcut unfractionated heparin or low-molecular weight heparin
All ischaemic stroke patients should receive thromboprophylaxis on admission (delayed 24hrs if rt-PA given)
Intracerebral haemorrhage stroke patients given thromboprophylaxis after 48-72hrs
Blood pressure management
Lower blood pressure but with caution, and addition of new antihypertensive therapy generally deferred for 7-10 days
Blood pressure should be reduced no more than 10-20%
Pre-existing antihypertensive therapy continued (orally or NGT)
For ICH
Surgical evacuation undertaken for cerebellar hemisphere haematomas> 3 cm diameter
Craniotomy for patient where haematoma is superficial
Nurses management for stroke patients
Administer thrombolysis early after stroke
Medication administration
FNO and monitoring
Swallowing screening, hydration monitoring and IV treatment if required
Comprehensive assessment of continence, skin integrity, pain control, development of management plans
Management of tracheostomies
Establish effective communication with pts who suffer from speech and language disturbances
Mobility assistance, falls prevention, personal care
Prevention of post-stroke complications
Pt education about prevention, including smoking cessation
Pathophysiology of a stroke
Brain receives approx 20% of total cardiac output each minute and accounts for 20% of the body's oxygen consumption
Blood flow to the cerebral vessels is self-regulated → autoregulation
Self-regulation is not effective when systemic blood pressure falls below 50mmHg or rises above 160mmHg
Pathophysiological changes at the cellular level take place in 4-5minutes when blood flow to and oxygenation of cerebral neurons are decreased or interrupted
Cellular metabolism ceases as glucose, glycogen and ATP are depleted and the Na-K pump fails
Cells and cerebral blood vessel walls swell as Na+ draws water into the cell, further decreasing blood flow
Vasospasm and blood viscosity also impede blood flow
Severe prolonged ischaemia leads to cellular death
Sepsis
Life-threatening organ dysfunction caused by a dysregulated host response to infection
Septic shock → subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher risk of mortality
The Quick Sequential Organ Failure Assessment (qSOFA) score
Bedside prompt that may identify patients with suspected infection who are at greater risk of a poor outcome outside the ICU
Uses 3 criteria:
1 point for hypotension → SBP < 100 mmHg
1 point for tachypnoea → > 22 breaths pm
1 point for altered mentation → GCS < 15
Score of 2 or more is associated with poor outcomes due to sepsis
Multiple organ dysfunction syndrome (MODS) refers to progressive organ dysfunction in an acutely ill patient, such that homeostasis cannot be maintained without intervention
Systemic inflammatory response syndrome (SIRS) → body-wide inflammatory response to infection, burns or trauma
Risk factors
ICU admission → increased risk of HAI and therefore high risk of sepsis
Bacteremia → often develops systemic consequences of infection
Advanced age → >65. Incidence of sepsis is higher in older adults
Immunosuppression → comorbidities that depress host defence, and immunosuppressant medication are common with sepsis
diabetes/obesity → alters the immune system
Cancer → most common comorbidity among sepsis
Previous hospitalisation → thought to induce an altered human microbiome, particularly in those treated with antibiotics
Genetic factors → increase risk of infection
Signs and symptoms
Arterial hypotension
SBP < 90, MAP < 70, SBP decrease of >40, or less than 2 standard deviations below normal for age
Temperature >38.3 or <36
Heart rate > 90bpm
Tachypnoea
Signs of end-organ perfusion
Diagnostic signs
Leukocytosis or leukopenia
WBC count >12,000 or <4,000
Hyperglycaemia in the absence of diabetes
Arterial hypoxaemia
Acute oliguria
<0.5ml/kg/hour for at least 2 hours despite adequate fluid resus
Creatinine increase
>0.5mg/dL or 44.2 micromoo/L
Thrombocytopenia
Platelet count <100,000microL
Hyperbilitubinemia
>70micromol/L
Hyperlactatemia
Imaging → infection at a specific site (e.g. pneumonia on chest radiography)
Treatment
Recommendation for initial resus
