Block 13 Flashcards
Define: dyspnoea
Breathlessness
An unpleasant sensation of a feeling of an increased demand for breathing
What are some causes for breathlessness?
Pulmonary oedema Pneumothorax Pulmonary embolism Acute: - Anaphylaxis - Acute asthma - Pneumonia
Subacute:
- heart failure
- pleural effusion
- lung cancer
- anaemia
Slowly progressive:
- chronic bronchitis and emphysema
- interstitial lung disease
- pneumoconiosis
- pulmonary arterial hypertension
What are some causes of cough?
Airway/lung infection Left heart failure Lung cancer Foreign body inhalation ACE inhibitors Asthma Pulmonary fibrosis COPD
Risk factors for TB
Elderly Immunocompromised Diabetes Hodgkin lymphoma Chronic lung disease Chronic kidney failure Malnutrition Alcoholism
What are the pathological manifestations of TB?
Caseating granulomas
Cavitation
Describe secondary TB
Arises in previously sensitised host
Appears when host immune system compromised
Cavitation occurs readily
Erosion of cavities = coughing up bacteria = INFECTIOUS
Reactivation of latent infection or exogenous reinfection
What are some of the carcinogens that can cause lung cancer?
Radon Arsenic Asbestos Outdoor air pollution Cigarette smoke Hydrocarbons
What are some of the carcinogenic substances in cigarette smoke?
43 known
Carcinogenic metals - arsenic, nickel, cadmium, chromium
Potential promoters - acetaldehyde, phenol
Irritants - nitrogen dioxide, formaldehyde
Cilia toxins - hydrogen cyanide
What are the targets of genetic damage in cancer?
Growth promoting oncogenes
Growth inhibiting cancer suppressor genes
Genes that regulate programmed cell death
Genes that regulate repair of damaged DNA
What is the histology of normal respiratory epithelium?
Pseudostratified, columnar, ciliated
Squamous if damaged
Describe what is seen in dysplasia
Disordered cell growth
Loss of normal architecture and of uniformity of cells
Pleomorphic, hyperchromic nuclei
Increase in mitotic figures often at abnormal locations
Precedes but does not necessarily lead to cancer
Squamous cell carcinoma
Develops from squamous metaplasia
Excessive growth of abnormal squamous cells
Locally invasive
Able to form metastases
How does carcinoma of the lung present?
Cough (75%)
Weight loss (40%)
Chest pain (40%)
Dyspnoea (20%)
What are the local effects of lung cancer, what causes them?
Pneumonia, lobar collapse, abscess - obstruction of airway
Lipid pneumonia- obstruction
Pleural effusion - spread to pleura
Hoarseness - invasion of recurrent laryngeal nerve
Dysphagia - oesophageal invasion
Diaphragm paralysis - phrenic nerve invasion
Rib destruction - chest wall invasion
SVC syndrome - SVC compression
Horners syndrome - invasion of sympathetic ganglia (Pancoast)
What are the systemic effects of lung cancer?
Metastatic spreak
Ectopic production of hormones - ADH, ACTH, Parathyroid hormone, calcitonin, gonadotropins, serotonin
Peripheral neuropathy
Dermatological abnormalities
Haematological abnormalities
What are the 2 main subtypes in lung cancer?
Non small cell carcinoma 80%
Small cell carcinoma 20%
What are the 3 sub groups of non small cell carcinoma?
Squamous cell carcinoma 25-40%
Adenocarcinoma 25-40%
Large cell carcinoma 10-15%
Describe adenocarcinoma (lung)
Infiltration of lung by abnorma glandular structures
Shows glandular differentiation
- tubular/acinar/papillary structures
- Mucin production
Precursor lesions - atypical alveolar cell hyperplasia (alveoli lined by atypical cuboidal epithelial cells)
Describe small cell carcinoma (lung)
Shows neuroendocrine differentiation
Crowded small cells with hyperchromatic glassy nuclei and extremely scanty cytoplasm
What are the 2 main factors for rapid spread of TB?
Crowded living conditions
A population with little native resistane
Where is prevalence of TB highest?
China
India
Southern Africa
What is the incidence of TB in the UK?
