Cardiology Flashcards
Class I anti arrhythmic Drugs:-
IA : intermediate sodium blocking activity that prolongs QRS complex duration and moderate potassium channel blocking activity that prolongs QT interval
IB: donot increase QRS duration nor QT prolongation because they rapidly dissociate from receptor
IC: strong sodium channel blocking activity that significantly increase QRS duration and a little bit increase in QT interval due to QRS widening
Class I anti arrhythmic drugs bind to sodium channel in inactive or open state and dissociate in resting state, the faster the heart rate, the more time sodium channels spend in open state the more they will be blocked (use dependence)
Class IB bind weakly to Na channels, they are more useful in ischemic myocardium bcoz of less negative potential of membrane which cause delay conversion of Na channel from open state to resting state, thus class IB drugs are good to prevent ischemia induced arrhythmia
Class IC are good to use in terminating tachyarrythmia but they also have proarhythmic effect
Subclavian steal syndrome:-
Causes atherosclerosis, takayasu arteritis, complication from heart surgery
Symptoms: arm ischemia (exercise induced pain, fatigue paresthesia), vertebrobasilar insufficiency (vertigo, dizziness, drop attacks)
Difference in blood pressure in both brachial artery more than 15mmHg drop,
Doppler ultrasound will confirm the diagnosis
Paroxysmal Atrial Fibrillation:-
Treatment includes rate and rhythm control
Rate control is achieved via AV nodal blocking drugs i.e beta-blockers and Ca channel blockers
Rhythm control is achieved via anti arrhythmic drugs
QT interval is mainly a measure of ventricular repolarization
Class III antiarrythmic drugs are K+channel blocker and prolong QT interval and predispose to development of torsade-de-pointes
Sotalol and dofetilide are more proarythmic than amiodarone.
Sotalol also has beta blocking activity so also causes bradycardia
Constrictive Pericarditis:-
Possible causes include TB, radiation to the chest, cardiac surgery
Symptoms usually mimic right heart failure, with progressive dyspnea, lower extremity edema, ascites and weight gain
A rapid Y descent (Fredrich sign) on the JVP is characteristic of constrictive pericarditis
Prinzmetal angina or Vasospastic Angina:-
Intermittent coronary artery vasospasm due to endothelial dysfunction and autonomic imbalance
Chest pain specially at night or sleep when vagal tone is peak and resolve within 15min
Smoking is the major risk factor
Diagnosis with ambulatory ECG which shows ST elevation during episode and followed by angiography to rule out CAD
Treatment with nitroglycerin and to prevent episode in future Ca channel blockers
Atrial Fibrillation:-
Rate control is achieved via blockade of conduction through AV node
1) beta-blockers : controlling sympathetic tone at rest and exercise
2)calcium channel blockers have same efficacy at rest and during exercise
3)Digoxin controls rate via increased parasympathetic tone in AV node so good to control heart rate at rest but during exercise sympathetic tone is high so it poorly controls the heart rate
Carcinoid Syndrome:-
Well-differentiated neuroendocrine tumors originate in gut and produce products like histamine, serotonin and VIP that are metabolized in liver
When metastasis occurs in liver these products are released in systemic circulation and cause Carcinoid Syndrome.
Carcinoid heart disease is caused by serotonin which stimulates fibroblast and cause fibrogenesis deposit on right sided heart valves because these products get metabolised in pulmonary circulation.
5-HIAA is by product of serotonin and 24 hr urinary production helps in diagnosis
Episodic flushing, secretory diarrhea, wheezing with fibrous plaque on right side valve causing tricuspid regurgitation and right heart failure
Cardiovascular changes during exercise:-
Vasoconstriction of capacitance veins increases venous return and preload and LV EDV
Vasoconstriction of splmachnic circulation and vasodilation of skeletal muscle cause shifting of blood towards muscle and overall decrease in Systemic vascular resistance
Increase in contractility increases stroke volume
Net increase in after load as LV has increased contractility so it generate maximum pressure
Net increase in SV and HR and Contractility increases cardiac output
Hypertriglyceridemia:-
Moderately elevated triglycerides (>500) requires pharmacologic therapy with lifestyle modifications such as increase aerobic exercise, decrease alcohol and caloric intake
Pharmacologic therapy includes fibrates which act via PPARalpha which decrease hepatic VLDL synthesis and increase lipoprotein lipase activity
Renal Artery Stenosis:—
Unilateral stenotic kidney will demonastrate parenchymal ischemia and morphologic changes include diffuse cortical thinning, tubules atrophic, crowded small glomeruli, interstitial fibrosis and enlargement of JG apparatus due to chronic stimulation of renin release which cause chronic hypertension
Nonstenotic kidney due to chronic HTN will develop hypertensive nephrosclerosis undergo arteriole wall thickening hyaline and hyperplastic arteriolosclerosis
Hyaline is caused by extravastion of plasma proteins and hyperplastic is caused by smooth muscle cell proliferation
