CVSR - Phase 1 Flashcards
Comparison of action potentials (skeletal muscle, cardiac muscle, autorhythmic)
- Membrane Potential
- Stimulus
- Depolarisation ion
- Repolarisation ion
- Hyperpolarisation
- Refractory period
Factors that influence rate of pacemaker cells
Tachycardia:
- SNS activity (A/NA) increases funny current activity
Bradycardia:
- increasing the threshold for Ca2+ channel opening
- inhibiting funny current activity
- hyperpolarising the resting membrane potential by increasing K+ permeability
Types of aneurysm
True aneurysms:
- fusiform: entire circumference of the vessel is distended
- saccular: pouch/pocket appearance as only one portion of the vessel circumference is affected
note: false aneurysms occur when there is a rupture but blood is contained as a haematoma which appears similar to an aneurysm
Three shunts of foetal circulation and how they close
Ductus Arteriosus – between the pulmonary trunk and the arch of the aorta, bypasses lungs,
- prostaglandin E produced by the placenta maintains the DA during foetal period, reduction of PGE2 following birth allows for closure
- increases in partial pressure of oxygen following the first breath induces closure
Ductus Venosus – between umbilical vein and IVC, bypassing the liver
- changes in blood flow and pressure following birth facilitate closure, prostaglandins also may be involved
Foramen Ovale – between right atrium and left atrium, bypassing pulmonary circulation
- first breath and functioning of the lungs decreases pulmonary vascular pressure and increases LA pressure which forces the septum primum against the septum secundum and functionally closes the foramen
Features of the tetralogy of Fallot
- overriding aorta
- large ventricular septal defect
- pulmonary valve stenosis
- right ventricle hypertrophy
Pathophysiology of Atherosclerosis
- Endothelial dysfunction occurs as a result of shear stress, infection, toxins (e.g. smoking) or autoimmune causes
- Endothelium constricts and releases chemokines + cytokines and upregulates adhesion molecules
- Accumulation of lipids occurs within the subintimal space, these become oxidised by ROS released by the damaged endothelium from LDL → mLDL, increasing toxicity
- Continued inflammation attracts macrophages to the subintimal space which take up mLDLs via scavenger receptor → foam cells which burst and become necrotic (fatty streak)
- Recruitment of smooth muscle cells to form fibrous cap via wound repair mechanism results in advanced plaque with a fibrous cap and necrotic core
Sliding filament theory of muscle contraction including the role of calcium
- Depolarisation of muscles cells opens VGCCs allowing Ca2+ ions to enter the cell
- Ca2+ binds to ryanodine receptors and trigger calcium-induced calcium release from the sarcoplasmic reticulum of the muscle cell
- Ca2+ binds to troponin-C causing a morphological change in the troponin-tropomyosin complex that exposes the myosin binding sites of actin
- Myosin heads bind to actin, ATP binds to myosin and is hydrolysed into ADP + Pi
- Release of ADP + Pi from myosin initiates the power stroke, sliding the filaments over each other and shortening the sarcomere
- Binding of another ATP to myosin causes the myosin head to detach and process repeats
- Cross bridge cycling continues until Ca2+ is returned to the sarcoplasmic reticulum by Ca2+ ATPases, causing contraction to stop
Starling’s forces
- Hydrostatic pressure: lateral pressure component of blood flow which pushes fluid out through capillary pores, decreases along the length of the capillary
- Colloid osmotic pressure: osmotic pressure created by proteins in a capillary
Virchow’s triad for blood coagulation
Endothelial damage/dysfunction – atherosclerosis, trauma, surgical procedures
Hypercoagulability – thrombophilia, sepsis, trauma, malignancy
Stasis – immobility/paralysis, venous obstruction, atrial fibrillation
Mechanism of haemostasis
- vasoconstriction – endothelial damage → vasoconstriction ↑ serotonin, TXA2 ↓ NO
- platelet plug formation – exposure of collagen or vWF activates platelets, morphological changes and release of PAF, ADP, serotonin, TXA2 recruits others
- coagulation cascade – formation of a fibrin mesh