13 per 100,000
Highest in London
What groups are most at risk of TB?
Alcoholics Intravenous drug users Homeless Prison inmates Urban poor
How is TB spread?
Inhalation of droplet nuclei
Aerosolised by coughing, sneezing or talking
8 hours of close contact required - prolonged exposure
Describe the process of TB infection
- Bacteria multiply freely in alveolar space or within macrophages
- Proceeds for weeks
- Development of tissue hypersensitivity
- CD4 recognise the antigens presented by macrophages
- Cytokine release
- Form Langhans giant cells (fused macrophages)
Describe caseous necrosis in TB
Inherently unstable
Liquifies and discharges through the bronchial tree producing a tuberculous cavity
Infectious material sloughed from a cavity can allow bronchogenic spread
What questions should be asked in taking a history from a patient with TB?
History of TB exposure Country of origin Age Ethnic or racial group Occupation
What is the presentation of TB?
Productive, prolonged cough (over 3 weeks) Chest pain Haemoptysis Fever Chills Night sweats Appetite loss Weight loss Fatigue
What happens in primary TB infection?
Rapid destruction of bacteria and the infective process is arrested (only evidence is positive ManToux test)
Ghon focus occurs but is stopped
What happens in post primary infection?
Immune deficiency which allows reactivation as macrophage and granuloma break up
Causes bronchial spread as necrosis occurs
Where are the main sites of spread for extra-pulmonary TB?
Can be to any organ
Abdomen Bone Brain Muscle Retina Lymph node
What percentage of TB cases are purely extrapulmonary?
19-30%
What is the stain used for acid fast bacilli?
Ziehl- Neelson
What tests can be used to check immunity to TB?
Man toux test (only specific for mycobacteria)
IFN-g (specific for TB)
What tests should be carried out if you suspect TB?
Chest X-ray Sputum specimens Routine drug susceptibility testing HIV testing Hepatitis testing
What are the first line drugs for TB treatment?
Isoniazid Rifampicin Pyrazinamide Ethambutol Rifabutin Rifapentine
Viractiv - one tablet for all 4 drugs
Name some occupational lung diseases
Occupational asthma COPD Pneumoconiosis Toxic pneumonitis Hypersensitivity pneumonitis Benign pleural disease e.g. asbestos Infective - TB
Outline occupational asthma
Underdiagnosed
Most common cause of occupational lung disease
Baker ,soldering, Paint spraying, animal housing.
Can prevent lifelong asthma if picked up early enough
Outline simple pneymoconiosis
Coal miners lung
Causes chronic bronchitis
Normal lung funtion
Cough and sputum
Outline silicosis
Coal workers (mixed) Sand blasters (pure)
Rare
Upper lobe nodules and lymph node calcification and enlargement
Predisposes to TB and lung cancer
Outline siderosis
Inhaled iron
Doesn’t cause disability or decrease lung function
Outline hypersensitivity pneumonitis
Form of pulmonary fibrosis (presents like pneumonia - breathing difficulties and fever)
Farmers lung (mouldy hay - fungal spores) and pigeon fanciers lung
Describe the pathogenesis of TB
- Macrophages are infected by mycobacterium tuberculosis
- Bacteria replicate within the macrophage
- 3 weeks post infection - TH1 response activates macrophages
- TH1 release IFN gamma.
- TH1 stimulates formation of granlomas and caseous necrosis
- Infection is controlled within the macrophages
- It can be reactivated or reexposed
Describe secondary TB
Arises in previously sensitised host
Reactivation when immune system decreased or re-exposure
What are the clinical features of secondary TB?
Insidious in onset Malaise Anorexia Weight loss Low grade fever Sputum Haemoptysis
Describe the morphology of TB
- Small area of white inflammation with consolidation - Ghon focus
- Centre undergoes caseous necrosis
- Ghon complex = lung lesion and node involvement
- It undergoes progressive fibrosis then calcification (Ranke complex)
Outline miliary pulmonary disease
Occurs when organisms drain through lymphatics
Consolidation scattered throughout lungs
Define chronic bronchitis
Defined clinically as persistent cough with sputum production for at least 3 months in at least 2 consecutive years
What can result from persistent chronic bronchitis?
