31 Flashcards
Cardiorespiratory
Epidemiology of ACS
Most common cause of death in the UK (1/5 men, 1/6 women).
More common in men.
Mortality equal in both sexes.
Increases with age.
Increased in South Asians.
Risk factors of ACS
Modifiable: smoking, diabetes, metabolic syndrome, hypertension, obesity, hyperlipidaemia, physical inactivity
Non-modifiable: male, increased age, FHx of premature CHD, premature menopause, south Asian
Definition of ACS
STEMI, NSTEMI and unstable angina
Symptoms of ACS
Central or epigastric chest pain, >15 minutes.
Radiates to arms, shoulders, neck or jaw.
- Sweating.
- Nausea and vomiting.
- Collapse/syncope.
- Dyspnoea.
- Fatigue.
- Palpitations.
Atypical presentation is seen in women, older men, diabetics and ethnic minorities - e.g. abdominal discomfort, jaw pain, altered mental state.
Signs of ACS
Tachycardia (sympathetic), Hypotension, Pallor, Sweating, Vomiting, Bradycardia (vagal), Pale, cool, clammy, Cold peripheries, 3rd heart sound, Oliguria, Narrow pulse pressure, Raised JVP, Lung crepitations.
Diagnostic criteria for MI
Detection of rise and/or fall of troponin and at least one of:
- Symptoms of ischaemia
- ECG changes
- Imaging evidence of new loss of myocardium or wall motion abnormality
Causes of MI
Atherosclerosis,
Infected cardiac valve,
Coronary occlusion secondary to vasculitis,
Coronary artery spasm.
Cocaine use.
Congenital coronary abnormality,
Coronary trauma,
Raised O2 requirement (hyperthyroid),
Decreased oxygen delivery (severe anaemia)
Investigations for ACS
Observations - stabilise
FBC - anaemia, CRP, ESR
U+Es - potassium and electrolytes
Lipid profile
Troponin
(can use CK-MB or myoglobin)
ECG (ST elevation, Q waves, T wave inversion)
ABG - high lactate and hypoxia
Echo for extent of infarction
Angiography
Myocardial perfusion scintigraphy (SPECT)
Cardiac enzymes
Troponin
- Increases within 3-12 hours from pain onset, peak at 48 hours, returns to baseline in 5-14 days
- Measure at presentation and 10-12 hours after onset
- T binds to tropomyosin, I binds to actin, C bind to calcium
Myocardial muscle creatine kinase (MB-CK) - Increase within 3-12 hours, peak at 24 hours, baseline within 3 days. Not as sensitive or specific.
Myoglobin - most sensitive early marker
Causes of raised troponin
ACS Congestive heart failure Sepsis PE CKD Myocarditis
ECG changes in anterior STEMI
Which artery is occluded?
LAD
V3-V4 (septal may be involved V1-V2)
Reciprocal ST depression in III and AVF
ECG changes in inferior STEMI
Which artery is occluded?
80% R coronary, 20% L circumflex
ST elevation, ST depression, T wave inversion, Q waves
II, III, aVF
ECG changes in lateral STEMI
Which artery is occluded?
V5-V6
1st diagonal branch of LAD or obtuse branch of L circumflex
Management for STEMI
- GTN
- Opioids
- 300mg aspirin
- Supplemental O2 if hypoxic
- PCI if able within 12 hours of onset
- Fibrinolysis if not - alteplase, reteplase or streptokinase.
Secondary prevention - ACEi, aspirin, 2nd anticoagulant (usually NOAC), beta blocker, statin.
Management of NSTEMI
- GTN
- Opioids
- 300mg aspirin
- Supplemental O2 if hypoxic
- Fondaparinux or unfractionated heparin within 24 hours
GRACE risk assessment
- Lowest risk - aspirin only (no angio)
- Low risk - aspirin + clopidogrel + consider angio
- High risk - aspirin + clopidogrel + urgent coronary angiography
Secondary prevention:
- ACEi
- Aspirin, + 2nd antiplatelet
- Beta blocker
- Statin
When is a coronary artery bypass graft (CABG) required?
Failed PCI (occlusion not amendable or refractory symptoms).
Cardiogenic shock.
Mechanical complications (rupture, mitral regurgitation).
Multivessel disease
What is the secondary prevention post ACS?
Aspirin +/- clopidogrel
Beta blocker
ACE inhibitor - check GFR and BP prior
Statin
Stop smoking, lower cholesterol, lower weight, increase exercise
Complications post-MI
Angina Re-infarct Heart failure Cardiogenic shock Valve dysfunction Cardiac rupture Arrhythmia
PE
Pericarditis
Depression
Epidemiology of angina
8% men, 3% women aged 55-64,
14% men, 8% women over 65
Increased in South Asian and Afro-Caribbean
Increasing age
Risk factors of angina
FHx Metabolic syndrome Smoking Diabetes Obesity Decreased exercise Hypertension Hyperlipidaemia Past CHD
Symptoms of angina
Constricting/heavy discomfort to the chest, jaw, neck, shoulders, or arms.
- Nausea
- Fatigue
- Dyspnoea
- Sweating
- Dizziness
“Stable angina:
- Symptoms brought on by exertion
- Relieved within 5min by rest or GTN
Unstable angina:
- Occurs even at rest
- May not be relieved by rest or GTN”
Different types of angina?
Stable - precipitated by predictable factors.
Unstable - symptoms occur at rest and occur at any time.
Refractory - symptoms cannot be controlled by medication.
Prinzmetal - occurs at rest and exhibits a circadian pattern - most episodes in the early hours of the morning.
Causes of angina
Atherosclerosis
Aortic stenosis
Hypertrophic
Obstructive cardiomyopathy
Hypertensive heart disease
Arrhythmias
Anaemia
Investigations for angina
12 lead ECG - LBBB, ST or T wave abnormalities (not NICE recommended)
FBC - rule out anaemia U+Es for renal function Fasting blood glucose LFTs Check TFTs Troponin
Echo
Exercise tolerance test
Estimate likelihood of coronary artery disease
- 90%+ treat as angina
- 61-90% - invasive coronary angiography
- 30-60% - non invasive functional testing for myocardial ischaemia
- 10-29% - CT calcium testing
Management of angina
Modify CV risk factors
Treatment should start before results
Advice - during attack - rest, use GTN (wait 5 mins), use up to 3 times, call 999
Beta blocker or calcium channel blocker
Add long acting nitrate e.g. nicorandil
Start aspirin
If diabetes + angina = ACEi
If symptomatic on 2 anti-angina meds then PCI or CABG
Differentials for chest pain
MI - NSTEMI or STEMI
Angina - stable or unstable
Prinzmetal angina
Acute pericarditis (constant pain, worse on inspiration, lying flat and movement)
PE
Pneumonia
MSK e.g. costochondritis
Aortic dissection
Gallstones
GORD
Prognosis of angina
1 in 10 will have MI within 1 year
Benign
Classification of angina
Canadian CV society functional classification
- No angina with ordinary activity, only strenuous
- Angina during ordinary activity e.g. walking up hill with mild limitations
- Angina with low level activity e.g. walking on flat, marked limitation
- Angina at rest or with any exercise
Identifying high risk ACS patients
QRISK2:
- Age, BP, smoking, diabetes, cholesterol, BMI, ethnicity, deprivation, FHx, CKD, RA, AF, diabetes, HTN
- If >10 start statin
- Number = % who will have CV event in 10 years
GRACE score:
Estimates 6 month mortality for those with ACS
TIMI score:
Likelihood of ischaemic event or mortality in UA or NSTEMI
Describe cardiac rehabilitation
Education, psychological support, exercise training and behavioural change
- Decreases morbidity and mortality
- NICE recommended
- Offer to all MI patients
- Only 40% uptake
- assess. reassure. educate. mobilise. discharge
- screen for anxiety/depression
- structured exercise and rehabilitation. graded exercise. aerobic low intensity.
- regular review of patients in primary care long term
What does a loud first heart sound (s1) suggest?
Hyperdynamic circulation
- Anaemia
- Pregnancy
- Hyperthyroidism
- Mitral stenosis
When would you hear a mid-systolic click?
Mitral valve prolapse
When would you hear an ejection systolic murmur?
Aortic stenosis
Pulmonary stenosis
Crescendo - decrescendo pattern
When would you hear a pansystolic murmur?
Mitral regurgitation
Ventricular septal defect
When would you hear an early diastolic murmur?
Aortic regurgitation
Pulmonary regurgitation
Soft blowing decrescendo pattern
Best hear when sitting forward in expiration
When would you hear a late diastolic murmur?
Mitral stenosis
Tricuspid stenosis
Associated with opening snap
Describe murmur associated with aortic stenosis?
Ejection systolic
Crescendo-descrescendo
Radiates into neck
Best heart at left sternal edge
Murmur of mitral regurgitation
Pansystolic Blowing Best heard at the apex Radiates to axilla best heard in left lateral position
Causes of mitral regurgitation
Rheumatic fever Degenerative calcification in elderly Congenital SLE RA Infective endocarditis
What happens to the heart with mitral stenosis?
Flow from LA to LV is restricted.
Left atrial pressure rises.
Pulmonary venous congestion (breathlessness) leading to pulmonary hypertension.
Dilation and hypertrophy of LA.
Can develop AF.
Exercise and pregnancy poorly tolerated as increase HR, shortens diastolic period with mitral valve open.
Presentation of mitral stenosis
Progressive breathlessness
Orthopnoea, PND, pulmonary oedema
Cough (pulmonary congestion)
Chest pain (pulmonary hypertension)
Oedema (right heart failure)
Fatigue (low cardiac output)
AF / Palpitations
Signs of mitral stenosis
Malar flush Raised JVP Right ventricular heave Laterally displaced apex beat Mid-late diastolic murmur best heard in left lateral position AF Signs of R heart failure - ascites, peripheral oedema Pulmonary oedema
Investigations and findings in mitral stenosis
CXR - LA enlarged, Kerley B lines (interstitial oedema)
ECG - AF, tall R waves in V1-3, may have bifid p waves
Echo - thickens immobile cusps
Doppler - increases pressure gradient across valve
Management of mitral stenosis
If asymptomatic - no intervention - yearly echos
- Diuretics or long acting nitrates (for dyspnoea)
- Beta blocker or calcium channel blocker
- Anticoagulation if AF
- If tachy, consider heart rate control
- Percutaneous mitral commissurotomy (valvotomy)
Epidemiology of heart failure
1-2% of adults.
