Nursing Year 2a

• infections microorganism reaches alveoli • macrophages overwhelmed, neutrophils recruited • Neutrophils engulf alveoli producing fibrin-rich exudate • Exudate fills infected and neighbouring alveoli • Exudate causes alveoli to stick together, reducing ventilation • Oedema increases diffusion distance for gases, impairing gas exchange

• virus enters respiratory tract binding to epithelial cells • Viral replication and limited immune response begins • Infection is contained at this stage in 80% of patients with viral clearance in 10-14 days • Migration into lower respiratory tract and invasion of the alveoli • Cytokine involvement and immune response causing injury to alveoli • Viral replication continues with damage and apoptosis to host cells • Adjacent healthy alveoli become infected causing death of pneumocystis • Diffuse alveolar damage results in Acute Respiratory Distress Syndrome (ARDS)

• irritant • macrophages release inflammatory mediators • neutrophils recruited, releasing elastase • elastase breaks down elastin causing destruction of elastic fibres • alveolar walls lose elasticity, increasing compliance (too stretchy) • Other proteases cause tissue damage too alveolar wall. • pulmonary capillary bed reduced, increasing pressure in pulmonary artery • T- lymphocytes cause further tissue damage • Cell apoptosis (death)

• Allergen (trigger) such as pollen, exercise, smoke, dust enters respiratory tract • Dendritic cells in epithelial layer engulf pathogen, stimulating immune response • Mast cells in bronchial smooth muscle activated and chemical mediators released • Eosinophils stimulated in bone marrow and attracted to local area • Vasodilation causes fluid to leak from vasculature into tissues = oedema • Airway hyper responsiveness causes bronchospasm • Increase mucous from goblet cells further obstructs air entry • Gas trapping from bronchoconstriction results in hypercapnia

• Thrombus formation in peripheral circulation dislodges • Thrombus travels to pulmonary circulation, causing partial or complete obstruction of PA • Increased pressure in RV causes dilation and septal deviation to LV • LV preload reduced, causing decreased CO • Systemic arterial hypotension leads to coronary hypo perfusion • RV hypoxia results causing schema and infarction • Further increased myocardial demand causes LV failure • Obstruction to blood flow in pulmonary capillary bed also results in VQ mismatch, worsening hypoxaemia

• vital signs • Peak flow • Chest assessment (IPPA) • COLDSPA (pain)

• bronchodilators (inhalers/nebuliser) • corticosteroids (oral/IV/inhaled) • Metered dose inhaler (MDI) spacer/neb use • Oxygen therapy • positioning • Reassurance to decrease anxiety which reduces SNS response

An acute or chronic condition in which the heart doesn’t pump blood as well as it should resulting in congestion (CHF) of blood backing up and unable to meet demands of the body

dyspnoea (difficulty breathing) orthopnoea (shortness of breath when lying down) paroxysmal nocturnal dyspnoea pulmonary congestion - cough, crackle, wheeze

renal failure peripheral oedema ascites enlarged liver and spleen distended JVP fluid weight gain

fluid balance IV Frusemide ACE inhibitors and beta blockers daily ECG

• An irritant is present e.g. lipids (LDL cholesterol), High blood pressure (HTN), toxins (cigarette smoke), diabetes • damage occurs to the endothelium - a crack or fissure is formed • LDL cholesterol deposits accumulate in the artery wall (tunica intima) known as fatty streaks • LDL oxidises (changes), sends signals to immune system and monocytes (WBC) arrive • Monocytes convert to macrophages and consume the cholesterol • Macrophages fill up on cholesterol and die = foam cells • Formation of foam cells = release of cytokines (inflammatory process - vicious circle) • Smooth muscle cells migrate into expanding fatty plaque forming a lipid cap (using collagen and elastin) • Smooth muscle cells also deposit calcium into the fatty plaque, hardening it and causing bulging into the artery lumen • Blood flow is decreased (resistance is increased) and compliance is reduced (less flexibility) • Ongoing inflammation = plaque rupture, thrombogenic material inside the cap is exposed = arriving platelets form a thrombus • A thrombus is formed (either partially or fully) and occludes the artery causing ischaemia, or ultimately infarction

Ventricular tachycardia, absence of P waves. needs defibrillation

Ventricular fibrillation, rapid disorganised contraction of the ventricles, needs defibrillating

complete absence of electrical activity, cannot defibrillate this

Atrial fibrillation, no P waves and its irregular

any condition that affects the structure function of the heart and bloods vessels CAD - angina, myocardial infarction CVD PVD HF HTN Rheumatic heart failure congenital heart disease

insufficient blood flow and blood volume to supply the 02 needs of the myocardium

is a symptom of reversible myocardial ischaemia, manageable, occurs die to a stable lesion/plaque in the coronary artery

ineffective myocardial oxygen perfusion

myocardial infarction, results from sustained ischaemia or sudden complete blockage of the coronary artery myocardial tissue distal to the obstruction dies can be partial thickness (NSTEMI) of full thickness (transmural, STEMI)

non ST-elevation myocardial infarction involves partial thickness myocardial wall damage. sudden complete blockage of a coronary artery, ECG finding is definitive

ST-elevation myocardial infarction involves full thickness myocardial wall damage (with/without necrosis). partial blockage of a coronary artery. not visible on an ECG

is the term for an imbalance of 02 supply and demand. the underlying pathophysiology is atherosclerosis which can lead to plaque rupture and thrombus formation. unstable angina pectons STEMI non - STEMI