FISDAP Cardiology P3 Exam - ADAME Questions With Correct Answers

Cardiac cellular action potential - Answer The cardiac action potential is a short-lasting event in which the membrane potential (the difference of potential between the interior and the exterior) of a cardiac cell rises and falls following a consistent trajectory, similar to the action potential in other types of cells. Cardiac action potentials are generated by the movement of ions through the transmembrane ion channels in the cardiac cells. Phase 4 is the resting membrane potential, and describes the membrane potential when the cell is not being stimulated. So in the standard myocyte model this phase will be a horizontal line. The resting membrane potential is caused by the difference in ionic concentrations and conductances across the cell membrane during phase 4 of the action potential. The normal resting membrane potential in the ventricular myocardium is about -85 to -95 mV. This potential is determined by the selective permeability of the cell membrane to various ions. The membrane is most permeable to K+ (mainly due to leak channels) and relatively impermeable to other ions. Phase 4 is associated with heart diastole (relaxation) so is called diastolic depolarization. Phase 0 is the rapid depolarization phase. Phase 1 of the myocyte action potential occurs with the inactivation of the fast Na+ channels. The transient net outward current causing the small downward deflection of the action potential is due to the movement of K+ and Cl− ions, carried by the Ito1 and Ito2 currents, respectively. Particularly the Ito1 contributes to the "notch" of some ventricular cardiomyocyte action potentials (image 1). Phase 2. This "plateau" phase of the cardiac action potential (absent in muscle cells-they had a peak not a plateau), is sustained by a balance between inward movement of Ca2+ (ICa) through L-type calcium channels (opened in response to large d Nitroglycerin's mechanism of action - Answer The principal pharmacological action of nitroglycerin is relaxation of vascular smooth muscle. Although venous effects predominate, nitroglycerin produces, in a dose-related manner, dilation of both arterial and venous beds. Dilation of postcapillary vessels, including large veins, promotes peripheral pooling of blood, decreases venous return to the heart, and reduces left ventricular end-diastolic pressure (preload). Nitroglycerin also produces arteriolar relaxation, thereby reducing peripheral vascular resistance and arterial pressure (afterload), and dilates large epicardial coronary arteries; however, the extent to which this latter effect contributes to the relief of exertional angina is unclear. Physiology of beta receptors - Answer Adrenaline is the original name for what we now call epinephrine. Stimulation of the adrenal medulla by the sympathetic nervous system causes the secretion of both epinephrine (E) (80%) and norepinephrine (NE)(20%) into circulation. Epinephrine is a hormone; norepinephrine is both a hormone and a neurotransmitter. There are two categories of receptors, alpha and beta. There are also subtypes of each. Useful generalizations concerning these are: • Activation of alpha 1 and beta 1 receptors cause stimulatory responses • Activation of alpha 2 , beta 2 & beta 3 receptors cause inhibitory responses •NE causes a greater response than E when activating alpha 1 receptors •E causes a greater or equal response than NE when activating alpha 2 receptors •E and NE cause equal responses when activating beta 1 receptors •E causes a significantly greater response than NE when activating beta 2 receptors Beta 1 Receptors Beta 1 receptors are located on: •cardiac pacemaker •myocardium •salivary gland ducts •eccrine and apocrine sweat glands The cardiac pacemaker responds by increasing the heart rate. Simultaneously the myocardium contracts more forcefully. The physiology of the response of salivary duct cells to beta 1 activation is unclear; it appears that beta 1 activation of certain duct cells reabsorbs some water in the slowly passing saliva making it more viscous. The secretory portion of both types of sweat gland is stimulated only by E and NE from the blood, not via nerves. Note that beta 1 activation in the heart is both neural and hormonal. In the salivary glands the activation is solely neural while in both type sweat glands it is solely due to E and NE in the blood. Beta 2 Receptors Beta 2 receptors are located on smooth muscle. The relationship between E (hormonal) / NE (neurologica Physiology of the coronary arteries - Answer The coronary arteries supply blood flow to the heart, and when functioning normally, they ensure adequate oxygenation of the myocardium at all levels of cardiac activity. Constriction and dilation of the coronary arteries, governed primarily by local regulatory mechanisms,regulate the amount of blood flow to the myocardium in a manner that matches the amount of oxygen delivered to the myocardium with the myocardial demand for oxygen. When CAD restricts blood flow to the myocardium (ischemia) there is an imbalance between oxygen supply and oxygen demand. When the oxygen supply is insufficient to meet the oxygen demand (reduced oxygen supply/demand ratio), the myocardium becomes hypoxic. This is often associated with chest pain (angina) and other clinical symptoms. Severe ischemia can lead