Increased in men.
Increases with age.
Increasing prevalence with increasing survival post MI and secondary prevention.
RFs:
- HTN
- IHD
- Valvular disease
- Cardiomyopathy
- Diabetes
- FHx
- Smoking
- Endocarditis
- Glitazones
- Sleep apnoea
- Alcohol
- Congenital defects
- Arrhythmia
Symptoms of heart failure
Dyspnoea Fatigue Orthopnoea Paroxysmal nocturnal dyspnoea (PND) Nocturnal cough Pink frothy sputum Wheeze Nocturia Weight loss Muscle wasting Nausea Anorexia
Signs of heart failure
Peripheral oedema Raised JVP Cardiomegaly Murmur Crackles on lung auscultation Displaced apex R ventricular heave Hypotension Narrow pulse pressure Tachycardia Tachypnoea
Aetiology of heart failure
HYPERTENSION
Valvular disease (10%) 2y to myocardial disease - CHD, HTN, cardiomyopathy.
Drugs: beta blockers, calcium channel blockers, anti-arrhythmics, cytotoxic drugs.
Toxins: alcohol, cocaine.
Endocrine: diabetes, hypothyroid, hyperthyroid, Cushings, adrenal insufficiency.
Nutritional deficiency - thalamine, selenium
Infiltrative: amyloidosis, sarcoidosis.
High output failure - anaemia, pregnancy, hyperthyroid,
Paget’s.
AF
Pathophysiology of heart failure
Heart failure with reduced ejection fraction:
- Heart unable to pump blood which prevents filling with new blood
- SYSTOLIC FAILURE
- Long term cardiac remodelling leads to ventricular dilation
- Increases preload and end diastolic volume
- Dilation is a compensatory mechanism to decrease preload
- Severe dilation is maladaptive
Heart Failure with Normal Ejection Fraction:
- Heart unable to relax fully preventing blood from entering or exiting the heart
- DIASTOLIC FAILURE
- Increased afterload, usually due to increased BP
- Ventricular wall hypertrophy to try to decrease afterload
- Decreased ventricular size, decrease compliance, decrease cardiac output
Investigations for heart failure
If no MI:
- Measure serum BNP and pro-BNP (they are released when myocardium stressed)
- NT-proBNP commonly used
- If over 400 then refer to specialist and Doppler echo
If previous MI refer to specialist and Doppler echo
- CXR for cardiomegaly, prominent upper lobe vessels, bat winging, kerley B lines, pleural effusions
- Blood tests: FBC, U+Es, creatinine, LFTs, glucose, fasting lipids, troponin
- ECG: for heart block, AF, IHD
- ABGs: acidosis or hypoxia
Signs of heart failure on CXR
Cardiomegaly Prominent upper lobe vessels Bat winging (alveolar oedema) Kerley B lines (interstitial oedema) Pleural effusions
Management of heart failure
Lifestyle changes: smoking cessation, dietary changes, regular exercise, reduce alcohol
First line: diuretic + ACEi + beta blocker
Second line: ADD aldosterone antagonist OR ARB or hydralazine + nitrate
3rd line: digoxin or cardiac resynchronisation therapy
Classification of heart failure
New York Heart Association
Class 1: no symptoms on ordinary physical activity
Class 2: slight limitation of physical by symptoms
Class 3: less than ordinary activity leads to symptoms
Class 4: inability to carry out any activity without symptoms
Management of acute heart failure
- IV diuretics bolus or infusion
- IV nitrates of myocardial ischaemia
- Start beta blockers
- Offer ACEi
- Monitor renal function and electrolytes
- Ionatropes for short term acute decompensation
Epidemiology of asthma
Very common 1 in 11 children, 1 in 12 adults Commonly starts at 3-5 years More common in boys, but more common in women FHx of atopy Increased in developed countries
RFs
- Personal history of atopy
- Inner city environment
- Obesity
- Prematurity and low birth weight
- Viral infections in early childhood
- Smoking
- Maternal smoking
- Early exposure to broad spec antibiotics
PROTECTIVE factors: breast feeding, vaginal birth, farming environment
Symptoms of asthma
Breathlessness
Wheeze
Chest tightness
Cough
Symptoms worse at night or early morning
Symptoms in response to exercise, allergen exposure or cold air
Symptoms present after taking aspirin or beta blockers.
Signs of asthma
Widespread wheeze on auscultation
Low FEV1 or PEFR
Peripheral blood eosinophilia
Pathophysiology of asthma
Airflow limitations, airway hyper-responsiveness and bronchial inflammation
Type 1 hypersensitivity reaction
Triggers cause inflammatory cascade.
Early: type 1. Preformed mediator release 0-90 minutes
Late: types 2. Inflammatory cell recruitment and activation. Mast cells, eosinophils, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage.
Raised IgE
- Antigen detected by dendritic cell which presents it to TH1 and TH2 cells via IL12
- TH2 cells recruit mast cells, basophils and eosinophils
- Release of inflammation mediators e.g. histamine, prostaglandins, leukotrienes
- Bronchial hyperresponsiveness and airway obstruction
Triggers for asthma
Allergens: grass pollen, dander Occupational sensitizers Viral infections Cold air Emotion Irritants: dust, vapour, fumes, smoker Genetic factors Drugs: NSAIDs, beta blockers Atmospheric pollution
Aspirin sensitive asthma
Aspirin inhibits cyclooxygenase which leads to arachidonic acid metabolism through lipo oxygenase pathway producing cysteinyl leukotrienes.
Extrinsic vs intrinsic asthma
The main difference is the level of involvement of the immune system:
In extrinsic asthma, symptoms are triggered by an allergen (such as dust mites, pet dander, pollen, or mold).
In intrinsic asthma, IgE is usually only involved locally, within the airway passages.
Causative agents for occupational asthma
Isocyanates - paint sprayers
Flour - bakers
Colophony and fluxes - soldering and printers
Latex - medical
Animal - vets
Aldehydes
Wood dust - carpentry
Investigations in asthma
SPIROMETRY for diagnosis
FEV1>15% increase following bronchodilator or steroid trial or >20% diurnal variation on 3+ days/week for 2 weeks
Peak flow - unreliable in under 5s
Nocturnal dips or work related
Should be measured every 15-30 minutes in acute attack
Histamine or methacholine provocation or exercise or inhaled mannitol challenge
Measure allergic status using skin prick test for attopy
FBC: may have eosinophilia
Brittle asthma
Exacerbations occur with little or no warning
Classification of asthma severity
Mild: PEFR 75-100%
Moderate: PEFR 50-75%
Acute Severe: PEFR 33-50%, RR>25, HR >110, inability to complete sentence
Life threatening: PEFR <33%, Sats <92%
- Normal or raised PaCo2
- Silent chest
- Cyanosis
- Bradycardia/arrhythmias
- Hypotension
- Exhaustion
- Confusion
Near fatal:
- Raised pCO2 requiring mechanical ventilation with raised inflation pressure
Treatment of acute asthma
Mild:
- Use inhaler
- Wait 60 minutes
Moderate:
- ABG,
- Nebulised 5mg salbutamol
- High flow O2
- Prednisolone 40mg PO.
- Wait 30 minutes, if PEFR<60% or higher home
Acute severe:
- ABG
- Nebulised 5mg salbutamol 2-4 hourly
- High flow O2
- Prednisolone 40mg PO or 200mg IV
- IV access, K+ levels, ADMIT
- Consider continuous nebuliser
- Consider IV mag sulphate
- Correct fluids and electrolytes - watch K+, often hypokalaemic
On discharge (for all):
- Oral prednisolone 40mg PO for 5/7
- Start or double inhaled corticosteroids
Treatment of chronic asthma
- Salbutamol inhaler
- Inhaled corticosteroid
- Long acting B2 agonist (should never be used without steroid)
- Increased inhaled steroid to 2000mcg/day
- Leukotriene receptor antagonist
- Theophylline
- Oral B2 agonist - Oral steroid while maintaining inhaled steroids
Once controlled, steroids should be lowered to the lowest possible dose to maintain symptom control.
Asthma in pregnancy
1/3 worsen
1/3 stable
1/3 improve
Uncontrolled asthma is biggest risk to foetus
ABG finding in asthma
Respiratory alkalosis
Hypoxaemia or hypercapnia secondary to hyperventilation
Risk factors for cardiovascular disease
Smoking Increasing age Family history (1st degree male under 55, or female under 65) Obesity Hypertension High cholesterol Ethnicity - South Asian or African T2DM Alcohol Low socioeconomic background Male Stress
Stages of hypertension
1 - Clinic BP >140/90 and ambulatory blood pressure (ABPM) >135/90
2 - Clinic BP > 160/110 |AND ABPM >150/95
3 - Clinic BP > 180 systolic or >110 diastolic
Diagnosing hypertension
BP in both arms, if difference >20mmHg then repeat
If BP >140/90 measure twice, if different then take 3rd. Record LOWEST of last 2 BPs
If over 140/90 offer ABPM
If stage 3 - >180 or >110 then treat without ABPM
Test for organ damage - LV hypertrophy, CKD, hypertensive retinopathy and CV risk
Pheochromocytoma (neuroendocrine tumor of the medulla of the adrenal glands)
Labile or severe hypertension Headache Palpitations Pallor Diaphoresis
When should secondary hypertension be considered?
