Cardiology PODs Full Review PDF

Cardiology PODs Prime Objectives for Didactic studies For graduate level professional medical programs (PA, NP) MS, MSPAS, PA-C This covers all objectives listed in the Physician Assistant National Cert...

Cardiology PODs Prime Objectives for Didactic studies For graduate level professional medical programs (PA, NP) MS, MSPAS, PA-C This covers all objectives listed in the Physician Assistant National Certifying Examination blueprint. All photos are attributed to their authors and are royalty free to public domain through their creative commons license. This video and powerpoint are intellectual property protected by an LLC. Any reproduction, resale, or distribution is STRICTLY PROHIBITED. PApods.weebly.com Thank you for buying this review video! Below are the links to the complete unit video reviews Part 1: https://youtu.be/i33hBLYvSnY Part 2 (starts on slide 49): https://youtu.be/MTslzjvow-o  Conduction Disorders (EKG) Congenital Heart Disease Normal sinus rhythm Atrial septal defect Sinus bradycardia Ventricular septal defect Sick sinus syndrome Coarctation of aorta Atrial tachycardia Patent ductus arteriosus Atrial fibrillation Tetralogy of Fallot Atrial flutter Transposition of great vessels Vascular Disease PSVT Hypoplastic left heart Hypertension Multifocal atrial tachycardia syndrome Hypotension Wolff-Parkinson-White Truncus arteriosus Dyslipidemia Objectives Ventricular tachycardia Torsades de pointes Atherosclerosis Aortic aneurysm Ventricular fibrillation Cardiac Disorders Rheumatic heart disease Aortic dissection Asystole Venous insufficiency Bacterial endocarditis Premature beats Varicose veins Acute pericarditis Bundle branch block Peripheral arterial disease Pericardial effusion Acute myocardial infarction Thromboembolism Cardiac tamponade Atrioventricular block Superficial thrombophlebitis Coronary artery disease Angina pectoris Temporal arteritis Valvular Disease Viral myocarditis Aortic stenosis/regurgitation Congestive heart failure Mitral stenosis/regurgitation Cor pulmonale Mitral valve prolapse Hypertrophic cardiomyopathy Tricuspid stenosis/regurgitation Dilated cardiomyopathy Pulmonary stenosis/regurgitation Restrictive cardiomyopathy  HEART & CIRCULATION Venules/Veins (-O) Vena Cava (-O) Right Atrium (-O) Tricuspid AV Valve (-O) Right Ventricle (-O) Pulmonary SL Valve (-O) Pulmonary Artery (-O) Lungs (+O) Pulmonary Vein (+O) Left Atrium (+O) Bicuspid AV valve (+O) Left Ventricle (+O) Aortic SL Valve (+O) Aorta (+O) Arteries/Arterioles (+O) Capillaries (+O/-O) If you “tri” you get it right ”Tri” before you “bi” Wapcaplet - CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253  aVL aVR I V6 V5 V1 V3 V4 V2 LEAD 2 STRONGEST IMPULSE FROM ELECTRICAL aVF PATHWAY EKG Leads View Left main coronary artery – Circumflex artery: Left atrium, posterior left side (lateral wall) – Left Anterior Descending: septal wall, Anterior left ventricle (anterior wall) Right main coronary artery (inferior wall): Right atrium and ventricle, SA/AV nodes, posterior right I aVR VI V4 II aVL V2 V5 III aVF V3 V6 I aVR V1 V4 V5 12 Lead EKG II aVL V2 Peaked T: hyperkalemia U wave: III aVF V3 V6 hypokalemia II- Rhythm Strip Lead 2: strongest impulse from electrical pathway of the heart Ptrump16, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=77817932  SA node Cardiac Conduction AV node Bundle of His Left/Right Bundle Branches Purkinje fibers 60-100 bpm 45-60 bpm L Bundle conducts faster Heart Diagram by Wapcaplet CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253 Conduction diagram by Angelito7 CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=29922595  