I hope everyone finds CVS Diseases In a Nutshell useful as I did. It's great for quick reading. Please note that it's highly recommended to correlate these notes with your reference.
I) Hypertension
Definition:
You cannot absolutely define hypertension, since its incidence is related to blood pressure which has a skewed normal distribution throughout the population.
Incidence:
Increases with age. Mild hypertension is 2% in ages 25 or less, 25% for those in their 50s, and 50% in those in their 70s.
Types and Causes:
1) Essential hypertension:
Incidence—95% of cases.
Causes—Lifestyle factors: Obesity, physical inactivity, alcohol, dietary; genetic factors; other CV factors: diabetes, smoking, cholesterol, age.
2) Secondary hypertension:
Incidence—2% of cases.
Uncommon Causes include:
Renal disease—75% of intrinsic origin (e.g. glomerulonephritis, PAN, polycystic kidneys), and 25% of renovascular origin (e.g. atheromatous)
Endocrine Disease—Cushing's syndrome, Conn’s Syndrome, acromegaly, hyperparathyroidism
Others—Pregnancy, steroids
3) Malignant hypertension:
Definition—severe hypertension (over 200/130) with bilateral hemorrhages and exudates (retinal changes)
Symptoms—headaches and visual disturbances, hypertensive emergencies like renal failure, heart failure, or encephalopathy are common.
Pathological hallmark is fibrinoid necrosis.
Consequences of hypertension:
The long-term risk is end-organ damage. Others include; stroke, coronary artery Disease, left ventricular hypertrophy, renal failure.
Signs and Symptoms:
It’s usually asymptomatic (except for the malignant type). Symptoms start appearing when end-organ damage occurs. Fully examine CVS and look for; signs of renal disease, Cushing, radiofemoral delay, weak femoral pulse, palpable kidneys, retinopathy and proteinurea.
Investigations:
Basic: Urea and Electrolytes.
Specific: renal ultrasound and arteriography, urinary free cortisol, renin, and aldosterone, ECHO, and 24-hour BP monitering.
Treatment:
Overall approach and aim: address CV risk factors and aim for 140/85 BP. All patients with sustained pressure of 160/100 or malignant hypertension should be treated.
Non-pharmacological measures: lifestyle modification.
Drugs: the "ABCD rule". It is better to "mix and match" the following drugs for initial therapy; if one matching fails, switch to another. It takes 4-8 weeks to produce their maximum effect:
1. ACE Inhibitors—used as first line of treatment for asthmatic patients, e.g. Captopril.
2. B-blockers—usually used as initial treatment unless patient is asthmatic, e.g. Atenolol and Metoprolol.
3. Calcium channel antagonists—used with B-blocker as initial treatment, e.g. Nifedipine.
4. Diuretics—thiazide diuretics, e.g. bendrofluazide.
Malignant hypertension treatment: most patients are managed with oral therapy (preferably a loop diuretic—furosemide), except for critical patients with encephalopathy. These patients should be given intravenous agents (preferably sodium nitroprusside) and monitored constantly to avoid sudden BP drops. BP drops should be controlled over days not hours, since stroke can be a serious complication in rushed treatment.
II) Heart Failure
Definition:
Cardiac output and BP are inadequate for the body’s requirements.
Factors and General Causes:
Pump Failure:
Heart muscle disease—IHD, cardiomyopathy
Restricted filling—constrictive pericarditis, restrictive cardiomyopathy
Inadequate heart rate—b-blockers, post MI.
Negatively inotropic drugs—e.g. most antiarrhythmic agents
Excessive preload: e.g. mitral regurgitation and fluid overload.
Chronic excessive afterload: e.g. aortic stenosis, hypertension.
Types:
1. Acute heart failure (LVF)
2. Chronic heart failure (RVF): specific causes include pulmonary hypertension and atrial septal defect.
3. Congestive Heart Failure: left and right ventricular heart failure together.
4. Low-output cardiac failure: inadequate or is only adequate with high pressures. Specific causes include ischemia, hypertension, valve disorders, and alcohol usage.
5. High-output cardiac failure: This is a rare type of HF. Evidently; this will later turn into LVF. Here, cardiac output only increases when needs increase, and the failure occurs when the output fails to meet the body's demand. Specific causes include heart disease with anemia or pregnancy, beri beri, thyrotoxicosis, vessel malformation, and Paget's disease.