Under 40s
Low potassium and high sodium (adrenal disease)
Raised creatinine or low GFR (renal disease)
Proteinuria or haematuria
With labile or worsening HTN
Long term complications of hypertension
LV hypertrophy
Congestive cardiac failure (CCF)
CAD
Arrhythmias - AF
Microvascular disease
Increased risk of stroke and dementia
Hypertensive retinopathy
Hypertensive nephropathy
End stage renal disease
Glomerular injury
Causes of secondary hypertension
RENAL
- chronic pyelonephritis
- diabetic nephropathy
- glomerulonephritis
- PKD
- Obstructive nephropathy
- Renal cell carcinoma
VASCULAR
- Renal artery stenosis
- Coarctation of aorta
ENDOCRINE
- Primary hyperaldosteronism (low potassium, high bicarbonate, high sodium)
- Phaeochromocytoma
- Cushing’s syndrome
- Acromegaly
- Hypothyroidism
- Hyperthyroidism
DRUGS
- Alcohol misuse
- Cocaine
- ciclosporin, COCP, corticosteroids, EPO, leflunomide, NSAIDs, liquorice, sympathomimetics (cough and cold meds), venlafaxine
Coarctation of aorta
Upper limb hypertension.
Large difference between arms.
Absent or weak femoral pulse.
Radio-femoral delay.
Suprasternal murmur, radiating to back.
Management of hypertension
Aim for under 140/90 in under 80s, or 150/90 in over 80s
Lifestyle: smoking cessation, weight loss, low salt diet, reduce alcohol.
- ACE inhibitor, unless over 55 or Black race (if so use calcium channel blocker)
- ACEi or ARB + CCB
- Add thiazide like diuretic
(Monitor U+Es) - Add spironolactone
No ACEi in pregnancy or renovascular disease.
ACEi best for heart failure and Type 1 diabetes.
Assessing CV risk
QRISK3
Used up to 84 year olds.
Age, sex, ethnicity, postcode, smoking, diabetes, FHx, CKD, AF, RA, cholesterol, BMI, BP.
Diagnostic criteria for metabolic syndrome
Clustering of CV risk factors relating to insulin resistance
1 in 5 adults
Any 3 or more of the following:
- Increased weight, BMI or waist circumference
- Raised triglycerides
- Low HDL
- Hypertension
- Raised fasting plasma glucose
Define COPD
Chronic obstructive pulmonary disease
Airflow obstruction, not reversible.
Airflow limitation if progressive and encompasses bronchitis and emphysema
Epidemiology of COPD
Affects men and women equally
Increases with age
RF Smoking Occupational exposure to dust/chemicals Air pollution alpha 1 antitrypsin deficiency Low birth weight Childhood infections Maternal smoking Recurrent infections Low socioeconomic status
Symptoms of COPD
Exertional breathlessness Chronic cough Regular sputum production Frequent winter bronchitis Wheeze Weight loss Ankle swelling
Signs of COPD
Tachypnoea Dyspnoea Increased use of accessory muscles Asterixis Confusion Pursed lip breathing Peripheral oedema Cyanosis Wheeze Hyperinflation of chest Quiet vesicular breath sounds
Pathophysiology of COPD
Loss of elastic recoil and collapse of small airways on expiration.
Abnormal enlargement of air spaces distal to terminal wall.
Enlargement of goblet cells and increased numbers.
Pulmonary vascular remodelling.
Unopposed action of proteases and oxidants leading to destruction of alveoli.
Infiltration of walls with inflammatory cells - CD8+.
Expiratory airflow limitation and decreased recoil = VQ mismatch
Patients rely on hypoxic drive due to persistent raised pCO2
If rely on hypoxic drive = renal hypoxia = fluid retension and polycythaemia
Alpha1 antitrypsin is an antiprotease deactivated by smoking
Investigations for COPD
Spirometry
- FEV1/FVC <70%
- FEV1 <80%
Chest x-ray can be normal
- low flattened diaphragm
- large bullae
- vessels may be large proximally
Bloods
- Hb may be raised with raised PCV (polycythaemia)
ABGs
- Hypoxia and hypercapnia if severe
Sputum culture if ? infection
- Can test alpha 1 antitrypsin
- CT
Management of COPD
- Pneumococcal and influenza vaccinations
- Smoking cessation
- Regular assessment of lung function
- Short acting B2 (salbutamol)
- Long acting B2 (salmetrol)
- Antimuscarinic (ipratropium)
- Add theophylline/phosphodiesterase inhibitor (moneleukast)
- Inhaled corticosteroid (never without long acting B2)
- Pulmonary rehab
- Home oxygen
Can add carbocysteine (antimucolytic)
If acute
- O2 where tolerated
- Removal of secretions
- Respiratory support
- Corticosteroids
- Antibiotics
Complications of COPD
Chronic hypoxia Cor pulmonale from pulmonary hypertension Pneumothorax Respiratory failure Arrhythmias - AF Infection Secondary polycythaemia
MRC dyspnoea grading
0 - only breathless on regular exercise.
1 - SOB on slight incline or hurried on flat.
2 - walks slower than others or has to stop.
3 - stops after 100m or few minutes on level.
4 - too breathless to leave the house or get dressed.
Classifying severity of COPD
GOLD or BODE index
BODE uses FEV1, GOLD FEV1/FVC
GOLD 1 - mild FEV1/FVC <70% but FEV1>80% 2 - moderate FEV1/FVC 50-79% 3 - severe FEV1/FVC 30-50% 4 - very severe FEV1<30% or respiratory failure
BODE 1 - mild FEV1>80% but symptomatic 2 - moderate FEV1 50-79% 3 - severe 30-49% 4 - <30% or respiratory failure
Factors that can destabilise heart failure patient
Ischaemia Hypertension Rapid AF Medication initiation Alcohol abuse Non-adherence Active infection PE Anaemia Hyperthyroidis
Assessing end organ damage from HTN
Urinalysis FBC (Hb and Hct) U+Es Fasting glucose Cholestrol work up ECG CXR
Signs of LV dysfunction
Hypotension Soft S1 S3 gallop Decreased volume carotid pulse LV apical enlargement Pulmonary congestion (rales) Mitral regurg
High risk patients with HTN
Older age Diabetes Renal disease LV hypertrophy Vascular disease CHD Cerebrovascular disease
Aim for 130/80 vs 140/90
Define bronchiectasis
Permanent dilation and thickening of airways characterised by chronic cough, excessive sputum production, bacterial colonisation and recurrent acute infections.
Classification of bronchiectasis
More than 1 type can be present in the same patient.
- Cylindrical: bronchi are enlarged and cylindrical (signet appearance of bronchi)
- Varicose: bronchi are irregular with areas of dilation and constriction.
- Saccular or cystic: dilated bronchi form clusters of cysts. Most severe form (often in CF patients).
Degree of bronchial dilation increased from proximal to distal.
Epidemiology of bronchiectasis
More common in women
Increases in age
3 per 1000
Increase in pacific nationality
RFs Cystic fibrosis Immunodeficiency PHx of infections Alpha 1 antitrypsin deficiency Connective tissue disorder Primary ciliary dyskinesia IBD Aspiration or inhalation injury Congenital disorder of bronchial airways
Aetiology of bronchiectasis
Caused by chronic inflammation
42% develop post-infection
No identifiable cause in up to 50%
Post infection - childhood viral infection (measles, pertussis, influenza), TB, bacterial pneumonia
Immunodeficiency e.g. HIV
Connective tissue disease - RA, Sjorgen’s, systemic sclerosis, SLE, Ehler’s Danlos syndrome, Marfan’s
Congenital defects - CF, primary ciliary dyskinesia, alpha 1 antitrypsin deficiency
Asthma Allergic bronchopulmonary aspergillosis Gastric aspirations Bronchial obstruction by lymphadenopathy, tumour or inhaled foreign body IBD
Pathophysiology of bronchiectasis
- Persistent airway inflammation
- Development of bronchial wall oedema and increased mucus production
- Recruitment of inflammatory cells
- Release of inflammatory cytokines, proteases and reactive oxygen mediators
- progressive destruction of airways
Vicious cycle - insult by primary infection, increased inflammation, bronchial damage, increase capacity for colonisation of airways
Symptoms of bronchiectasis
Vary from intermittent episodes of expectoration to persistent daily expectoration of large volumes of purulent sputum.
Dyspnoea Chest pain Haemoptysis Wheezing Cough Rhinosinusitis
Signs of bronchiectasis
Coarse crackles - early in inspiration and in lower zones.
Large airway rhonchi
Wheeze
Fever
Clubbing
When should bronchiectasis be considered
Persistent productive cough AND ONE OF:
- Young age at presentation
- Hx of symptoms spanning years
- Absence of smoking history
- Daily expectoration of large volumes of sputum
- Haemoptysis
- Colonisation of P. aeuroginosa
- Unexplained haemoptysis
Investigations for bronchiectasis
CXR - baseline in all patients, 90% are abnormal. Ring or tubular opacities, tramlines, fluid levels
HRCT - high resolution CT is GOLD STANDARD
- Bronchial wall dilation
- Bronchial wall thickening
Sputum microbiology
FBC - raised WCC or polycythaemia
Immune function testing
CF in all under 40 - CFTR genetic mutation analysis or sweat chloride
Lung function tests - FEV1, FVC, peak flow (annual repeat)
Tests for CF
CFTR genetic mutation analysis
Sweat chloride
Management of bronchiectasis
Smoking cessation
Immunisation against influenza and pneumococcus
Healthy diet and physical exercise
Physiotherapy - airway clearing techniques with or without sterile water
Antibiotics (in acute exacerbations) - amoxicillin or clarithromycin - send of sputum and culture
If more than 3 exacerbations per year requiring antibiotics then long term antibiotics (azithromycin)
Beta 1 agonists and anticholinergic bronchodilators (theophylline and aminophylline)
No steroids. No mucolytics.
Oxygen
Surgery - lung resection if not controlled by medical treatment.
