Posted by: Johnson Francis on: 31 May, 2009
Non modifiable cardiovascular risk factors
Male gender
Advancing age
Family history of premature coronary artery disease
Modifiable cardiovascular risk factors
Diabetes mellitus
Body mass index
Abdominal obesity
Hypertension
Dyslipidemia – high LDL and low HDL
Smoking
Posted by: Johnson Francis on: 31 May, 2009
Ventricular remodeling is the changes in geometry of the left ventricle which occurs in the long term following a myocardial infarction. As time progresses, there is progressive infarct expansion and dilatation of the rest of the ventricle. The ellipsoid shape of the left ventricle gets converted to a more globular shape. This progressive change in shape and size of the left ventricle leads to heart failure. Ventricular remodeling can be prevented by unloading the left ventricle with angiotensin converting enzyme inhibitors or angiotensin receptor blockers which reduce the afterload of the left ventricle. Though ventricular remodeling is initially beneficial by increasing the stroke volume by the Frank-Starling mechanism which mentions that force of contraction increases with increasing myocardial fibre length to a certain extent. But increase in fibre length beyond an optimal level leads to ventricular failure. A patent infarct related coronary artery is also thought to influence the ventricular remodeling in a favourable way, meaning less of left ventricular dysfunction.
Posted by: Johnson Francis on: 01 Apr, 2009
Tricuspid regurgitation jet on colour Doppler echo
Tricuspid regurgitation jet seen on colour Doppler echocardiography from the apical four chamber view. RV right ventricle; LV left ventricle; LA left atrium; RA right atrium. The mosaic colour indicates high velocity with aliasing while the proximal most portion of the jet in right atrium is blue indicating flow away from the transducer. The tricuspid regurgitation in this case was moderate to severe. The right atrium and right ventricle are dilated due to pulmonary hypertension. Left atrium is also dilated due to mitral regurgitation.
Posted by: Johnson Francis on: 01 Apr, 2009
Tall sharp P waves in lead II measuring 0.25 mV (2.5 mm) or more
Sharp initial deflection of P wave in V1 of 0.1 mV (1 mm) or more
Sharp intrinsicoid deflection of P wave (atrial intrinsicoid deflection) is suggestive of right atrial enlargement even in the presence of a prominent negative deflection in V1 (pseudo left atrial enlargement pattern, often seen in atrial septal defect)
Posted by: Johnson Francis on: 25 Mar, 2009
Heparin
Heparin is found in the secretory granules of mast cells. Heparin is a catalytic template for the interaction of anti thrombin and thrombin. Heparin produces a conformational change in anti thrombin making it more reactive to thrombin. Heparin prolongs activated partial thromboplastin time (aPTT). Heparin causes release of lipoprotein lipase into the circulation and clears lipemic plasma. Heparin is degraded and cleared by the reticuloendothelial system.
Protamine sulphate is the heparin anti dote. 1 mg for 100 units of heparin left is needed. Dose of protamine for neutralisation can be calculated taking into account the initial dose administered, time elapsed and the half life of heparin.
Low molecular weight heparin (LMWH)
Low molecular weight heparin has more anti factor Xa activity than heparin. The incidence of heparin induced thrombocytopenia is lesser with low molecular weight heparin. But LMWH cannot be used as an anticoagulant in a person who has already developed heparin induced thrombocytopenia syndrome (HIT). The bioavailability of LMWH is more predictable than that of unfractionated heparin. LMWH activity can be measured by factor Xa activity. No anti dote is available for neutralization of LMWH.
Posted by: Johnson Francis on: 27 Feb, 2009
Prexcitation
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This ECG has a superficial resemblance to left bundle branch with tall slurred QRS complexes in lateral leads. The QS complexes in inferior leads mimick inferior wall infarction. Actually it is a non infarction Q wave or pseudo infarction pattern. The PR interal is short and is immediately followed by the slurred initial portion of the QRS in lateral leads, which is the positive delta wave. The delta wave is negative in inferior leads and V1. The tall QRS in lateral leads also mimick left ventricular hypertrophy.
Posted by: Johnson Francis on: 27 Feb, 2009
Arm lead inversion / technical dextrocardia
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Arm lead inversion (right arm lead placed on left arm and vice versa) can be recognized by inverted P waves, negative QRS and T waves in lead I. The same pattern can be seen in true dextrocardia as well. But in true dextrocardia, the chest electrodes will not show the usual progression of R waves, instead the QRS amplitude will progressively decrease from V1 to V6 as the heart is on the opposite side. Simple option is to get a repeat ECG for verification, if possible under direct supervision. Arm lead inversion or technical dextrocardia is one of the commonest errors in ECG recording.
This ECG also shows narrow Q waves and prominent T waves in lateral leads with mild concave upwards ST segment elevation. The S waves in lead V1 is deep and the R waves in V6 are tall, possibly an evidence of left ventricular hypertrophy by voltage criteria.
Posted by: Johnson Francis on: 22 Feb, 2009
Aims of cardiac rehabilitation
The primary aim of cardiac rehabilitation is to enable the patient to regain full physical, psychological and social status after a cardiac event. Cardiac rehabilitation can optimize the long term prognosis by secondary prevention.
