Problem 7. (10 points) A patient arrives to the ER complaining on unusually rapi
ID: 3511123 • Letter: P
Question
Problem 7. (10 points) A patient arrives to the ER complaining on unusually rapid heart rate. History is unremarkable with the exception of a recent usage of a "Z-pack" antibiotic (azithromycin) for sinus infection. His bloodwork shows mild hypomagnesemia. While at the ER, the patient starts feeling dizzy, his blood pressure drops and he develops syncope. ECG is shown below. What is your diagnosis? What is the possible etiology? What is the conduction abnormality that this patient likely has hadtwas unaware of? What is the most likely outcome? If this condition persists, what is the possible worse outcome? What kind of treatment would you recommend? V4 V2 vs V3 veExplanation / Answer
From the given question
In a patient who is hemodynamically unstable or unconscious however the DIAGNOSIS of VENTRICULAR TACHYCARDIA is made from the physical findings and ECG strip
VT may be MONOMORPHIC OR POLYMORPHIC. IF THE QRS morphology changes from beat to beat the VT is classified as polymorphic.
presence of.AV Technically ventriculoatrial dissociation in which ventricles fire at a faster rate than the atria
fusion beats and capture beats
The symptoms and ECG shows POLYMORPHIC VENTRICULAR TACHYCARDIA LIKE TORSADES DE POINTES
1.DIAGNOSIS : TORSADES DE POINTES
2.ETIOLOGY : most common setting for VT is ischemic heart disease.,in which myocardial scar tissue is the substrate for electrical re-entry
Also dilated and hypertrophic cardiomyopathy
Also triggered by
1. electrolyte deficiencies like hypokalemia, hypocalcemia, hypomagnesemia
2.systemic diseases that affect myocardium like sarcoidosis, amyloidosis, SLE, RA, hemochromatosis
3.sympathomimetic agents including iv inotropes and ilicit drugs like cocaine
4.digitalis toxicity which can lead to biventricular tachycardia
5.drugs that prolong QT interval class1A and class3 anti arrythmics, azithromycin levofloxacin etc cause TORSADES DE POINTES
6.inherited channelopathies LONG QT SYNDROME, BRUGADA SYNDROME
3.CONDUCTION ABNORMALITY THAT PATIENT WAS UNAWARE was hypomagnesemia..
4.MOST LIKELY OUTCOME: Predicted best by left ventricular function.patients with VT may suffer heart failure and its attendant morbidiy as a result of hemodynamic compromise. major risk being injury incurred during syncopal spells
patients with LONG QT SYNDROME, RIGHT VENTRICULAR DYSPLASIA OR HYPERTROPHIC CARDIOMYOPATHY May be at increased risk for sudden death despite well preserved left ventricular function.
POSSIBLE WORST OUTCOME: SUDDEN CARDIAC DEATH Patients with sustained VT develop hemodynamic instability with hypotension or even unresponsiveness
pulseless VT form of pulseless arrest and is treated emergently with defibrillation and CPR in accordance with advanced cardiac life support (ACLS) algorithms.
TREATMENT : if VT persist after one defibrillation and two minutes of CPR AMIODARINE is the preferred agent, but lidocaine may be given if amiodarone is not availabe.
BETA BLOCKER theraphy can reduce the risk of sudden cardiac death from VT And implantable cardioverter defibrillators can terminate malignant arrythmias.