Complications of bronchiectasis
Repeated infection Decreased lung function Empyema Lung abscess Pneuomothorax Life threatening haemoptysis Respiratory failure Cor pulmonale Decreased quality of life
Normal pH
7.35-7.45
Base excess
-2 to +2
Positive numbers = alkalotic
Negative number - acidosis
ABG findings and causes of respiratory acidosis
Low pH < 7.35
Raised pCO2
Normal bicarbonate (if no compensation)
Raised bicarbonate (if compensated)
- COPD, late stage asthma
- Respiratory depression
- Sleep disordered breathing
- Neuromuscular disorders
- Increased CO2 production: seizures, hyperthermia
ABG findings and causes of respiratory alkalosis
High pH > 7.45
Low CO2
Low bicarbonate (if compensating)
Breathing off too much CO2
- Fever
- Sepsis
- Anxiety
- Aspirin poisoning
- Pulmonary oedema
- Pneumonia
- Profound anaemia
- Pleural effusion
- PE
- Hyperthyroidism
ABG findings and causes of metabolic acidosis
Low pH < 7.35
Low bicarbonate
Low CO2 (if compensating)
- DKA
- Sepsis
- Renal failure
- Tissue ischaemia
- GI loss of bicarbonate (diarrhoea)
- Renal tubular disease
- Uraemia
ABG findings and causes of metabolic alkalosis
High pH
Raised bicarbonate
High CO2 if compensating
- GI loss of H+ (vomiting)
- Renal loss of H+ (loop/thiazide diuretics)
- Hypovolaemia
What would ACE inhibitors do to BNP?
B-type natriuretic peptide is released by LV in response to ventricular strain
ACE inhibitors are used to treat heart failure and would decrease the amount of BNP produced.
Effects of BNP?
- Vasodilator
- Diuretic and natriuretic
- Suppresses both sympathetic tone and the RAAS
Which one of the following types of beta-blocker is the most lipid soluble?
Bisoprolol Atenolol Propranolol Carvedilol Sotalol
Propranolol
Lipid-soluble are more likely to cause side-effects such as sleep disturbance by crossing BBB
Type 1 respiratory failure and causes
Hypoxaemic respiratory failure
Low O2 with normal or low CO2
- High altitude
- Pulmonary embolism
- Neuromuscular disease
- Pneumonia
- Acute respiratory distress syndrome (ARDS)
- Cyanotic congenital heart disease (right to left shunt)
Type 2 respiratory failure and causes
Hypercapnic respiratory failure
High pCO2 and low O2
- COPD
- Asthma
- Drug OD
- Extreme obesity
- Myasthenia gravis
- Polyneuropathy
- Polio
- Motor neuron disease
- Guillain-Barre syndrome
- Pulmonary oedema
- Acute respiratory distress syndrome (ARDS)
- Kyphoscoliosis
Non-respiratory causes of respiratory failure
- Hypovolaemia
- Shock (septic or cardiogenic)
- Severe anaemia
- Drug OD
- Neuromuscular disease
- Spinal/head injury
Signs and symptoms of respiratory failure
- Dyspnoea
- Confusion
- Tachypnoea
- Cyanosis
- Stridor
- Accessory muscle use
- Anxiety
- Headache
- Retraction of intercostal spaces
- Hypoventilation
- Polycythaemia (chronic)
- Cor pulmonale
- Cardiac arrhythmia
Investigations in respiratory failure
Pulse Oximetry ABGs ECG D-dimer for PE CXR Pulmonary function tests LFTs and U&Es TFTs Echo
Management of respiratory failure
ABCDE
- Supplemental o2 to sats >90%
- Treat underlying cause
- BiPap
- Intubation and mechanical ventilation - RSI
- Bronchodilators, corticosteroids, antibiotics, opioids
Target O2 saturations
94-98%
For COPD 88-92%
Indications for humidifying oxygen prior to delivery
Flow rate > 4l/min for several days Tracheostomy CF Bronchiectasis Chest infection training secretions
Risk factors for community acquired pneumonia
Extremes of age Smoking Alcohol Previous recent viral illness (predisposes to strep pneumonia) Asthma COPD (increased H. influenza or morexella) Malignancy Bronchiectasis CF Immunosuppression - AIDS, chemo etc. (increased gram negatives, S.aureus or P.jiroveccii) IV drug use (S. aureus) Diabetes CV disease Nursing home (H. influenza)
Decreased consciousness, neurological disease = aspiration
Signs and symptoms of pneumonia
Productive cough Purulent sputum Breathlessness Fever Malaise
Focal chest signs Increased temperature Tachypnoea. Tachycardia. Bronchial breathing + crepitations Dullness on percussion pleural rub Pleuritic chest pain
Confusion, myalgia, anorexia, fatigue (in elderly)
Non-specific symptoms + abdo pain (children)
Typical pathogens for CAP
- Streptococcus pneumonia (66%)
- Haemophilus influenzae
- Klebsiella pneumonia
- Staphylococcus aureus
Streptococcus pneumonia
Gram positive
Diplococci
Common in winter
Common in creasing age, comorbidities, CV disease, a
Haemophilus influenzae
Gram positive
Coccobacillus
Klebsiella pneumoniae
Gram negative
bacillus
More common in men - can cause decreased platelets and leukopenia
Staph aureus
Gram positive
Coccus
More common after influenza like illness
Atypical pathogens for CAP
Mycoplasma pneumonia
- More common in young patients or prior antibiotics
- Slower onset, neurological complications, dry cough
Chlamydia pneumoniae
- Initial upper RTI leading to bronchitic or pneumonitic features
- Cough with scanty sputum
- Hoarseness, headache
Legionella pneumoniae
- Sever infection
- Water sources in Mediterranean
- Abnormal LFTs, raised CK
- Mild headache, myalgia, chills, rigors, haemoptysis, GI upset
Pneumocysitic jirovecci
- only in immunocompromised
Investigations for CAP
FBC - Raised WCC
Raised CRP
LFTs (decreased albumin)
U&Es - if high urea then poor prognosis
Blood cultures
Urinary antigen tests - legionella or pneumococcus (c-polysaccharide)
CXR
- Consolidation. May have effusions or collapse
Sputum examination and culture
Pulse oximetry or ABGs
Aspiration of pleural fluid for culture
Severity of CAP
CURB65 Confusion Urea >7 Respiratory rate >30 BP < 90 (systolic) Age over 65 All worth one point
0 or 1 - LOW
2 = moderate
3 = severe
Management of CAP
Smoking cessation
Oxygen for hypoxia
Fluids for dehydration
Analgesics - care with opiates RE respiratory depression
LOW (CURB 0 or 1)
- Treat at home
- 5 day course oral amoxicillin
- If penicillin allergic = clarithromycin or doxycycline
MODERATE (CURB 2)
- Hospital
- Amoxicillin and clarithromycin
Severe (CURB 3+)
- Co-amoxiclav and clarithromycin IV
- Add levofloxacin if ? legionella
- ? ITU admission
Complications of CAP
Pleural effusion Empyema Lung abscess pneumothorax DVT Bronchiectasis AKI Sepsis - pericarditis, endocarditis, osteomyelitis, meningitis
Define hospital acquired pneumonia
New radiographic infiltrate in presence of infection with onset 48 hours after admission
RF for hospital acquired pneumonia
Over 70 Chronic lung disease Comorbidities Decreased consciousness Chest or abdominal surgery Mechanical ventilation NG feeding PHx of antibiotic exposure Poor dental hygiene Steroids Chemotherapy
Causes of hospital acquired pneumonia (bacteria)
Gram negative enteric bacilli and pseudomonas
- Pseudomonas aeruginosa - intubation
- E. Coli
- Klebsiella
Strep pneumonia and H. influenza
Staph aureus - neurosurgery patients and trauma
Anaerobes e.g. enterobacter after abdo surgery
Antibiotics used in hospital acquired pneumonia
Co-amoxiclav Ceftriaxone Tazocin Carbapenem Gentamicin
Define pleural effusion
Increase in fluid volume between visceral and parietal pleura
Types of pleural effusion
Benign (more common) or malignant
Transudate - disruption of hydrostatic and oncotic forces operating across pleural membranes
LOW PROTEIN <30
Exudate - increased permeability of pleural surface - usually due to inflammation
HIGH PROTEIN >30
Causes of transudate pleural effusions
Heart failure Cirrhosis Hypoalbuminaemia Peritoneal dialysis Atelectasis Hypothyroidism Nephrotic syndrome Mitral stenosis PE SVC obstruction Constrictive pericarditis Ovarian Hyperstimulation Meigs syndrome - benign ovarian tumour, ascites, pleural effusion
Meig’s syndrome
TRIAD
Pleural effusion
Ascites
Benign ovarian tumour
Causes of exudate pleural effusion
Pneumonia Malignancy Pulmonary infarction PE Autoimmune - RA Asbestos exposure Pancreatitis TB Complication of acute MI (Dressler's syndrome) Drugs - methotrexate, Amiodarone, nitrofurantoin
Signs and symptoms of pleural effusion
SOB Cough Dyspnoea Pleuritic pain Dullness on percussion Decreased breath sounds Decreased chest expansion Decreased tactile and vocal fremitus
Investigations for pleural effusion
CXR
- Blunting of costophrenic angles
- 200ml needed to see PA, 50ml on lateral
Thoracocentesis/pleural aspiration
- Only if exudate
- Cytology, protein, LDH, pH, gram stain, culture and sensitivity, lipids, amylase (pancreatitis)
- Not if bilateral
ESR CRP Albumin Amylase TFTs Blood cultures D-Dimer CT
CT of thorax +/- abdomen
Pleural biopsy
Thoracoscopy/Bronchoscopy
Causes for bloody thoracocentesis
Malignancy PE Infraction Trauma benign asbestos Post cardiac injury syndrome
Causes for low pH or glucose in thoracocentesis
Infection and empyema RA SLE TB Malignancy Oesophageal rupture
Management of pleural effusion
Aimed at treating underlying cause
If small then observe
If large the tapping fluid can give symptomatic relief and is useful for diagnosis but recurrence common
DO NOT DRAIN MORE THAN 1.5L in one go
Chest drain (Can use long term indwelling pleural draining in malignant effusions)
Pleurodesis - injection of sclerosing agent to cause pleural adhesion and prevent recurrence - sterile talc, tetracycline, bleomycin
Pleurectomy if all other options failed
Indications for a chest drain
Pneumothorax Traumatic pneumothorax Pleural effusion Hemopneumothorax Peri-operative - oesophageal or cardiothoracic surgery
Safe triangle for chest drain insertion
Between
- Lateral edge of pec major
- Base of axilla
- Lateral edge of lat dorsi
- Above 5th IC space
If apical pneumothorax - 2nd intercostal space
Process of chest drain
Patient lying at 45 degrees. arms raised.
