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(BQ) Part 2 book ECG short rapid review for non-Cardiologists presents the following contents: Ventricular arrythmias, heart blocks, myocardial infarction, junctional arrythmias, premature ventricular contractions, miscellaneous, P&Q wave relationships.
CHAPTER : VENTRICU LAR ARRYTHMIAS IDIOVENTRICULAR RHYTHM If the ventricle does not receive triggering signals , the ventricular myocardium itself becomes the pacemaker (escape rhythm) This is called Idioventricular Rhythm Ventricular signals are transmitted cell-to-cell between cardiomyocytes and not by the conduction system, creating wide sometimes bizarre QRS complexes(> 0.12 sec) Rate : 20-40 bpm Rhythm : Regular P waves : None PR interval : None QRS : Wide (>0.10 sec) Bizzare type appearance Idioventricular rhythms occur when all of the heart’s other pacemakers fail to function or when supraventricular impulses can’t reach the ventricles because of a block in the conduction system Ventricular arrhythmias originate in the ventricles below the bundle of His and fires at the rate of 20-40 bpm Idioventricular rhytm may also be called as agonal rhythm If the rate is >40 bpm, it is called accelerated idioventricular rhythm The rate of 20-40 is the 61 | P a g e "intrinsic automaticity" of the ventricular myocardium Bizzare appearance : The T wave and the QRS complex deflect in opposite directions because of the difference in the action potential during ventricular depolarization and repolarization P wave is absent because depolarization of atria does not occur The arrhythmias may accompany third-degree heart block or be caused by anything which damages AV node like infarction or blocks it like digoxin ACCELETATED IDIOVENTRICULAR RHYTHM Same as Idioventricular rhytm , only difference is , heart rate Here it’s 40-100 bpm , while in IVR it’s been 20-40 bpm Rate : 40-100 bpm Rhythm : Regular P waves :None PR interval :None QRS : Wide (>10 sec) , Bizzare appearance Idioventricular rhythms appear when supraventricular pacing sites are depressed or absent If the heart rate 62 | P a g e become slow , diminished cardiac output is expected History is helpful for identifying the underlying etiology for AIVR Most patients with AIVR presents with chest pain or shortness of breath (symptoms related to myocardial ischemia with history of myocardial reperfusion with drugs or coronary artery interventions.) ,Plus Peripheral edema, cyanosis, clubbing, (With the history of cardiomyopathy, myocarditis, and congenital heart diseases ) Treatment : Idioventricular rhythm should never be treated with lidocaine or other antiarrhythmics that would suppress that safety mechanism If the symptoms develops , immediate treatment required to increase his heart rate, improve cardiac output and establish a normal rhythm Treat the Underlying Cause In life-threatening situations in which time is critical, a transcutaneous pacemaker may be used to regulate heart rate VENTRICULAR TACHYCARDIA (MONOMORPHIC) Ventricular tachycardia refers to any rhythm faster than 100 beats per minute, with or more irregular beats in a row, arising distal to the bundle of His In Monomorphic type , The shape, size and amplitude of QRS complex will be same 63 | P a g e Rate : 100-250 bpm Rhythm : Regular P waves : None or not associated with the QRS PR interval : None QRS : Wide (>0.10sec) , Bizzare appearance It is important for a physician to confirm the presence or absence of pulses because monomorphic VT may be perfusing or non perfusing Sustained SVTs requiring immediate treatment to prevent death, monomorphic VT will probably deteriote into VF or unstable VT if sustained and not treated Ventricular tachycardia usually results from increased myocardial irritability, which may be triggered by enhanced automaticity or reentry within the Purkinje system or by PVCs Conditions that can cause ventricular tachycardia include: Myocardial ischemia & Infarction Coronary artery disease Valvular heart disease Heart failure, Cardiomyopathy Hypokalemia Drugs like digoxin , procainamide, quinidine or cocaine 64 | P a g e VENTRICULAR TACHYCARDIA (POLYMORPHIC) The difference between monomorphic and polymorphic is the presence of different type of complexes in polymorphic Rate : 100-250 bpm Rhythm : Regular P waves : None or not associated with the QRS PR interval : None QRS : Wide (>0.10sec) , Bizzare appearance Electrolyte