Showing posts with label CVS. Show all posts
Showing posts with label CVS. Show all posts

Valvular Heart Diseases : Aortic Regurgitation/Insufficiency


Aetiology (Causes)

Congenital-
     Bicuspid valve or disproportionate cusps
Acquired
     Rheumatic disease
     Infective endocarditis
     Failure of prosthetic heart valve
     Aortic dilatation (Marfan's syndrome, aneurysm, dissection, syphilis, ankylosing spondylitis)


Pathophysiology

Symptoms
   
Mild to moderate AR
     
Often asymptomatic
     Awareness of heart beat, 'palpitations'
     Severe AR
     Breathlessness
     Angina
Signs
     Pulses-
       Large volume or ‘collapsing pulse’
       Low diastolic and increased pulse preassure
       Bounding peripheral pulses- A rapidly rising "water-hammer" pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and diastole (Corrigan's pulse)
       Capillary pulsations, an alternate flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail (Quincke's pulse/sign)
       Femoral bruit (‘pistol shot’)- Duroziez’s sign/ Traube’s sign
       Head nodding with pulse- de Musset’s sign
     


Murmurs-
          Early diastolic murmur
          Systolic murmur (increased stroke volume)
          Austin Flint murmur (soft mid-diastolic)
Other signs
          Displaced, heaving apex beat (volume overload)
          Pre-systolic impulse
          Fourth heart sound
          Pulmonary venous congestion (crepitations)


Investigatons


ECG –
           Initially normal, later LV hypertrophy and T-wave inversion
Chest X-ray –
           Cardiac dilatation, maybe aortic dilatation
           Features of left heart failure
Echo Dilated left ventricle
           Hyperdynamic left ventricle
           Fluttering anterior mitral leaflet
           Doppler detects reflux
Cardiac catheterisation (may not be required)
          Dilated LV
          Aortic regurgitation
          Dilated aortic root


Treatment

Treat the cause- underlying conditions like endocarditis or syphilis.
Nefidipine or ACE inhibitors to lower the systolic blood preassure.
If end systolic dimension of left ventrical is =>55mm then- Aortic valve replacement is undertaken.
Aortic root replacement – in aortic root dilatation (eg. Marfan syndrome)

Essentials of Diagnosis
Usually asymptomatic until middle age; presents with left-sided failure or chest pain.
Wide pulse pressure.
Hyperactive, enlarged LV.
Diastolic murmur along left sternal border.
ECG shows LVH; radiograph shows LV dilation.
Echocardiography/Doppler is diagnostic.
Afterload reduction is beneficial if the LV is dilated (LV end-diastolic dimension > 5.0 cm).
Surgery indicated for symptoms, EF < 55%, or LV end-systolic dimension > 5.0 cm.

Rx of Coronary hear disease (CHD)


Coronary hear disease (CHD)/Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium.
It typically occurs when there is an imbalance between myocardial oxygen supply and demand.
The most common cause of myocardial ischemia is atherosclerotic disease - which results in inadequate perfusion of the myocardium.
the single most important cause of premature death in Europe, the Baltic states, Russia, North and South America, Australia and New Zealand.
By 2020 it is estimated that it will be the major cause of death in all regions of the world.
Abnormal constriction or failure of normal dilation of the coronary resistance vessels can also cause ischemia. When it causes angina, this condition is referred to as microvascular angina.


Factors influenting myocardial oxygen supply and demand/Pathophysiology

Oxygen demand

Cardiac work
Heart rate
Blood pressure
Myocardial contractility
Left ventricular hypertrophy
Valve disease, e.g. aortic stenosis


Oxygen supply

Coronary blood flow
Duration of diastole
Coronary perfusion pressure (aortic diastolic minus coronary sinus or right atrial diastolic pressure)
Coronary vasomotor tone
Oxygenation
Haemoglobin
Oxygen saturation


Coronary Atherosclerosis-

Epicardial coronary arteries are the major site of atherosclerotic disease.
The major risk factors for atherosclerosis disturb the normal functions of the vascular endothelium:
high plasma low-density lipoprotein (LDL),
low plasma high-density lipoprotein (HDL),
cigarette smoking,
hypertension, and
diabetes mellitus

These functions include local control of vascular tone, maintenance of an antithrombotic surface, and impairment of inflammatory cell adhesion and diapedesis.
The loss of these defenses leads to inappropriate constriction, luminal thrombus formation, and abnormal interactions with blood leukocytes, especially monocytes, and platelets.
This leads to atherosclerosis.