Local anaesthetic
Thoracostomy or seldinger technique used to insert tube
Insert into safe triangle
Aspirate fluid and/or air
Open incision with blunt dissection of deep tissue
Connect drainage system
DO NOT REMOVE MORE THAN 1.5L
Suture to skin
CXR to confirm placement
Complications of chest drain
Incorrect placement
Injury to intercostal muscles
Perforation of other vessels
Pain
Define pneumothorax
- Collection of air in the pleural cavity resulting in the collapse of the lung on the affected side
- Extent of collapse depends on amount of air
Types of pneumothorax
Primary spontaneous Secondary spontaneous Traumatic Iatrogenic Catamenial Tension
Primary spontaneous pneumothorax
Occurs in healthy people Increased in: Tall, thin and healthy Male Marfan's Pregnancy Smokers
Occurs from ruptures of blebs and bullae
Secondary spontaneous pneumothorax
Associated with underlying lung disease
Consequences are greater and management more difficult
Associated with: Smoking COPD Asthma HIV TB Sarcoidosis CF Cancer Idiopathic pulmonary fibrosis Ehler's Danlos syndrome RA Marfan's FHX Ankylosing spondylitis
Iatrogenic pneumothorax
Following certain medical procedures
- Lung biopsy
- Transthoracic needle aspiration
- Thoracocentesis
- Central line insertion
- Intercostal nerve block
- Tracheostomy
- APR
- NG tube placement
Catamenial pneumothorax
At time of menstruation
- 30-40 years old with pelvic endometriosis
- 90% in R lung and within 72 hours of onset of menstruation
Tension pneumothorax
MEDICAL EMERGENCY
Occurs in: ventilated patients, trauma, CPR, lung disease, blocked or clamped chest drain, hyperbaric oxygen treatment
- Usually follows penetrating chest trauma
- Stabbing/gun shot/fractured rib
Signs and symptoms of pneumothorax
Sudden onset pain - stabbing, radiating to shoulder, increased on inspiration
SOB - depends on size
Cyanosis
Distressed
Sweating
Decreased breath sounds or absent over affected area
Hyper resonance
Trachea deviates AWAY from pneumothorax
Symptoms can be minimal in primary
Tension:
- Hypotension
- Raised JVP
- Tachycardia
- Pulsus paradoxicus (pulse slows on inspiration)
Pathophysiology of pneumothorax
In normal respiration, pleural space has negative pressure
As chest wall expands, surface tension of pleura expands lung outwards
If pleural space invaded by gas then llung collapses until equilibrium is achieved or rupture sealed
Decreased vital capacity
Decreases PaO2
Tension
- Injured tissue forms one way valve
- Air allowed in but not out
- Increases pressure, lung collapses and hypoxia
- Decreased venous return to heart
- Respiratory insufficiency, CV collapse and death
Investigations for pneumothorax
CXR
- Lung edge and absent lung markings peripherally
- Blunting of ipsilateral costophrenic angle
- Width of rim of air is used to classify size
(Small <2cm, Large >2cm) 2cm= 50% of lung volume
US
Chest CT in complicated or uncertain cases
ABGs - hypoxia more disturbed in secondary
Occasionally hypercapnia
Management of pneumothorax
Is tension pneumothorax suspected? - YES then immediate needle decompression followed by chest drain insertion
PRIMARY
- Depth less than 2 cm - discharge and follow up
- > 2 cm aspirate. In then under 2 cm with clinical improvement then discharge and follow up
- If no improvement then Admit and fit chest drain
SECONDARY
- > 2 cm or SOB - admit and fit chest drain
- Depth 1-2 cm - aspirate, if <1 cm then admit, high flow O2 and observe, if >1 cm then admit and fit chest drain
- If <1 cm then admit, high flow O2 and observe
Aspirate = thoracocentesis
- 2nd or 3rd intercostal space, midclavicular line
- OR 4th or 5th intercostal space over superior rib margin in anterior axillary line
- Enter just above a rib
Pleurodesis if risk high
Surgery
- If persistent air leak or failure of lung to expand
Open thoracotomy and pleurectomy
OR VATS - video assisted thoracoscopic surgery and pleurectomy is better tolerated but higher recurrence
Surgical emphysema
subcutaneous emphysema
- Occurs as air tracks below skin under pressure from pleural space
- Results from large air leaks or blocked chest drain
Harmless
treat with high flow oxygen
Risk factors for PE
- Major abdo/pelvic surgery
- Post-op ITU
- Late pregnancy
- Malignancy
- Fractures
- C-section
- Varicose vein surgery
- Decreased mobility
- Hospitalisation
- Spinal cord injury
- IV drug use
- Major trauma
- Central venous lines
MINOR: - congenital heart disease - congestive heart failure = hypertension - COCP - Stroke - myeloproliferative disorders - thrombotic disorders - HRT - COPD - Sedentary travel - Obesity - IBD
Virchow’s triad
Venous stasis
Vessel wall damage
Hypercoagulability
Pathophysiology of PE
Virchow’s triad:
- Venous stasis
- Vessel wall damage
- Hypercoagulability
- Endothelial damage promotes thrombus formation, usually at valves.
- Poor blood flow and stasis also promotes thrombus formation.
- Thrombus forms and dislodges, becomes trapped in pulmonary vasculature.
- Obstruction increased pulmonary resistance
Increased work of right ventricle. - R ventricle over distension, increased end diastolic pressure and decreased output.
Symptoms of PE
Dyspnoea Pleuritic pain Cough Haemoptysis Dizziness Syncope Any chest symptoms with signs of DVT
Signs of PE
Tachypnoea Tachycardia Hypoxia Pyrexia Raised JVP Pleural rub Hypotension Cardiogenic shock Gallop heart rhythm
Investigations for PE
Wells PE Score
- If more than 4 points then likely then CTPA
- If 4 or less points then unlikely - D-dimer, if positive then CTPA
CTPA first line
Baseline investigations -
- O2 sats
- FBC, U&Es, clotting, troponin
ECG
- S1Q3T3 deep s waves in I, Q waves in III, inverted T waves in III
- Right axis deviation
- RBBB
- Right ventricular strain
- Sinus tachycardia
- AF
CXR - usually normally, may have decreased vascular markings
Late sign = Hampton’s hump
ABGs = low PaO2, low PaCO2 if hyperventilation
D-dimer - raised in VTE, not specific
Leg US - if suspected DVT
If no cause found - need to investigate for an undiagnosed cancer
Wells PE Score
Suspected DVT - 3
Alternative diagnosis less likely than PE - 3
Tachycardia - 1.5
Immobilisation >3 days or surgery in last 4 weeks - 1.5
Hx of DVT or PE - 1
Haemoptysis - 1
Malignancy - 1
If 4 points or less UNLIKELY (D-dimer)
If OVER 4 points LIKELY (CTPA)
Management of a PE
Resuscitation - oxygen, IV access, analgesia
Anticoagulation:
- LMWH, fondaparinux ASAP unless renal impairment, significant bleeding risk or haemodynamic instability
- Continue for 5 days
- Warfarin or rivaroxaban once confirmed within 24 hours and continue for 3 months
- Only thrombolysis with alteplase if hypotensive
If not suitable for anticoagulation - IVC filters.
Surgical embolectomy if high risk or failed or contraindicated thrombolysis.
Signs/symptoms of DVT
Limb pain and tenderness along line of deep veins
Unilateral swelling of calf or thigh
Pitting oedema
Distension of superficial veins
Increased skin temperature
Skin discolouration (red)
Palpable cord - hard thickened, palpable vein
Investigations of DVT
Wells score for DVT
Likely 2 or more
Unlikely <2
Likely = Proximal leg vein US
Positive = DVT
Negative D-dimer
Unlikely = D-dimer
If positive then proximal leg vein US
CT/MRI venography Contrast venogram (old gold standard)
If no diagnosis of cancer and first DVT over 40 - CT abdo and chest + mammogram
Wells score for DVT
Likely 2 or more
Unlikely <2
Active cancer - 1 Paralysis or immobilisation - 1 Recently bedridden - 1 Localised tenderness in leg veins - 1 Entire leg swelling - 1 Calf swelling >3cm - 1 Unilateral pitting oedema - 1 Previous DVT - 1 Collateral superficial vein - 1
If alternative cause at least as likely - MINUS 2
Management of DVT
Anticoagulation
- LMWH, fondaparinux ASAP unless renal impairment, significant bleeding risk or haemodynamic instability
- Continue for 5 days
- Warfarin or rivaroxiban once confirmed within 24 hours and continue for 3 months
- Only thrombolysis with alteplase if hypotensive
If not suitable for anticoagulation - IVC filters
Consider extending anticoagulant >3m if high risk of recurrence and no increased bleeding risk
Below knee compression stockings after swelling gone down or 1 week
Post-thrombotic syndrome
Post-thrombotic syndrome (in 20-40%):
- Chronic venous hypertension
- Pain
- Swelling
- Hyperpigmentation
- Dermatitis
- Ulcers
- Gangrene
DVT prophylaxis
High risk patients -0
- GA with surgery > 90 minutes
- Acute surgical admission
- Decreased mobility
- 1 or more risk factors for DVT/PE
- Avoid dehydration
- Early mobilisation
- Graduated compression stockings
- Intermittent pneumatic compression devices
LMWH/Fondaparinux/Unfractionated heparin (if CKD)
Macule
Completely flat lesion
Smooth small area of colour change <1.5cm
Papule
Discrete raised palpable lesion <1cm
Nodule
Discrete raised palpable lesion >1cm
Pustule
Small raised lesion filled with purulent fluid
Plaque
Raised area of skin with flat top and clear edge
Circumscribed, superficial, elevated plateau 1-2cm
Lichenification
Hard thickening of skin with accentuated skin markings
Results from inflammation or rubbing
Vesicles
Small superficial circumscribed containing serous fluid < 0.5cm
Bulla
Large superficial circumscribed containing serous fluid > 0.5cm
Wheal
Transient circumscribed elevated papules or plaques with erythematous borders and pale centres
FEV1
Volume of air the patient is able to exhale in the first second of forced expiration
FVC
Forced vital capacity
Total volume of air a patient can forcibly exhale in 1 breath
FVC and FEV1 in
Obstructive lung disease FEV1<80% FEV1/FVC <70%% 294 FVC and FEV1 in Restrictive lung disease FEV1<80% FVC<80% FEV1/FVC>70%
Define TB
Notifiable disease
Chronic granulomatous disease caused by Mycobacterium tuberculosis
It is spread via inhalation of infected droplets
Epidemiology of TB
14 per 100,000
Increased in ethnic minorities
Increased in elderly
Increased in Non UK born population
RDs
- Healthcare worker
- Alcoholic
- Close contact of TB patient
- Homeless / poor housing / over crowding
- Poverty
- Drug use
- Malnutrition
- Prison
- Immunocompromised
- HIV (60% have TB)
- Haematological cancers
- Diabetes
- long term steroids
- Silicosis
Aetiology of TB
Causes by mycobacterium tuberculosis
Can be:
- Multi-drug resistant: resistant to more than 1 drug
- Extensively drug resistant: resistant to more than 3 drugs
Pathophysiology of TB
- Primary infection host macrophages in lung engulf organisms and carry to hilar lymph nodes which forms GHON FOCUS
- Some organisms disseminate via lymph nodes to distant sites
- Small granulomas are formed around the body to contain the bacteria
- 80% heal spontaneously and bacteria are eliminated
- OR bacterial remain encapsulated in defensive barrier but persist
- DORMANT DISEASE
Secondary TB - activation of dormant disease
usually preceded by immunosuppression, malnutrition, aids.
