HNN227: Respiratory + Cardiovascular Flashcards
Upper vs Lower Respiratory Tract
Upper Respiratory Tract: nose, naval cavity, oral cavity, pharynx, epiglottis, upper trachea.
Lower Respiratory Tract: lower trachea, bronchi, bronchioles, alveoli ducts, alveoli.
Pneumonia Pathophysiology
- Inflammatory condition of the lung affecting the bronchioles and the alveoli
- Usually the result of an infection by pathogens (bacteria/viruses)
- Severity is related to the type and amount of bacteria
Normal Conditions:
* The alveoli are sterile, air-filled sacks covered by capillaries
* The cells lining the airway secrete mucous which traps pathogens and particles. Some cells have cilia which sweep the mucous up the respiratory tract to be expelled.
Normal Inflammatory Response:
* Fluid, WBC, RBC enter the alveoli
* Consolidation: fluid (puss) instead of liquid fills the alveoli
○ Puss is produced as a biproduct of the body fighting infection
○ Consolidation leaves portions of tissue unventilated = O2/CO2 diffusion is blocked impairing gas exchange
* Inflammation causes the lung tissue to stiffen resulting in decreased lung expansion
Pneumonia SS
- Rapid, shallow, laboured breathing
- Use of accessory muscles
- Crackles and decrease air entry
- Decreased SpO2
- Productive cough
- Difficulty speaking
- Chest pain
- Rapid pulse
- Cyanosis
- Clammy
- Drowsy, restless, confused
- Fever
Pneumonia Risk Factors
- Immunocompromised
- Inability to effectively DB+C
- Hx of smoking
- Chronic respiratory disease
- Altered consciousness
- General anaesthetic
- Intubation
- Elderly
- Difficulty swallowing
- Immobility
- NG tube
- Aspiration
Pneumonia Nursing Management
- Pt to rest in bed during acute phase
- Get pt out of bed and mobilising ASAP
- Maintain hydration and nutrition
- Manage pain
- O2 therapy
Assessments
* Blood tests
* Chest x-ray
* Sputum sample
* Respiratory assessment
Coronavirus pathophysiology
- Caused by SARS-COV2 virus
- Virus invades the nasal epithelial cells first before migrating through the respiratory tract to the alveoli
- Virus binds to the protein angiotensin converting enzyme 2 (ACE2) found on alveolar epithelial cells
- This damages the alveoli and other infected tissues
- The immune system triggers an inflammatory response
Coronavirus SS
- Fever and chills
- Headache
- Myalgia
- Loss of taste
- Sore throat
- Cough
- Dyspnoea
- GIT disturbances
Coronavirus Nursing Management
- Rest
- Hydration
- Identify any abnormal signs of clotting e.g. microvascular thrombosis; DVT
Medication
* Analgesics
* Anti-pyrectics
* Anti-histamines
* Anti-viral
* Glucocorticoids
* SpO2 92-96% (high flow O2)
Assessments
* Respiratory assessment
* Bloods: normal or low WBC; increased LDH, CRP, CK, AST, ALT, D-Dimer; abnormal coagulation e.g. increased INR, PT.
* CT
* Chest x-ray
* Urinalysis
Coronavirus Complications
- Acute respiratory distress syndrome
- Cardiovascular or thromboembolic events
- Sepsis
- Acute kidney injury
- Disseminated intravascular coagulation
○ Thrombocytopenia
○ Increased D-Dimer
○ Increased fibrin degradation products
○ Prolonged PT
Pulmonary Embolism Pathophysiology
Blockage of the pulmonary artery by a substance delivered in the bloodstream.