Ventricles Depolarize Basic EKG Ventricles Atria Repolarize Depolarize SA Node PR segment ST segment QRS Complex 0.08-0.1 sec PR interval 0.12-0.20 sec QT interval 0.40-0.43 sec  Ventricles Depolarize Ventricles Repolarize Atria Depolarize SA Node AV Junction Heart Diagram by Wapcaplet CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253  Determining Rate: Regular Rhythms Find where a QRS complex falls on a thick line Count the number of thick lines between the first R and the next R 300bpm (0 lines), 150bpm (1 line), 100bpm (2 lines), 75bpm (3 lines), 60bpm (4 lines), 50bpm (5 lines) Or use a calculator… 1500 150 50 # small boxes between R-R 75 300 100 60  Determining Rate: Irregular Rhythms Each large box is 0.2 seconds. There are 5 large boxes in 1 second. 3 second method: count all QRS complexes in 3 seconds (15 boxes, 1 hash mark) and multiply by 20. OR 6 second method: count all QRS complexes in 6 seconds (2 hash marks) and multiply by 10. (Use only if hash marks– otherwise inefficient) Total 8 QRS x 20 = 160 bpm 2 QRS 1 sec 3 QRS 2 sec 3 QRS 3 sec Simplifying Axis Deviation  -90 -90 Left Axis Left Axis Deviation Deviation Extreme Axis -30 toto-90 -30 Extreme Axis Deviation -30 -90 Deviation -90 to 180 -90 to 180 180 0 Right Axis Normal Axis Deviation -30 to 90Axis Normal 90-180 -30 to 90 Right Axis Deviation 90-180 NORMAL AXIS OF THE +90 +90 HEART  -90 -90 LEFT AXIS DEVIATION LeftAxis Left Axis Extreme Axis Deviation Deviation -30 Extreme Axis Deviation -30toto-90 -30 -90 Deviation -90 to 180 -90 to 180 180 0 Right Axis Normal Axis Deviation -30 to 90Axis Normal 90-180Right Axis -30 to 90 Deviation 90-180 NORMAL RIGHT AXIS AXIS OF THE DEVIATION +90 +90 HEART  -90 -90 aVR aVL Left Axis Left Axis Deviation Extreme Axis Deviation -30 -30 to -90 Deviation -30 to -90 Extreme Axis -90 to 180 Deviation -90 to 180 180 0 Lead I Normal Axis Right Axis -30 to 90 Deviation Normal Axis 90-180Right Axis -30 to 90 Deviation 90-180 Lead III +90 aVF Lead II  Simplify into 4 quadrants Find the two perpendicular leads: Lead 1 and aVF -90 Determine if the QRS is Left Axis R Extreme Deviation -30 Positive S Axis -30 to -90 Deviation R longer than S -90 to 180 0 180 Lead I R Negative S Right Axis Normal Axis Deviation -30 to 90 R shorter than S 90-180 A positive QRS indicates that the axis is in line +90 with this lead aVF  -90o 180o -QRS +QRS 0o Lead 1 -90o -QRS +90o 180o 0o -90o +QRS Lead I +90o 180o 0o Positive aVF aVF Positive +90o Normal Axis -30 to 90  -90o aVF 180o -QRS +QRS 0o Lead 1 -90o -QRS Left Axis +90o 180o 0o Deviation -90o -30 to 90 +QRS Lead I +90o 180o 0o Positive aVF Negative +90o  -90o 180o -QRS +QRS 0o -90o -QRS Lead 1 +90o 180o 0o +QRS -90o Lead I +90o Negative aVF 180o 0o aVF Positive Right Axis Deviation 90-180 +90o  -90o aVF 180o -QRS +QRS 0o -90o -QRS Lead 1 +90o 180o 0o +QRS Extreme Axis Deviation -90o -90 to 180 Lead I +90o Negative 180o 0o aVF Negative +90o Lead 1 Lead aVF Quadrant Axis Positive Positive Normal 0o-90o Positive Negative Possible Left Axis Deviation 0o-90o (-30o to 90o) Negative Positive Right Axis Deviation +90o to 180o Negative Negative Extreme Axis -90o to 180o  Conduction Disorders & EKGs Normal sinus rhythm Ventricular tachycardia Sinus bradycardia Torsades de pointes Sick sinus syndrome Ventricular fibrillation Cardiac arrest (asystole) Supraventricular Tachycardia (SVT) Premature beats Atrial tachycardia Bundle branch block Atrial fibrillation Acute myocardial infarction Atrial flutter Atrioventricular block Paroxysmal supraventricular tachycardia Multifocal atrial tachycardia Wolff-Parkinson-White  Normal