Reactivation usually occurs in APEX of lungs and can spread
Miliary TB
When primary infection is not adequately contained it enters the bloodstream and causes severe disease
Presentation of TB
Most cases occur from latent infection from previous exposure
Onset is insidious
1y infection - asymptomatic
2y infection is variable and non-specific
TB can affect all organs and body systems
- General symptoms: fatigue, weight loss, anorexia, pyrexia
- Pulmonary symptoms: chronic productive cough +/- haemoptysis, lobar collapse, bronchiectasis, pleural effusion, pneumonia, pneumothorax
- GU: most common site outside of lung. infertility, pyuria, swelling of epididymis
- MSK: pain, arthritis, osteomyelitis, nerve compression
- CNS: meningitis
- GI: ileocecal regions: abdo pain, bloating, obstruction
- Lymph nodes: tender, firm, discrete
- Skin
- pericardial effusion
Investigations for TB
CXR (even if no pulmonary symptoms)
- Primary: central apical portion + lower lobe infiltrate or effusion
- Severe = millet seeds
- patchy nodular shadows
- upper zones
- Loss of volume
- fibrosis +/- cavitation
Microbiology - 3 sputum samples for culture
- Analysed using Ziehl-Neelson stain to test for acid/alcohol fast bacteria
- 4-8 weeks for culture as slow growth
lab tests for HIV, Hep B and C
FBC, U&Es, CRP, ESR, U&Es
What is the Ziehl-Neelson stain used for?
TB
Screening and vaccination for TB
Mantoux test or IGRA (interferon gamma release assay)
If had vaccine: Mantoux +, IGRA -
If have TB - Mantoux +, IGRA +
If no vaccine, no TB - Mantoux -, IGRA -
Mantoux measures response to tuberculin - <5mm is negative, 5-10mm is positive, 10-15mm is strongly positive
For contact screening use Mantoux
Management of TB
Notify public health
Most managed as outpatients but some need admitting to monitor drug adherence.
Well ventilated single room, away from immunocompromised
- 6 months, 4 drugs
- Isoniazide, rifampicin
- Ethambutol and pyrazinamide (only for first 2 months)
- If meningeal then 12 months with 2-3 weeks of steroids
- Regularly check LFTs due to drug toxicity
- Avoid ethambutol in renal failure
- Compliance is a large problem
Fibroepithelial polyps
Skin tags/acrochordons
- small pedunculated skin coloured papules
occur most frequently with skin folds
- 0.2-0.5mm
Causes of lung fibrosis in upper zones
TB Extrinsic allergic alveolitis Coal workers pneumoconiosis Silicosis Sarcoidosis Ankylosing spondylitis Histocytosis
Causes of lung fibrosis in lower zones
- Bleomycin
- Idiopathic pulmonary fibrosis
- Connective tissue disorder
- Drug induced: methotrexate, amiodarone
- Asbestosis
Epidemiology of aortic stenosis
Most common valve disease
2-7% of population over 65, 10% over 80s
Can be congenital
Aged 30-60 in rheumatic disease, 50-60 with bicuspid valves, 70-90 with calcific changes
Aetiology of aortic stenosis
Congenital aortic stenosis
Congenitally bicuspid valve
Rheumatic disease
Degenerative - calcified
Pathophysiology of aortic stenosis
- Cardiac output is maintained at the expense of steadily increasing gradient.
- LV becomes hypertrophied and coronary blood flow may then become inadequate.
- Fixed outflow obstruction limits and increase in cardiac output with exercise .
- Eventually LV cannot overcome obstruction and pulmonary oedema occurs.
Presentation of aortic stenosis
Tend to be asymptomatic for years and deteriorate rapidly
SOB on exertion Angina Dizziness Syncope (on exertion) Predisposition to angina - 50% have coronary artery disease Risk of sudden death so avoid exertion
TRIAD - chest pain, heart failure and syncope
Episodes of acute pulmonary oedema
Signs of aortic stenosis
Ejection systolic murmur Radiates to carotids Most commonly heard in aortic area Slow rising pulse - pulsus parvus et tardus Narrow pulse pressure Thrills 4th heart sound if severe Thrusting apex beat from LV pressure overload Crepitations from pulmonary oedema
Investigations for aortic stenosis
ECG: LVH and LBBB
Left ventricular strain pattern, down slowing ST segments, ST depression, T wave inversion
CXR - may be normal
Cardiomegaly, enlarged LV and dilated ascending aorta
Echo: calcified valve with restricted opening, hypertrophied LV
Doppler to measure degree of stenosis
Cardiac catheterisation - identify coronary artery disease and measure gradient across the valve
No exercise testing unless they are asymptomatic
CT and cardiac resonance imaging for quantifying calcification and used in prognosis
Management of aortic stenosis
Avoid heavy exertion
Early surgical intervention as no medical management can improve outcome
- Statins
- Modify atherosclerotic risk factors
- Digoxin, diuretics and ACEi if awaiting or not suitable for surgery
- Manage hypertension and maintain sinus rhythm
- If severe, monitor every 6 months and echo, mild-moderate review yearly
Aortic valve replacement
- Definitive therapy, mortality 1-3%,
Transcatheter aortic valve implantation
- Under general or local
- Balloon valvuloplasty followed by insertion of specialised valve device
- Fluoroscopy guided
Complications of aortic stenosis
LV dysfunction Heart failure Infective endocarditis Small systemic emboli Sudden death
Epidemiology of aortic regurgitatoin
Most commonly caused by rheumatic disease
Peak age 40-60
2%
RFs Marfan's SLE Ehler's Danlos syndrome Turners Ankylosing spondylitis Reactive arthritis Takayasu's disease Behcet's disease Acute severe follows infective endocarditis or aortic dissection
Aetiology of aortic regurgitation
- Rheumatic disease
- Bicuspid aortic valve
- Infective endocarditis
- Collagen vascular disease
- Degenerative aortic valve disease
- Aortic dilatation: Marfan’s, aneurysm, dissection, ankylosing spondylitis
Pathophysiology of aortic regurgitation
- Regurgitation leads to an increase in LV end-diastolic pressure
- Which leads to LV dilatation and hypertrophy to compensate for regurg
- Stroke volume can be doubled/tripled
- As disease progresses LV diastolic pressure rises and causes breathlessness
Symptoms of aortic regurgitation
Often asymptomatic Palpitations breathlessness Angina PND Peripheral oedema
Signs of aortic regurgitation
Waterhammer pulse - large volume collapsing,
Wide pulse pressure,
S3 heart sound,
Diastolic thrill,
De Musset’s sign – head nodding in time with heartbeat,
Quincke’s sign – pulse felt in the nail,
Traube’s sign - ‘pistol shots’ over femoral arteries
Murmur:
- Soft blowing early decrescendo pattern
- Best heard when sitting forward in expiration
Musset’s sign
Head bobbing with each pulse
Seen in aortic regurgitation
Quincke’s sign
Capillary pulsation in nail beds
Seen in aortic regurgitation
Investigations in aortic regurgitation
ECG:
- LV hypertrophy and strain (T wave inversion),
- Left axis deviation
ECHO:
- Dilated LV
- Hyperdynamic LV
- Fluttering anterior mitral leaflet
CXR – LV enlargement
Cardiac catheterisation:
- Dilated LV
- Aortic regurgitation
- Dilated aortic root
Management of aortic regurgitation
Medical:
- Treatment aimed at symptoms (diuretics, ACE inhibitors, vasodilators)
- Nifedipine/ACE inhibitors may delay the need for surgery
Surgery if symptomatic:
- Aortic valve replacement
- Valve sparing aortic replacement
Types of mitral regurgitation
Primary
Intrinsic lesions affect one or several components of the valve
Degenerative mitral regurgitation is the most common cause
Acute can be caused by papillary muscle rupture, infective endocarditis or trauma
Secondary (functional)
Valve leaflets normal but MR results from distortion of subvalvular apparatus due to LV enlargement
May be due to cardiomyopathy
Epidemiology of mitral regurgitation
2nd most prevalent valve disease after aortic stenosis.
Increased in females
increases with age.
