CVS Disease
Hypertension
Hypertension
Chronically elevated BP
Presentation
Usually asymptomatic (except malignant HTN)
Cardiac enlargement
Causes
Primary/Essential/Idiopathic -95%
Secondary
1. Renal
- Intrinsic renal disease(75%)- glomerulonephritis, PAN, systemic scelosis, chronic pyelonephritis, PKD
- Renovascular disease(25%) –atheromatous, fibromascular dysplasia
- Renin producing tumour
2. Endocrine
- Thyroid disease – hyperparathyroidism
- Adrenal – Cushing, Conn (Primary aldosternism), Phaechromocytoma
3. Others
- Coarctation of aorta, pregnancy, sleep apnea, stress, drugs(alcohol, cocaine)
Investigation
U&E
Creatinine
cholesterol
glucose
ECG
urine analysis
Specific: (exlclude secondary cause)
- renal US
- renal arteriography
- 24h ambulatory BP monitoring (always lower, add-on 12/7 mmHg)
Hypertensive retinopathy
I Tortuous arteries with thick shiny walls (silver or copper wiring)
II A-V nipping (narrowing where arteries cross veins)
III Flame haemorrhages and cotton wool spots
IV Papillodema
Management
Category | Systolic (mmHg) | Diastolic (mmHg) | |
Normal | <120 | <80 | - |
Pre-hypertension | 120-139 | 80-89 | Reassess in 5 years, advice on healthy lifestyle |
Stage 1 | 140-159 | 90-99 | CHD+stroke risk |
Stage 2 | >160 | >100 | |
isolated systolic hypertension | >140 | <90 |
Heart Failure
Problem with the structure or function of the heart impairs its ability to supply sufficient blood flow to meet the body's needs.
Presentation
Left ventricular failure | Right ventricular failure | |
Symptoms |
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New York Classification of HF
Class I asymptomatic
Class II symptoms at routine activity
Class III symptoms at less than routine activity
Class IV symptoms at rest
Causes
Heart disease with anaemia or pregannacy
hyperthyroidism
Paget’s disease
atreoalvenous malformation
Risk Factor
Previous MI
Hx of arrhythmia, valvular/ vascular disease
HTN
Family hx of cardiomyopathy
DM
Obesity
Prior exposure to cardiotoxic agents
Investigation
FBC
U&E
B-type Natriuretic Peptide(BNP)
- secreted by the heart in response to excessive stretching of heart muscle cells
- 100pg/ml, HF likely, sensitivity = 90%, specificity = 76%
- ↓ aldosterone, endothelin-1 (vasoconstrictor)& noradrenaline, ↑diuresis, lusitropic, anti-fibrotic, anti-remodelling
- Caveats: lower with ↑ BMI, affected by renal fn, ↓ by ACEi, diuretics,
ECG –usually shows abnormality (causes) – MI
If ECG and BNP are normal, heart failure is unlikely
Echocardiography – not diagnostic, indicate the causes (MI, valvular disease, LV dysfunction), performed if BNP ↑. Findings:
Ejection fraction: EDV-ESV > 50% + 5%
valvular disease
Diastolic dysfunction - ↑ wall thickness, LA dimension
CXR- eg: features in LVF:
- Alveolar oedema – perihilar bat’s wing shadowing
- Kerley B lines (interstitial oedema)
- Cardiomegaly -cardiothoracic ratio >50%
- Dilated prominent upper lobe vessels
- Pleural Effusion
Cardiac CT, MRI
Coronary angiogram
Management
Acute HF (emergency) | Chronic HF |
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- reassess the cause, compliance - bed rest - metolazone,frusemide, opiates, nitrates - DVT prophylaxis: heparin and TED - consider heart transplant. Jarvik thumb-sized titanium axial flow impeller pump. |
Valve Disease
Mitral Stenosis | Mitral Regurgitation | Aortic stenosis | Aortic regurgitation | |
Causes | Rheumatic, congenital parachute valve- all chordate insert into 1 papillary muscle., mucopolysacharide | Functional (LV dilatation) annular calcification, Rheumatic, IE, HOCM | senile calcification, bicuspid valve, William’s syndrome | congenital, rheumatic fever, IE, RA, aortic root disease |