CORONARY HEART DISEASE: CLINICAL MANIFESTATIONS AND PATHOLOGY

Angina

Angina pectoris is the symptom complex caused by transient myocardial ischaemia and constitutes a clinical syndrome rather than a disease.
It may occur whenever there is an imbalance between myocardial oxygen supply and demand.
Coronary atheroma is by far the most common cause of angina.
The symptom may also be a manifestation of other forms of heart disease, particularly aortic valve disease and hypertrophic cardiomyopathy.


Stable Angina

Occurs when coronary perfusion is impaired by fixed or stable atheroma of the coronary arteries.

Activities precipitating angina
Common
Physical exertion
Cold exposure
Heavy meals
Intense emotion
Uncommon
Lying flat (decubitus angina)
Vivid dreams (nocturnal angina)



Clinical Features

Chest discomfort/pain-
                       
usually described as heaviness, pressure, squeezing, smothering, or choking, and only rarely as frank pain.
typically lasts 2–5 min, and can radiate to either shoulder and to both arms (especially the ulnar surfaces of the forearm and hand).
typically caused by exertion (e.g., exercise, hurrying, or sexual activity) or emotion (e.g., stress, anger, fright, or frustration) and are relieved by rest, they may also occur at rest.
Physical findings-

Usually negative
Evidence of valve disease (particularly aortic)
Important risk factors (eg. Hypertension, diabetes.)
Evidence of left ventricular dysfunction (cardiomegaly and gallop rhythm)
Other conditions- carotid bruits, peripheral vascular disease, anemia and thyrotoxicosis (unrelated conditions)


Cardiovascular Disease Classification Chart



Investigations

Resting ECG- Ischemia causes characteristic changes in the electrocardiogram.
Repolarization abnormalities, as evidenced by inversion of T waves and, when more severe, by displacement of ST segments.
Transient T-wave inversion likely reflects nontransmural, intramyocardial ischemia.
Transient ST-segment depression often reflects subendocardial ischemia.
 ST-segment elevation is thought to be caused by more severe transmural ischemia.


Exercise ECG- is performed using a standard treadmill or bicycle ergometer protocol while monitoring the patients ECG, BP and general condition.
Planar or down-sloping of ST segment depression of 1 mm or more is indicative of ishemia.
Up-sloping ST depression is less specific.



A positive exercise test. The resting 12-lead ECG shows some minor T-wave changes in the inferolateral leads but is otherwise normal. After 3 minutes' exercise on a treadmill there is marked planar ST depression in leads II, V4 and V5 (right offset). Subsequent coronary angiography revealed critical three-vessel coronary artery disease.


Other forms of stress testing

Myocardial perfusion scanning-

Stress echocardiography-

Coronary arteriography-

A technetium scan showing reversible anterior myocardial ischaemia. The images are cross-sectional tomograms of the left ventricle. The resting scans (right) show even uptake of technetium and look like doughnuts; during stress (in this case a dobutamine infusion) there is reduced uptake of technetium, particularly along the anterior wall (arrows), and the scans look like crescents (left).




Coronary angiogram from a patient with stable angina. There is severe stenosis of the left main stem (arrow).




Management

Assessment of the likely extent and severity of arterial disease
Identification and control of signifiacant risk factors
The use of measures to control symptoms
The identification of high-risk patients and application of treatments to improve life expectancy


Advice to patients with stable angina

Do not smoke
Aim at ideal body weight
Take regular exercise (exercise up to, but not beyond, the point of chest discomfort is beneficial and may promote collateral vessels)
Avoid severe unaccustomed exertion, and vigorous exercise after a heavy meal or in very cold weather
Take sublingual nitrate before undertaking exertion that may induce angina



Medical Therapy

Antiplatelet therapy-   Low-dose (75-150 mg) aspirin, Clopidogrel (75 mg daily) is an equally effective antiplatelet agent that can be prescribed if aspirin causes troublesome dyspepsia or other side-effects.
Anti-anginal drug treatment-