abnormality is a possible etiology behind this Patient in VT will present with Palpitation, lightheadedness, and syncope (from diminished cerebral perfusion) Chest pain (due to ischemia or to the rhythm itself Anxiety usually present Some patients describe a sensation of neck fullness, which may be related to increased central venous pressure and cannon a waves “Cannon A” waves are related to right atrial contraction against a closed tricuspid valve (Jugular Venous Pressure Graph is Discussed later on) Dyspnea (due to increased pulmonary venous pressures when left atrial contraction 65 | P a g e against a closed mitral valve) Ventricular Tachycardia can convert into Ventricular Fibrillation if not treated V fib is a medical emergency It is important to confirm the presence or absence of pulses because polymorphic VT may be perfusing or non perfusing Treatment of VT: They are Treated aggressively by Anti arrythmimc drugs Coronary revascularization is indicated to reduce the risk of SCD in patients with VF when there is presence of direct evidence of acute myocardial ischemia Amiodarone or lidocaine are usually used VENTRICULAR FIBRILLATION Is when ventricles fire rapidly and asynchronously at rate more than 300.Most common cause of death in cardiac ER Massive hypoperfusion will occur throughout the body Rate : 300-600 Rhythm : Extremely Irregular P wave : Absent PR interval : N/A QRS : Fibrillatory baseline 66 | P a g e Ventricular fibrillation is defined when Ventricles beat >250bpm V-fib, is a pattern of electrical activity in the ventricles in which electrical impulses arise from many different foci It produces no effective muscular contraction and no cardiac output Untreated ventricular fibrillation causes most cases of sudden cardiac death in people outside of a hospital The ventricular rate, P wave, PR interval, QRS complex, T wave, and QT interval cannot be determined Patient will present with Prodrome of symptoms of chest pain, fatigue, palpitations, and other nonspecific complaints (50% patients visit in week before death) , A history of Left Ventricular impairment (LV ejection fraction < 30-35%) is the single greatest risk factor for sudden death from VF Otherwise , symptoms depend upon the underlying cause of V-Fib : Coronary artery Disease , Hypertrohpic or dilated cardiomyopathy , valvular pathology , Myocarditis , Congenital Heart Disease (All this pathology are discussed in Pathology Section) Treatment : if pulseless , treat with immediate defibrillation followed by epinephrine , vasopressin , amiodarone or lidocaine If pulse is present treat with amiodarone and synchronized cardioversion 67 | P a g e TORSADE DE POINTES Characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line Rate : 200-250 bpm Rhythm : Irregular P waves : None PR interval : None QRS : Wide (>0.10sec) , Bizzare appearance The main causes of Torsades are Drugs that prolong QT interval and electrolyte abnormalities such as Hypomagnessemia This rhythm is unusual variant of polymorphic VT with the normal or long QT intervals It may deteriotes to Ventricular fibrillation or asystole Patient usually present with recurrent episodes of palpitations, dizziness, and syncope; however, sudden cardiac death can occur with the first episode Nausea, cold sweats, shortness of breath, and chest pain also may occur but are nonspecific and can be produced by any form of tachyarrhythmia HALLMARK : QRS complexes that rotate about the 68 | P a g e baseline, deflecting downward and upward for several beats Treatment : Magnesium (Decreases the influx of calcium, thus lowering the amplitude of Action Potentials ) Beta-1 Agonist Drugs (to increase Heart rate and decrease Prolonged QT interval) If torsades convert into V-Fib – Direct Current Cardioversion is required PULSELESS ELECTRICAL ACTIVITY When you try to measure pulse ,you will not detect them , but , when you will perform ECG , identifiable electrical rhythms are produced Rate , Rhythm , P waves PR interval ,QRS - All reflects the underlying rhythm Rhythm may be sinus , atrial , juinctional , or ventricular in origin PEA is also called as electromechanical dissociation 69 | P a g e In pulseless electrical activity, the heart muscle loses its ability to contract even though electrical activity is preserved As a result, the patient goes into cardiac arrest On an electrocardiogram, you’ll see evidence of organized electrical activity, but you