Sinus Rhythm (NSR) Rate: 60-100 (SA node) Rhythm: regular, normal intervals P:QRS: 1 to 1 P-R-T: same direction P-R interval: 0.12-0.20 seconds QRS complex: less than 0.12 seconds  Sinus Bradycardia Hx: conditioned athlete, freediver PE: peripheral and pulmonary edema (if severe) Etiology: slow SA conduction. Increased vagal tone (athletes), medications (beta blockers, calcium channel blockers, cardiac glycosides (digitalis, digoxin)), hypothermia, hypothyroid, hypoglycemia Dx: less than 60 bpm, regular rhythm, 1:1 P:QRS Tx: less than 50 bpm gets atropine and pacemaker  Sick Sinus Syndrome (Tachy-Brady) Hx: history of heart disease Etiology: dysfunctional SA node, conduction system does not excite atria uniformly Epidemiology: rare, elderly Dx: alternating tachycardia/bradycardia Tx: pacemaker  Atrial Tachycardia Hx: palpitations PE: hypotension (if severe) Etiology: fast SA conduction. Exercise, fever, dehydration, hypoxia, caffeine, albuterol, cocaine Dx: 120-250 bpm, regular rhythm, T may run into next P (camel humps), 1:1 P:QRS Tx: valsalva, carotid rub, rate control (beta blockers, verapamil), antiarrhythmic (Class I), adenosine (if severe, pause heart to reset to normal sinus rhythm), synchronized cardioversion (shock during R part of QRS complex to avoid stimulation during the refractory period, which could cause ventricular fibrillation)  Atrial Fibrillation Hx: dyspnea, angina Etiology: atrium only quivers. Valvular disease, EtOH (holiday heart), drugs (stimulants, methamphetamines, cocaine), coronary artery disease, thyroid storm, pheochromocytoma Epidemiology: most common arrhythmia, most common cause of cerebrovascular accident Dx: 110-140 bpm, irregularly irregular rhythm, no P waves Tx: anticoagulation (warfarin, heparin) for 3 weeks before cardioversion and 4 weeks after, rate control (beta blocker, calcium channel blocker), antiarrhythmic (amiodarone, flecainide, propafenone, sotalol), synchronized cardioversion (during R)  Atrial Flutter PE: jugular venous distention, lungs (rales, crackles) Etiology: AV conduction block. Heart disease (congenital, rheumatic, pericarditis), cardiac surgery, diabetes, EtOH, COPD, hyperthyroid, pheochromocytoma Epidemiology: less common than atrial fibrillation Dx: 250-350 bpm, negative sawtooth pattern, flutter (F) waves Tx: anticoagulation (warfarin, heparin) prior to cardioversion if present for more than 48 hours, rate control (beta blocker, calcium channel blocker), antiarrhythmic (amiodarone, flecainide, propafenone, sotalol), radiofrequency ablation, synchronized cardioversion (during R)  Paroxysmal Supraventricular Tachycardia (PSVT) PE: jugular venous distention, S3 murmur, lungs (rales, crackles) Etiology: differs from atrial tachycardia because it is episodic and due to AV node reentrant pathways or accessory tracts. Prior myocardial infarction, mitral valve prolapse, rheumatic heart disease, pericarditis, COPD, EtOH, digitalis or digoxin toxicity. Dx: rate changes abruptly, 150-250 bpm, regular rhythm, 1:1 P:QRS Tx: vagal maneuver (carotid rub, valsalva), rate control (beta blocker, calcium channel blocker), adenosine (pause heart to reset to normal sinus rhythm), radiofrequency ablation, synchronized cardioversion (during R)  Multifocal Atrial Tachycardia (MAT) PE: rapid irregular pulse Etiology: multiple sites of competing atrial activity. Cor pulmonale due to COPD (most common), coronary artery disease, diabetes, hypokalemia, sepsis Epidemiology: elderly males Dx: over 100 bpm, irregular rhythm, more than three morphologically distinct P waves Tx: rate control (verapamil, metoprolol), antiarrhythmic (amiodarone, flecainide), radiofrequency ablation, synchronized cardioversion (during R)  Wolff Parkinson White (WPW) Hx: episodic palpitations, syncope Etiology: genetic accessory electrical pathways, associated with congenital Ebstein anomaly (dysmorphic tricuspid valve is further into right ventricle + atrial septal defect) Epidemiology: diagnosis usually during adolescence Dx: Holter monitor, episodic tachycardia, regular rhythm, wide QRS, short PR, delta wave (when accessory tract is firing) Tx: radiofrequency ablation, antiarrhythmic (Class Ic, Class III), avoid digoxin  Ventricular Tachycardia PE: altered mental status, hypotension, jugular venous distention (cannon A waves) Etiology: conduction block distal to bundle of His. Hypo (K, Mg, Ca), cardiomyopathy, cardiac surgical scar, drugs (methamphetamines, cocaine, digoxin), lupus, sarcoid Epidemiology: 6% of all sudden death, high mortality Dx: over 100 bpm, no P, very long QRS, tombstones in V1 -V6 Tx: CPR → alternate epinephrine with antiarrhythmic according to ACLS. Synchronized cardioversion (if pulse present, lower shock more effective), defibrillator (if pulseless, larger shock resets the heart)  Torsades de Pointes Hx: triggered by fear, exercise, stress Etiology: polymorphic ventricular tachycardia. Antiarrhythmic, antipsychotic, anticonvulsant, hypo (K, Mg, Ca), macrolides, fluoroquinolone, cocaine, Takotsubo cardiomyopathy, myocardial infarction, AV block, hypothyroid, pheochromocytoma, hyperaldosteronism, anorexia nervosa Epidemiology: rare, 5% of sudden death Dx: 150-250 bpm, QRS twists around baseline, QT >600ms, preceded by ventricular tachycardia, may degenerate into ventricular fibrillation Tx: magnesium sulfate. Synchronized cardioversion (if pulse present), defibrillator (if pulseless, larger shock resets the heart). Pacemaker if recurrent.  Ventricular Fibrillation Hx: family history of sudden cardiac death Etiology: ventricles only quiver. Reversible causes H’s (Hypovolemia, Hypoxia, Hypo/Hyperkalemia, Hypocalcemia) and T’s (Toxins (cocaine, antiarrhythmic overdose) Thrombosis (PE, AMI, CVA). Other (valvular diseases, myocarditis, WPW) Epidemiology: 80% leads to asystole, 80% mortality Dx: over 300 bpm, irregularly irregular rhythm, usually preceded by ventricular tachycardia Tx: defibrillation only (no synchronized cardioversion). CPR, intubation, epinephrine/antiarrhythmic according to ACLS  Cardiac Arrest (Asystole) PE: unconscious, agonal gasps, no pulse Etiology: cardiac ischemia. Reversible causes H’s (Hypovolemia, Hypoxia, H+ (acidosis), Hyperkalemia, Hypothermia) and T’s (Toxins, Tamponade, Tension pneumothorax, Thrombosis (PE, AMI, CVA). Other (heart block, suffocation, drowning, sedative overdose, lightning strike) Epidemiology: 90% of pediatric cardiac arrest Dx: flat line in 2 perpendicular leads, preceded by bradyarrhythmia or ventricular fibrillation Tx: CPR, intubation, epinephrine/antiarrhythmic according to ACLS  Premature Atrial Contraction Premature Ventricular Contraction Hx: palpitations Hx: feel heart stop Etiology: atrial ectopy (not SA), normal Etiology: ventricular ectopy, normal Epidemiology: common Epidemiology: common Dx: Holter monitor. Intermittent extra, Dx: Holter monitor. Intermittent extra, skipped, or early atrial contraction. 