Symptoms | dyspnoea, PND, haemoptysis (ruptured bronchial vein), ascites | dyspnoea, fatigue | Exertional chest pain/dyspnoea/ syncope | Exertional dyspnoea, angina, palpitation |
General | tachypnoea, mitral stenosis | tachypnoea | - | Marfan, ankylosin. spondilytis |
Pulse, BP | normal/↓ | normal/ sharp upstroke | Pulse: Plateu/ anacrotic/ late peaking/ small volume | Pulse :collapsing, water hammer/ bisfirens Corrigan sign |
Palpation | tapping apex beat (palpable S1 | displaced apex beat, pansystolic thrill, parasternal impulse | apex beat hyperdynaamic, slightly displaced | apex beat displaced & hyperkinetic |
Auscultation | Loud S1, mid-diastolic murmur over mitral area using bell, louder with isometric handgrib and left lateral position | Soft/ no S1 pansystolic murmur maximal at the apex and radiating to the axilla, louder with isometric handgrib and left lateral position | narrowly split/ reversed S2 Ejection systolic murmur, radiates to carotid arteries, louder when pt squats rapidly from standing position | Soft S1 Early diastolic murmur, maximal at the left sternal border with diaphragm and pt leans forward in full expiration |
Severe | valve area<1cm. longer murmur, early opening snap, soft S1 | larger left ventricle, loud S3 | valve area<1cm, valve gradient >50mmHg,delayed carotid upstroke,late peaking murmur | collapsing pulse, wide pulse pressure, soft A2, Austin Flint murmur, systolic 80mmHg > than diatolic BP |
Complication | Pulm. HTN, emboli, pressure effct | |||
Test | ECG(AF, P-mitrale if in sinus rhytm, RVH) CXR(large left atrial, pulm edema, valve calcification), Echo. Indication for cardiac catheter: prev. valvotomy, other valve disease, angina, severe pulm HTN | ECG(AF, P-mitrale if in sinus rhytm, RVH) CXR(large LA & LV), Echo, Doppler echo, cardiac catheterisation | ECG(P-mitrale, LVH, LAD, LBBB), CXR(LVH, calcified aortic valve), Echo: (dx, measure valve gradient) Cardiac cathter: LV function | ECG:(LVH), CXR; (cardiomegaly), Echo, cardiac catheter |
Management | control AF, warfarin, diuretics. if fail:balloon valvuloplasty, open valvulotomy/valve replacement, penicillin for recurrent rheumatic fever if <30 Indication for surgey LVEF >60%, LVESD <45mm | symptomatic: Prompt valve replacement, except for unfit: percutaneous valvuloplasty. Asymptomatic: regular monitor Poor prognosis: 2-3y if angina, | Valve replacement |
MYOCARDIAL INFARCTION
Pathophysiology
90% caused by artherosclerosis
nonatherosclerotic c in younger patients: infected cardiac valve through a patent foramen ovale (PFO), coronary occlusion secondary to vasculitis, primary coronary vasospasm (variant angina), cocaine use, or other factors leading to mismatch of oxygen supply and demand, as may occur with a significant gastrointestinal bleed.
Epidemiology
- 5/1000 per year for ST segment elevation
- African American, Hispanic, and white populations in the United States.
- male, age 70 years when the sexes converge to equal incidence.
- Premenopausal women appear to be somewhat protected from atherosclerosis, possibly owing to the effects of estrogen.
- Incidence increases with age.
- Most patients who develop an acute myocardial infarction are older than 60 years. Elderly people also tend to have higher rates of morbidity and mortality from their infarcts.
Risk Factor
- Non modifiable: age, gender, family hisyory
- Modifiable: smoking, hypertension, DM,, hyperlipidaemia, obesity, sedentery lifesyle
- Controversial: stress, type A personality, ↑ of apoprotein A & fibrinogen, hyperinsulinaemia, homocystein, ACE genotype, cocaine
Presentation
- acute central chest pain > 20min ass with sweatiness, nausea, SOB, palpitations.