- extrinsic: tissue factor 3 in subendothelium → factor 7 → 10
- intrinsic: collagen → factor 12 → 11 → 9 → 8 → 10
- common: factor 10 → thrombin (+ve feedback on 5, 8, 9) → fibrin
Risk factors and pathogenesis of IHD (including four types)
modifiable: smoking, diet high in saturated fat and salt, alcohol, sedentary lifestyle, stress
non-modifiable: male sex, advanced age, ethnicity, genetics, FHx
IHD occurs as a result of an imbalance between myocardial oxygen demand and coronary supply, due to occlusion of the coronary arteries typically from atherosclerosis
Types of IHD:
- stable angina
- unstable angina
- myocardial infarction
- sudden cardiac death
Types of angina
- Stable: due to atherosclerotic occlusion, symptoms on exertion when occlusion >70%
- Unstable: plaque rupture and thrombosis, symptoms at rest
- Variant/Prinzmetal: idiopathic cause due to vasospasm
Principles of analysing ECGs
- Leads and artery
- Method to interpret
- Rhythm: regular, regularly irregular, irregularly irregular
- Rate: R-R distance counted on rhythm strip or 300/no. large squares
- Intervals: PR < 1 large box, QRS < 0.5 large boxes
- Axis: thumb rule (lead I = left, aVF = right)
- P wave character
- QRS appearance
- ST-elevation
- T wave inversion
Electrical conduction of the heart
- Signal originates in the pacemaker cells of the SA node at the superior end of the crista terminalis within the RA
- Travels through the atria to the AV node, causing atrial depolarisation
- Slows through AV node before travelling down the septum through the Bundle of His then the left/right bundle branches to the apex of the heart
- Jumps across to right ventricle papillary muscles via moderator band (septomarginal trabeculae)
- Depolarises ventricles via the Purkinje fibres which travel back towards the base
Structure of blood vessels
Lumen (larger in veins)
Tunica Intima = endothelium, basement membrane
Tunica Media = smooth muscle, collagen, elastin in arteries (thicker in arteries)
Tunica Externa = loose CT, vasa vasorum, nerva vasorum (thicker in veins)
Basic embryology of the heart
- Progenitor cells of the splanchnic mesoderm differentiate into myoblasts in ‘blood clusters’ that form a horseshoe shape
- Canalisation, lateral + craniocaudal folding results in a midline tube with vessels developing around it
- Atria: two sinus venosus horns shift to become predominately right sided (venae cavae) while left becomes coronary sinus, septum primum and septum secundum grow down from the roof of the atrium to divide into left and right with a foramen ovale
- Endocardial cushions grow in the atrioventricular canal to isolate and form the AV valves, superior, inferior and lateral (x2) – superior + inferior grow faster
- Ventricles: membrane grows up from the floor to divide the ventricles and apoptosis occurs to enlarge lumen and form endocardial structures
- Rotating spiral shaped membrane grows to isolate great vessels and endocardial cushions grow to create semilunar valves (aorta – PLR, PT – ALR)
Types of congenital heart disease
Cyanotic:
deoxygenated blood flowing from the right side of the heart into the left, reducing arterial blood oxygenation leading to cyanosis
e.g. tetralogy of Fallot, transposition of the great arteries
Acyanotic:
not affecting blood oxygenation, generally L to R shunts in which oxygenated blood re-enters the pulmonary circulation leading to right heart overload and pulmonary hypertension
e. g. ASD, VSD, PDA
* note: untreated L to R shunts typically reverse due to Eisenmenger syndrome*
Classification of aortic dissections
Aortic dissection occurs when blood begins tracking along the planes of the vessel wall typically in the tunica media, occurs in hypertension and Marfan syndrome
- Type A: ascending aorta involved
- I: ascending only
- II: spread to other regions
- Type B: ascending aorta not involved
Thrombosis vs. embolism
Thrombosis = process of blood clotting which is essential for haemostasis but can become pathological due to occlusion or embolism
Embolism = movement of a mass through circulation resulting in eventual obstruction, potential emboli include thrombi, fat, tumour cells, gas/air, amniotic fluid
Serum diagnostics used in assessment of cardiac disease