Nitrates GTN  (in the form of metered dose aerosol and sublingual tablets), transdermal and oral (isosorbide dinitrate and mononitrate).
Beta blockers
Calcium channel blockers
Potassium channel activators-  eg Nicorandil

Invasive Treatment

Percutaneous Coronary Intervention

Coronary Artery Bipass Grafting

Severe stenosis of the circumflex artery (arrow). A balloon has been advanced into the stenosis, over a guidewire, and has been inflated. (Note the waisting caused by the lesion.) Residual stenosis and dissection (tramline shadow-arrow) after balloon dilatation. A stent is deployed on a balloon. The stent is visible on plain fluoroscopy (arrow). Angiogram after stenting. A short balloon is used to dilate the stent at high pressure. Final result.

Coronary artery bypass graft surgery. Narrowed or stenosed arteries are bypassed using saphenous vein grafts connected to the aorta, or by utilising the internal mammary artery.

A scheme for the investigation and treatment of stable angina on effort. (PCI = percutaneous coronary intervention; CABG = coronary artery bypass grafting)

A silent killer : Hypertension


In children and adolescents, hypertension is generally defined as systolic and/or diastolic blood pressure consistently >95th percentile for age, gender, and height.
Blood pressures between the 90th and 95th percentiles are considered prehypertensive and are an indication for lifestyle interventions.
A recent classification recommends blood pressure criteria for defining normal blood pressure, prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a common occurrence among the elderly.

Blood Pressure Classification

Causes of secondary hypertension

Alcohol
Obesity
Pregnancy (pre-eclampsia)
Renal disease (Ch. 17) Renal vascular disease,Parenchymal renal disease, particularly glomerulonephritis , Polycystic kidney disease
Endocrine disease Phaeochromocytoma, Cushing's syndrome, Primary hyperaldosteronism (Conn's syndrome), Hyperparathyroidism, Acromegaly, Primary hypothyroidism, Thyrotoxicosis, Congenital adrenal hyperplasia due to 11-β-hydroxylase or 17-hydroxylase deficiency, Liddle's syndrome,11-β-hydroxysteroid dehydrogenase deficiency.
Drugs e.g. Oral contraceptives containing oestrogens, anabolic steroids, corticosteroids, non-steroidal anti-inflammatory drugs, carbenoxolone, sympathomimetic agents


Measurement of Blood Pressure

Use a machine that has been validated, well maintained and properly calibrated
Measure sitting BP routinely, with additional standing BP in elderly and diabetic patients and those with possible postural hypotension
Remove tight clothing from the arm
Support the arm at the level of the heart
Use a cuff of appropriate size (the bladder must encompass > two-thirds of the arm)
Lower the mercury slowly (2 mm per second)
Read the BP to the nearest 2 mmHg
Use phase V (disappearance of sounds) to measure diastolic BP
Take two measurements at each visit


Patient's Relevant History

Duration of hypertension
Previous therapies: responses and side effects
Family history of hypertension and cardiovascular disease
Dietary and psychosocial history
Other risk factors: weight change, dyslipidemia, smoking, diabetes, physical inactivity
Evidence of secondary hypertension: history of renal disease; change in appearance; muscle weakness; spells of sweating, palpitations, tremor; erratic sleep, snoring, daytime somnolence; symptoms of hypo- or hyperthyroidism; use of agents that may increase blood pressure
Evidence of target organ damage: history of TIA, stroke, transient blindness; angina, myocardial infarction, congestive heart failure; sexual function.


History and Examination

History- family history, life style (exercise, salt intake, smoking habit), and other risk factors. Drug or alcohol consumption, other features of secondary hypertension causes eg. Pheochromocytoma (paroxysmal headache, palpitation and sweating.)
Examination- measure blood pressure, look for radio-femoral delay, enlarged kidneys (PKD), abdominal bruits (renal artery stenosis), and characteristic facies and habitus of Cushing’s syndrome, central obesity and xanthomas.


Target organ damage

Retinal changes in hypertension.   Grade 4 hypertensive retinopathy showing swollen optic disc, retinal haemorrhages and multiple cotton wool spots (infarcts).   Central retinal vein thrombosis showing swollen optic disc and widespread fundal haemorrhage, commonly associated with systemic hypertension.