Symptoms:
LVF: dyspnoea, poor exercise tolerance, fatigue, weight loss, muscle wasting, orthopnoea, paroxysmal nocturnal dyspnoea, nocturnal coughing and wheezing, nocturia.
RVF: peripheral edema, ascites, nausea, anorexia, facial engorgement, tricuspid regurgitation.
Signs:
Patient looks ill and exhausted, cool peripheries, peripheral cyanosis, tachycardia, raised JVP, displaced apex, murmurs, respiratory crackles, plural effusion.
Investigations:
Key Investigation: echocardiography, since it can indicate the cause.
Basic: if ECG and BMP are normal, then heart failure is unlikely. If either abnormal, then echo is required.
Blood tests: FBC, U&E, BMP.
Chest X-ray: ABCDE—Alveolar edema, B lines Kerley, cardiomegaly, dilated upper lobe vessels, effusion (plural effusion).
Treatment:
Acute Heart Failure: medical emergency. Continuous monitoring and IV management is needed. Investigations are done after the initial treatment.
Chronic Heart Failure:
1. Treat exacerbating factors—e.g. anemia, thyroid disease, infection, elevated BP.
2. Avoid exacerbating factors—e.g. NSAID and verapamil.
3. Maintain lifestyle—eat less salt, avoid smoking, and maintain weight and nutrition.
4. Drugs—loop diuretics, ACE inhibitors, beta-blockers, digoxin, and vasodilators.
Intractable Heart Failure: reassess the cause and manage in hospital.
III) Infective Endocarditis
Classification
50% occurs on normal heart valves, following an acute course and presenting with acute heart failure.
On abnormal heart valves, it tends to run on a subacute course. Predisposing cardiac lesions; valvular heart disease, tricuspid valves in IV drug users, patent ductus arteriosus, VSD, prosthetic valves (early or late phase).
Causes:
Bacteria: Any cause of bacteraemia exposes valves to the risk of colonization, e.g. dental work, UTI, respiratory infection, skin disease, surgery, fractures, etc. Commonest organism is streptococcus viridans (30-50%). Others include; staphylococcus aureus/epidermis, enterococci, gram-negative organisms (HACEK group—rare).
Fungi: rare—Candida, Aspergillus, and Histoplasma.
Others: SLE and malignancy.
Clinical features:
Signs of infection: fever, rigors, night sweats, malaise, weight loss, etc.
Cardiac lesions: new murmurs, vegetations, severe regurgitation, valve obstruction.
Immune complex deposition: vasculitis, microscopic haematuria, glomerulonephritis and acute renal failure.
Pathognomonic signs: roth spots, splinter hemorrhages, Osler’s nodes, Janeway lesions.
Embolic: pulmonary abscesses may occur in right-sided endocarditis.
Diagnosis:
Use Duke Criteria—evidence of 2 major criteria, or 1 major and 3 minor, or all 5 minor.
1. Major criteria:
Positive blood culture: typical organism in 2 separate cultures or persistently positive blood cultures (hours apart).
Endocardium: positive echocardiogram or new valvular regurgitation.
2. Minor criteria:
Predisposition (cardiac lesion, IV drug abuse)
Fever over 30C
Vascular/immunological signs
Positive blood culture and echocardiogram which do not meet major criteria
Treatment:
Antibiotics: intravenous, continues for 4-6 weeks, drug combinations recommended.
Surgery: removal and replacement of infected valve. Consider if; severe valve obstruction, heart failure, abscess formation, persistent bacteraemia, prosthetic valve endocarditis.
Prophylaxis: for patients with known valvular disease or prosthetic valves.
IV) Rheumatic Fever
Definition:
It’s a systemic infection which is still common in the Third World but rare in the West. Pharyngeal infection with group A beta-haemolytic streptococci triggers this disease 2-4 weeks later. Antigenic mimicry mechanism between strep and valve tissue causes permanent damage. Incidence: 5-15 years. It tends to recur if not prevented.
Clinical Features and Diagnosis:
Revised Jones criteria—evidence of recent strep infection plus 2 major criteria, or 1 major + 2 minor.