Progress to COPD
Lead to cor pulmonale and heart failure
Cause atypical metaplasia and dysplasia of respiratory epithelium
What is the pathogenesis of chronic bronchitis?
Long standing irritation of inhaled substances
Hypersecretion of mucus in large airways (hypertrophy of glands)
Proteases released from neutrophils
Marked increase in goblet cells
Damage to cilia and epithelium
Outline the morphology of chronic bronchitis
- Hyperaemia, swelling and oedema of mucous membranes
- Excessive mucinous secretions
- Hyperplasia of mucous glands
- Increased Reid index
- Marked narrowing of bronchioles
- Obliterations of lumen due to fibrosis (extreme)
What are the clinical features of chronic bronchitis?
Persistent cough, productive of sputum Dyspnoea on exertion Hypercapnia Hypoxaemia Mild cyanosis Impairment of respiratory function
What are the changes seen in chronic bronchitis?
Squamous metaplasia Glandular hyperplasia Goblet cell hypertrophy Smooth muscle cell hypertrophy Mucociliary dysfunction
LYMPHOCYTES not eosinophils
What is the incidence of lung cancer?
Occurs most frequently between 40-70 years
Peak incidence at 50-60
5 year survival rate = 16%
Incidence and mortality rates have been decreasing
Outline pathogenesis of lung cancer
Stepwise accumulation of genetic abnormalities
- 87% are smokers
- Heavy smokers (10 pack years) are 60x increased risk
- Gene mutations: KRAS, EGFR, p53, RB1, p16
What are the features of a lung adenocarcinoma?
Malignant epithelial tumour with glandular differentiation
Most common in women and non-smokerss
Peripheraly located and tend to be smaller
Slow growth - wide and early metastasis
KRAS mutation
What are the features of a small cell carcinoma?
Highly malignant with distinctive cell type - high mitotic count
No cell differentiation, necrosis is common and extensive
Neuroexcretory granules
Strong relationship to cigarette smoking
p53 and RB1
What are the features of a squamous cell carcinoma (lung)
Most common in men
Closely correlated with smoking
Keratinisation
p53 mutations
What are the uses of radiotherapy in lung cancer?
External radiotherapy (more common) and internal during bronchoscopy
Shrink tumour blocking an airway
SE: fatigue, anaemia, skin soreness, hair loss in area, difficulty swallowing
What are the uses of chemotherapy in lung cancer?
Small cell lung cancer
Can be used for non-small cell after surgery
SE: tiredness, nausea and vomiting, mouth ulcers, diarrhoea, constipation, hair loss, increased infection
What are the uses of surgery in lung cancer?
Non-small cell lung cancer Lobectomy Sleeve resection Pneumonectomy Segmentectomy
Mycobacterium tuberculosis
large non-motile baccili obligate aerobe (upper lobes) Intracellular parasite of macrophages Acid fast High lipid content
Why is the high lipid content of M. tuberculosis important?
Impermeability to stains and dyes
Resistance to many antibiotics
Resistance to killing by acidic and alkaline compounds
Resistance to osmotic lysis via complement deposition
Resistance to lethal oxidations and survival inside macrophages
Define multi-drug resistant TB
Resistant to at least 2 of the best anti-TB drugs
Isoniazid and rifampicin
Define extensively drug resistant TB
XDR TB
Rare
Resistant isoniazid and rifampicin plus resistant to any fluroquine and at least 1 of 3 injectable 2nd line drugs e.g. kanamycin, capremycin
Define asthma
Chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and//or in early morning.
What are the hallmarks of asthma?
Increased airway responsiveness to various stimuli
Causing episodic bronchoconstriction
Inflammation of bronchial walls
Increased mucus secretion
What are the common triggers of asthma?
Respiratory infections Environmental exposure to irritants (smokes, fumes) Cold air Stress Exercise
What are the 4 different types of asthma?
Atopic
Non-atopic
Drug-induced
Occupational
What is atopic asthma?
Type 1 IgE mediated hypersensitivity reactions
- Begins in childhood
- Positive family history common
- Triggered by allergens
What is non-atopic asthma?