won’t be able to palpate a pulse or measure the blood pressure This condition requires rapid identification and treatment Causes include : Hypovolemia , Hypoxia, Acidosis, Tension pneumothorax, Cardiac tamponade, massive pulmonary embolism Hypothermia, hyperkalemia, Overdose of drugs such as tricyclic antidepressants , calcium channel blockers , digoxin Treatment : Cardiopulmonary resuscitation is the immediate treatment, along with epinephrine Atropine may be given to patients with bradycardia Subsequent treatment focuses on identifying and correcting the underlying cause 70 | P a g e Blocks inactivated Na+ channel On ECG : Decrease QT interval , Increases Heart Rate , No effect on SA/AV node Use is Post MI , Digoxin toxicity – works best in Hypoxic tissues Tocainide side effect : Agranulocytosis Class Ic antiarrhythmics : Flecainide, Propafenone , Moricozine Blocks Fast NA+ channel , especially of HisPurkinje Tissue Highly proarrythmogenic , Last choice drugs when all other option fails On ECG : Prolongs QRS , Heart rate is variable Class ll : B-Blockers : Acebutalol , propranolol , Sotalol , Esmolol Decreases SA & AV nodal activity On ECG – Slight increase in PR interval and decreases Heart rate Use : Post MI , Anigna (except Prinzmetal angina ) , Anti hypertensive and in Supraventricular tachycardia , thyrotoxicosis (Propranolol) , migraine prophylaxis , anxiety Esmolol (IV) is use in acute SVTs Carvedilol : Beta1 & Alpha blocker (Vasodilates + decrease Heart rate) Side-effect :bronchospasm , cold peripheries , fatigue , sleep disturbances, including nightmares 119 | P a g e Contraindications: uncontrolled heart failure , asthma , sick sinus syndrome , concurrent verapamil use: may precipitate severe bradycardia Class lll : Potassium Channel Blockers : Amiodarone , Sotalol Amiodarone : half life is more than 80 Days , High tissue binding ( Decrease metabolism of Warfarin) Act like class l , ll ,lll ,lV antiarrythmic drugs Side effects : Blue pigmentation of skin , Pulmonary fibrosis , Corneal deposits , hepatotoxic , Thyroid dysfunction , thrombophlebitis (because ideally given I.V) , Peripheral Neuropathy , Prolongs QT interval (Torsades ) Use : Any arrhythmia Sotalol : Potassium + B-Blocker , so decreases Heart rate , decreases AV conduction Use : Life threaning Ventricular arrhythmias Class lV : Calcium Channel Blockers : Verapamil , Diltiazam Blocks cardiac calcium channel , decreases SA and AV nodal activity Use : SVTs , Angina , Anti-hypertensive Side effects are : Heart failure, constipation, hypotension, bradycardia B-blockers , Ca+ channel blocker , digoxin – have additive AV node block effect If given in combination there is high risk for AV nodal blockage 120 | P a g e dihydropyridines (eg Nifedipine , Amlodipine) family of calcium channel blockers have more action on vasculature (vasodilation) than on the heart and so use as a antihypertensive agents , Angina & Reynauds Phenomenon They will cause reflex tachycardia Side effects are : Flushing, headache, ankle swelling Unclassified : Adenosine , Atropine , Digoxin , Epinephrine , Magnessium Sulphate Adenosine : Decreases SA & AV nodal activity by decreasing cAMP (Hyperpolarize the cell by Potassium efflux) , Duration of action is 10 Sec only Drug of choice in Paroxysmal Supraventricular tachycardia & AV nodal arrythimia Effects of adenosine are enhanced by dipyridamole (anti-platelet agent) and blocked by theophyllines It should be avoided in asthmatics due to possible bronchospasm Adverse effects : chest pain ,bronchospasm , can enhance conduction down accessory pathways resulting in increased ventricular rate (e.g WPW syndrome) Magnessium : Use in Torsades Digoxin : is a cardiac glycoside , increases intracellular Ca+ by inhibiting cardiac Na-K+ ATPase , increases contractile force and blocks AV node by indirectly increasing vagal activity (by inhibiting neuronal Na-K+ ATPase) 121 | P a g e Use : Congestive Heart failure , SVTs (except Wolf Parkinson White Syndrome) Moniter Potassium level when patient is on Digoxin Digoxin toxicity : lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision , arrhythmias (e.g AV block, bradycardia) Precipitating factors are : Hypokalaemia (Classic) Increasing age , Renal failure , Myocardial ischemia , hypomagnesemia, hypercalcemia, hypernatremia, acidosis , hypoalbuminemia , hypothermia , hypothyroidism Drugs ike amiodarone, quinidine, verapamil, diltiazem, spironolactone (compete for secretion in distal convoluted tubule therefore reduce excretion) Also drugs which cause hypokalaemia e.g thiazides and loop diuretics In Toxicity – use Digibind (Fab antibodies toward digoxin) and supportive electrolyte therapy + lidocaine Atropin – As a antimuscarinic – Increases Heart Rate useful to pace up the heart Epinephrine : Low dose : increases Heart Rate and Vasodilates (Beta , Beta action) Medium dose : Increases Heart Rate only (Alpha-1 , Beta , Beta action Alpha-1 & B-2 action cancel each other High Dose : Alpha –action predominates , so vasoconstrict and increase Blood pressure (useful in Shock , Hemorrage and many other condition Please Read adrenergic-noradrenergic receptor pharmacology for more detail) 122 | P a g e Nesiritide : Recombinant form of Human Beta-type Natriuretic Peptide BNP is synsthesize in right atrium when there is overload/stretch on atrium and will help to get rid of extra volume by diuresis.Used in Decompensated Congestive Heart Failure Angina pectoris: Drug management The management of stable angina comprises lifestyle changes, medication, percutaneous coronary intervention and surgery Medication : 1) All patients should receive aspirin and a statin in the absence of any contraindication 2) Sublingual glyceryl trinitrate to abort angina attacks 3) A beta-blocker or a calicum channel blocker is generally used first-line 4) If a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used If used in combination with a beta-blocker then use a longacting dihydropyridine calcium-channel blocker (e.g modified-release nifedipine) Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block) 5) If there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose 6) If a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa 7) If a patient is on monotherapy and cannot tolerate the addition of a calcium channel 123 | P a g e blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine 8) If a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for Percutaneous Coronary Intervation or Coronary Artery Bypass Grafting Nitrates : Have vasodilating effects : Dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand Mainly use is in the management of angina and the acute treatment of heart failure Sublingual Glyceryl trinitrate is the most common drug used in patients to relieve angina attacks Side-effects : hypotension , tachycardia , headaches Nitrate tolerance : Some patients who develop tolerance should take the second dose of isosorbide mononitrate after hours, rather than after 12 hours this effect is not seen in patients who take modified release isosorbide mononitrate Ivabradine : A new class of anti-anginal drug which works by reducing the heart rate , acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity Adverse effects: visual effects, particular luminous phenomena, are common Bradycardia, due to the mechanism of action, may also be seen 124 | P a g e ANTIHYPERTENSIVE DRUGS Beta Blockers (Atenolol , Acebutolol , Propranolol , Metaprolol ) Calcium channel blockers (Nifedipine , Amlodipine) Diuretics (Loops , Thiazides ) Vasodilators : Hydralazine , Isosorbide Dinitrate , nitroprusside , nitroglycerin , ACE- inhibitors , ARBs are other Antihypertensive and antianginal agents Hydralazine : used for hypertension in pregnancy and for severe hypertension, act by increasing cGMP leading to arterial smooth muscle relaxation Contraindication : Systemic lupus erythematous , ischemic heart disease Side effect : tachycardia , palpitations , flushing , fluid retention , headache , drug-induced lupus Diuretics (Furosemide , Ethacrynic acid ,Thiazides , Spironolactone etc) Loop diuretics (Furosemide and bumetanide, Ethacrynic Acid) Inhibiting the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl 125 | P a g e Uses in : heart failure: both acute (usually intravenously) and chronic (usually orally) , Resistant hypertension, particularly in patients with renal impairment Adverse effects : Hypotension , Hyponatremia , Hypokalemia , Hypochloremic Alkalosis , Ototoxicity (Except Ethacyninc Acid) , Hypocalcemia , Renal impairment (from dehydration + direct toxic effect) , Hyperglycemia (less common than with thiazides) , Gout Thiazides (Hydrocholorothiazide , Indapamide) : Inhibit Na+/Cl- transporter on distal tubules , Increases Calcium (+ve charge) absorbtion by inhibiting Sodium (+ve Charge ) Uses : Hypertension , CHF , Nephrolithiaisis (Calcium stone) ,Nephrogenic Diabetic Insipedus Side effects : Sulfonamide hypersensitivity , Hypokalaemia & Alkalosis, Hypercalcemia , Hyperuricemia , Hyperglycemia , Hyperlipidemia Avoid in Patients with Diabetes Potassium Sparing Diuretics (Spirinolactone , Amiloride, Triampterene) Spirinolactone : Aldosterone Receptor Antagonist (On collecting duct) Uses : Hyperaldosteronic state , Adjunct to Potassium wasting diuretics , Antiandrogenic uses , CHF 126 | P a g e Side effect : Hyperkalaemia & Acidosis , Anti androgenic (Gynaecomastia in males, hirsuitism , acne in female) Amiloride & Triampterene : Na+ Channel blocker (on collecting duct) Use : Adjunt to K+ wasting diuretics , lithium induced Diabetes insipedus Side effect : Hyperkalaemia , acidosis Other diuretics like Carbonic Anhydrase inhibitors (Acetazolamide , dorzolamide- Use : Glaucoma , Acute Mountain Sickness , Metabolic Alkalosis ) & Osmotic diuretics (Mannitol - use to decrease intraocular pressure in Glaucoma , to decrease intracerebral pressure , Oliguric states – eg Rhabdomyolysis) are not typically use in Cardiology Angiotensin-converting enzyme (ACE) inhibitors : Act by inhibiting the conversion angiotensin I to angiotensin II in Lungs Uses : Hypertensive (Young patients ) , heart failure , Diabetic nephropathy They are less effective in treating hypertensive black patients and have a role in secondary prevention of ischemic heart disease Side-effects: Cough (due to increased bradykinin levels) , Angioedema , hyperkalemia (because of decreased aldosterone) , first-dose hypotension: more common in patients taking diuretics Contraindications : pregnancy and breastfeeding (Class 127 | P a g e IV drug) , Bilateral Renal artery stenosis , Aortic stenosis - may result in hypotension , patients receiving high-dose diuretic therapy - significantly increases the risk of hypotension due to hypovolemia , Hereditary of idiopathic angioedema Monitor : Urea and electrolytes should be checked before treatment is initiated and after increasing the dose , a rise in the creatinine and potassium may be expected after starting ACE inhibitors Acceptable changes are an increase in serum creatinine, up to 30% from baseline ARBs (Angiotensin Receptor Blockers) are used when patient develops side effects of ACE inhibitors arises They blocks AT1 Receptors , Same mechanism & Uses as ACEIs & not interfere with bradykinin degeneration ANTIHYPERLIPIDEMIC DRUGS Atherosclerosis which is the main cause of Cardiovascular & Cerebrovacular diseases is associated with Hypercholesterolemia HMG-CoA Reductase Inhibitors : Statins (Atorvastatin , Lovastatin , - statins) Inhibit HMG-CoA Reductase which results in Decrease in Liver Cholesterol Production , Increase in LDL – Receptor expression and decrease in Plasma LDL Also decreases Triglyceride synthesise Myalgia , Rhabdomyolysis , Hepatotoxic are common side effects Increase risk of Rhabdomyolysis if combined with other antihyperlipidemic like Gemfibrozil (use to decrease Triglyceride) 128 | P a g e Bile Acid Sequetrants : Cholestyramine & Colestipole: Binds to the Bile salts in the gut , which results in decrease entero hepatic circulation of bile salts , which leads to increase in new bile salts by the liver by the use of cholesterol , thus decreasing Liver cholesterol, which leads to increase in LDL Receptor expression and thus Decreases Blood Cholesterol Side effect : Increase VLDL and so , Triglyceride., Malabsorbtion of Lipid Soluble vitamins and so related problems Contraindication - Hypertriglyceridemia Niacin : Inhibit VLDL synthesis – so , decreases VLDL & LDL , while main effect is Increase in HDL Side effect : Flushing , Rashes , which are controlled by use of Aspirin before taking Niacin Gemfibrozil : Induction of Lipoprotein Lipases Decreases VLDL , LDL – so Use in Hypertriglyceridemia , and not in HyperCholesteremia Side effect : Gallstone , myositis (on combination with Statins) , Thromboenbolism Ezetimibe : Prevent intestinal absorption of Cholesterol , so , decrease in LDL ,Nowadays , it is mostly replaced by Statins 129 | P a g e NON PHARMACOLOGICAL TREATMENTS For symptomatic arrhythmias : treatment is choosen based on the type of arrhythmia, the severity of symptoms being experienced, and the presence of other conditions (such as, diabetes, kidney failure, or heart failure) which can affect the course of the treatment Lifestyle