1. Remote thrombus embolises lodges in pulmonary vascular tree 2. Obstruction of blood flow distal to the embolism increased pulmonary vascular resistance increased pulmonary artery pressure increased right ventricular pressure 3. Regional decrease in lung perfusion dead space (ventilation but no perfusion) hypoxaemia and tachypnoea
Source of the Embolus
* Lower DVT: iliofemoral vein above the knee (most common), pelvic vein
* Upper DVT: very rare
* Air, fat, amniotic fluid
Pulmonary Embolism SS
- Dyspnoea
- Pleuritic chest pain
- Cough
- Haemoptysis (coughing up blood)
- Signs of DVT: tender, swollen, erythematous extremity
- Syncope
- Low SpO2, tachypnoea, tachycardia
- Low grade fever
- Shock
Pulmonary Embolism Nursing Managemen
Medication
* Anticoagulants
○ Acute: heparin, fondaparinux
○ Chronic: warfarin, acenocoumarol, phenprocoumon
* Thrombolytics
Assessment
* Well’s Score
* Chest x-ray
* CT pulmonary angiography
* Venous duplex ultrasound
* Ventilation perfusion scan
* ECG
* Bloods: FBE, clotting, ESR, EUC, LFT
ABG:
Hypoxaemia (low PaO2)
Hyperventilation (high PaCO2, high pH, respiratory alkalosis)
D-Dimer: negative result rules out pulmonary embolism
Pneumothorax Pathophysiology
Caused by air entering the pleural cavity.
* In normal conditions, negative pressure exists between the visceral pleura (surrounding the lungs) and the parietal pleura (lining the thoracic cavity), that allows to effective chest wall expansion. * When air enters the pleural cavity there is a change to positive pressure causing partial or total lung collapse.
Pneumothorax Types
Spontaneous Pneumothorax
Occurs due to the rupture of small blebs (air-filled blisters) at the apex of the lung. Can be caused by COPD, asthma, cystic fibrosis, pneumonia, smoking.
Iatrogenic Pneumothorax
Occur due to laceration or puncture of the lung during medical procedures.
Traumatic Pneumothorax
Occur from penetrating (stab, gunshot) or non-penetrating (rib fracture, blunt force) chest trauma.
Tension Pneumothorax
Occurs when air enters the pleural space and cannot escape. The accumulation of air leads to the gradual increase in pressures.
Pneumothorax SS
- Chest pain
- SOB
- Tachycardia
- Tachypnoea
- Dry cough
Haemothorax Pathophysiology
Accumulation of blood in the pleural space resulting from injury to the chest wall, diaphragm, lung, blood vessels, or mediastinum.
Haemothorax SS
- SOB
- Tachypnoea
- Tachycardia
- Chest pain.
- Low blood pressure (shock)
- Pale, cool and clammy skin.
Pleural Effusion Pathophysiology
Abnormal collection of fluid in the pleural space.
* The pleural space normally contains 5-15mL of fluid that acts as lubricant. * Pleural effusion is not a disease but an indication of a disease. Can result from increased pulmonary capillary pressure, decreased oncotic pressure, increased pleural membrane permeability, or obstruction of lymphatic flow.
Pleural Effusion Types
Transudative
Occurs primarily in non-inflammatory conditions. Accumulation of protein-poor, cell-poor fluid.
Fluid is clear and pale yellow.
Caused increased hydrostatic pressure (e.g. heart failure) or decreased oncotic pressure (e.g. hypoalbuminemia).
Exudative
Results from increased capillary permeability characteristic on inflammation.
Often associated with infection or malignancy.
Empyema
Collection of purulent fluid in the pleural space.
Pneumonia, TB, lung abscess, infection of surgical wounds.
Ischemia
Oxygen deprivation to tissues which can cause cell death infarction or necrosis.
Causes
* Vasoconstriction
* Vasospasm
* Atherosclerosis
* Anaemia
* Haemorrhage
Ischemia Management
- Ensure sufficient O2 supply
- Ensure good coronary blood flow
- Decrease O2 demand
- Decrease blood viscosity
Atherosclerosis
The thickening of an artery wall due to the accumulation of fatty substances. Plaque deposits cause narrowing of the artery.
Can cause cardiac arrest; stroke; peripheral vascular disease.