- Respiratory infections are common triggers
- Hyperirritability of bronchial tree
- Virus induced inflammation lowers threshold of the subepithelial vagal receptors to irritants
Describe the pathogenesis of asthma
- Genetic predisposition for atopy
- Initial sensitisation to allergen which stimulates production of TH2 cells
- TH2 cells secrete cytokines IL4, 5 and 13
- Promotes inflammation and stimulates B cells to produce IgG and the antibodies
- IgE, eosinophils and mucus secretion
- IgE coats mast cells, repeat exposure to release granule contents
Describe the early phase reaction in asthma?
Bronchoconstriction - triggered by direct stimulation of subepithelial vagal receptors
Increased mucous production
Variable degrees of vasodilation
Increased vascular permeability
Describe the late phase reaction in asthma?
Inflammation with recruitment of leukocytes and eosinophils, neutrophils and T cells
Eotaxin activates eosinophils
Prolonged bronchoconstriction - leukotrienes C4.D4.E4. ACh, histamine. prostaglandin D2.
What are the features of airway remodelling?
- Hyperplasia and hypertrophy of bronchial smooth muscle
- Epithelial injury
- Increased airway vascularity
- Increased mucus gland hypertrophy
- deposition of subepithelial collagen
Epidemiology of asthma
1 in 10 children
1 in 12 adults
What are the clinical features of asthma?
Chest tightness
Dyspnoea
Wheezing
Cough with or without sputum production
Define emphysema
Condition of the lung characterised by irreversible enargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis
What are the different types of emphysema?
Centriacinar
Panacinar
Paraseptal
Irregular
Outline centriacinar emphysema
Central or proximal parts of acini (respiratory bronchioles)
Terminal alveoli are spared
Lesions are more common and more severe in upper lobes
Inflammation around bronchi and bronchioles common
Occurs predominantly in heavy smokers
Outline panacinar emphysema
Acini are uniformly enlarged from the level of respiratory bronchiole to the terminal blind alveoli
Entire acinus
Occurs more commonly in lower zones and anterior margins
Associated with alpha 1 antitrypsin deficiency
Outline paraseptal/ distal acinar emphysema
Proximal part of the acinus is normal Distal part is predominantly involved At margins of lobules and adjacent to pleura More severe in upper part of lungs Forms cyst like structures Underlies most spontaneous pneumothorax
Outline the pathogenesis of emphysema
- Activated inflammatory cells release mediators - IL8, TNF that damage lung structures and sustain neutrophilic inflammation
- Protease antiprotease mechanism and imbalance of oxidants and antioxidants (deficiency of antiprotease alpha 1 antitrypsin)
- Increased neutrophil elastase
- Causes tissue damage
- Loss of elastic tissue which causes respiratory bronchioles to collapse during expansion
What are the cellular findings in emphysema?
Goblet cell metaplasia
Inflammatory infiltration of walls with neutrophils, macrophages, B cells, CD4 and 8 T cells
Thickening of bronchiolar wall due to smooth muscle hypertrophy and peribronchial fibrosis
Loss of elastic recoil
Outline the morphology of emphysema
Voluminous lungs overlapping heart Upper 2/3 of lung more affected Large alveoli separated by thin septa Loss of attachment of alveoli to outer wall of small airways Decrease in capillary bed
What are the clinical features of emphysema?
No symptoms until at least 1/3 is damaged Dyspnoea Cough or wheeze Expectoration Weight loss Barrel chest and dyspnoic Prolonged expiration Sits hunched over with pursed lip breathing
What is type 1 respiratory failure?
Hypoxaemic
Low O2
Normal or low CO2
Caused by ventilation-perfusion mismatch
- Underventilated alveoli
- Venous blood bypasses ventilated alveoli
Hyperventilation increases CO2 removal but does not increase oxygenation
What is type 2 respiratory failure?
Hypercapnic
Increased CO2
Indicated inadequate alveolar ventilation
Can be acute or chronic
Causes of type 1 respiratory failure
COPD Pneumonia Pulmonary oedema Pulmonary fibrosis Asthma Pneumothorax PE Pulmonary hypertension
Causes of type 2 respiratory failure
COPD Severe asthma Drug overdose Myasthenia gravis Obesity
Define forced vital capacity
Volume of lungs from full inspiration to forced maximal expiration
Reduced in restrictive disease
Define FEV1
Forced expiratory volume in one second
Volume of air expelled in the first second of forced expiration
Define FER
Forced expiratory ratio
FEV1/FVC x100
What would you expect in a FEV1/FVC to be in obstructive disease?