- Creatine Kinase: CK-MB isoenzyme primarily present in myocardium, fall quickly
- Myoglobin: useful as an early marker of an infarction and to gauge size, however it is not specific for myocardium (used to rule out)
- Troponin: I and T highly specific for myocardial injury, levels begin to rise 3–12 hours after infarction, falls gradually over days/weeks
- LDH: isoenzymes 1 and 2 associated with myocardial injury
Cellular changes which occur in myocardial infarction
- Hypoxia due to coronary blockage leads to a shift from glycolysis to favour beta-oxidation which decreases ATP synthesis efficiency
- Impaired Na/K ATPase function leads to Na+ build up within the cell while anaerobic metabolism creates excess H+ (lactate)
- Reversal of Na/Ca channel occurs to remove Na+ but results in Ca2+ build up
- Excess calcium further depletes ATP, leads to contracted myocardium and apoptosis
Sequelae of myocardial infarction
DARTHVADER
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valvular disease
Aneurysm
Dressler’s syndrome
Embolism/thrombosis
Regurgitation
Placement of ECG leads
limb leads:
right arm, left arm, left leg
precordial leads:
- V1 + V2 first, either side of sternum in 4th ICS
- place V4 in same location as apex beat
- place V3 halfway between V2 and V4
- place V5 and V6 extending around the 5th ICS to the MAL
Types of coagulation studies
Prothrombin Time (PT) – evaluates extrinsic (play tennis outside)
Activated Partial Thromboplastin Time (aPTT) – evaluates intrinsic (play table tennis inside)
International Normalised Ratio (INR) – adjusted form of PT used to evaluate blood thinners
Types of hypoxia
Hypoxic – decreased oxygenation of the blood due to low availability or respiratory disease
Anaemic – diminished oxygen carrying capacity of the blood
Histotoxic – inability for tissues to utilise delivered oxygen
Circulatory – normal oxygenation and tissue function but impaired blood delivery
Cardiac determinants of mean arterial pressure
Mechanisms of blood pressure regulation
Autonomic Nervous System:
- SNS – increases blood pressure by increasing heart rate and contractility as well as peripheral vasoconstriction
- PNS – decreases blood pressure by decreasing heart rate at the SA node
Renin Angiotensin Aldosterone System:
Multistep process which synthesises angiotensin II in response to decreased blood pressure, ATII causes vasoconstriction and increases sympathetic tone
Local signalling:
variation based on which vascular bed however various vasoactive chemicals and metabolites can induce changes in arteriolar radius to influence blood pressure:
- constriction: serotonin, ADH
- dilation: NO, bradykinin, histamine, ANP, carbon dioxide
Types of adrenergic receptors
- Receptor
- Location
- Mechanism
- Effect
Baroreceptor reflexes
High pressure baroreceptors – in carotid body and aortic arch, increased stretch in this region indicates high blood pressure and leads to increased PNS activity and vice versa
Low pressure baroreceptors – in SVC/IVC/RA, increased stretch in this region indicates high venous return and induces an increase in SNS activity to compensate
Classifications of hypertension by severity and cause
primary/essential = idiopathic cause
secondary = result of another condition
classification of severity:
- mild: 140-59/90-99
- moderate: 160-79/100-109
- severe: >180/>110
hypertensive urgency = severe category with risk factors for end organ damage
hypertensive emergency = severe category with evidence of end organ damage
Pharmacology of hypertension and compliance issues
- β-blockers: reduce cardiac output by decreasing HR and contractility
- ACE inhibitors: inhibit RAS resulting in decrease in TPR
- ARBs: inhibit RAS resulting in decrease in TPR
- Ca<u>2+</u> channel blockers: reduce contractility of heart and constriction of vessels
- Thiazide diuretics: increase loss of fluid via urine resulting in reduced blood volume
- α-antagonists: inhibit peripheral vasoconstriction therefore decreasing TPR
- Central acting mimetics: decrease SNS tone
Patients with hypertensive medications often have compliance issues as the effects of HTN are not immediately recognisable, they must be taken indefinitely, may have side effects etc.