RFs
- Lower BMI
- Renal dysfunction
- Prior MI
- Prior mitral stenosis or mitral valve prolapse
Aetiology of mitral regurgitation
Coronary artery disease (papillary muscle dysfunction)
Infective endocarditis
Following mitral valve surgery
Myxomatous degeneration - Ehler’s Danlos, Marfan’s, SLE, scleroderma
Cardiac tumours - atrial myxoma
Rheumatic fever
Acute LV dysfunction
Congenital heart disease
Drug related
Pathophysiology of mitral regurgitation
- Chronic mitral regurg causes gradual dilation of LA with little increase in pressure causing few symptoms
- LV dilates slowly and LV diastolic and LA pressures increase gradually as a result of chronic volume overload
Symptoms of mitral regurgitation
Pulmonary oedema (acute)
- Dyspnoea,
- R-sided heart failure,
- Orthopnoea,
- Fatigue
- Palpitations if in AF,
- Symptoms of infective endocarditis
Sign of mitral regurigation
- Jerky pulse,
- Soft S1
- Displaced apex beat
- Apical thrill
- S3
- Pulmonary oedema
- Irregularly irregular pulse (AF),
Murmur:
- Harsh pansystolic murmur
- Axilla radiation
Investigations for mitral regurg
CXR
Enlarged LA, enlarged LV, pulmonary venous congestion, pulmonary oedema if acute
ECG
Left atrial hypertrophy, broad P wave, LV hypertrophy
Echo: dilated LA, LV. structural abnormalities of mitral valve
Cardiac catheterisation - dilated LA, LV, mitral regurg, pulmonary hypertension, co-existing coronary artery disease
Angiography for CAD
Management of mitral regurgitation
Surgery if signs of LV dysfunction, new onset AD or pulmonary hypertension
Follow up yearly with echo every 2 years, severe every 6 months with echo annually
Medical:
- Nitrates, diuretics, positive inotropic agents (Digoxin)- Anticoagulation if AF present
Surgery:
- Urgent if acute severe
- Valve replacement, repair where possible
- Percutaneous not recommended
Complications of mitral regurgitation
Pulmonary hypertension
LV dysfunction
AF
Thromboembolism due to AF
Define aortic aneurysm
Permanent and irreversible dilation of the aorta by at least 50% its normal diameter
Normal diameter of the aorta is 2cm, but increases with age
AAA is >3cm
Most arise from above the renal arteries
Epidemiology of aortic aneurysms
1-12% of the population
More common in men
Aetiology of aortic aneurysms
Risk factors:
- Hypertension
- FHx (minimal)
- Severe atherosclerotic changes to vessel wall
- Smoking
- COPD
- Hyperlipidaemia
Most have no specific cause:
- Trauma
- Infection: HIV, TB, Brucellosis, salmonellosis
- Inflammatory disease:behcet’s and takaysau’s
- Connective tissue disorders: Marfan’s, Ehler’s Danlos syndrome
Pathophysiology of aortic aneurysms
- Degradation of elastic lamellae
- Leukocytic infiltrate
- Enhanced proteolysis
- Smooth muscle cell loss
- Dilation affects all 3 layers of the cell wall
- The larger the AAA the larger the growth rate and the greater the risk of rupture
Presentation of unruptured aortic aneurysm
Most have no symptoms
Incidental finding on examination
Can have pain in back, abdomen or groin (? due to pressure on nearby structures)
Pulsatile abdominal swelling
Distal embolization can produce features of limb ischaemia
Hydronephrosis
Abdominal bruits
Presentation of ruptured aortic aneurysm
Hypotension
Atypical abdominal symptoms
Sudden and severe abdominal pain (or back or loin)
Syncope
Shock or collapse
Cold, sweaty, faint
Vomiting
Degree of shock depends on site of rupture and whether it is contained
Retroperitoneal bleeding may cause
Grey Turner’s sign - flank bruising
TRIAD - pain in flank or back, hypotension, abdominal pulsatile mass
If thoracic - then chest pain, cardiac tamponade and haemoptysis
Grey Turners sign
Flank bruising (due to retroperitoneal bleeding)
Investigations for AAA
Bloods - FBC, clotting screen, renal function, LFTs, cross match units for surgery ESR or CRP if ? inflammatory cause ECG CXR Lung function tests
Scans
US
CT - crescent sign (blood within thrombus which may predict immanent rupture)
MRI angiography
Management for aortic aneurysm
If UNCOMPLICATED: - Monitor if <5.5cm, consider surgery in over 5.5cm - US monitoring frequency depends on size, 3-4.5 every year, >4.5 every 3 months - Change RFs where possible Surgery - If over 5.5 - High risk of rupture - Rapid expansion - Symptomatic
Open repair with aortic and iliac clamping, replacement of segment with prosthetic graft
OR endovascular repair: stent-graft system through femoral arteries
Complications and prognosis of aortic aneurysm
Death
AKI
Multi-organ failure
Respiratory failure
Risk determined by diameter
2.4% mortality with elective repair
20% annual survival rate if over 5.5vm
80% mortality with ruptured AAA
Normal electrical activity in the heart
Initiated by electrical discharge in SA note
Atria and ventricles depolarise sequentially.
SA node acts as pace maker, intrinsic rate determined by autonomic nervous system
Passes through AV node, into bundles of His then pirkinje fibres
Define sinus bradycardia
Causes
HR under 60bpm in sinus rhythm
MI Sinus node disease (sick sinus syndrome) Hypothermia Hypothyroidism Cholestatic jaundice Raised ICP Drugs - beta blockers, digoxin, verapamil
NORMAL in athletes
Symptoms of sinus bradycardia
Often asymptomatic
Fatigue
Lightheadedness
Syncope
Management of sinus bradycardia
Normally responds to IV atropine
If recurrent or persistent then cardiac pacing
Causes of sinus tachycardia
Anxiety Fever/Sepsis Thyrotoxicosis Anaemia Phaeochromocytoma heart failure Drugs - beta agonists Pregnancy Exercise
Sick sinus syndrome (sinoatrial disease)
- Most common in elderly
- Underlying pathology can be fibrosis, degenerative changes or ischaemia
- Characterised by a number of arrhythmias
- May have palpitations, dizzy spells, syncope
- Intermittent tachycardia, bradycardia or pauses with no atrial or ventricular activity
Features:
- Sinus bradycardia
- Sinoatrial block
- Paroxysmal AF
- Paroxysmal atrial tachycardia
- AV block
Treat symptomatic patients with pacing
Atrial ectopic beats
Extrasystoles, premature beats
usually causes no symptoms
ECG shows a premature but otherwise normal QRS
If the visible p wave has a different morphology, from abnormal site
No consequence, however, very frequent atopics can lead to onset of AF
Atrial flutter
Large re-entry circuit within the RA
Atrial rate 300bpm, usually associated with 2:1, 3:1 or 4:1 block (producing HR 150, 100 or 75)
- Sawtooth flutter waves
- Should always be suspected if narrow complex with 150bpm
Management:
- Carotid sinus pressure or IV adenosine can slow rate to see sawtooth waves
- Treat with digoxin/beta blockers/verapamil
- Can try to restore rhythm through DC cardioversion or IV Amiodarone
- Beta blocker or Amiodarone can help prevent recurrence
- Catheter ablations can give chance of complete cure and is treatment of choice with persistent symptoms
AF
Most common sustained cardiac arrhythmia
0.5% prevalence, increases to 9% in over 80s
Abnormal automatic firing with presence of multiple atrial re-entry circuits
Becomes sustained after re=entry conduction
Atria beat rapidly, ineffectively and in-coordinated
Ventricles activated irregularly determined by conduction through AV node
Irregularly irregular pulse
Normal but irregular QRS
No p wave
Can be paroxysmal or permanent
Initial physical changes - electrical remodelling
After a few months - structural remodelling with atrial fibrosis and dilation
Causes of AF
Idiopathic MI Valvular heart disease (particularly mitral disease) Hypertension SA node disease Hyperthyroidism Alcohol Cardiomyopathy Congenital heart disease Chest infection PE Pericardial disease
Symptoms of AF
Palpitations Breathlessness Fatigue Lightheadedness Chest pain (if coronary artery disease) May have reduced BP
Often asymptomatic
Stroke/TIA
Investigations for AF
12 lead ECG
- Irregular QRS
- No p waves
- Fast ventricular rate 120-160, slows with chronic
Bloods
- FBC (anaemia may precipitate)
- U&Es (potassium is a culprit)
- LFTs and coag screen prior to anticoagulation
- TFTs
CXR - may show structure causes
Echo - baseline needed for longer term management, if considering cardioversion or high risk of functional or structural heart disease
Management of AF
- Treat any underlying cause
- Control of arrhythmia (rate and rhythm)
- Thromboprophylaxis
Rate control is first line unless: reversible cause of AF, heart failure caused by AF or new onset AG
- beta blocker or rate limiting CCB
- Consider digoxin if permanent AF and sedentary patient
- If monotherapy fails, try combining
- No Amiodarone
Rhythm control - if AF continues post rate control or unsuccessful
- Cardioversion (electrical, Amiodarone therapy for 4 weeks before and 12 months after to maintain sinus)
- Drug treatment:
- 1st line: beta blocker
- Dronedarone or Amiodarone is LV impairment of HF
- Left atrial ablation if drugs unsuccessful
- Pacing and ablate strategy
Anticoagulation
- Apixaban, rivaroxaban or warfarin or dabigatran
- Use CHA2DS2-Vasc score
Assessing risk of stroke in AF
CHA2DS2 Vasc score Congestive heart failure Hypertension Age>75 - 2 points Diabetes past Stroke or TIA - 2 points
Vascular disease
Age 65-75 - 1 point
Sex - female
If males score 1 or more, or females 2 or more - start anticoagulation, proving consideration of bleeding risk
HAS-BLED
Complications of AF
Stroke
Can precipitate acute heart failure or aggravate established heart failure
Cardiomyopathy
Premature death
Management of acute AF
If life threatening haemodynamic instability then emergency electrical cardioversion and resuscitation.
Rhythm control if within 48 hours of start, rate control if unsure or longer.
Types of AF
Paroxysmal - intermittent episodes that self-terminate in 7 days
Persistent - prolonged episodes which can be terminated with chemical or electrical cardioversion
Permanent
Atrioventricular nodal reentrant tachycardia
Re-entry circuit involving AV node and its 2 right atrial input pathways
- Produces tachycardia at 120-140bpm
- Occurs in absence of structural disease
- Rapid, forceful regular heart beat
- Chest discomfort
- Breathlessness
- Lightheadness
- Tachycardia with normal QRS complexes
- Adenosine or verapamil will restore sinus rhythm in most cases
Wolff-Parkinson White syndrome signs
- ECG changes
- Shortened PR interval
- Slurred initial deflection of QRS - DELTA WAVE
- Broad QRS complex
Wolff-Parkinson White syndrome
Abnormal band of conducting tissue connects atria and ventricles.