FVC normal or reduced
FEV1 reduced <80%
Ratio reduced below 70%
What would you expect in a FEV1/FVC to be in restrictive disease?
FVC reduced <80%
FEV1 reduced
Ratio remains the same
What are the 5 steps in asthma treatment?
Step 1 - short acting beta agonist (salbutamol)
Step 2 - Inhaled steroid (beclometasone)
Step 3 - Long acting beta agonist (salmetrol)
Step 4- Leukotriene receptor antagonist and increased steroid (montelukast)
Step 5- Oral steroid (prednisolone)
What are the symptoms of life threatening asthma?
Severe breathlessness Unable to complete sentences Tachypnoea Tachycardia Silent chest Cyanosis Collapse
Define MI
Death of cardiac muscle due to prolonged severe ischaemia
What is the incidence of MI?
Frequency rises with age
Men at more risk
10% under 40
45% in over 65s
What is the pathogenesis of MI
Sudden change in atheromatous plaque which causes coronary artery occlusion
- exposed subendothelial collagen, platelets adhere and become activated
- Release of granule contents (aggregation)
- Vasospasm stimulated by mediators released from platelets
- Tissue factor activates coagulation pathway
- Thrombus occludes lumen
Myocardial response
- Ischaemia and myocyte death
- Cessation of aerobic metabolism
- Accumulation of noxious metabolites (lactic acid)
- Loss of contractility
- Cell death (if ischaemia longer than 20-30 minutes)
What are the 2 forms of MI?
Transmural
Subendocardial
Describe transmural infarction
Ischaemic necrosis involves full or nearly full thickness of ventricular wall in the distribution of coronary artery
ST elevation
Describe subendocardial infarction
Ischaemic necrosis limite to inner 1/3 or 1/2 of ventricular wall which is the area most vulnerable to decreased blood flow
non ST elevation
Which arteries are most commonly affected in MI?
Left anterior descending 40-50%
Right coronary artery 30-40%
Left circumflex 15-20%
What are the dangers of reperfusing the heart after MI?
Arrythmias Haemorrhage Irreversible cell damage Microvascular injury Prolonged ischaemic dysfunction
What are the clinical features of an MI?
Rapid weak pulse
Profuse sweating
Dyspnoea
10-15% asymptomatic
How would you diagnose an MI?
Cardiac troponins T and I
MB fraction of creatine kinase
ECG
What are the complications of MI?
Contractile dysfunction (pulmonary oedema, ventricular failure, cardiogenic shock)
Arrythmia - VT, VF, tachycardia, asystole
Myocardial rupture
Pericarditis
What is the mortality after MI?
30% in the first year
3-4% with each year after
Define angina
Angina pectoris
Characterised by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by transient myocardial ischaemia
Doesn’t cause myocyte necrosis
Stable and unstable
Outline stable angina
Most common
Caused by an imbalance in coronary perfusion due to chronic stenosing coronary atherosclerosis relative to myocardial demand
Pain caused by increased cardiac load - physical activity and emotional excitement
Outline unstable angina
Pattern of increasingly frequent pain, often of prolonged duration that is precipitated by progressively lower levels of physical activity
Can occur at rest
Caused by disruption of atherosclerotic plaque with thrombosis, possibly embolisation or vasospasm
Outline the conduction system of the heart
SA node (pacemaker) Bachmanns bundle Anterior, middle, posterior to AV node Bundle of His Left and right bundle branch Purkinje fibres
What is the arterial supply tot he AV node?
Right coronary artery 85-90%
Left circumflex artery 10-15%
What is the arterial supply to the SA node?
Right coronary artery 55-60%
Left circumflex artery 40-45%
Define ventricular tachycardia
Broad complex tachycardia originating from a ventricular ectopic focus
3 or more ventricular extrasystoles in succession at a rate of more than 120bpm
What are the features of ventricular tachycardia?