Hypertensive encephalopathy-

A rare condition characterised by high blood pressure and neurological symptoms.
Includs transient disturbances of speech or vision, paraesthesiae, disorientation, fits and loss of consciousness. Papilloedema is common.
A CT scan of the brain often shows haemorrhage in and around the basal ganglia; however, the neurological deficit is usually reversible if the hypertension is properly controlled.


‘Malignant’ or ‘accelerated’ phase hypertension

A rare condition which may complicate hypertension of any etiology.
Characterized by accelerated microvascular damage with necrosis in the walls of small arteries and arterioles (fibrinoid necrosis) and by intravascular thrombosis.
Diagnosis based on- high blood pressure and
Rapidly progressive end organ damage- such as retinopathy of grade 3 or 4, renal dysfunction (proteinuria), and/or hypertensive encephalopathy.
Left ventricular failure may occur and if not treated death may occur within months.


Investigation of all patients

Urinalysis for blood, protein and glucose
Blood urea, electrolytes and creatinine
Blood glucose
Serum total and high-density lipoprotein (HDL) cholesterol
12-lead ECG (left ventricular hypertrophy, coronary artery disease)


Investigations in selected patients

Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta
Ambulatory BP recording: to assess borderline or 'white coat' hypertension
Echocardiogram: to detect or quantify left ventricular hypertrophy
Renal ultrasound: to detect possible renal disease
Renal angiography: to detect or confirm presence of renal artery stenosis
Urinary catecholamines: to detect possible phaeochromocytoma.


Treatment

Lifestyle Modifications to Manage Hypertension



Antihypertensive drugs

Thiazide and other diuretics- mechanism of action is incompletely understood. A daily dose of 2.5 mg bendroflumethiazide or 0.5 mg cyclopenthiazide is appropriate. Furosemide(loop diuretics) have few advantages over thiazides in hypertension.
Beta-adrenoceptor antagonists (β-blockers)- Metoprolol (100-200 mg daily), atenolol (50-100 mg daily) and bisoprolol (5-10 mg daily) are cardioselective.


Labetalol and carvidilol- are combined β- and α-adrenoceptor antagonists. Labetalol (200 mg-2.4 g daily in divided doses) and carvedilol (6.25-25 mg 12-hourly).
Angiotensin-converting enzyme (ACE) inhibitors: e.g. enalapril 20 mg daily, ramipril 5-10 mg daily or lisinopril 10-40 mg daily. They should be used with particular care in patients with impaired renal function or renal artery stenosis because they can reduce the filtration pressure in the glomeruli and precipitate renal failure. Electrolytes and creatinine should be checked before and 1-2 weeks after commencing therapy.
Side-effects include first-dose hypotension, cough, rash, hyperkalaemia and renal dysfunction.


Angiotensin receptor blockers- These drugs (e.g. losartan 50-100 mg daily, valsartan 40-160 mg daily) block the angiotensin II type I receptor and have similar effects to ACE inhibitors but do not cause cough and are better tolerated.
Calcium antagonists- The dihydropyridines (e.g. amlodipine 5-10 mg daily, nifedipine 30-90 mg daily) are effective and usually well-tolerated antihypertensive drugs that are particularly useful in the elderly.
Side-effects include flushing, palpitations and fluid retention.
Diltiazem 200-300 mg daily, verapamil 240 mg daily can be useful when hypertension coexists with angina but they may cause bradycardia. The main side-effect of verapamil is constipation.


Other drugs- These include the α1-adrenoceptor antagonists (α-blockers), such as prazosin (0.5-20 mg daily in divided doses), indoramin (25-100 mg 12-hourly) and doxazosin (1-16 mg daily), and drugs that act directly on vascular smooth muscle, such as hydralazine (25-100 mg 12-hourly) and minoxidil (10-50 mg daily).
Side-effects include first-dose and postural hypotension, headache, tachycardia and fluid retention.
Centrally acting drugs, such as methyldopa (initial dose 250 mg 8-hourly) and clonidine (0.05-0.1 mg 8-hourly), are effective antihypertensive drugs but cause fatigue and are usually poorly tolerated.
Adjuvant drug therapy – Aspirin and Statins.