to anoxia and infarction of the tissue. Furthermore, acute or chronic ischemia caused by CAD can impair cardiac mechanical and electrical activities leading to heart failure and arrhythmias. CAD results in myocardial ischemia, which leads to chest pain (angina) and cardiac mechanical and electrical dysfunction. The goal in treating CAD is to restore normal coronary perfusion, or if that is not possible, then to reduce the oxygen demand by the heart (i.e., normalize the oxygen supply/demand ratio) so as to minimize myocardial hypoxia. In severe CAD in which one or more coronary arteries is very stenotic, some patients will have a stent implanted within the coronary artery to open up the lumen and restore blood flow. Other patients may undergo coronary artery bypass grafts in which the diseased segment is bypassed using an artery or vein harvested from elsewhere in their body (i.e., internal mammary artery). If the coronary is occluded by a blood clot, a thrombolytic drug may be administered to dissolve the clot. Anti-platelet drugs an Treating a patient with a tachycardic rhythm - Answer Tachycardia/tachyarrhythmia is defined as a rhythm with a heart rate greater than 100 bpm. An unstable tachycardia exists when cardiac output is reduced to the point of causing serious signs and symptoms. Serious signs and symptoms commonly seen with unstable tachycardia are: chest pain, signs of shock, SOA (short of air), altered mental status, weakness, fatigue, and syncope The most common causes of tachycardia that should be treated outside of the ACLS tachycardia algorithm are dehydration, hypoxia, fever, and sepsis. There may be other contributing causes and review of the H's and T's of ACLS should take place as needed. Administration of OXYGEN and NORMAL SALINE are of primary importance for the treatment of causative factors of sinus tachycardia and should be considered prior to ACLS intervention. There are several rhythms that are frequently associated with stable and unstable tachycardia these rhythms include: •Atrial fibrillation •Atrial flutter •Supraventricular tachycardia (SVT) •Monomorphic VT •Polymorphic VT •Wide-complex tachycardia of uncertain type The fist question that should be asked when initiating the ACLS tachycardia algorithm is: "Is the patient stable or unstable?" The answer to this question will determine which path of the tachycardia algorithm is executed. Unstable Tachycardia Patients with unstable tachycardia should be treated immediately with synchronized cardioversion. If a pulseless tachycardia is present patients should be treated using the cardiac arrest algorithm. The initial recommended synchronized cardioversion voltage doses are as follows: •narrow regular: 50-100 J; i.e., SVT and atrial flutter •Narrow irregular: 120-200 J biphasic or 200 J monophasic; i.e., atrial fibrillation •Wide regular: 100 J; i.e., monomorphic VT •Wide irregular: de Identify and treat pulseless electrical activity - Answer For a patient in whom PEA is suspected, the American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines protocol (revised in 2010[15, 16] ) recommends the following:[17] • Initiate CPR • Place an intravenous line • Intubate the patient • Correct hypoxia by administering 100% oxygen Once these basic measures are in place, reversible causes should be sought and corrected. These include the following: • Hypovolemia • Hypoxia • Acidosis • Hypokalemia/hyperkalemia • Hypoglycemia • Hypothermia • Toxins (eg, tricyclic antidepressants, digoxin, calcium channel blocker, beta-blockers) • Cardiac tamponade • Tension pneumothorax • Massive pulmonary embolus • Acute myocardial infarction Once reversible causes are identified, they should be corrected immediately. This process involves needle decompression of pneumothorax, pericardiocentesis for tamponade, volume infusion, correction of body temperature, and administration of thrombolytics or surgical embolectomy for pulmonary embolus Identify and treat wide complex tachycardia - Answer Patients who present with electrocardiograms (ECGs) demonstrating wide complex tachycardias (WCTs) are often challenging to clinicians. Not only may the patient present with (or be at risk for) hemodynamic compromise, but their treatment may result in hemodynamic collapse if the incorrect pharmacologic agent is selected. In Part 1 of this article,1 the identification, epidemiology, and electrophysiology of WCTs were discussed. In this article, treatment of WCTs and miscellaneous causes of this condition will be described. In patients presenting with WCTs, correct interpretation of the ECG should not be the primary concern of emergency physicians. In fact, it is appropriate (and may be preferred) to "diagnose" the ECG as "wide complex tachycardia of unknown (or uncertain) etiology." This may allow the treating clinician to focus on the patient and his or her hemodynamic status, rather than the academic exercise of ECG interpretation. The most important aspect of treating patients who present with WCTs is to select a therapeutic approach that does no harm. Several diagnostic algorithms were provided for the interpretation of WCTs, although none have proven superior over others, and great debate continues among researchers as to the preferred approach. Given this circumstance of uncertainty, proper treatment will be described for conditions resulting in WCTs.