Rate >120bpm
Broad QRS complexes
Can be monomorphic - regular rhythm from single focus
Can be polymorphic - irregular with different QRS complexes
What is sustained VT associated with?
Late phase MI Cardiomyopathy Right ventricular dysplasia Myocarditis Drugs e.g. class 1 anti-dysrhythmic
What is the presentation of VT?
Chest pain Palpitations Dyspnoea Dizziness Syncope
What are the risk factors for VT?
Coronary heart disease
Structural heart disease
Triggered by electrolyte deficiency
Sympathomimetic agents e.g. caffeine
What is VF?
Ventricular fibrillation - cause of cardiac arrest and sudden cardiac death.
Ventricular muscle fibres contract randomly causing a complete failure of ventricular function
What are the risk factors for VF?
Anti-dysrhythmics Ischaemia Shock during cardioversion Hypoxia AF Electrical shock
What is the presentation of VF?
Chest pain
Fatigue
Palpitations
What is an ectopic pacemaker?
Abnormal pacemaker sites within the heart (outside SA node) that display automaticity
Can cause additional beats or take over the SA node
Generally produce a rhythm of 30-40bpm
Spread of depolarisation is not normal as it takes longer to spread
Prolongs duration of QRS complex
What is ischaemic heart disease?
Leading cause of death worldwide
Myocardial ischaemia is reduced blood flow due to obstructive athersclerotic lesions in coronary arteries
What is the presentation of ischaemic heart disease?
Myocardial infarction
Angina pectoris
Chronic IHD with heart failure
Sudden cardiac death
What is the pathogenesis of IHD?
Insufficient coronary perfusion relative to myocardial demand due to chronic progressive atherosclerotic narrowing of coronary arteries, superimposed acute plaque change, thrombosis and vasospasm.
What are the risk factors for atheroma/ CVD?
Increasing age Male Family history Race - south Asians Smoking Lack of exercise High fat diet High alcohol intake Psychological factors e.g. depression, stress Hypertension Diabetes Hyperlipidaemia Obesity Systemic inflammation
What is the management for obesity?
Dieting Exercise Weight loss programs Orlistat - inhibits pancreatic lipase Bariatric surgery
What are the physical consequences of obesity?
Increased risk of: CHD Hypertension Stroke Type 2 diabetes Cancer Fertility problems/ high risk pregnancy Decreased life expectancy Joint problems
What are the psychological consequences of obesity?
Depression Anxiety Low quality of life Low self-esteem Body dissatisfaction Poor concentration Lower academic success Social exclusion
What are the social consequences of obesity?
More likely to suffer from discrimination
- in employment, travel, school, healthcare, retail
Less friends
Lower educational achievement
Lower employment
Where are the 3 main places that myocardial rupture can take place?
Myocardial rupture of L ventricular wall
Myocardial rupture of ventricular septum
Myocardial rupture of papillary muscle
What are the features of a myocardial rupture of the ventricular septum?
Size of defects determine magnitude of Left to right shunt
Haemodynamic compromise
Harsh, loud, holsystolic murmur
What are the 4 classes in the New York Heart Classification?
Class 1 - no limitation of physical exercise. No symptoms on ordinary physical activity
Class 2 - slight limitation of physical activity. Symptoms on ordinary activity
Class 3 - Marked limitation of physical activity. Symptoms on less than ordinary activity
Class 4 - inability to carry out any physical activity without discomfort
What is cardiac neurosis?
Occurs in relative or friend of individual who has recently been diagnosed with cardiac condition or in the period following myocardial infarction
Dyspnoea, fatigue, rapid pulse, palpitations and chest pain with exertion
Psychological disorder associated with exhaustion and emotional strain
Describe the cardiac action potential
Phase 0 - rapid depolarisation, fast inflow of Na+
Phase 1 - short initial rapid repolarisation due to closure of Na+ channels, Cl- influx and outflow of K+
Phase 2 - Plateau, delay repolarisation, slow inward movement of Ca2+ and continual outflow of K+
Phase 3 - second period of repolarisation caused by continual flow of K+ and inactivation of Ca2+ inflow
Describe the waves on an ECG
P wave - spread of excitation through atria
PR interval - atria contract, excitation within AV node
QRS complex - spread of excitation through ventricles
QT interval - ventricles contract, action potential pahse 2
T wave - ventricles repolarise
What are the average lengths of the peaks in an ECG?