It is unwise to lower blood pressure too quickly because this may compromise tissue perfusion (due to altered autoregulation) which may lead to cerebral damage, including occipital blindness, and precipitate coronary or renal insufficiency.
Even in the presence of cardiac failure or hypertensive encephalopathy, a controlled reduction, to a level of about 150/90 mmHg, over a period of 24-48 hours is ideal.
Intravenous or intramuscular labetalol (2 mg/min to a maximum of 200 mg), intravenous glyceryl trinitrate (0.6-1.2 mg/hour), intramuscular hydralazine (5 or 10 mg aliquots repeated at half-hourly intervals) and intravenous sodium nitroprusside (0.3-1.0 μg/kg body weight per minute) are all effective remedies but require careful supervision, preferably in a high-dependency unit.

Treatment of Acute Rheumatic Fever


Acute Rheumatic Fever

Acute rheumatic fever (ARF) is a multisystem disease resulting from an autoimmune reaction to infection with group A streptococci.
Although many parts of the body may be affected, almost all of the manifestations resolve completely.
The exception is cardiac valvular damage [rheumatic heart disease (RHD)], which may persist after the other features have disappeared.
Acute rheumatic fever (ARF) usually affects children (most commonly between 5 and 15 years) or young adults.
 It remains endemic in parts of Asia, Africa and South America. It is still the most common cause of acquired heart disease in childhood and adolescence.

Pathogenesis

Organism factors- exclusively caused by infection of the upper respiratory tract with group A streptococci. Any strain of group A streptococcus has the potential to cause ARF.
Host factors- Approximately 3–6% of any population may be susceptible to ARF. Presence of familial susceptibility.
The immune response- When a susceptible host encounters a group A streptococcus, an autoimmune reaction results, which leads to damage to human tissues as a result of cross-reactivity between epitopes on the organism and the host.
Epitopes present in the cell wall, cell membrane, and the A, B, and C repeat regions of the streptococcal M protein are immunologically similar to molecules in human myosin, tropomyosin, keratin, actin, laminin, vimentin, and N-acetylglucosamine.

Antibodies developed against group A streptococcal M proteins cross react with similar proteins in human tissue (endocardium, myocardium and pericardium as well as joint and skin).
Also results in T-cell sensitization. These T cells are then recalled following subsequent exposure to group A streptococci bearing immunologically similar epitopes.
Histologically, fibrinoid degeneration is seen in the collagen of connective tissues. Aschoff nodules are pathognomonic and occur only in the heart. They are composed of multinucleated giant cells surrounded by macrophages and T lymphocytes, and are not seen until the subacute or chronic phases of rheumatic carditis.



Typically follows an episode of streptococcal pharyngitis and usually presents with fever, anorexia, lethargy and joint pains.
Symptoms characteristically occur 2-3 weeks after the initial attack of pharyngitis but the patient may not give history of sore throat.
Arthritis- The most common major manifestation and is characterised by acute, painful, asymmetric and migratory inflammation of the large joints (typically the knees, ankles, elbows and wrists). Occurs in approximately 75% of patients, usually an early feature that tends to occur when streptococcal antibody titres are high.

Carditis- a 'pancarditis' that involves the endocardium, myocardium and pericardium to varying degrees.
May manifest as breathlessness (due to heart failure or pericardial effusion),
Palpitations or chest pain (usually due to pericarditis or pancarditis).
Tachycardia, cardiac enlargement and new or changed cardiac murmurs.
Murmurs- A soft systolic murmur due to mitral regurgitation is very common. A soft mid-diastolic murmur (the Carey Coombs murmur) is typically due to valvulitis, with nodules forming on the mitral valve leaflets.
Pericarditis may cause chest pain, a pericardial friction rub and precordial tenderness.

Skin lesions- Erythema marginatum occurs in less than 5% of patients. Occur mainly on the trunk and proximal extremities but not the face.
Subcutaneous nodules occur in 5-7% of patients. They are small (0.5-2.0 cm), firm and painless, and are best felt over extensor surfaces of bone or tendons.
Appear more than 3 weeks after the onset of other manifestations and are therefore a feature that helps to confirm rather than make the diagnosis.

Sydenham's chorea (St Vitus dance)- a late neurological manifestation that typically appears at least 3 months after the episode of ARF when all the other signs may have disappeared.
Emotional lability may be the first feature and is typically followed by purposeless involuntary choreiform movements of the hands, feet or face. Spontaneous recovery usually occurs within a few months.
Other systemic manifestations are rare, but include pleurisy, pleural effusion and pneumonia.

