Pathologies Flashcards
Symptoms of emphysema? (5)
SoB Fatigue Recurrent chest infections Weight loss Decreased O2 increased CO2
Explain INTRINSIC PEEP in terms of emphysema.
Decreased expiratory flow > prevents all air being expelled from lungs before next inspiration starts > air is trapped distal to obstruction > extra thresold to overcome > INTRINSIC PEEP.
Effects of Intrinsic PEEP.
Extra threshold load at start of insp.
Hinders cardiac output.
Impairs perfusion.
Stabilization occurs at higher than usual vols and pressures > Reduces lung compliance.
Characteristics of emphysema. (5)
DEDLH
Destruction of elastic fibres. Erosion of alveolar septa. Dilation of distal airspaces. Loss of radial traction. Hyperinflation.
Passive hyperinflation.
Reduced elastic recoil > airways collapse on expiration > gas trapping.
Dynamic hyperinflation.
Actively needs to sustain inspiratory muscle contraction to hold open airways >
WoB
Barrel chest
Chronic bronchitis diagnosis.
Constant cough and sputum production for 3 months of 2 consecutive years. Originally classed as smokers cough.
Chronic bronchitis causes.
Repeated inhalation of tobacco smoke irritates sensitive lining of airways.
Chronic bronchitis symptoms.
Inflammation - narrowing in small distal airways >proximal, fibrotic changes and scarring.
Mucus hypersecretion - increase in size and number of goblet cells.
Breathlessness - inflammatory damage and airway narrowing.
Bronchospasm - acetylcholine release due to inflammatory stimulation of parasympathetic NS.
Clinical features of chronic bronchitis.
Breathlessness - disturbs sleep. Decreased exercise tolerance. Fatigue. Cyanosis. Hypoxaemia.
Rib #.
Healing Stage 1 - Heamotoma formation.
Clot produced 6-8 hrs.
Inflammation results in phagocytic cells invading injury.
New capillaries grow.
Rib #.
Healing Stage 2 - Fibrocartilaginous callus formation.
Fibroblasts lay down collagen.
Contrablasts produce fibrocartilaginous callus.
Rib #.
Healing Stage 3 - Bony callus formation.
Osteoblasts secrete spongy bone to join the broken bone ends lasting 3-4 months.
Rib #.
Healing Stage 4 - Bone remodelling.
Compact bone replaces the spongy bone callus.
Remodelling bone back to normal shape.
Rib # Pulmonary complications.
Pain (restrictive) Pneumothorax Surgical emphysema Haemothorax Intra abdominal injury
Cystic fibrosis
Cystic fibrosis is an inherited disease of the mucus and sweat glands. It affects exocrine glands. CF causes your mucus to be thick and sticky. The mucus clogs the lungs, causing breathing problems and making it easy for bacteria to grow. This can lead to problems such as repeated lung infections and lung damage.
(Na and Cl cannot escape epithelial cells to maintain hydration of mucus - thick and sticky)
Clinical features of cystic fibrosis.
Incessant coughing Small stature and delayed puberty Breathlessness Pleural inflam, muscle strain (coughing), pneumothorax, chest pain Reproductive problems Decreased FEV1 Decreased O2 Increased CO2.
Physiotherapy for cystic fibrosis.
Sputum clearance ACBT AD Flutter Abdominal breathing Postural drainage Little and often exercise.
Primary ciliary dyskinesia clinical features.
Inherited disease characterised by uncoordinated ciliary beat, excess secretions and recurrent infections of ears, sinuses and lungs > scarring.
PCD treatment.
Selective antibiotics and regular physio to delay onset of bronchiectasis. More maintenece than cure, query deafness.
Bronchiectasis.
Irreveresable distortion and dialation of bronchi > extra mucus production, prone to infection > damages elastic and muscular components of subsegmental airways > thick mucus sits on tender cilia > further damage > fibrosis and bronchospasm.
Bronchiectasis symptoms.
Bronchospasm Fibrosis Distortion and dilation of bronchi Sputum production Cough.