First 6 hours should include CVP 8-12mmHg, MAP >65mmHg, urine output >0.5mL/kg/hr
Antibiotics
IV antimicrobials within the first hour
Empiric combination therapy → using at least 2 antibiotics of different antimicrobial classes
Fluid therapy
Crystalloids are the recommended fluid of choice
Albumin in addition to crystalloids when a large amount of crystalloids is required
Young children → 80-100ml/kg of isotonic solution
Early aggressive fluid resus in children even with normal BP
Children maintain SBP despite significant volume depletion
Vasoactive agents
Norepinephrine → first choice
Norepinephrine and dobutamine
Mechanical ventilation
Higher PEEP is recommended
Glucose control
Insulin dosing when 2 consecutive blood glucose levels are >7 mmol
BGL monitored every 1-2 hrs until glucose values and insulin infusion rates are stable
Then every 4 hrs thereafter in patients receiving insulin infusion
Paediatric antibiotics
Antimicrobial agents should be given ASAP
according to the most likely pathogens
The following therapies are commonly employed:
Newborns and infants in the first 6-8 weeks of life: Ampicillin and gentamicin, ampicillin and cefotaxime, or ampicillin and ceftriaxone
Older infants and children with sepsis of unclear aetiology: A third-generation cephalosporin plus vancomycin. Add clindamycin if S aureus
Patients with indwelling catheters or at high risk for MRSA infection: As above, with the addition of vancomycin.
Patients who have fever and neutropenia: Broad-spectrum coverage with an emphasis on Gram-negative bacteria
Surgical intervention
Adjunctive therapies of corticosteroids and IVIG
Pathophysiology of sepsis
Bacterial pathogen enters a sterile site where resident cells detect the invader and initiate the host response
Host response → initiated by binding of macrophages to microbial components, resulting in phagocytosis of invading bacteria, bacterial killing and phagocytosis of debris from injured tissue
Production and release of proinflammatory cytokines by macrophages
Response is highly regulated by proinflammatory and anti-inflammatory mediators
When a limited number of bacteria invade, local host responses are sufficient, resulting in tissue repair and healing
Sepsis occurs when the release of proinflammatory mediators in response to an infection exceeds the boundaries of the local environment, leading to a more generalised response
Proinflammatory mediators interact with endothelial cells, causing injury to the endothelium and activation of coagulation factors
Coagulation factors and endothelial damage may impede blood flow, leading to leaky blood vessels and clot formation
Cytokines cause vasodilation, and excessive nitric oxide production leads to hypotension
Fluid and microorganisms escape into the surrounding tissues; the tissues begin to swell in the lungs, which can lead to pulmonary oedema
Inadequate tissue perfusion leads to cellular hypoxia and lactic acidosis
Widespread cellular injury occurs as a result of ischaemia, cytopathic injury and an altered rate of apoptosis
Cellular injury with release of proinflammatory and anti-inflammatory mediators causes organ dysfunction
Pathogen enters the body → activation of immune cells (macrophages, monocytes, neutrophils) → release of inflammatory mediators → proinflammatory mediators exceed local area → generalised response/systemic inflammatory response → mediators cause endothelial activation and injury → activation of coagulation factors → increases vascular permeability and causes vasodilation → fluid leaving blood vessels, causing oedema, decrease in BP, and impaired microcirculation → impaired cellular metabolism and dysfunction → decreased tissue perfusion → cellular hypoxia → organ dysfunction
Acute Kidney Injury
Rise in the serum creatinine concentration or a decline in urine output that has developed within hours to days
Increase in serum creatinine by >0.3mg/dL (27 micromol/L) within 48 hours
Increase to >1.5 times the presumed baseline value that is known or presumed to have occurred within the prior 7 days
Decrease in urine volume to <0.5ml/kg/hour over 6 hours
Aetiology
Ischaemia
Exposure to nephrotoxic agents
Risk factors
Major trauma
Surgery