Investigations

Evidence of a systemic illness (non-specific)
Leucocytosis, raised ESR, raised CRP

Evidence of preceding streptococcal infection (specific)
Throat swab culture: group A β-haemolytic streptococci (also from family members and contacts)
Antistreptolysin 0 antibodies (ASO titres): rising titres, or levels of > 200 U (adults) or > 300 U (children)

Evidence of carditis
Chest X-ray: cardiomegaly; pulmonary congestion
ECG: first- and rarely second-degree heart block; features of pericarditis; T-wave inversion; reduction in QRS voltages
Echocardiography: cardiac dilatation and valve abnormalities

Jones Criteria for the Diagnosis of Rheumatic Fever

Major manifestations
Carditis
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules

Minor manifestations Fever
Arthralgia
Previous rheumatic fever
Raised ESR or CRP
Leucocytosis
First-degree AV block (ECG changes)

PLUS  Supporting evidence of preceding streptococcal infection: recent scarlet fever, raised antistreptolysin 0 or other streptococcal antibody titre, positive throat culture.

Treatment

Bed rest and supportive therapy -
Antibiotics-
Penicillin is the drug of choice and can be given orally (as penicillin, 500 mg PO twice daily for 10 days) or as a single dose of 1.2 million units IM benzathine penicillin G.
Erythromycin, 250 mg bid, may be used for patients with penicillin allergy.
Salicylates and NSAIDs- for the treatment of arthritis, arthralgia, and fever, once the diagnosis is confirmed.
Aspirin is the drug of choice. An initial dose of 80–100 mg/kg per day in children (4–8 g/d in adults) in 4–5 divided doses is often needed for the first few days up to 2 weeks.
Corticosteroids- prednisolone 1-2mg/kg per day in divided doses.


Secondary prevention-

Early medical management of MI


Myocardial Infraction
Myocardial infarction occurs when cardiac myocytes die due to prolonged myocardial ischaemia.
The diagnosis can be made in patients with an appropriate clinical history together with findings from repeated 12-lead ECGs and elevated biochemical markers - troponin I and T, CK-MB.
STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury.
This injury is produced or facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation.
A mural thrombus forms at the site of plaque disruption, and the involved coronary artery becomes occluded.
Histologic studies indicate that the coronary plaques prone to disruption are those with a rich lipid core and a thin fibrous cap.

Clinical Features

Symptoms
Prolonged cardiac pain: Chest, throat, arms, epigastrium or back (pain is not uniformly present in patients with STEMI).
Anxiety and fear of impending death
Nausea and vomiting
Breathlessness
Collapse/syncope

Physical signs
Signs of sympathetic activation
Pallor, sweating (The combination of substernal chest pain persisting for >30 min and diaphoresis strongly suggests STEMI), tachycardia
Signs of vagal activation (up to one-half with inferior infarction)
Vomiting, bradycardia
Signs of impaired myocardial function (physical signs of ventricular dysfunction )
Hypotension, oliguria, cold peripheries
Narrow pulse pressure
Raised jugular venous pressure
Third heart sound
Quiet first heart sound
Diffuse apical impulse
Lung crepitations
Signs of tissue damage
Fever
Signs of complications, e.g. mitral regurgitation, pericarditis.

Investigations
Electrocardiogram
Serum cardiac biomarkers-
 Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI)
 CKMB
Cardiac Imaging-
 Echocardiography: estimation of left ventricular (LV) function is useful prognostically; detection of reduced function serves as an indication for therapy with an inhibitor of the renin-angiotensin-aldosterone system.
 Identify the presence of right ventricular (RV) infarction, ventricular aneurysm, pericardial effusion, and LV thrombus.



Typical ECG changes in myocardial infarction (STEMI)

Cardiac biomarkers

Typical cardiac biomarkers that are used to evaluate patients with STEMI include the MB isoenzyme of CK (CKMB) and cardiac-specific troponins. The black horizontal line depicts the upper reference limit (URL) for the cardiac biomarker in the clinical chemistry laboratory.