Structure and function of lymphatic capillaries
Lymphatic capillaries are blind-ended vessels made up of endothelial cells anchored by tethering filaments which expand with the interstitium creating low pressure to generate flow
Pharmacology of angina management
- Aspirin: antiplatelet agent by inhibiting COX synthesis of TXA2
- Nitrates: metabolised to NO which causes vasodilation
- β-blockers: reduce cardiac output by decreasing HR and contractility
- Ca2+ channel blockers: reduce contractility of heart and constriction of vessels
- Statins: inhibit HMG-CoA reductase to prevent endogenous cholesterol synthesis
- Fibrinolytics: catalyse plasminogen → plasmin to dissolve blood clots
Overview of the RAAS
- angiotensinogen synthesised by the liver
- decreased afferent arteriolar stretch stimulates renin release by juxtaglomerular apparatus which converts angiotensinogen → angiotensin I
- ACE in pulmonary vasculature converts angiotensin I → angiotensin II
- Angiotensin II causes vasoconstriction and increases sympathetic tone, stimulates Aldosterone and ADH (Na + H2O retention to increase Blood Volume)
Physiological zones of the lung
Zone 1 – at lung apex, arterial pressure low and alveolar pressure high leads to vascular collapse and physiological dead space, only in positive pressure ventilation and hypotension
Zone 2 – low arterial pressure (gravity) leads to partial collapse and reduced flow
Zone 3 – adequate arterial pressure gradient allows for normal flow, majority of healthy lungs
Zone 4 – high interstitial pressure compresses extra-alveolar capillaries at the extreme base
Regulation of blood pressure in different vascular beds
- Coronary
- Cerebral
- Skeletal muscle
- Skin
- Renal
Categorisation of ischaemic limb pain
Stage I: viable
Stage II: immediately threatened
Stage III: not viable
Six Ps of acute limb ischemia
Pallor
Paraesthesia
Pain
Pulselessness
Paralysis
Perishingly cold or poikilothermia
Features of a cardiovascular risk chart
The factors used in calculating estimated CVD risk are:
- sex
- age
- blood pressure
- smoking status
- total cholesterol:HDL ratio
- diabetic status
Principles of ambulatory blood pressure monitoring
Ambulatory blood pressure monitoring involves use of a device that measures blood pressure at regular intervals over a 24-hour period
- May be used to diminish circumstantial increases in blood pressure such as exercise or white coat hypertension
- Expect to see a nocturnal dip in blood pressure in healthy patients (10% lower)
- Highest blood pressures expected in the morning between 6am and 12pm
Pathophysiology of Asthma
Primary exposure: sensitisation to allergen, results in production of IgE which binds to mast cells and sensitises them for a second exposure
Secondary exposure: cross-linking of allergen with bound IgE triggers degranulation
- early phase (0-2 hours) – release of spasmogens and inflammatory mediators including histamine, prostaglandins, leukotrienes causes vasodilation and bronchospasm
- delayed phase (4-12 hours) – ongoing inflammation mediated by T cell response, eosinophils and mast cells
- goblet cell hyperplasia
- oedema
- smooth muscle proliferation
- chronic asthma leads to airway remodelling and fibrosis due to fibroblast activation
Common asthma triggers
Some common asthma triggers include:
- Viral respiratory infections
- Exercise
- Specific allergen exposure – dust mites, pollen, mould, pets
- Environmental/occupational triggers – pollutants, smoke, cold air, dry air
- Dietary triggers including foods and additives
- Some medications e.g. NSAIDs
Examples of atopic disease
An atopic Hx or FHx may include – asthma, allergic rhinitis, eczema (atopic dermatitis)
Factors influencing gas exchange in the lungs
- Diffusion distance e.g. pulmonary oedema
- Surface area for gas exchange e.g. emphysema
- Ventilation e.g. asthma
- Perfusion e.g. pulmonary embolism
Types of respiratory failure and sequelae
Type I:
Oxygenation failure, low oxygen (<60mmHg)
- damage to lung tissue that prevents adequate oxygenation but is still sufficient to excrete carbon dioxide
- pneumonia, pulmonary embolism, altitude
Type II:
Ventilatory failure, low oxygen with high carbon dioxide
- decreased alveolar ventilation such that oxygenation and excretion of carbon dioxide are both compromised
- PTX, pleural effusion, pulmonary fibrosis, kyphoscoliosis, motor neuron disease
Acute consequences: tachycardia, hypertension, agitation, death
Chronic consequences: polycythaemia, right heart failure
non-respiratory functions of the lung
- Immune surveillance: tonsillar ring, BALT, alveolar macrophages, mucociliary elevator
- Conversion of angiotensin II