1:1 skipped, or early ventricular contraction. P:QRS, abnormal P, no compensatory No P, compensatory pause after T, T pause after T, short QRS opposite QRS, long QRS Tx: beta blocker, calcium channel blocker Tx: beta blocker, calcium channel blocker if if frequent frequent  Bundle Branch Block (BBB) Etiology: block in bundle branch slows impulse across ventricles, W M causing loss of synchrony and cardiac output LEFT – LBBB: myocardial infarction, myocarditis, cardiomyopathy, hypertension V1 WILLIAM V6 – RBBB: myocardial infarction, myocarditis, congenital defect, pulmonary hypertension, pulmonary embolus Dx: “bunny ears,” long QRS, T opposite QRS – LBBB: W in V1 & M in V6 (WiLLiaM MoRRoW) (LL=left) M W – RBBB: M in V1 & W in V6 (WiLLiaM MoRRoW) (RR= right) RIGHT Tx: pacemaker if LBBB, cardiologist monitor if RBBB V1 MORROW V6  Acute Myocardial Infarction STEMI NSTEMI Progression 1 2 3 4 5 6 1. MI Onset: tall positive T wave 4. 24h post: T inversion (remains days-months) 2. 1h post: ST elevation (onset of necrosis) 5. ST return to normal, small R 3. Q enlarged, R smaller 6. Persistent deep Q, T return to normal  Acute Myocardial Infarction Hx: malaise, chest pain for days prior. Severe retrosternal pressure at rest, not relieved with nitroglycerin, lasting longer than 30 minutes, radiates to left shoulder, arm, jaw. Syncope, cough, feeling of doom, elephant on chest PE: pallor, diaphoresis, Kussmaul sign (JVD on inspiration), tachycardia, weak pulse, S3/S4, Levine sign (clutching chest) Etiology: atherosclerotic plaque causes thromboembolus and myocardial necrosis from ischemia (NSTEMI is partial occlusion). Smoker, diabetes, hypertension, hyperlipidemia, obesity, sedentary, type A personality, family history AMI age 40-50. Epidemiology: males, post-menopausal women (estrogen is protective), over age 60, early morning (platelet aggregation) Dx: ↑troponin (peak 1-2 days, normal 5-14 days), ↑CK-MB (peak 1 day, normal 2-3 days, evaluate new infarct). EKG (STEMI has ST elevation >1mm in 2 contiguous leads or new Q wave; NSTEMI has ST depression). EKG inferior infarct (leads II, III, avF) lateral (I, aVL, V4-V6), anterior (V1-V6). Tx: First line: aspirin (give first, chewable works faster) + antiplatelet (clopidogrel (Plavix), ticagrelor (Brilinta), prasugrel (Effient)), anticoagulation (unfractionated heparin, enoxaparin (LMWH)) Within 90 minutes: IV fibrinolytic (tPA, rPA, TNK-tPA) OR Percutaneous Coronary Intervention (PCI; stent) Coronary bypass: if unstable, PCI or fibrinolytic unsuccessful, or full left main artery blockage. Others: nitroglycerin (vasodilator for chest pain, contraindicated if hypotension, bradycardia, or right ventricular infarct), oxygen (only if less than 90% sat), morphine (only severe pain). Within 24 hours: beta blocker (reduce contractility and arrhythmias; metoprolol, carvedilol, bisoprolol) OR calcium channel blockers (if contraindication to beta blocker; verapamil, diltiazem). Long term (reduce recurrence and mortality): ACE inhibitor or ARB, beta blocker, statin  Heart Is there a P for every QRS? Block 1st degree YES NO Algorithm PR interval is long  First Degree AV Block QRS QRS QRS P P P Hx: asymptomatic Etiology: AV node block. Increased vagal tone (athletes), myocardial infarction (inferior), infectious (myocarditis, endocarditis, Lyme disease), hypo (K, Mg), antiarrhythmics, aortic/mitral valve stenosis, collagen disease (Lupus, scleroderma) LONG DISTANCE between R and P; Is heart block of FIRST DEGREE Dx: 1:1 P:QRS with a fixed, prolonged PR >200 ms R and P are in a long distance relationship (prolonged PR) and spend every weekend Tx: none together (fixed pattern)  Heart Is there a P for every QRS? Block 1st degree YES NO Algorithm PR interval is long Is P to P distance always the same? 2nd degree, Mobitz Type 1 NO YES PR interval long-longer-longest-drop  Mobitz I Wenckebach 2o AV Block PR PR PR NO QRS Hx: asymptomatic Etiology: block at AV node, more common and less pathologic