Early medical management

brief history/risk factors. Examination
intravenous access + blood for markers (plus FBC, biochemistry, lipids, glucose)
12 lead ECG
intravenous opiate, e.g. morphine sulphate 5-10 mg or diamorphine 2.5-5 mg + anti-emetic, e.g. metoclopramide 10 mg
aspirin 150-300 mg chewed
sublingual glyceryl trinitrate 0.3-1 mg. Repeat
oxygen - nasal cannula 2-4 L/min
beta-blocker (if no contra-indication) for ongoing chest pain, hypertension, tachycardia
if primary PCI available give GP IIb/IIIa inhibitor. Alternatively give thrombolysis.

Fibrinolysis/Thrombolysis
Fibrinolytic agents enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin.
The initial thrombolytic agent used in clinical trials was streptokinase. Others are tissue plasminogen activator (alteplase), Newer-generation analogues of tPA (tenecteplase (TNK))
This agent is derived from bacteria, which can lead to the development of neutralizing antibodies that limit its repeated use.
Given as early as possible: <30 mins of onset of symptoms.

Streptokinase, 1.5 million U in 100 ml of saline given as an intravenous infusion over 1 hour, is a widely used regimen.
Alteplase (human tissue plasminogen activator or tPA) is a genetically engineered drug that is not antigenic and seldom causes hypotension.
The standard regimen is given over 90 minutes (bolus dose of 15 mg, followed by 0.75 mg/kg body weight, but not exceeding 50 mg, over 30 minutes and then 0.5 mg/kg body weight, but not exceeding 35 mg, over 60 minutes).

Contraindications to thrombolysis

Primary percutaneous coronary intervention (PCI)
In institutions that are able to offer rapid access (within 3 hours) to a 24-hour catheter laboratory service, percutaneous coronary intervention is the treatment of choice.
In comparison to thrombolytic therapy, it is associated with a 50% greater reduction in the risk of death, recurrent myocardial infarction or stroke.
Intravenous thrombolytic therapy remains the first-line reperfusion treatment in many hospitals with advanced cardiac unit.

Valvular Heart Diseases : Tricuspid Stenosis


Tricuspid Stenosis

Etiology-

Generally rheumatic in origin
Females more than in males
Usually associated with Mitral Stenosis
Clinicallly evident Tricuspid Stenosis occurs in 5-10% of cases
Rheumatic Tricuspid Stenosis is commonly associated with some degree of Tricuspid Regurgitation
Nonrheumatic causes of TS are rare.

Pathophysiology
A diastolic pressure gradient between the Right Atrium and Right Ventricle defines Tricuspid Stenosis.
A mean diastolic pressure gradient of 4 mmHg is usually sufficient to elevate the mean RA pressure to levels that result in systemic venous congestion.
This results in a reduced cardiac output, which is restored towards normal when the right atrial pressure increases.
The elevated Right Atrial preassure and Systemic venous congestion gives the clinical features of Tricuspid Stenosis

Clinical Features

Symptoms-
Since the development of MS generally precedes that of TS, many patients initially have symptoms of pulmonary congestion.
Spontaneous improvement of these symptoms should raise the possibility that TS may be developing.
Fatigue secondary to low cardiac output.
Discomfort due to edema, ascitis and hepatomegaly.

Signs-
The jugular veins are ditended. In cases of sinus rhythm (i.e. in absence of atrial fibrillation and other arrhythmias) there is prominent a wave and a slow y descent.
Mid-diastolic murmur- usually best heard at the lower left sternal border. Augmented during inspiration and reduced during expiration.
Features of right heart failure- hepatic congestion (hepatomegaly), ascitis and bilateral pitting edema.

Investigations
The ECG features of RA enlargement include tall, peaked P waves in lead II, as well as prominent, upright P waves in lead V1.
The chest x-ray in patients with combined TS and MS shows particular prominence of the RA and superior vena cava without much enlargement of the PA and with less evidence of pulmonary vascular congestion than occurs in patients with isolated MS.
On echocardiographic examination, the tricuspid valve is usually thickened and domes in diastole.
The transvalvular gradient can be estimated by Doppler echocardiography.

Management

Medical management consists of diuretic therapy and salt restriction. Specially during preoperative period.
Tricuspid valvotomy is occasionally possible, but tricuspid valve replacement is often necessary.
Other valves usually also need replacement because tricuspid valve stenosis is rarely an isolated lesion.