Atherosclerosis Management
- Diet control
- Lifestyle change
- Statins/cholesterol drugs
- BP management
- Anti-platelet therapy
- Diabetes management
- Surgical intervention
Peripheral Arterial Disease
Ischaemic disorder of the arteries supplying the lower limbs.
Insufficient blood and O2 supply due to ischemia and atherosclerosis.
Stroke
Reduced or blocked blood supply to the brain causing tissue death.
Causes
* Blood clot
* Atherosclerosis
* Intercranial bleeding
Haemorrhagic stroke: blood vessel in or near the brain ruptures, causing blood to leak into the brain.
Ischemic stroke: blood vessel to the brain becomes blocked.
1. Thrombotic: blood clot/thrombosis formed in an atherosclerotic artery. 2. Embolic: blood clot/embolism forms elsewhere in the body and travels to the brain.
Stroke Management
Diagnostic Tests
* CT
* MRI
* EKG
Intervention
* Antiplatelet therapy (warfarin)
* Surgical intervention
* Manage atherosclerosis risk factors:
*Hypertension * Diabetes * Smoking * Dyslipidaemia
Coronary Artery Disease
Hyperlipidaemia
Hypertension
DM
Smoking
Obesity
Hyperhomocysteinaemia
CAD Detailed
Hyperlipidaemia
* Elevated LDL promote atherosclerosis
* Low HDL = reduced transport of cholesterol to the liver
Hypertension
* Pro-atherogenic as it increase vascular inflammation
Diabetes Mellitus
* Pro-atherogenic
* Increased free radicals and cytokines
Smoking
* Promotes vasoconstriction and oxidative stress
* Increases platelet aggregation
* Disrupts lipid metabolism increasing LDL
Obesity
* Increased fat mass causes white adipose tissue dysfunction insulin resistance, increased SNS activity endothelial dysfunction
Hyperhomocysteinaemia
* Cysteine is important for cellular function and metabolism of zinc, iron, and copper
High levels of homocysteine reduced nitric oxide; increased reactive O2; increased platelet aggregation.
Angina
Stable angina: result of atherosclerotic plaque and inappropriate vasoconstriction within one of more blood vessels. Blood flow is adequate at rest but compromised on exertion.
Unstable angina: result of atherosclerotic plaque and associated thrombus causing vascular obstruction. Blood flow is compromised at rest.
Variant (Prinzmetal) Angina: unexplained vasospasms causing angina pain.
Angina SS
Stable
* Chest pain on exertion
Unstable
* N+V
* SOB
* Diaphoresis
Variant
Sudden chest pain associated with increased exertion
Myocardial Infarction
Significant reduction in blood flow such that myocardial cells die.
Non-ST elevation MI (NSTEMI): partial or transiently obstructive thrombus in the coronary artery resulting in ischemia and necrosis.
ST elevation MI (STEMI): complete obstruction by a thrombus in the coronary artery resulting in ischemia and necrosis.
MI Management
Diagnostic Tests
* Angiogram
* Elevated circulating lipid levels
* Chest pain on exertion or at rest
* Troponin levels
* ECG
* CT
Intervention
* Aspirin
* Nitro-glycerine
* Thrombolytic medication
* PCI
* Stenting
* CABG
MI SS
Common
* Increased HR; RR
* Diaphoresis
* N+V
* Chest pain
* Radiating jaw or arm pain
Atypical
* Syncope
* Fatigue
* Epigastric, back, right-arm pain
ECG
P wave = atrial depolarisation (usually 0.08s)
PR interval = time from atrial depolarisation to ventricular polarisation (0.12s, should not be >0.2s).
QRS complex = ventricular depolarisation + atrial repolarisation (0.12s).
ST segment = period of no net current; ventricles contract
T wave = ventricular repolarisation (0.16s)
ECG
P wave = atrial depolarisation (usually 0.08s)
PR interval = time from atrial depolarisation to ventricular polarisation (0.12s, should not be >0.2s).
QRS complex = ventricular depolarisation + atrial repolarisation (0.12s).
ST segment = period of no net current; ventricles contract
T wave = ventricular repolarisation (0.16s)
