Medicine Hack

As soon as a diagnosis of VTE / PE is strongly suspected, anticoagulant therapy should be started unless there are contraindications. Parenteral drugs like unfractionated heparin (standard heparin) and low molecular weight heparin (lovenox) are started and therapy shifted to a long term stable vitamin K antagonist like warfarin. Unfractionated heparin The anticoagulant action is by binding to and accelerating the activity of antithrombin III. This inactivates thrombin, factor IXa and Xa and thus prevents further clot formation. The classical regimen for the dosage is a loading dose of 5000 - 10000 units followed by a continuous infusion of 1000 - 1500 units/hour. Unfortunately we all do not have the same weight. So, a more appropriate dosage is a loading dose of 80 units/kg and a continuous infusion of 18 units/kg/hr. The aim is to achieve a target activated partial thromboplastin time (aPTT) aka partial thromboplastin time with kaolin (PTTK) of 2-3 times the normal laboratory val

1) First detected AF - It is the designation given when diagnosis has only recently been made. 2) Recurrent AF - When patient has experienced two or more episodes of AF. 3) Paroxysmal AF - Self terminating episodes that generally last less than 7 days (mostly <24 hr) 4) Persistent AF - Last more than 7 days and requires electrical or pharmacologic cardioversion. 5) Permanent AF - It has failed cardioversion and has been sustained for more than a year.

The use of I.V morphine in dyspnea from pulmonary edema due to left ventricular failure produces remarkable relief. The proposed mechanisms include:  1) reduced anxiety ( decreased perception of shortness of breath ),  2) reduced cardiac preload ( reduced venous tone ) and  3) decreased cardiac afterload (decreased peripheral resistance ).  However frusemide remains the treatment of choice.  Side effect is respiratory depression at a higher dosage which occurs because of inhibition of the brainstem respiratory mechanism.

LMNOP L - Lasix (frusemide) M - Morphine N - Nitrates O - Oxygen (If Sp02 < 95 %) P - Pulmonary ventilation (If patient bad)

The ECG changes in hypokalemia is mainly due to a delayed ventricular repolarisation. The changes normally do not correlate well with the plasma concentration. Early changes include flattening or inversion of the T wave, a prominent U wave, ST-segment depression k/a thumbprint-like ST depression, and a prolonged QU interval but the QT interval will be normal. Severe K + depletion may result in a prolonged PR interval, decreased voltage and widening of the QRS complex, and an increased risk of ventricular arrhythmias, especially in patients with myocardial ischemia or left ventricular hypertrophy. The QT interval may be normal or lengthened.

1) P wave - atrial depolarisation, < 120 ms 2) PR segment - end of P wave till beginning of QRS complex i.e. time taken between atrial and ventricular activation. 3) PR interval - onset of P wave till onset of QRS complex, 120-200 ms 4) QRS complex - ventricular depolarisation, <110 ms 5) T wave - ventricular repolarisation 6) U wave - repolarisation of Purkinje fibres 7) QT interval - beginning of QRS complex till end of T wave

The action potential of a cardiac muscle fiber can be broken down into several phases: 0- depolarization, 1- initial rapid repolarization, 2- plateau phase, 3- late rapid repolarization, 4- baseline. Many persons find it hard to understand why the curve is as such. I'll try to give a simple explanation in phases. The diagram shows the action potential and below it is what happens to the different ions. By convention, influx is shown by downward deflection while efflux by upward deflection. If positive ions get inside the curve will show an increase and it will show a decrease if ions get out. Phase 0 Unlike in skeletal muscles where there is only the fast sodium channels, in cardiac muscles there are both fast sodium channels and slow calcium-sodium channels. Both open simultaneously. Phase 0 is due to the rapid opening of the voltage gated sodium channels that leads to a massive influx of sodium ions that cause the initial rapid depolarisation. The slower calcium-sodiu

Cardiac muscle is striated same as a typical skeletal muscle. The muscle fibrils are surrounded by numerous and elongated mitochondria since the heart needs energy supply continously. The muscle fibres branch and interdigitate. They lie parallel to one another but at the end of each muscle fibres there are extensive folds of the cell membrane that are called as intercalated disks/discs . The intercalated discs act as gap junctions that is very permeable and allow almost free diffusion of ions. They always occur at the Z lines i.e. the dark middle section of the light (I) band of the muscle. They provide a strong union between fibers, maintaining cell-to-cell cohesion, so that the pull of one contractile cell can be transmitted along its axis to the next. The heart muscle thus acts as a syncytium. i.e. a multinucleated mass. Therefore when one of the cells is excited, the action potential spreads from cell to cell through the latticework interconnections fast and the syncytium as

The conducting system of the heart consists of: 1) Sino-Atrial Node (SAN), 2) Internodal tract, 3) Atrio-Ventricular Node (AVN), 4) Bundle of His or A-V Bundle, 5) Right and left Bundle branches, 6) Fascicles and  7) Purkinje fibres. In the human heart, the SA node is located at the junction of the superior vena cava with the right atrium.  The AV node is located in the right posterior portion of the interatrial septum.  There are three bundles of atrial fibers that contain Purkinje-type fibers and connect the SA node to the AV node:  a) the anterior internodal tract of Bachman,  b) the middle internodal tract of Wenckebach, and  c) the posterior internodal tract of Thorel.  Conduction also occurs through atrial myocytes, but it is more rapid in these bundles.  The AV node is continuous with the bundle of His, which gives off a left bundle branch at the top of the interventricular septum and continues as the right bundle branch.  The

It is a condition whereby the patient will have well perfused pink upper extremities evident by the pink finger nails while the lower extremities will both have cyanosis and clubbing in the toes, as shown in the picture above. In adults, it is commonly seen in patients of Patent Ductus Arteriosus (PDA) who have Pulmonary Hypertension at the same time. This occurs because venous blood shunts through the ductus and enters the aorta distal to the subclavian arteries.  In newborns, it can also occur in pre-ductal coarctation of aorta along with PDA. 