than Mobitz II. Athletes (increased vagal tone), infectious (myocarditis, endocarditis, Lyme, rheumatic), hyper (K, Mg), antiarrhythmics, hyperthyroid, collagen disease (Lupus, scleroderma, sarcoidosis, amyloidosis) Dx: gradually elongating PR prior to dropped QRS PR before dropped QRS is longest PR after dropped is shortest LONG-LONGER-LONGEST-DROP Commonly occurs in P:QRS cycles of 3, 4 or 5 (long-longer, longest- is heart block called WENCKEBACH drop; long-longer-longer-longest, drop; etc.) QRS usually narrow After time together (long-longer- longest), R and P break up (dropped QRS) and go wink at other singles Tx: no progression to third degree block  Heart Is there a P for every QRS? Block 1st degree YES NO Algorithm PR interval is long Is P to P distance always the same? 2nd degree, Mobitz Type 1 NO YES PR interval long-longer-longest-drop 2nd degree, Mobitz Type 2 PR constant, randomly dropped QRS  Mobitz II 2o AV Block PR PR PR NO QRS Hx: asymptomatic to lightheaded/syncope Etiology: block usually occurs distal to bundle of His, more pathologic than Mobitz I. Infectious (myocarditis, endocarditis, Lyme, rheumatic), hyper (K, Mg), antiarrhythmics, hyperthyroid, collagen disease (Lupus, scleroderma, sarcoidosis, amyloidosis) Dx: constant PR interval to randomly dropped QRS. Every so often week R bids ADIEU; QRS usually wide (slows conduction through ventricles) in heart block called MOBITZ TWO Can be random or cyclical R spends every weekend with P (fixed PR) except when he travels for work once in a while (dropped QRS) Tx: pacemaker, can progress to third degree block  Heart Is there a P for every QRS? Block 1st degree YES NO Algorithm PR interval is long Is P to P distance always the same? 2nd degree, Mobitz Type 1 NO YES PR interval long-longer-longest-drop 2nd degree, Mobitz Type 2 PR constant, randomly dropped QRS Is P always followed by QRS? NO P-P constant, QRS-QRS constant rd degree No association of P-QRS 3  Third-degree AV block (complete block) P P P P P P QRS QRS QRS Hx: syncope, angina PE: respiratory distress, hypotension Etiology: no conduction through the AV node, complete dissociation of atria and ventricles. Myocardial infarction, infectious (myocarditis, Lyme, rheumatic), hyper (K, Mg), antiarrhythmics, hyperthyroid, collagen disease (sarcoidosis, amyloidosis) Dx: regular P-P, regular R-R, but QRS does not follow P When R and P DO NOT AGREE; That is heart block THIRD DEGREE (each is beating separately) R and P have split and are not speaking Tx: pacemaker (atria and ventricles contract separately)  Cardiac Disorders Hypertension Hypotension Hyperlipidemia Atherosclerosis Angina (Stable, Unstable, Prinzmetal) Venous insufficiency Peripheral arterial disease Peripheral arterial thromboembolism Peripheral venous thromboembolism  Hypertension Hx: headache, nausea, blurry vision PE: fundoscopy (AV nicking, copper/silver wiring, papilledema) Normal: less then 120/80 (2017 American Heart Association), less than 130/85 (2020 International Society of Hypertension) Elevated: 120-129/less than 80 (2017 AHA), 130-139/85-89 (2020 ISH) Stage 1: 130-139/80-89 (2017 AHA), 140-159/90-99 (2020 ISH) Stage 2: >140/>90 (2017 AHA), >160/>100 (2020 ISH) Urgency: >180/120 + no end organ damage Emergency: >180/110 + end organ damage (renal failure, seizure) Etiology: angiotensinogen (+ renin) → angiotensin 1 (+ ACE) → angiotensin 2 → vasoconstriction, increased aldosterone (causes Na + H20 resorption) Essential (primary) (95%): genetic, obesity, diabetes, heart disease Secondary (5%): renal artery stenosis (#1), pheochromocytoma, Addison’s disease, sleep apnea, hyperthyroid