Accessory pathway - bundle of Kent contains rapidly conducting fibres rich in sodium channels.
As the AV node and accessory pathway have different conduction speeds and refractory periods - therefore a re-entry circuit can develop causing tachycardia.
- If AF occurs very dangerous as no rate limitation from AV node (emergency)
Describe ventricular ectopics
Broad, premature and bizarre QRS complexes
Ventricles are activated sequentially and not simultaneously
Unifocal or multifocal
Pulse irregular with weak or missed beats
Generally asymptomatic but can have irregular heartbeat, missed beats or unusually strong beats
More prominent at rest and decreases with exercise
No treatment unless symptomatic - use beta blockers or catheter ablations
Bigeminy
Alternating between ventricular ectopics and sinus rhythm between on each beat
S - E - S - E - S - E
When are ectopic beats more common
At rest
In patients with heart failure and cardiomyopathy
Increases in age
Digoxin toxicity
ECG findings in VT
- Tachycardia, rate over 120bpm
- Broad, abnormal QRS complexes
- Marked left axis deviation
- Can be difficult to distinguish between this and SVT with BBB
Ventricular tachycardia
- Occurs most commonly in MIs and cardiomyopathy, where there is extensive ventricular disease
- May cause haemodynamic compromise and progress to VF
- It is caused by abnormal automaticity or triggered activity in ischaemic tissue
Symptoms and features in keeping with VT
Symptoms:
- Syncope
- Palpitations
- Lightheadedness
- Dyspnoea
Features
- History of MI
- AV dissociation
- Capture or fusion beats
- Extreme left axis deviation
- Very broad QRS > 140ms
- No response to carotid sinus massage or IV adenosine
Management of VT
Prompt action to restore sinus rhythm
- DC cardioversion if BP<90
- IV Amiodarone if arrhythmia well tolerated
- Correct: hypokalaemia, hypoxia, hypomagnesaemia, acidosis
- Avoid class 1c antiarrhythmic
ECG findings in Torsade de Pointes
Rapid irregular complexes the oscillate from upright to inverted position and twists around the baseline as mean QRS axis changes
Non sustained, repetitive, but can degenerate into VF
Prolonged QT interval
Causes of long QT and Torsade de pointes
Bradycardia Hypokalaemia Hypomagnesaemia Hypocalcaemia Class 1a and class 1c antiarrhythmic drugs Amitriptyline and other TCAs Chlorpromazine Congenital syndromes
Congenital long QT syndromes
Long QT1 - triggered by exercise
Long QT2 - triggered by sudden noise
Long QT3 - common during sleep
Management of torsade de pointes
Treat underlying cause
IV magnesium in all cases
Atrial pacing
If very long >500ms then implanted defibrillator
Brugada syndrome
Genetic disorder which can present with polymorphic VT or sudden death
Due to a defect in the sodium channel function
RBBB and ST elevation in V1 and V2 with no prolongation of QT interval
First degree heart block
AV conduction delayed
Prolonged PR interval > 200ms
Second degree heart block
2:1
Mobitz type 1 Wenckeback
PR interval increases until QRS dropped
2:2 - mobitz type 2
PR interval remains constant but some QRS complexes are not conducted, Regular p waves
Third degree heart block
QRS and p waves do not correlate
Occurs when AV conduction fails completely
Slow regular pulse 25-50bpm
Pulse does not vary with exercise
Causes of 3rd degree heart block
- Congenital
- Idiopathic fibrosis
- MI
- Inflammation: infective endocarditis, sarcoidosis, Chagas disease
- Cardiac surgery
- Drugs: digoxin, beta blockers
Stokes-Adams attacks
Episodes of ventricular asystole that can complicate 3rd degree or mobitz type 2 heart block.
Sudden loss of consciousness that occurs without warning and results in collapse.
Brief anoxic seizure if prolonged.
Pallor and death like appearance during attack followed by characteristic flushing.
Rapid recovery unlike epilepsy.
Causes of RBBB
- Normal variant
- Right ventricular hypertrophy or strain
- PE
- Congenital heart disease e.g. atrial septal defect
- Coronary artery disease
Causes of LBBB
- Coronary artery disease
- Hypertension
- Aortic valve disease
- Cardiomyopathy
Bundle branch block
Depolarisation goes through a smaller myocardial route rather than fast Purkinje fibres.
Causes delayed conduction into one of the ventricles.
Broad QRS > 120ms
WilliaM - LBBB has W in V1 and M in V6
MarroW - RBBB has M in V1 and W in V6
Reversible causes of cardiac arrest
Hypovolaemia Hypoxia Hydrogen ions (acidosis) Hypothermia Hypokalaemia/ hyperkalaemia Hypoglycaemia
Toxins Tamponade (cardiac) Tension (pneumothorax) Thrombosis (coronary or pulmonary) Trauma
Arteries in the brain
Vertebral arteries:
- Enter the cranial cavity via foramen magnum
- Lie in the subarachnoid space
- Ascend on anterior surface of medulla oblongata
- Unite to form the basilar artery at the base of the pons
Branches:
Posterior spinal artery
Anterior spinal artery
Posterior inferior cerebellar artery
Basilar artery: Branches: - Anterior inferior cerebellar artery - Labyrinthine artery - Pontine arteries - Superior cerebellar artery - Posterior cerebral artery
Internal carotid arteries: Branches: - Posterior communicating artery - Anterior cerebral artery - Middle cerebral artery - Anterior choroid artery
QT interval and electrolytes
Hypocalcemia is associated with QT interval prolongation;
Hypercalcemia is associated with QT interval shortening
Bendroflumethiazide
Inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule
JVP waveform
- A wave – atrial systole
- X descent – atrial relaxation
- C wave – tricuspid valve bulging into atria with ventricular contraction
- V wave – passive atrial filling
- Y descent – atrial empty into ventricle (tricuspid valve opens)
Note:
- Giant V waves = tricuspid regurgitation
- Large A wave = Pulmonary hypertension, Tricuspid stenosis, Cannon waves in CH8 or VT
- No A wave = AF
Loud S1
“Hyperdynamic circulation:
- Anaemia,
- Pregnancy,
- Hyperthyroidism,
- Mitral stenosis,
- Left to right shunts
- Short PR interval, atrial premature beats
- Hyperdynamic states”
Soft S1
”- Mitral regurgitation
- Long PR interval”
Loud S2
”- Hypertension: systemic (loud A2) or pulmonary (loud P2)
- Hyperdynamic states
- Atrial septal defect without pulmonary hypertension”
Soft S2
Severe aortic stenosis
S3
“Caused by diastolic filling of the ventricle
- Physiological < 30 years old
- Left ventricular failure (dilated cardiomyopathy, constrictive pericarditis)
- Mitral regurgitation
- Pulmonary oedema”
S4
”- Aortic stenosis
- HOCM
- Hypertension
Caused by atrial contraction against a stiff ventricle”
Systolic ejection murmur
crescendo-decrescendo pattern
- Aortic stenosis,
- Pulmonary stenosis
Systolic click
heard early or mid-systole
- Aortic stenosis,
- Pulmonary stenosis,
- Prosthetic heart valve
Pansystolic murmur
- Mitral regurgitation
- Ventricular septal defect
Early diastolic murmur
- Pulmonary regurgitation
- Aortic regurgitation
Late diastolic murmur
- Mitral stenosis
- Tricuspid stenosis
Continuous murmurs
- Patent ductus arteriosus
- Arteriovenous fistula
- Ruptured sinus of Valsalva”
Left axis deviation
- Left anterior hemiblock
- Inferior MI
- VT from a left ventricular focus,
- WPW
- LVH
Right axis deviation
- Left posterior hemiblock
- Anterolateral MI
- PE
- WPW
- RVH
Left bundle branch block (WiliaM)
- Aortic stenosis
- Ischaemic heart disease
- Hypertension
- Dilated cardiomyopathy
- Anterior MI
- Lenegre disease
- Hyperkalaemia
- Digoxin toxicity
Right bundle branch block (MarroW)
- Right ventricular hypertrophy (cor pulmonale)
- Pulmonary embolism
- Ischemic heart disease
- Rheumatic heart disease
- Myocarditis or cardiomyopathy
- Lenegre disease
- Atrial septal defect
Enlarged Virchow’s node (left supraclavicular lymph node)
- Lymphoma,
- Various intra-abdominal malignancies,
- Breast cancer,
- Infection (e.g. of the arm)
Enlarged right supraclavicular lymph node
- Thoracic malignancies (lung and oesophageal cancer)
- Hodgkin’s lymphoma
Monophonic wheeze (large airways)
- ETT malposition
- Foreign body
- Blood
- Secretions
- Tumour
- Compression by lymph nodes
Polyphonic wheeze (small airways + multiple sites)
- Aspiration
- Unilateral emphysema
- Contralateral pneumothorax
- Asthma in a pneumonectomy patient
Respiratory acidosis
- CNS depression: coma, drug OD, head injury
- Thoracic injury: pneumothorax, flail chest
- Airway obstruction: asthma, COPD
- Severe pneumonia
- Pulmonary oedema
- Obesity-hypoventilation syndrome (Pickwickian)
- Neuromuscular weakness: myasthenia, Guillain-Barre
- Interstitial fibrosis
Metabolic alkalosis
- Diuretics
- Vomiting / aspiration
- Hypokalaemia
- Cushing’s syndrome
- Primary hyperaldosteronism
- Bartter’s syndrome
Metabolic acidosis
Raised anion gap:
- Renal failure
- Alcohol poisoning
- Hypoxia
- Diabetic ketoacidosis
- Shock
- Salicylate poisoning
Normal anion gap:
- Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
- Renal tubular acidosis
- Drugs: e.g. acetazolamide
- Ammonium chloride injection
- Addison’s disease
Respiratory alkalosis
- Hyperventilation
- Sepsis
- Stroke
- Salicylate toxicity
- Interstitial lung disease
- Pregnancy
- Hepatic encephalopathy