Class New York Heart Association (NYHA) Functional Classification I Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain. II Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain. III Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain. IV Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increas

Hyperkalemia is a very dangerous and potentially lethal condition because it will eventually affect the heart. With mild increase in plasma K + level, the first change in the ECG is the appearance of tall peaked T waves, which is a manifestation of altered repolarization. As plasma K + levels rise further, there is the paralysis of the atria and QRS complexes are prolonged and slurred.  Ventricular arrhythmias may develop. The resting membrane potential of the muscle fibers decreases as the extracellular K + concentration increases. The fibers eventually become unexcitable, and the heart stops in diastole.

It is a nice diagramatic representation of how the content of the diet of individuals varies with increase their income. This clearly causes an increase in the risk for cardiovascular diseases. As the income increases, there is a drastic increase in the intake of saturated animal fats and hydrogenated vegetable fats both of which contain atherogenic trans fatty acid. Simple carbohydrates are taken in more and vegetables are less eaten.

T ransposition of the great arteries T otal anomalous pulmonary venous return T runcus arteriosus T ricuspid atresia T etralogy of Fallot E bstein's anomaly E isenmenger physiology Critical pulmonary stenosis or atresia Functionally single ventricle Note there are 5 Ts and 2 Es.

The most characteristic finding is increased amplitude of the QRS complex. R waves in leads facing the left ventricle (i.e., leads I, aVL, V 5 , and V 6 ) are taller than normal, whereas S waves in leads overlying the right ventricle (i.e., V 1 and V 2 ) are deeper than normal. In many patients, the ST segment is depressed and followed by an inverted T wave. In most cases, the ST segment slopes downward from a depressed J point and the T wave is asymmetrically inverted (formerly called a “strain” pattern). A widening of the QRS complex may be there i.e. more than 110 ms and also the QRS complex may be notched. Common diagnostic criteria include: 1) Sokolow - Lyon index : SV 1 + (RV 5 or RV 6 ) > 3.5 mV                                        : RaVL > 1.1 mV 2) Cornell voltage criteria : SV 3 + SaVL ≥ 2.8 mV (for men)                                        : SV 3 + SaVL ≥ 2.0 mV (for women)

1) Increase dietary potassium intake 2) Limit dietary sodium intake to < 2.4 gm/day 3) Increase physical activity 4) Weight loss 5) All antihypertensive medications and combinations are effective 6) Multiple drug combinations may be required to achieve control 7) Angiotensin-converting enzyme (ACE) inhibitors and beta blockers as monotherapy may be less effective but should be used when indicated (e.g., renal disease, heart failure, post–myocardial infarction) 8) Thiazide diuretics and calcium channel blockers may have greater blood pressure–lowering efficacy 9) A higher incidence of angioedema occurs when using ACE inhibitors

In this condition there is exaggerated vagal discharge following carotid sinus stimulation when doing simple tasks like shaving or buttoning a tight shirt collar or even head rotation. There is reflex vasodilation and decrease in the pulse. These may combine to reduce blood pressure and cerebral perfusion in some elderly patients, causing loss of consciousness. Carotid sinus hypersensitivity is diagnosed by applying gentle pressure over the carotid pulsation just below the angle of the jaw, where the carotid bifurcation is located. Pressure should be applied for 5 to 10 seconds. It should be done in both supine and upright position. A normal response to carotid sinus massage is a transient decrease in the sinus rate, slowing of atrioventricular (AV) conduction, or both. Carotid sinus hypersensitivity is defined as a sinus pause longer than 3 seconds in duration and a fall in systolic blood pressure of 50 mmHg or more.

This is caused by autonomic overactivity, usually provoked by emotional or painful stimuli, less commonly by coughing or micturition. It is also called as neurocardiogenic syncope. The mechanism is that directly or indirectly, the nucleus tractus solitarius is activated by the triggering stimuli and this leads to increased parasympathetic tone and decreased sympathetic tone. The vagal parasympathetic tone leads to negative chronotropic and negative inotropic effects. This causes a slowing in the heart rate and decreased contractility that leads to a drop in the cardiac output. The decreased sympathetic tone on the other hand leads to vasodilation which leads to a decrease in the total peripheral resistance. Both cause a decrease of blood pressure significant enough to lead to loss of consciousness. 'Malignant' vasovagal syndrome is a rare condition where syncopal attacks so frequent that they are significantly disabling . Recovery is rapid if the patient lies down.

ACE inhibitors e.g enalapril remain one of the drug of choice to initiate anti hypertensive therapy. It acts by inhibiting the angiotensin converting enzyme and thus prevent the conversion of angiotensin I to angiotensin II. The latter is a potent vasoconstrictor. Since it is not being produced there is a resulting vasodilation and thus a decrease in the blood pressure. At the same time ACE inhibitors prevent the breakdown of bradykinin and sunbstance P. These 2 agents are potent protussive mediators in the respiratory tract and thus will cause dry cough. This is an indication to shift to angiotensin receptor blocker e.g. losartan.

The signs are caused by deposition of immune complex in the capillary circulation. These include: 1) Splinter hemorrhages : These are linear, subungual, dark red streaks especially in the fingers, less commonly in the toes. They are probably due to embolism to the linear capillaries in the nail bed. 2) Osler's nodes  : These are painful, tender, pea-sized erythematous nodules in the pulps of fingers. They tend to occur in crops and are indicator of either embolism to distal digital arteries or an immunological phenomenon. 3) Janeway lesions : These are painless erythematous lesions on the palms. They blanch on pressure.