1) Evidence of strep infection:
Recent strep infection
History of scarlet fever
Positive throat swab
Increase in AOST above 200U/mL
Increase in DNase B titer
2) Major criteria:
Carditis: conduction defects (45-70%), tachycardia, cardiomegaly, murmurs (Carey Coombs’ murmur).
Arthritis: ‘fitting’ polyarthritis usually affecting the larger joints (75%).
Subcutaneous nodules: small, mobile, painless, on extensor surfaces of joints and spine (2-20%).
Erythema marginatum: geographical-type rash. Reddish edges but clear in the center. The 'white' spreads all over. It occurs in the trunk, thighs and arms, NOT in face or below knees/elbow. (2-10%)
Chorea: unilateral or bilateral involuntary semi-purposeful movements (10%).
3) Minor criteria:
Fever
Raised ESR or CRP
Arthralgia
Prolonged P-R interval
Previous rheumatic fever
Treatment:
Bed rest until CRP is normal, benzylpenicillin IM then penicillin, aspirin doses with monitoring for carditis/arthritis, haloperidol for chorea, and steroids for symptom improvement.
V) Deep Vein Thrombosis
Incidence:
DVT occurs in 20% of surgical patients, and many non-surgical ones. 65% below-knee DVTs are asymptomatic; they rarely embolize to the lung.
Risk:
Factors include increased age, pregnancy, surgery, malignancy, obesity, immobility, past DVT, thrombophilia, and synthetic estrogen.
Signs:
Signs include calf warmth/tenderness/swelling, mild fever, pitting edema. Do NOT perform Homans’ sign.
Differential diagnosis:
Cellulitis or ruptured Baker’s cyst (both may coexist).
Tests:
a) Guidelines:
Use D-dimer blood tests and pretest clinical probability score.
If test is negative and score is low, exclude DVT.
If vice versa on both tests, do compression ultrasound.
If this is negative, then repeat ultrasound in a week just in case.
Do thrombophilia tests in recurrent DVT, positive family history DVT, and if there are no predisposing factors.
b) D-dimer blood tests: sensitive but not specific to DVT—raised in infection, pregnancy, malignancy and post-op.
c) Pretest clinical probability scoring:
In patients with symptoms in both legs, the more symptomatic one is used. Points are graded for each clinical feature; a total of 3 or more points has high probability, 1-2 points has intermediate probability, and 0 or less points has low probability:
Active Cancer—1 point
Paralysis or recent plaster immobilization of leg—1 point
Major surgery or bedridden for more than three days within the last 4 weeks—1 point
Local tenderness along leg—1 point
Entire leg swollen—1 point
Calf swelling more than 3 cm compared to normal leg (10 cm)—1 point
Pitting edema—1 point
Collateral superficial veins—1 point
Alternative diagnosis as or more likely than DVT—(-2) points
VI) Aortic Valve Disease (Aortic Stenosis and Regurgitation)
a) Aortic Stenosis
*Definition:
Impaired systolic flow of blood from left ventricle to aorta by narrowed aortic valve.
*Causes:
Senile calcification is the commonest (tricuspid from 60-100 years). Other causes congenital (bicuspid valve, William’s syndrome).
*Symptoms:
These include angina, dyspnoea, dizziness, faints, systemic emboli if infective endocarditis.
*Signs:
Slow rising pulse with narrow blood pressure, forceful displaced apex beat, ejection systolic murmur, soft or absent A2, ejection click if valve mobile.
*Investigations:
Cardiac ultrasonography is the key investigation, as it allows assessment of LV function, valve function, and severity of stenosis. Doppler echo estimates gradient across valves. Cardiac catheter and ECG are also useful tests.
*Differential diagnosis:
AS can be mistaken for hypertrophic obstructive cardiomyopathy.
*Treatment and Management:
Poor prognosis; 2-3 year survival if angina, 1-2 year survival with cardiac failure. Valve replacement is recommended.
b) Aortic Regurgitation:
*Causes:
Congenital valve disease: rheumatic fever, infective endocarditis, rheumatoid arthritis, SLE.
Aortic root disease: hypertension, trauma, aortic dissection, Marfan’s syndrome, syphilitic aortitis.
*Symptoms:
These include dyspnoea, palpitations, cardiac failure.