- Respiratory compensation for acidosis/alkalosis
- Production of surfactant – Clara cells and type II pneumocytes
Principles of spirometry
Four volumes: inspiratory reserve, tidal, expiratory reserve, residual
Four capacities: functional residual, inspiratory, vital, total lung
Lung function diagnostics for asthma and COPD
spirometry diagnostics:
- Asthma: FEV1/FVC < 0.7 of predicted, 12% and 200mL improvement after a bronchodilator
- COPD: FEV1/FVC < 0.7 with minimal change after a bronchodilator, FEV1 used for staging
Factors affecting oxygen-haemoglobin affinity (including Bohr and Haldane effect)
Factors that decrease oxyhaemoglobin affinity (promoting release):
- temperature
- pH
- 2,3–BPG
- carbon dioxide
Bohr effect = describes the effect of CO2 and H+ on oxygen-haemoglobin affinity, high CO2 and H+ promote unloading (at tissues)
Haldane effect = describes the effect of oxygen on carbaminohaemoglobin affinity, high O2 concentrations promote unloading (at lungs)
Methods of carbon dioxide and oxygen transport
Carbon dioxide:
- bicarbonate ions (85%)
- carbaminohaemoglobin (10%)
- dissolved gas (5%)
Oxygen:
- oxyhaemoglobin (99%)
- dissolved gas (1%)
Innervation of the lungs
- System
- Description
- Effect
Principles of arterial blood gas analysis (acidosis vs. alkalosis)
- Determine if the pH is acidotic or alkalotic (normal range = 7.35–7.45)
- Assess if the bicarbonate (22–26) and carbon dioxide (35–45) are acidotic/alkalotic to determine the origin of the acid-base imbalance
- if bicarbonate imbalance aligns with pH = metabolic cause
- if carbon dioxide aligns with pH = respiratory cause
- Determine if there is compensation, this may be full if the pH is normal or partial otherwise
Overview of cough reflex
- Irritant receptors in lungs/airways sense chemical/mechanical stimuli
- Signal is relayed to medulla via vagus afferents
- Efferent signals sent to muscles to coordinate cough response, this involves forced expiration against a closed glottis to build pressure before the glottis opens to expel air
Pharmacology of respiratory disorders (relievers, preventers)
- Class
- Mode of Action
- Side effects
- Examples
Principles of tuberculosis infection including testing and management
Latent TB
Diagnostic test options for latent TB include
- Mantoux test: measuring reaction to tuberculin skin challenge, cheap but can only be performed a limit number of times and is based on probability of infection (risk factors)
- IGRA: in vitro measurement of IFNγ released when WBC sample challenged with TB antigens, expensive but highly specific
Treatment is with 9 months of isoniazid with pyridoxine (vitamin B6) to prevent neurotoxicity, hepatotoxicity is an issue in older patients so risk must be weighed with benefit
Active TB
Diagnosis is based on history, CXR and tissue/sputum culture of M. tuberculosis which can take weeks
Treatment is a multi-drug regimen (isoniazid, rifampicin, pyrazinamide, ethambutol)
- 2 months of 4 drugs, followed by 4-7 months of 2 drugs
- drugs and duration modified based on sensitivity/resistance
Types of pneumonia
The type of pneumonia will influence the most likely causative organisms and therefore the treatment and prognosis
- Community acquired: half of all cases are Strep. pneumoniae
- Typical pneumonia – sudden onset, chest pain and sputum
- Atypical pneumonia – longer prodrome with non-respiratory symptoms, causative organisms include Legionella pneumophila, Chlamydophila pneumoniae and Mycoplasma pneumoniae
- Aspiration pneumonia due to inhalation of vomit, contains GIT bacteria
- Nosocomial/hospital-acquired
- Ventilator associated pneumonia
Phases of embryological lung development
- Embryonic – initial budding and branching from primitive foregut
- Pseudoglandular – branching to the level of terminal bronchioles, pulmonary vasculature develops alongside
- Canalicular – extensive angiogenesis and maturation of lung tissue
- Terminal sac – stromal thinning, surfactant (now viable)
- Alveolar – further maturation of alveoli (continues for several years after birth)
Pathophysiology of cystic fibrosis
Mutation results in a defective CFTR transport protein which regulates movement of chloride ions out of mucous epithelial cells, results in dysfunction of several organs
- Lungs: thick mucus that narrows airways and cannot be cleared, chronic bacterial infection, inflammation, fibrosis
- Pancreas: thick mucus blocks pancreatic ducts → pancreatitis and malabsorption
- Male reproductive tract: absence of vas deferens causing male infertility
- Sweat glands: high chloride and sodium in sweat, basis of sweat test
Common types of URTI and LRTI and their causative organisms
URTI:
- oral infections: commensal bacteria/fungi due to microflora imbalance
- pharyngitis: adenovirus, EBV, CMV, HSV. group A Streptococcus
- sinusitis: commensal nasopharyngeal organisms
- epiglottitis: Haemophilus influenzae
LRTI:
- laryngitis: Haemophilus influenzae, rhinovirus, RSV, influenza
- bronchitis/bronchiolitis: RSV, rhinovirus, adenovirus,
- pneumonia: (see above) Strep. pneumoniae, Haemophilus influenzae
Overview of Arachidonic Acid Pathway
Arachidonic acid is mobilised from membrane phospholipids by phospholipase A2, arachidonic acid is used in several pathways to produce a number of paracrine factors including leukotrienes, thromboxanes, prostacyclins and prostaglandins
- there are two forms of cyclooxygenase – COX1 is constitutive and has constant basal activity while COX2 is inducible in inflammatory conditions, modern NSAIDs are typically COX2 selective to limit side effects
- final biologically active compounds are often formed in their specific tissues
Control of ventilation (receptors, respiratory centres)
Receptors involved in respiratory control:
- Central chemoreceptors in the floor of the fourth ventricle respond to carbon dioxide indirectly due to it passing across the blood brain barrier and producing H+ ions
-
Peripheral chemoreceptors send signals to the brainstem via CNIX and CNX
- Carotid body: respond to H+, O2 and CO2 (CNIX)
- Arch of aorta: respond to O2 and CO2 (CNX)
-
Pulmonary receptors send signals to the brainstem via CNX
- Stretch receptors – airways and lung in general
- J receptors – distension of the capillaries, alveolar expansion
- Irritant receptors
Respiratory centres involved:
- DRG: main control of inspiration, receives input from receptors above and outputs via the phrenic and intercostal nerves to respiratory muscles
- VRG: activated by the DRG for active expiration (abdominals, internal intercostals) and forced inspiration using accessory muscles
- Apneustic: prolongs breathing by acting on the lower centres, deep breathing
- Pneumotaxic: turns off inspiration, breath hold
Effects of diving and altitude on lung physiology
Altitude:
- hypoxaemia detected by peripheral chemoreceptors and relayed to DRG which coordinates an increase in the rate (DRG) and depth (VRG) of breathing
- chronic hypoxaemia leads to ↑EPO in kidneys, results in polycythaemia
Diving:
- increased pressure increases gas solubility, main concern is nitrogen narcosis which involves bubbling and gas emboli as pressure decreases on ascent
Pathophysiology of COPD
Emphysema – occurs due to imbalance between elastases/anti-elastases in the lung acini
- smoking causes immune response which increases elastase production
- alpha-1-antitrypsin deficiency
result is structural changes with destruction of elastic walls and dynamic airway collapse on expiration → hyperinflation, hypoxaemia, wheeze, pursing lips to prolong expiration
Chronic bronchitis – irritation due to smoking/pollutants causes goblet cell hyperplasia and increased mucus production as well as decreased ciliary function
- excess build-up of mucus obstructs airways
- poor mucus clearance increases predisposition to infection
result is expiratory wheeze, gas trapping, hyperinflation, barrel chest, cyanosis
Types of emphysema
- centriacinar* – affects only the more proximal alveoli surrounding the respiratory bronchioles, associated with smoking
- panacinar* – affects the entire alveolar network around both respiratory bronchioles and alveolar ducts, associated with α1-antitrypsin deficiency
Classification of lung cancers
Non-small cell lung cancers: (85-90%)
- squamous cell carcinoma – proximal airway epithelium, central
- adenocarcinoma – small airway epithelium + type II pneumocytes, peripheral
- large cell undifferentiated cancer, peripheral
Small cell lung cancer (10-15%), central lesions
Obstructive vs. restrictive lung diseases
- Summary
- Spirometry
- CXR
- Signs/symptoms
- Examples
Transudate vs. exudate
Transudate = fluid leaking from capillaries due to increased hydrostatic pressure or decreased oncotic pressure, low in protein and LDH
Exudate = fluid leaking due to increased capillary permeability or inflammatory processes, high in protein and LDH
Immune defence of the lungs
- Tonsillar ring – lymphoid tissue that protects the airways, pharyngeal + palatine + lingual
- Goblet cells – secrete mucus to capture inhaled substances, part of mucociliary elevator
- Cilia – apical projections of epithelium which beat to remove particles trapped in mucus
- BALT – bronchi associated lymphoid tissue, immune tissue within lung submucosa
- Alveolar macrophages – phagocytic cells which circulate within alveoli