Tricuspid Regurgitation

Etiology-

Primary- Rheumatic heart disease
                 Endocarditis, particularly in IV drug abusers
                 Ebstein’s congenital anomaly

Secondary- Right ventricular dilatation due to chronic heart failure.
                     Right ventricular infraction
                     Pulmonary Hypertension (eg. Cor pulmonale)

Clinical Features
Symptoms-
Nonspecific related to reduced forward flow like tiredness.
Signs-
Features of systemic venous congestion. Ascitis, bilateral pitting edema, hepatic enlargement and raised JVP.
JVP- systolic wave a cv wave replacing normal x descent.
A pansystolic murmur at the left sternal edge.
Investigations
ECG- right axis deviation
Chest X-ray- right ventricular enlargement
Echo- reveals dilated right ventricles, thickened tricuspid valve of Rheumatic origin, Endocarditis vegetation and Ebstein anomaly.
Management
Often improves when the cause of right ventricular overload is corrected. Eg. Diuretics and vasodilator treatment of CCF.
Patient with normal pulmonary artery pressure tolerate isolated tricuspid reflux well so the valve replavement is not always necessary.
Annuloplasty ring- with marked dilatation of tricuspid annulus
Tricuspid valve replacement in rheumatic damage.

ACUTE CORONARY SYNDROMES and its types ?


ACUTE CORONARY SYNDROMES

Acute coronary syndromes (ACS) include:
Non-ST-elevation myocardial infarction (NSTEMI), and
Unstable angina,
ST-elevation myocardial infarction (STEMI)

Myocardial infarction occurs when cardiac myocytes die due to myocardial ischaemia, and can be diagnosed on the basis of:
appropriate clinical history,
12-lead ECG and
elevated biochemical markers - troponin I and T, creatinine-kinase-MB (CK-MB).


The spectrum of acute coronary syndromes. The relation between ECG changes, biochemical markers of damage and the extent of myocardial necrosis. (CK = creatine kinase)



The above figure explains ECG changes in ischemis with regard to extent of myocardial damage:
Ischemia with no myocardial damage- Unstable angina- ST and T wave changes (like ST depression and T wave inversion)
Ischemia with minimal myocardial damage,
Partial thickness (non ST elevation or non-Q wave) myocardial infraction, and
Full thickness (Q wave myocardial infraction)

Pathophysiology
The common mechanism to all ACS (Acute coronary syndrome- unstable angina, non ST elevation MI and ST elevation MI) is rupture or erosion of the fibrous cap of a coronary artery plaque.
This leads to platelet aggregation and adhesion, localized thrombosis, vasoconstriction, and distal thrombus embolization.
The presence of a rich lipid pool within the plaque and a thin fibrous cap, are associated with an increased risk of rupture.
Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2, results in myocardial ischaemia due to reduction of coronary blood flow.

Unstable Angina

Unstable angina (UA) is defined as- angina pectoris or equivalent ischemic discomfort with at least one of three features:
(1) it occurs at rest (or with minimal exertion), usually lasting >10 min;
(2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
(3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.

Clinical Findings


The clinical hallmark of UA/NSTEMI is (symptoms)
chest pain, typically located in the substernal region or sometimes in the epigastrium, that radiates to the neck, left shoulder, and left arm.
Anginal "equivalents" such as dyspnea and epigastric discomfort may also occur.

The examination resembles that in patients with stable angina and may be unremarkable.
If the patient has a large area of myocardial ischemia or a large NSTEMI, the physical findings can include
diaphoresis,
pale cool skin,
sinus tachycardia,
a third and/or fourth heart sound,
basilar rales, and
sometimes hypotension, resembling the findings of large STEMI.

Investigations

ECG- In UA, ST-segment depression, transient ST-segment elevation, and/or T-wave inversion, depending on the severity of the clinical presentation.
T-wave changes are sensitive for ischemia but less specific, unless they are new, deep T-wave inversions.

Cardiac Biomarkers (bichemical test)- Creatinine Kinase (CKMB) and Troponin.
Elevated levels of these markers distinguish patients with NSTEMI from those with UA.
In patients with an unclear history, small troponin elevations may not be diagnostic of an ACS.


A guide to the investigation and treatment of unstable angina and non-ST segment elevation myocardial infarction (NSTEMI).