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