- Surfactant – major function is to improve compliance but has a role in lung immunity
Pathophysiology of pulmonary embolism and potential sequelae
A PE occurs when an embolus lodges within the pulmonary arterial tree, embolus may include thrombus, fat, air bubbles, amniotic fluid, tumour cells
Signs and Symptoms:
- tachycardia,
- tachypnoea,
- pleuritic chest pain,
- syncope,
- sudden death
Potential sequelae:
- asymptomatic PE
- sudden death due to saddle embolus at pulmonary artery bifurcation
- infarction of a lung segment
- emphysema of infarcted lung tissue
- chronic pulmonary hypertension from recurrent PE
Five A’s of smoking in medical practice
- ASK smoking status
- ADVISE smokers to quit
- ASSESS willingness to quit
- ASSIST in a quit attempt
- ARRANGE a follow up
Stages of sleep
Non-REM sleep – idle brain activity, movement possible
- stages 1 + 2: relatively light
- stage 3: deep, slow wave patterns
REM sleep – brain and eyes are very active, body is paralysed, dreaming
Histology of respiratory and pulmonary epithelia
Respiratory histology (nasal cavity, pharynx, auditory tube, paranasal sinuses, trachea, bronchi)
pseudostratified columnar epithelium with three major cell types
- ciliated columnar epithelial cells
- goblet cells
- basal stem cells
The walls of the trachea and bronchi contain submucosal mucous glands as well as hyaline cartilage for strength and maintaining patency
note: the vocal folds and epiglottis have stratified squamous epithelium to resist abrasion
Pulmonary histology (functional lung tissue – alveoli)
The alveoli are arranged in an acinar structure with large airspaces and very thin walls consisting only of a type I pneumocyte epithelial cell, endothelial cell and a fused basement membrane
other cells present include:
- type II pneumocytes: scattered cuboidal cells that secrete surfactant, can differentiate into type I pneumocytes
- alveolar macrophages: immune cells for surveillance of the alveoli
Interpretation of pressure-volume loops
Pressure and volume within the left ventricle are measured to generate pressure-volume loop which illustrates LV function and can be used to identify and describe pathology
ESPVR = end-systolic pressure-volume relationship, demonstrates the maximal pressure that can be produced by the LV at a given volume, represents inotropic state of the ventricle
Pressure volume loop description
- Aortic Stenosis
- Aortic Regurgitation
- Mitral Stenosis
- Mitral Regurgitation
Different classes of shock (causes, examples)
- Hypovolaemic: loss of fluid volume e.g. traumatic blood loss, GI bleeding, burns
- Cardiogenic: inability of the heart to function as an effective pump e.g. arrhythmias, myocardial infarction, valvular disease, chest trauma, toxicity/infection
- Obstructive: barriers that prevent filling of the heart such as pulmonary embolism, cardiac tamponade, fibrous pericarditis, tension pneumothorax
-
Distributive: failure of vasoregulation → systemic vasodilation and peripheral pooling
- septic – systemic inflammation due to infection e.g. bacteraemia
- anaphylactic – systemic inflammation due to allergic reaction, release of histamines causes vasodilation e.g. drug/food allergy, insect bites
- neurogenic – loss of SNS tone causes peripheral vasodilation e.g. spinal cord injury, cerebral stroke, anaesthesia
Types of hypertrophy
Concentric hypertrophy – adding sarcomeres in parallel due to pressure overload, weightlifter
Eccentric hypertrophy – adding sarcomeres in series due to volume overload, swimmer
Pathophysiology of heart failure
Heart failure can affect either the left heart, right heart or both sides
- LHF: MI, cardiomyopathy, valvular disease, systemic HTN
- RHF: cor pulmonale, left heart failure
One of the major classifications for causes and pathogenesis of heart failure is systolic versus diastolic heart failure:
Systolic heart failure – inability of the ventricle to effectively eject blood due to dysfunction in contraction or elevated afterload, results in ↑EDV ↓CO, ejection fraction is therefore not preserved
- MI or dilated cardiomyopathy causes myocardial failure, cannot generate force
- systemic hypertension and aortic stenosis increase afterload
Diastolic heart failure – dysfunction of heart filling during diastole means that ↓EDV ↓CO however ejection fraction is usually preserved
- cardiac tamponade or pericarditis can restrict ventricular relaxation
- MI can lead to fibrosis which limits relaxation
- hypertrophic cardiomyopathy will reduce the lumen volume of the ventricle
The overall principle of these mechanisms is the inability of the heart to maintain sufficient cardiac output to meet the needs of the body, during heart failure there are a number of compensatory mechanisms