- Silent infarct in elderly and diabetics- syncope, pulmonary oedema, epigastric pain and vomiting, post-op hypotension, oliguria, acute confusional state, stroke, diabetic hyperglyceamic state
- distress, anxiety, pallor, pulse & BP ↑ or ↓, S4, sign of heart failure (↑ JVP, S3 and basal crepitations) or a pansystolic mumur (papillary muscle dysruption, rupture)
- low grade pyrexia
- later: pericardial rub or peripheral oedema
WHO criteria: 2 out of 3
- Typical history of ischaemic type chest pain lasting for more than 20 minutes
- Changes in serial ECG tracings
- Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin + typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
Investigation
ECG
- hyperacute (tall) t waves, ST elevation or new LBBB within hours of acute Q wave (transmural infarction). T wave inversion and development of pathological Q wave follows over hours to days.
- St depressiion, T inversion, non-specific changes, or normal
- normal in 20% of MI
CXR
Cardiomegaly, pulmonary odema, widened mediastinum (?aorta dissection)
Blood
FBC, U&E, glucose ↑, lipids ↓,
Cardiac enzyme
(CK, AST, LDH, troponin) ↑, CK is found in myocardial and skeletal muscle: ↑ in MI, after trauma, prolonged exercise, myositis, afro-carribeans, hypothermia, hypothyroidism
Check CK-MB isoenzyme levels if there is doubt as to the source (normal CK-MB:CK ratio <5%)
Troponin T better shows MI (peaks at 12-24H, elevated for >1wk) If normal >6h after onset of pain, and ECG mormal, risk of missing Mi is tiny (0.3%). peak post MI levels also help risk stratification.
Differential Diagnosis
Angina, pericarditis, myocarditis, aortic dissection, pulmonary embolism, PE, oesophageal reflux
Management
Pre-hosp
Arrange emergency ambulance.aSPIRIN 300MG chewed and GTN sublingual
Analgesia (morphine 5-10mg IV + metoclopramide 10mg IV (not IM- risk of bleeding)
Hospital
Morphine, O2, Aspirin, IVI
check for ST elevetaion
ST-segment elevation | No ST segment elevation |
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Subsequent management: bed rest for 48H, continuous ECG monitoring
- Daily examination of heart, lungs anfd legs complications
- Daily 12-lead ECG, U&E, cardiac enzymes for 2-3d
- Prophylaxis against thromboembolism, eg heparin 5000u/12h, until,fully mobile. If large anterior MI, consider warfarin anticoagulation for 3months as prophylaxis against systemic emnolism from LV mural thrombus. Continue daily low-dose aspirin (75-150mg) -reduce vascular events (MI, stroke, vascular death) by 29%
- oral B-blocker (metoprolol 50mg/6h decrease pulse <60, continue for at least 1 year. Long term- reduce mortality by 25% in pt who had previous MI. If CI: verapamil or diltiazem
- ACEi in all pt ↓ 2y mortality by 25-30%
- Statin - ↓ cholesterol for all pt or if total cholesterol >4mmol/L
- discourage smoking, encourage exercise, treat DM, HTN and hyperlipidaemia
- exercise EC: in risk stratification 3-4wk post MI, in non STEMI or troponin rise
- if uncomplicated : discharged after 5-7d.
- Return to work after 2M, x start post MI: airline traffic, divers. Lighter jobs. Diet: oily fish, veg, fibre, low in saturated fat. Exercise. Avoid sex for 1 month, avoid air travel for 2 months
- Review symptoms at 5wks
- Review at 3 months: check fasting lipids
Complications
Cardiac arrest
Unstable angina
bradycardia or heart block
Tachyarryhtmias
LVF/RVF
Pericarditis
DVT, PE, systemic embolism
Cardai tamponade
Mitral regurgitation, VSD
Late malignant ventricular arryhtmias
Dressler's syndrome – recurrent pericarditis
Left ventricular aneurysm
Mortality
50% deaths occur within 2h onset of symptom
ATRIAL FIBRILLATION
supraventricular tachyarrhythmia characterized by disorganized atrial electrical activity and progressive deterioration of atrial electromechanical function. absence of P waves; rapid oscillations (or fibrillatory [f] waves)
Epidemiology
5% of the population older than 69 years, 8% of persons older than 80 years.