Patient groups for cardiac rehabilitation
Following patient groups may benefit by cardiac rehabilitation programs:
Following an acute cardiac event
Awaiting or post revascularisation
Stable angina
Stable heart failure
Post valve surgery
Post heart transplantation
Post ICD (implantable cardioverter defibrillator) insertion
Benefits of cardiac rehabilitation
Benefits from a cardiac rehabilitation program will include a reduction in angina, blood pressure, anxiety and depression as well as hospital admissions. There is an improvement in the lipid profile, functional capacity, better compliance with lifestyle modification, increase in level of confidence, earlier return to work and leisure activities.
Myocardial effects of exercise
Myocardial oxygen consumption (MO2) depends on the double product. Double product = HR x SBP (heart rate multiplied by systolic blood pressure; double product determines the myocardial work load).
Rise in HR and SBP is determined by the VO2 (oxygen consumption) expressed as a percentage of the VO2max (maximum oxygen consumption) rather than the absolute value of VO2. VO2max increases with exercise training. Hence the rise in heart rate and systolic blood pressure and consequently the myocardial oxygen consumption for a given level of activity decreases as the exercise training program progresses.
Metabolic equivalent
1 MET (metabolic equivalent) = 3.5 ml oxygen/Kg/min. 1 MET is the basal metabolic oxygen consumption. Cardiac output can increase almost 6 times with maximal exercise. Oxygen extraction from arterial blood can increase almost 3 times with peak exercise. Hence oxygen consumption can increase about 18 times (VO2max). But in case of coronary circulation, oxygen extraction is maximum even at rest so that increase in oxygen supply can occur only by an increase in flow. A person with maximum exercise capacity of less than 2 METs will be in class IV. Those with an exercise capacity of 2-5 METs will be in class III and those with a capacity between 5-7 METs will be in functional class II. If a person has more than 7 METs of exercise capacity, the functional class will be I.
Phases of cardiac rehabilitation
Conventionally there are 4 phases for cardiac rehabilitation. The first phase starts during the hospital stay for the acute event or surgery. Phase II is after discharge from hospital and is usually carried out at home as per the advice of the rehabilitation team. Phase III, typically after 2-6 weeks, is either at the hospital cardiac rehabilitation facility or a community based program. Phase IV is long term maintenance, most often taken care of by leisure services.
Components of a cardiac rehabilitation program
A comprehensive cardiac rehabilitation program can include proper medications for secondary prevention and symptom limitation, graded exercise programs, advice on healthy eating, including participation in weight loss support groups, relaxation / stress management, general information on the disease process and a training on cardiopulmonary resuscitation for the relatives.
Potential risks of exercise program
Exercise programs do carry risks of worsening of ischemia, left ventricular dysfunction and potential for life threatening arrhythmias. Hence a proper risk stratification is needed prior to initiation of the exercise component of cardiac rehabilitation.
Contraindications to the exercise component of cardiac rehabilitation
Exercise component of the cardiac rehabilitation should be deferred in case of unstable angina, resting BP above 200 / 110mmhg, significant drop in BP during exercise, resting tachycardia > 100 bpm, uncontrolled atrial or ventricular arrhythmias, unstable heart failure, unstable / uncontrolled diabetes and febrile illness. Program can be resumed after stabilization of these situations.
Posted by: Johnson Francis on: 16 Feb, 2009
Anterior wall myocardial infarction
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the “Pardee’s sign” [Pardee HEB. An electrocardiographic sign of coronary artery obstruction. Arch Intern Med 1920; 26: 244– 257]. The current ECG show QS complexes in V1 and V2 and poor R waves in V3 and V4. ST segment elevation is maximum in lead V2. T waves are inverted in leads I, aVl and V1 to V5.
Posted by: Johnson Francis on: 13 Feb, 2009
Hypertension is an important risk factor for stroke, renal disease, coronary artery disease, peripheral arterial disease, left ventricular hypertrophy and congestive heart failure. Various cardiovascular complications of hypertension can cause significant morbidity and mortality.
Benefits of lowering blood pressure
Good control of hypertension reduces the stroke incidence by 35–40%, myocardial infarction by 20–25% and heart failure by 50%.
Blood pressure control rates
Inspite of increasing awareness of hypertension and the availability of better drugs, the control rates of hypertension is far from satisfactory.
While the awareness percentage rose from 51 in 1980s to 70 in 2000, the control rates were only 34 percent in 2000.
Joint national committee on prevention, detection, evaluation, and treatment of high blood pressure (JNC 7)
Joint national (US) committee on prevention, detection, evaluation, and treatment of high blood pressure (JNC 7) has classified hypertension as follows:
Normal: sysolic BP <120 mm Hg and diastolic BP <80 mm Hg.
Prehypertension: systolic BP between 120 – 139 mm Hg and diastolic BP betwen 80 and 89 mm Hg.
Stage 1 hypertension: systolic BP between 140 – 159 mm Hg and diastolic BP between 90 – 99 mm Hg.
Stage 2 hypertension: systolic BP > 160 mm Hg and disatolic BP > 100 mm Hg.
Key messages from JNC 7:
Systolic BP is a more important cardiovascular risk factor in those who are 50 years or more. Cardiovascular risk doubles with each increment of 20/10 mm Hg of BP. Prehypertensives require therapeutic life style modifications to prevent cardiovascular disease.