modification : Elimination of caffeine, alcohol, or any other substances believed to be causing the problem, stress-reduction measures, such as meditation, stress-management classes, an exercise program, or psychotherapy Cardioversion In this procedure, an electrical shock is delivered to the heart through the chest to stop certain very fast arrhythmias such as atrial fibrillation, supraventricular tachycardia, or atrial flutter The patient is connected to an ECG monitor which is also connected to the defibrillator The electrical shock is delivered at a precise point during the ECG cycle to convert the rhythm to a normal one Ablation This is an invasive procedure done in the electrophysiology laboratory, which means that a catheter (a very thin, flexible hollow tube) is inserted into the heart through a vessel in the groin or arm The procedure is done in a manner similar to the electrophysiology studies (EPS) described above Once the site of the arrhythmia has been determined by EPS, the catheter is moved to the site By use of a technique, such as radiofrequency ablation (very high frequency radio waves are applied to the site, heating the tissue until the site is destroyed) or cryoablation (an ultra-cold substance is applied to the site, freezing the tissue and 130 | P a g e destroying the site), the site of the arrhythmia may be destroyed Pacemaker A permanent pacemaker is a small device that is implanted under the skin (most often in the shoulder area just under the collar bone), and sends electrical signals to start or regulate a slow heart beat A permanent pacemaker may be used to make the heart beat if the heart's natural pacemaker (the SA node) is not functioning properly and has developed an abnormal heart rate or rhythm or if the electrical pathways are blocked Pacemakers are typically used for slow arrhythmias such as sinus bradycardia, sick sinus syndrome, or heart block Implantable cardioverter defibrillator An implantable cardioverter defibrillator (ICD) is a small device, similar to a pacemaker, that is implanted under the skin, often in the shoulder area just under the collarbone An ICD senses the rate of the heartbeat When the heart rate exceeds a rate programmed into the device, it delivers an electrical shock to the heart in order to correct the rhythm to a slower more normal heart rhythm ICDs are combined with a pacemaker to deliver an electrical signal to regulate a heart rate that is too slow ICDs are used for life-threatening fast arrhythmias such as ventricular tachycardia or ventricular fibrillation Surgery Surgical treatment for arrhythmias is usually done only when all other appropriate options have failed Surgical ablation is a major surgical procedure requiring general anesthesia The chest is opened, exposing the heart The site of the arrhythmia is located, the tissue is destroyed or removed in order to eliminate the source of the arrhythmia 131 | P a g e REFERENCES www.Wikipedia.org Robin’s Pathology 8th edition ECG Interpretations : Lippincott Williams and Wilkins Brochert’s Crush Step Some ECG images – freely available on Internet (If you own that image , please let us know from our website) Dr Najeeb’s Electrocardiogram lectures USMLEstat Secret Pathology Notes – USMLE High yields www.mayoclinic.org www.heart.org USMLE First AID step ECG Made Easy If you didn’t liked anything inside the book and want us to change something , please Message us through our Website www.medicaids22.info Dr Chirag Navadia 132 | P a g e Kindle book available on Amazon for Just $4.99 ECG Short Rapid Review : Edition 2.2 New Inclusions to this Edition : - Cardiology Summary - 20 ECG Practice Strips - Book Size Increased to 6*9 - 15 Clinical USMLE Style Q&A - 150+ Super High Yield Points for USMLE STEP & *~~~*~~~*~~~*~~~*~~~*~~~*~~~*~~~*~~~*~~ ~*~~~* 133 | P a g e ... rate 62 | P a g e become slow , diminished cardiac output is expected History is helpful for identifying the underlying etiology for AIVR Most patients with AIVR presents with chest pain or shortness... treatment for asystole is CPR 71 | P a g e CHAPTER : HEART B L OCKS ATRIOVENTRICULAR BLOCKS (FIRST DEGREE BLOCK) It is the prolongation of the PR interval on an electrocardiogram (ECG) to more than 20 0... ventricular rate is slow 74 | P a g e Treatment : For asymptomatics – No Rx For symptomatics : Atropine may improve AV node conduction For long term relief : Temporary Pacemaker N D DEGREE