- SNS and RAS activate to maintain CO however they become overactivated and lead to further pathology of the heart
- cardiac natriuretic peptides counteract SNS/RAS but soon fatigue
NYHA classifications of heart failure
Stage I – asymptomatic
Stage II – mild symptoms e.g. fatigue, dyspnoea with physical activity
Stage III – symptoms appear with any physical activity
Stage IV – symptoms appear at rest and significant discomfort with activity
Pharmacological management of heart failure
- Drug Class
- Description
- Example
Mechanisms of peripheral oedema (pitting vs. non-pitting)
Pitting oedema = residual indentation left by pressure on the swollen site due to lymphatic drainage of the oedema fluid
- Increased hydrostatic pressure (fluid retention in heart failure) or reduced oncotic pressure (hypoalbuminaemia)
- Increased blood vessel wall permeability (inflammation)
Non-pitting oedema = peripheral swelling where indentation does not persist after pressure removed
- obstruction of lymphatic vessels (lymphoedema)
- thyroid disorders (myxoedema)
Common causes of syncope
Syncope = unexpected LOC and loss of postural tone due to lack of cerebral perfusion
- Thermoregulatory vasodilation and stillness → diminished venous return
- Compression of IVC e.g. pregnancy
- Tachycardia, due to decreased time for diastolic ventricular filling
- Vasovagal syncope → unknown cause of massive PNS activity
- Heart blocks and conduction disorders
Four heart sounds
S1: AV valve closure (mitral then tricuspid)
S2: semilunar valve closure (aortic then pulmonary)
S3: during rapid filling of early diastole, mitral regurgitation
S4: during atrial contraction of late diastole, reduced LV distensibility
Types of heart murmurs and their causes
Neural vs. humoral control of cardiac output
Neural control
- PNS*: ↓CO
- innervates SA node, ↓HR
- SNS*: ↑CO
- innervates SA node and myocardium, ↑HR ↑contractility
- causes peripheral vasoconstriction, ↑TPR
Humoral control
- RAS*: circulation of angiotensin II synthesised via the RAS causes peripheral vasoconstriction and stimulates SNS activity, ↑CO
- natriuretic peptides*: primarily ANP and BNP ↓CO
secreted in response to atrial (ANP) or ventricular (BNP) stretch
- dilation of afferent arterioles, ↓renin
- inhibition of sodium reabsorption in the convoluted tubule, ↓BV
- increased capillary permeability and peripheral vasodilation, ↓TPR
Common arrhythmias
Bradyarrhythmias
- Sinus bradycardia – due to intrinsic/extrinsic factors influencing the SA node
- Heart blocks
- atrioventricular block: first, second- or third-degree block in AV node
- bundle branch block: left or right
Tachyarrhythmias
Supraventricular tachycardias
- sinus tachycardia – abnormal SA node or abnormal ANS regulation
- AV junctional tachycardia – AV re-entry (AVRT) or AV nodal re-entry (AVNRT)
- atrial tachyarrhythmias – atrial fibrillation, atrial flutter, atrial ectopic beats
Ventricular tachycardias
- sustained ventricular tachycardia or non-sustained ventricular tachycardia
- ventricular fibrillation
- ventricular premature beats
Effect of respiration on blood pressures including pulsus paradoxus
During inspiration: ↓BP ↑HR
changes in intrathoracic pressure will lead to changes in both right atrial pressure and pulmonary vascular pressure due to the expansion of the lungs
- ↓ RA pressure increases the gradient for venous return
- ↓ pulmonary vascular pressure will decrease left heart filling and therefore cardiac output, triggering a compensatory baroreceptor reflex that increases HR
Pulsus Paradoxus = exaggeration of these respiratory changes in blood pressure which has two potential causes:
- greater drop in intrathoracic pressure due to status asthmaticus
- restriction of the ventricle which exaggerates septal shift, so the greater filling of the right heart impinges on the filling of the left e.g. cardiac tamponade
Principles of CXR interpretation
Details – type of film, patient details, orientation, date and time, indication
RIPE – (quality of film) rotation, inspiration, picture, exposure
Soft tissues and bones – assess the bones, breast shadows, masses
Airways/mediastinum – trachea midline, bronchial changes, hila
Breathing – lung fields appear the same, opacities/lesions, pleural reflections
Circulation – cardiac position, CTR, great vessels
Diaphragm – right hemidiaphragm higher, smoothness, costophrenic angles, air in peritoneum
Extras – e.g. , ET tube, NG tube, catheters, electrodes, chest tube
Signs of heart failure on CXR
A: alveolar oedema (bat wing opacity)
B: Kerley B lines
C: cardiomegaly
D: dilated upper lobe vessels (cephalisation)
E: pleural effusion