*Signs:
Collapsing pulse, wide pressure pulse, displaced hyperdynamic apex beat, high-pitched early diastolic murmur, Corrigan's sign, Duroziez's sign, de Musset's sign, Quincke's sign, Traube's sign.
*Investigations:
Cardiac ultrasonography is diagnostic. Cardiac catheterization is used to assess. X-ray may show cardiomegaly (unlike AS, CXR is NOT used). CT and MRI are used on thoracic aorta.
*Management:
ACE inhibitors and diuretics to maintain severe AR
AV replacement surgery is recommended, possibly with root replacement. Indications include increasing symptoms, enlarging heart, ECG deterioration.
VII) Mitral Valve Disease (Stenosis, Prolapse, Regurgitation)
a) Mitral Stenosis
*Definition:
Impaired diastolic flow of blood from left atrium into left ventricle through narrow mitral valve.
*Causes:
Rheumatic is the commonest cause (99%). Other causes include SLE, congenital, malignant carcinoid, and prosthetic valve.
*Symptoms:
These include dyspnoea, fatigue, palpitations, chest pain, haemoptysis, and chronic bronchitis-like picture.
*Signs:
These include malar flush, low-volume pulse, AF, tapping apex beat (palpable S1), low-pitched rumbling mid-diastolic murmur, and opening snap.
*Differential Diagnosis:
Atrial myxoma may cause similar signs.
*Tests/Investigations:
Cardiac ultrasonography confirms the diagnosis.
ECG for AF
CXR shows left atrial enlargement, pulmonary edema, and mitral valve calcification. Use chest catheterization if one of these is present: signs of other valve disease, angina, valve calcification, and severe pulmonary hypertension.
*Treatment:
Drugs: diuretics, beta-blockers, digoxin, warfrin.
Surgery: mitral valvotomy or mitral valve replacement.
Penicillin prophylaxis against RF.
b) Mitral Regurgitation
*Definition:
Abnormal systolic flow of blood from left ventricle back into left atrium from leaking valve.
Causes:
Mitral Valve Disease: MV prolapse, rheumatic valve disease, papillary muscle dysfunction/rupture, endocarditis.
Functional MR (secondary): LV dilatation from any cause
Connective Tissue Disorders: Ehlers-Danlos, Marfan’s Syndrome
Congenital: associated with other defects, e.g. ASD
Symptoms:
These include dyspnoea, fatigue, palpitations, and infective endocarditis.
Signs:
These include AF, hyperdynamic displaced apex, soft S1, split S2, loud P2, pansystolic murmur radiating to the axilla.
Tests/Investigations:
Cardiac ultrasonography to confirm MR and monitor LV function
Echocardiography to check severity (transthoracic or transesophageal)
CXR (shows big LA and LV), ECG, and cardiac catheterization as in MS
Treatment: as in MS but use antibiotics for prophylaxis against endocarditis.
c) Mitral Prolapse
Definition:
Mitral valve is larger than usual (possible congenital deformity, may occur with others). Because of that, part of the valve prolapses back into the left atrium during ventricular systole. It has 5% prevalence. It occurs alone or with MR.
Symptoms: WITHOUT MR it’s asymptomatic but may cause chest pain and palpitations.
Signs: WITHOUT MR there is a mid-systolic click and/or late systolic murmur.
Tests: Echocardiography is diagnostic. ECG may show inferior T-wave inversion.
Complications: MR, cerebral emboli, arrhythmias, sudden death, and endocarditis WITH MR.
Treatment: b-blockers prevent symptoms and endocarditis prophylaxis WITH MR.
VIII) Congenital Heart Disease
Definition:
Abnormal embryological cardiac development or persistence of some parts of the fetal circulation after birth resulting in structural cardiac defects.
Incidence:
Major defects account for 8/1000 live births. Minor defects more common.
Main Classification:
Four major categories: 1) shunt defects, 2) valvular defects, 3) complex lesions, 4) associated syndromes.
1) Shunt defects:
Three main defects: a) ventricular septal defect, b) atrial septal defect, c) patent ductus arteriosus.
a) Ventricular septal defect:
Incidence—25% of CHD
Definition—a defect in the interventricular septum allowing blood to shunt from left to right.