stroke risk 2.5%
Causes
Heart failure/ischaemia, HTN, MI, mitral valve disease, PE, pneumonia
hyperthyroidism, alcohol, post-op, K+ and Mg+ ↓
rare: Cardiomyopathy, constrictive pericarditis, sick sinus syndrome, lung cancer, atrial myxoma, endocarditis, haemochromatosis, sarcoid, Lone AF= no cause found
Presentations
may be asymptomatic
chest pain, palpitations, SOB,or faintness
irregularly irregular pulse, the apical pulse rate is greater than the rate
variable S1 intensity
sign of LVF
Investigation
ECG – absent p waves, irregular QRS complex
Blood: U&E, cardiac enzyme, TFT
Echo to look for left atrial enlargement, mitral valve disease, poor LV function
Management
Acute AF (<AF) | Chronic AF |
Controlling ventricular rate:
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Controlling ventricular rate: B-blocker or rate limiting CCB if fail, add Digoxin (monotherapy only ok in sedentary pt), then consider amiodarone |
Paroxysmal AF
Pill-in-the-pocket
If not,try B-blocker
If fails and no LV dysfunction, sotalol 40mg/12h. S/E:↑QT interval, so monitor QT
If LV sydfunction: amiodarone
INFECTIVE ENDOCARDITIS
Classifications
50% endocarditis occurs in normal valve. It follows acute course -present with heart failure
endocarditis occurs in abnormal valve → subacute course
Causes
- Bacteraemia – dentistry, UTI, urinary catheterization, cystoscopy, resp infection, endoscopy
- Colon cancer, gall bladder disease, skin disease, IV cannulation, surgery, abortion, fractures.
- Streps viridans commonest(35-50%), enterococci, staph aureus/ epidermidis, diphteroids, HACEK group, Coxiella burnetti, chlamydia
- Candida, aspergillus, Histoplasma
- SLE (libman-Sacks endocarditis), malignancy
Presentations
- septic signs: fever, rigors, night sweats, malaise, weight loss, anaemia, splennomegaly, clubbing
- cardiac lesions: any new murmur, or change in the nature of pre-existing murmur
- vegetation may cause valve destruction, and severe regurgitation, or valve obstruction.
- An aortic root abscess causes prolongation of the P-R interval, and may lead to complete AV
- Immune complex deposition: vasculitis may affect any vessel.
- Microscopic haematuria,glomerulonephritis and ARF
- Roth spots(boat shaped retinal haemorrhage with pale centre), splinter haemorrhage, Osler nodes, Janeway's lesion.
- Embolic phenomena: abscess in relevant organ- brain, kidney, lung (in R-sided endocarditis)
Diagnosis
- Blood cultures: take 3 sets at different time and from different site at peak fever. 85-90% are diagnosed from the first 2 sets. 10% culture negative.
- Blood test: normochromic, normocytic anaemia, neutrophil leucocytosis, high ESR/CRP. Also check U&E, Mg, LFT
- Urinalysis- microscopic haematuria
- CXR(cardiomegaly)
- ECG (prolonged P-R interval)
- Echo TTE may show vegetation, but only if >2mm, TOE is more sensitive and better for visualizing mitral lesions and possible development of aortic root abscess.
Duke Criteria
Major Criteria | Minor Criteria |
Positive blood culture
Endocardium involved
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Definite IE: 2 major or 1 major and 3 minor or all 5 minor criteria
Management
- Liase early with microbilogist and cardiologist
- Empirical therapy: benzylpenicilin 1.2g/4h IV + gentamicin eg 1mg/kg/8h IV (serum peak 3-5mg/L & a pre-dose trough of <1mg/L) for 4wks. If acute, add flucloxacilin to cover staphylocicci
- Enteroccoci: amoxicilin 1g/6h iv + gentamicin as above
- Streptococci: benzylpenicilin 1.2g/4h IV 2-4wks, then amoxicilin 1g/8h PO for 2wks. Monitor minimum inhibitory concentration (MIC). Add gentamicin
- Staphilococci : flucloxacilin 2g/6h IV + gentamicin as above IV. Treat for 6-8wks, stop gentamicin after 1wk. If prosthetic valve or MRSA suspected, substitute flucloxacilin with vancomicin + rifampicin
- Coxiella: doxycilin 100mg/12h PO indefinitely + co-trimoxazole, rifampicin or ciprofloxacilin
- Fungi: flucytosine 50mg/kg/6h IVI over 30min followed by fluconazole 50mg/24h PO (higher dose may be needed) Amphotericin if flucytosine or Aspergillus. Miconazole if renal fn is poor
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