Infection
Haemorrhage
Severe heart failure
Severe liver disease
Lower urinary tract obstruction
Drugs
Categories of AKI
Prerenal
Occur as a result of impaired blood flow that leads to hypoperfusion of the kidney and a drop in GFR
Main causes → haemorrhage, MI, HF, sepsis, anaphylactic shock
Intrarenal
Result of actual parenchymal damage to the glomeruli
Conditions such as burns, crush injuries, infections and nephrotoxic agents (NSAIDs and ACE inhibitors), may lead to acute tubular necrosis and cessation of renal function
With burns and crash injuries → myoglobin and haemoglobin are released, causing renal toxicity, ischaemia or both
Postrenal
Usually result of an obstruction somewhere distal to the kidney
Pressure rises in the kidney tubules, eventually, GFR decreases
Common causes → calculi, tumours, benign prostatic hyperplasia, strictures, blood clots
Clinical manifestations
Decreased urine output, occasionally urine output remains normal
Fluid retention, causing swelling in legs, ankles or feet
Frowsiness
SOB
Fatigue,
Confusion
Nausea
Seizures or coma in severe cases
Chest pain or pressure
Anaemia from blood loss due to uremic GI lesions, reduced RBC lifespan, reduced erythropoietin production
Rise in blood urea nitrogen (BUN)
Hyperkalaemia
Muscle twitching
AKI management
Elimination of potential insults, including hypotension, contrast agents, or meds (NSAIDs, ACE inhibitors, ARBs) and nephrotoxins
IV fluid therapy
1-3L of crystalloid should be administered to patients with a clinical history consistent with fluid loss
Should be avoided in pts with pulmonary oedema or clear evidence of anuria
IV furosemide 80-120mg single dose
To pts with AKI and hypervolaemia who are haemodynamically stable and not anuric to augment the urine output and relieve symptoms
Manage electrolyte imbalances
E.g. hyperkalaemia, hyperphosphataemia, hypocalcaemia, hypermagnesaemia, hypermagnesaemia, hyperuricaemia
Initiate RRT
in pts with oliguric or anuric AKI who are volume overloaded and have severe metabolic acidosis
May benefit from diet restrictions on potassium, phosphorous, sodium and fluid intake
1-1.5L per day, except in volume depleted
At least nutrition consult
Daily assessment of uremic signs and symptoms
E.g. anorexia, N+V, metallic taste, altered mental status
To determine if RRT may be indicated
Monitor serum creatinine, electrolytes, albumin, and measures of fluid balance daily
Weight, fluid intake, urine output
Emergency renal replacement therapy (RRT) should be performed in pts with AKI who have one or more of the following:
Hypervolemia with pulmonary oedema that does not promptly respond to diuretics
Severe hyperkalemia
serum potassium >6.5 mEq/L or those with symptoms or signs of hyperkalemia
Signs of uremia, such as pericarditis, encephalopathy, or an otherwise unexplained decline in mental status
Severe metabolic acidosis
pH <7.1
Certain alcohol and drug intoxications
Renal Replacement Therapy
Haemodialysis
Pts blood pumped through the blood compartment of a dialyser, exposing it to a partially permeable membrane
Dialyser is composed of thousand of tiny synthetic hollow fibres
The fibre wall acts as the semipermeable membrane
Blood flows through the fibres, dialysis solution flows around the outside of the fibres, and water and wastes move between these 2 solutions
The cleansed blood is then returned via the circuit back to the body
Haemofiltration
Similar treatment to haemodialysis
Blood is pumped through a dialyser or haemofilter but no dialysate is used
A pressure gradient is applied
As a result, water moves across the very permeable membrane rapidly, dragging along with it many dissolved substances, including ones with large molecular weights which are not cleared as well by haemodialysis
Pathophysiology of AKI
Sudden and almost complete loss of kidney function over a period of hours to days
Glomerular injury, vasoconstriction of capillaries or tubular injury due to sepsis, trauma, nephrotoxins can lead to:
Oliguria → less than 400ml/day
Anuria → less than 50ml/day
High serum creatinine and blood urea nitrogen levels → azotemia
retention of other metabolic waste products normally excreted by the kidneys