Types—small and large
Murmurs—smaller holes are haemodynamically less significant and give louder murmurs (Maladie de Roger)…classically, you can hear a harsh pansystolic murmur with systolic thrill and possible parasternal heave at the left sternal edge. Larger holes give quiet murmurs.
Complications—High risk endocarditis is especially present in smaller holes. Larger holes have more serious complications; can lead to pulmonary hypertension and Eisenmenger's syndrome if untreated.
b) Atrial septal defect:
Incidence—10% of CHD
Definition—a defect in the interatrial septum allowing blood to shunt from left to right.
Murmurs—ASD produces systolic pulmonary flow murmur and splitting of the 2nd heart sound.
Types—Ostium secundum (70%) and ostium primum (30%)
Presentation—secundum is often asymptomatic until adulthood. Primum presents early.
Complications—primum is often associated with AV valve anomalies and other defects (like VSD).
c) Patent ductus arteriosus:
Incidence—15% of CHD
Definition—Ductus arteriosus fails to close after birth, resulting in left-to-right shunting from the aorta to pulmonary artery.
Murmur—Continuous (machinery) murmur can be heard.
Complications—large ducts with significant shunt leads to complications (refer to ‘general shunt pathophysiology’)
*Associations:
Down’s Syndrome and Klinefelter’s Syndrome.
*Investigations/tests for shunt defects:
Echocardiography is diagnostic.
ECG showings in ASD: primum defect—left axis deviation (LAD), RBBB, and prolonged P-R interval, secundum defect—right axis deviation. Both are associated with RVH.
ECG showings in VSD: normal (small VSD), LAD + LVH (moderate VSD), LVH + RVH (large VSD).
Cardiac catheterization: O2 saturation in the right atrium (ASD) or right ventricle (VSD).
CXR: heart size, pulmonary plethora, enlarged arteries…all which depend on the size of the shunt.
*Treatment for shunt defects:
Surgical closure of the shunts before complications develop, precutaneous dilatation as an alternative.
*General shunt pathophysiology:
Mild-to-moderate shunt defect à left-to-right shunting à increase pulmonary blood flow à possible right heart hypertrophy
Large shunts à Eisenmenger’s Syndrome (i.e. irreversible pulmonary hypertension + shunt reversal from ‘left-to-right’ to ‘right-to-left’) à severe pulmonary hypertension signs (i.e. cyanosis, clubbing) à severe complications may develop (LVH, HF)
*Common complications to shunt defects:
These include bacterial endocarditis, heart hypertrophy (right or left), Eisenmenger’s Syndrome, heart failure, pulmonary hypertension, respiratory infections.
2) Valvular defects:
Definition:
Abnormal valve development, usually resulting in stenosis or atresia of valves
Types:
Three main types: a) aortic stenosis, b) bicuspid aortic valve, c) tricuspid atresia.
Bicuspid aortic valve:
Description—functions well at birth and go undetected. Most cases develop into AS and/or AR.
Associations—coarctation of aorta: the congenital narrowing of the descending aorta.
Coarctation of aorta:
Compensation—blood flow is maintained by increased collateral flow via mammary and intercostal arteries.
Associations—bicuspid aortic valve and Turner’s syndrome.
Signs—weak femoral pulse, radiofemoral delay, palpable collaterals around the scapulae, systolic murmur
Tests—echocardiography, CT or MRI, CXR shows rib notching
Complications—heart failure, infective endocarditis
Treatment—surgical correction or precutaneous dilatation
3) Complex lesions:
Definition:
These consist of abnormal relationships between various individual defects, including great vessels, arteries, chamber development, septal/valvular defects.
Types:
Three main types: a) Fallot’s tetralogy, b) Ebstein’s anomaly, c) transposition of the great vessels.
Fallot’s tetralogy:
Incidence—10% of CHD, most common complex lesion
Definition—combination of VSD and ‘right-to-left’ shunt due to; pulmonary stenosis, RVH, and dextro-position of the aorta which in turn overrides the VSD.
Features—children have breathlessness, dizziness, growth retardation
Signs—cyanosis, clubbing, pulmonary systolic murmur
Treatment—surgery aims to correct the defects and increase pulmonary blood flow via systemic-to-pulmonary artery shunts. The three main surgical shunts are; Blalock-Taussig (subclavian-to-pulmonary artery), Waterston (ascending aorta-to-right pulmonary artery), and Potts (descending aorta-to-left pulmonary artery).