Cor pulmonale.
An alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. (As a result of pulmonary hypertension).
Effects of general anesthetic.
Impairs CNS - affects regulation of breathing, hypoventilation in supine.
Decreased surfactant production and surface tension - collapse and increase WoB.
Paralysis of cilia - build up of mucus.
Decreases FRC.
Increases sputum retention.
Risk of atelectasis and shunt.
Loss of cough reflex- diaphragm.
Shunt.
Fraction of cardiac output that is not exposed of gas exchange in the pulmonary capillary bed.
Fibrosing alveolitis.
Interstitial lung disease, affects supporting structures of the lung rather than airspaces. Can be caused by pollutants. Increase in lung stiffness - increases WoB. Decreased surface area of alveolar-capillary membrane - impairs gas exchange.
Interstitial lung disease symptoms. (Fibrosing alveolitis).
Rapid breathing to sustain ventilation Decreased O2 due to V/Q mismatch Decreased CO2 due to rapid breathing Dyspnoea Hypoxaemia Fatigue.
Oestophagogastrectomy.
Removal of lower esophagus and upper stomach.
Three ways to do it - through chest, stomach or neck.
Complications: lung complications (especially pneumonia)
severe infection in the chest
injury to the stomach, intestines, lungs, or other organs during surgery
leakage from your esophagus or stomach where the surgeon joined them together
narrowing of the connection between your stomach and esophagus.
Surgery complications.
Primary haemorrhage.
Basal atelectasis.
Shock: blood loss, acute myocardial infarction, pulmonary embolism or septicaemia.
Low urine output: inadequate fluid replacement intra-operatively and postoperatively.
Acute confusion: exclude dehydration and sepsis.
Nausea and vomiting: analgesia or anaesthetic-related.
Fever.
Secondary haemorrhage: often as a result of infection.
Pneumonia.
DVT.
Acute urinary retention.
UTI.
Postoperative wound infection.
Bowel obstruction.
CABG.
Sternotomy. Diverts blood around narrowed/clogged parts of major arteries to improve blood flow and O2 supply.
Mitral valve replacement.
Mitral/biscuspid valve seperates upper/lower left chambers. During each heartbeat, the smaller upper chambers of the heart (atria) contract to push blood into the larger lower chambers (ventricles).
The mitral valve opens to allow this passage of blood from the left atrium, and closes when the left ventricle is full of blood, to prevent backflow.
When the valve closes, its two leaflets (flaps) normally seal the valve shut.
Elective AVR.
The aortic valve is located between the left ventricle (lower heart pumping chamber) and the aorta, which is the largest artery in the body. Valves maintain one-way blood flow through the heart.
Sternotomy or minimally invasive.
Types of pneumonia.
Community acquired pneumonia (CAP)
Health care associated pneumonia (HCAP) - occurs in patients hospitalised within 90 days usually
Hospital acquired pneumonia (HAP) - acquired within 48 hours or more of admission and not incubating at the time
Ventilator associated pneumonia (VAP)
Inflammatory process pneumonia.
Congestion: This stage is characterized by vascular
engorgement, intra-alveolar fluid, and numerous bacteria; the lung is heavy, boggy, and red.
Red hepatization: In this stage, massive exudation develops, with red blood cells, leukocytes, and fibrin filling the alveolar spaces; the affected area appears red, firm, and airless, with a liver like consistency.
Gray hepatization: This stage is characterized by progressive disintegration of red blood cells and the persistence of a fibrin exudate.
Resolution: The consolidated exudate within the alveolar spaces undergoes progressive enzymatic digestion to produce debris that is later reabsorbed, ingested by macrophages, or coughed up.
Bronchial breathing indicates…
Audible gap between the inspiratory and expiratory phase sounds. If heard in the chest they are abnormal and suggest the presence of consolidation or fibrosis.
Vital signs (BP, RR, HR)
BP: 90/60 mm/Hg to 120/80 mm/Hg
Resp rate: 12 - 18 breaths per minute
Pulse: 60 - 100 beats per minute
Norm pH.