PR = 0.12-0.2s QRS = 0.08-0.12s QT = 0.3-0.46s
How do you measure HR using an ECG?
300/ number of large boxes between successive R wave peaks
What time is represented by 1 ECG grid box (small square)?
0.04s
What are the different types of heart block?
1st degree 2nd degree - Mobitz type 1 - Mobitz types 2 3rd degree (complete)
Describe 1st degree heart block
PR interval >0.2s
Asymptomatic, no treatment required
Describe Mobitz type 1 heart block
2nd degree
Wenckebach
Progressive PR interval prolongation until P wave fails to conduct
No treatment unless symptomatic
Describe Mobitz type 2 heart block
Sinus rhythm with normal PR interval but occasionally the p wave is not followed by QRS complex
Close monitoring - could progress to complete heart block
Describe a 3rd degree heart block
Complete heart block
Normal p wave
No QRS complex
ICU or CCU
What is bundle branch block?
Block of either the right or left bundles that branch from the bundle of His
In right BBB - right heart activation follows left
In left BBB - left heart activation follows right
Wide double peaked QRS complex and inverted T wave
What are the symptoms of heart block?
2nd and 3rd degree Fainting Dizziness Fatigue SOB Chest pain
Outline AF
Atrial fibrillation Atrial activity poorly defined Ventricular response is irregularly irregular Atrial rate = 350-650bpm P wave is fibrillatory. QRS <0.12s
How can you manage arrythmias?
Treat cause (if possible) Vagotonic manoeurves DC cardioversion Pacemakers Surgery Medication
What are the causes of bradycardia?
HR < 60bpm
Physiological - athletes
Cardiac - AV block or sinus node disease
Non-cardiac - vasovagal, hypothermia, hypothyroidism, hyperkalaemia
Drugs - Beta blocker, diltazem, digoxin, amiodarone
How can you treat bradycardia?
atropine
glucagon
digoxin specific antibody fragments
external pacing
What are the causes of haemopysis?
Lung cancer TB Bronchiectasis Pulmonary oedema Pulmonary embolism Pneumonia
What are the causes of stridor?
Whooping cough Epiglottitis Foreign body Laryngeal/tracheal tumour Laryngeal oedema
What would you expect to find on examination of consolidation?
Mediastinal shift - NO Percussion note - DULL Added sounds - CRACKLES Chest expansion - NORMAL OR DECREASED Breath sounds - BRONCHIAL Vocal resonance - INCREASED
What would you expect to find on examination of pleural effusion?
Mediastinal shift - NONE OR AWAY Percussion note - STONY DULL Added sounds - NONE Chest expansion - DECREASED Breath sounds - DIMINISHED/ABSENT Vocal resonance - DECREASED
What would you expect to find on examination of airway obstruction?
Mediastinal shift - NONE Percussion note - NORMAL Added sounds - WHEEZE Chest expansion - SYMMETRICAL Breath sounds - NORMAL Vocal resonance - NORMAL
What would you expect to find on examination of pneumothorax?
Mediastinal shift - AWAY Percussion note - HYPER RESONANT Added sounds - NONE Chest expansion - DECREASED ON SIDE OF Breath sounds - ABSENT/DIMINISHED Vocal resonance - INCREASED
What would you expect to find on examination of collapse?
Mediastinal shift - TOWARDS Percussion note - DULL Added sounds - NONE OR CRACKLES Chest expansion - REDUCED Breath sounds - DIMINISHED Vocal resonance - REDUCED
What would you expect to find on examination of unilateral fibrosis?
Mediastinal shift - TOWARDS Percussion note - DULL Added sounds - CRACKLES Chest expansion - REDUCED Breath sounds - NORMAL Vocal resonance - NORMAL
What is congestive heart failure?
Occurs when the heart is unable to pump blood at a rate sufficient to meet metabolic demands of tissues or can only do so at an elevated filling pressure
- Ischaemic heart disease
- Chronic work overload
- Acute haemodynamic stresses e.g. large MI
What is the Frank-Starling mechanism?