Ebstein’s anomaly:
Tricuspid valve is displaced into the right ventricle, resulting in a small RV cavity and a large right atrium. It is associated with ASD and Wolf-Parkinson-White syndrome.
Transposition of the great arteries:
Definition—aorta arises from the right ventricle and pulmonary artery from the left ventricle.
Fate—incompatible with life unless there’s an ASD (shunting)
Treatment—balloon septostomy, interartiral shunt, congenitally corrected transposition.
IX) Coronary Syndromes/Ischemic Heart Diseases
Classification:
Acute Coronary Syndrome—unstable angina and evolving myocardial infarction
Chronic Coronary Syndrome—chronic stable angina
1) Angina Pectoris
*Definition:
This is due to myocardial ischemia and presents as a central chest tightness or heaviness, brought by exertion and relieved by rest. It may radiate to the arms, the neck, jaw, or teeth. Other precipitants include: emotion, cold weather, heavy meals.
*Associated symptoms:
Dyspnoea, nausea, sweatiness, faintness
*Causes:
Atheroma is the commonest. Anemia, AS, and arteritis are rare causes.
*Types:
a) Stable angina:
Definition—pain induced by effort, relieved by rest.
Risk stratification—outlook of chronic stable angina is worsened by; increasing age, exercise intolerance, impaired LV function, severe coronary disease, peripheral vascular disease, diabetes, etc.
Tests—Bruce protocol on exercise testing, four stages descending to ascending, 10-16% gradient, 0-12 minutes. ECG changes on exercise include; planar or downsloping ST depression (compared to the normal upsloping ST depression)
Treatment—anti-ischemic therapy, revascularization, coronary angioplasty, coronary artery bypass surgery (CABS)
b) Unstable angina:
Definition—pain of increasing frequency or severity, occurs on minimal excretion or at rest, unpredictable symptoms.
Risk stratification—factors associated with high-risk include: recurrent chest pain, impaired LV function, heart failure.
Tests—ECG shows ST depression and/or T wave inversion. Elevated cardiac markers (e.g. troponin, creatine kinase, AST, LDH), cholesterol, glucose
Treatment—emergency...aspirin, analgesia, IV b-blocker, LMW heparin, anti-platelet drugs to high-risk patients and cardiac catheterization
c) Crescendo angina: amount of effort provoking symptoms decreases, do not occur at rest. It can result from unstable angina.
2) Myocardial Infraction
*Definition:
Ischemic necrosis of the mydocardium as a result of acute occlusion of a coronary artery
*Causes:
Most common cause is atheromatous coronary artery disease. Rare causes include; coronary artery embolism/spasm/thrombosis/aneurysm/dissection, arteritis.
*Types:
a) Acute MI: otherwise known as ‘acute coronary syndrome with ST-elevation’.
b) Severe MI: ACS without ST-elevation. ECG can show; t-wave inversion (minutes or hours), and q-waves (days or months)
*Pathogenesis:
Basically, it’s plague rupture, thrombosis, and inflammation.
*Regions involved in MI:
a) Anterior: LAD artery occluded
b) Inferior: right CA
c) Posterior: right or circumflex
d) Lateral: circumflex or diagonal branch of LAD
*Clinical presentation:
a) Classic presentation: crushing central chest pain for more than 20 minutes, associated with sweating, pallor, and nausea.
b) Other presentations: arrhythmia, cardiac arrest, or heart failure
c) Elderly: collapse or confusion. "Silent infract" may occur
d) Diabetic: metabolic worsens or heart failure. “Silent infract” may occur.
*Differential Diagnosis:
Aortic Dissection and pericarditis
*Treatment:
Monitering in CCU, aspirin (chewed), masked oxygen, analgesia, thrombolysis
*Complications:
a) immediate/hours: AF, failed reperfusion
b) hours/days: cardiac rupture, cardiac arrest, re-infarction is common after thrombolysis
c) days/weeks: thromboembolism, chronic heart failure, tachycardia, Dressler’s syndrome.
No comments:
Post a Comment