The normal pH value for the body fluids is between pH 7.35 and 7.45. When the pH value of body fluids is below 7.35, the condition is called acidosis, and when the pH is above 7.45, it is called alkalosis.
Upper lobectomy.
Thorocotomy.
Gastrectomy.
Partial/whole/sleeve(L side).
Open/keyhole. (open - abdomen or chest cut)
Techniques to increase lung vols. (4)
Abdominal breathing
Thoracic expansion
Mobilisation
Incentive spirometry.
Techniques to clear secretions. (4)
Flutter
Percussion
ACBT
AD.
Techniques to reduce breathlessness. (1)
Positioning.
Effects of deep breathing/TEE.
Increase lung vols
Increase ventilation
Increase surfactant secretion - improving compliance
Decrease dead space, airway resistance, air way turbulance
Improve V/Q matching, O2 sats.
Effects of exercise.
Increase ventilation, CO, maximum O2 uptake.
Decrease dead space.
Maintain O2 and pH.
Increase mucus transport.
Effects of precussions.
Clear peripheral lung regions
Speeds mucociliary transport.
Effects of AD.
Increase airflow in small airways
Clear distal secretions
Fast mucus clearance
Greater O2, decrease CO2.
Holding breath and TEE effects.
Disperses O2 and open alveoli to clear secretions, air gets behind collateral channels to open after atelectasis. Called pauls of cone, channels of lambert, cannals of martin.
Effects of L heart failure.
Causes a back pressure into the lungs which increases hydrostatic pressure and changes concentration. osmotic pressure of blood changes and more water is drawn into lungs leading to pulmonary oedema.
Pulmonary oedema.
Extravascular water in the lungs which leads to pleural effusion.
Pleural effusion.
Excess fluid in the pleural cavity caused by disturbed osmotic/hydrostatic pressure in plasma or membrane permeability.
Equal pressure points.
Pleural pressure becomes positive and equals alveolar pressure called equal pressure point. Towards mouth, transmural pressure is reversed so pressure outside airway is higher than inside which squeezes airway = DYNAMIC COMPRESSION.
Respiratory acidosis.
Retention of CO2. Hypoventilation.
pH < 7.35.
PaCO2 > 6kPa.
Respiratory alkalosis.
pH > 7.45
PaCO2 < 4.7kPa
Hyperventilation, removes CO2 faster.
Type 1 Respiratory failure.
Failed oxygenation.
Type 2 Respiratory failure.
Failed ventilation caused by failure of respiratory pump - hypoxaemic and hypercapnic.
Autogenic drainage phases.
UNSTICKING PHASE: Breathe as much air out of your chest as you can then take a small breath in through your nose, feeling the breath at the bottom of your chest. Hold your breath for 2-3 seconds, then exhale all the air back out like an active ‘sigh’. Repeat 5-6 times or until you can HEAR or FEEL your secretions. Resist any desire to cough and move onto the next phase.
COLLECTING PHASE: Breathe a middle-sized breath in, feeling the breath in the middle of your chest. Hold your breath for 2-3 seconds, then exhale actively, but not all the way out. Repeat 5-6 times or until you can HEAR or FEEL your secretions. Resist any desire to cough and move onto the next phase.
EVACUATION PHASE: Breathe in as big a breath as possible, feeling the breath right up to the top of your chest. Hold your breath for 2-3 seconds, then exhale actively, but only a third of the way out. Repeat 5-6times or until you can HEAR or FEEL your secretions.
Causes of emphysema.
Smoking
Alpha1 antitrypsin deficiency.
Crackles.
Secretions or parenchymal disorder.
Air forced through airways narrowed by oedema, inflamm or secs/when airless alveoli or peripheral airways snap open.
Wheezes.
Vibration of walls of narrowed airways.
Expiratory = bronchospasm.
Inspiration and expiration = airway obs - mucosal oedema, pulmonary oedema, sputum, tumours.
Increased WoB.