Increased filling volumes dilate the heart and increases functional cross bridge formation, enhancing contractility
What mechanisms maintain perfusion and pressure?
Frank-Starling mechanism Myocardial adaptations - hypertrophy and ventricular remodelling Activation of neurohumoural systems - Release of NA by ANS - Activation of RAAS - Release of ANP
Outline the formation of cardiac hypertrophy
Increase mechanical work due to pressure or volume overload - cause myocytes to increase in size
Pressure overload hypertrophy -
Response to increase in pressure. Concentric increase in wall thickness. Expanding cross sectional area of myocytes
Volume overload hypertrophy -
Ventricular dilatation. Wall thickness can be: increased, decreased or stay the same.
Describe how cardiac dysfunction occurs
Hypertension (pressure overload)
Vascular disease (pressure +/- volume overload)
MI (volume overload)
- Increased cardiac load
- Increased wall stretch
- Cell stretch
- Hypertrophy +/- dilation
- Cardiac dysfunction
What are the characteristics of congestive heart failure?
Variable degrees of decreased cardiac output and tissue perfusion
Pooling of blood in venous system
What are the causes of left sided heart failure?
Ischaemic heart disease
Hypertension
Aortic and mitral valvular disease
Myocardial diseases
Define left sided heart failure
Congestion of pulmonary circulation, stasis of blood in the left sided chambers and hypoperfusion of tissues leading to organ dysfunction
What are the consequences of left sided heart failure?
Left ventricle is hypertrophied and often dilated
Can cause dilation of left atrium and increase risk of AF
Pulmonary congestion and oedema
Perivascular and interstitial oedema (Kerley B lines)
Progressive oedematous widening of alveolar septa
Accumulation of fluid in alveolar spaces
RBC in fluid = phagocytosed = iron in macrophages
Decreased output causes decrease in renal perfusion
Activation of RAAS
Induces retention of salt and water
Expansion of interstitial and intravascular fluid volumes
What are the clinical signs of left sided heart failure?
Cough
Dyspnoea (initially in exertion, later at rest)
Orthopnoea
Paroxysmal noctural dyspnoea
What is systolic dysfunction?
Failure of the pump function
Decreased ejection fraction (less than 45%)
Destruction or dysfunction of cardiac myocytes
Ventricle inadequately emptied
Ventricular end-diastolic pressures and volume increases
Pressure transmitted to atrium then pulmonary vasculature
What is diastolic dysfunction?
Failure of the ventricle to adequately relax - stiff ventricle wall
Heart can’t increase output without demand
Any increase in pressure causes pulmonary oedema
What is right sided heart failure?
Most commonly caused by left sided heart failure
Increased pressure in pulmonary circulation burdens the right
Pure right sided heart failure is from lung disorders
What are the causes of right sided heart failure?
Parenchymal diseases of lung
Primary pulmonary hypertension
Recurrent pulmonary thromboembolism
Hypoxia
What is the incidence of hypertension?
35 years - 30%
45-54 years - 30%
Over 75 years - 70%
What are the different stages of hypertension?
Stage 1 - BP in surgery 140/90+
Stage 2 - BP in surgery 160/100+
Severe hypertension - BP in surgery 180/110+
What are the causes of hypertension?
Primary - essential hypertension (unknown 95%))
Secondary 5% Renal disease Endocrine (cushings, crohns, acromegaly, hyperparathyroidism) Coarction Pre-eclampsia Drugs and toxins
What are the long term consequences of hypertension?
Atherosclerosis Stroke MI Aneurysm Kidney disease Vascular dementia Eye damage
Define preload
Filling pressure, pressure in ventricle just before it starts to contract
Define afterload
Pressure at which the heart has to eject blood
What is Starlings Law?
Increase in preload leads to increased heart work and increased force of contract
Caused by increased cross linking of myofibrils in syncytium
What are the precipitants of heart failure?
acute ischaemia arrythmia AF, VT mechanical disaster intercurrent illness non-compliance PE Stress Drugs
What is chronic heart failure?
Cardiac dysfunction at rest
Symptoms of heart failure
Responds to treatment