Urgency/Emergency: medication noncompliance, diet pills, cocaine, eclampsia Epidemiology: 35% of Americans, smokers, sedentary. Leads to renal failure, retinopathy, AMI, CVA Dx: >130/>80 on three visits. Thyroid panel, urine catecholamines (if suspect pheochromocytoma), renal ultrasound (if unresponsive to several medications), polysomnography (if suspect OSA), drug screen (if suspect cocaine) Tx: DASH diet, limit EtOH and salt, exercise (150 minutes per week). ACE inhibitor/ARB, diuretic, beta blocker, calcium channel blocker. Goal is 130/80 or less. Emergency: nitroprusside sodium, labetolol, phentolamine for cocaine overdose.  Hypotension Hx: dizzy, blurry vision, lightheaded, palpitations, syncope with standing PE: tachypnea, tachycardia, clammy skin, orthostatic hypotension (↓20 mmHg systolic or ↓10 mmHg diastolic within 3 minutes of standing) Etiology: Orthostatic: sympathetic failure of SA node pools blood in legs. Dehydration, diuretics, distress, standing too long in a hot room. Cardiogenic syncope: vasoconstriction fails → partially filled ventricles contract → low brain perfusion Cardiogenic shock: heart cannot pump blood to organs. Myocardial infarction, ventricular tachycardia, ventricular fibrillation, severe supraventricular tachycardia Epidemiology: elderly Dx: EKG or Holter (possible arrhythmia), urinalysis (high specific gravity if dehydration) Tx: fluids, support hose, stand slowly, increase blood pressure (fludrocortisone, desmopressin), cardiac defibrillator/pacemaker (if cardiogenic)  Dyslipidemia Hx: asymptomatic until advanced atherosclerosis PE: xanthelasma, arterial bruits, arcus senilis (gray ring around iris) Etiology: LDL over 100, HDL under 40, Total cholesterol over 200, triglycerides over 150. Genetic, diabetes, smoking, anorexia nervosa (liver cannot metabolize cholesterol since in Xanthelasma starvation mode), high fat diet. Leads to atherosclerosis, Klaus D. Peter, CC BY 3.0 de, https://commons.wikimedia.org/w/index.php?curid=3784435 pancreatitis (if extremely high triglycerides) Epidemiology: 15% of Americans Dx: lipid panel Tx: HMG-CoA reductase inhibitors (-statin), bile acid sequestrants (if unable to tolerate statins), fibrates (if only has Arcus senilis high triglycerides) Loren A Zech Jr and Jeffery M Hoeg - Correlating corneal arcus with atherosclerosis in familial hypercholesterolemia, CC BY 2.0, https://commons.wikimedia.org/w/index.php?curid=7630894  Atherosclerosis (Coronary and Noncoronary) Hx: asymptomatic, reduced exercise tolerance, angina (stable → unstable) PE: bruits if severe (renal, abdominal, carotid) Stent Etiology: arterial narrowing. Fatty streak → foam cells → fibrous plaque → inflammation → vascular remodeling → cap rupture. Family history, smoking, hyperlipidemia, hypertension, obesity, diabetes, EtOH, sedentary, high fat diet Epidemiology: 36% of Americans. Male over age 60, female over 65. Most common cause of myocardial infarction Dx: lipid panel, carotid ultrasound, coronary (nuclear stress test, coronary angiography) Tx: lifestyle modification, nitroglycerin, antiplatelet (aspirin, clopidogrel (Plavix)), hypertension (beta blocker, calcium channel blocker, diuretic, ACE inhibitor), statin, endarterectomy (noncoronary), stent, coronary artery bypass graft (CABG) Npatchett CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=39235257 Medical gallery of Blausen Medical 2014. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=33041225  Stable Angina and Unstable Angina Hx: Stable: retrosternal pain consistently caused by stress or exertion, always relieved by rest or nitroglycerin, lasts less than 15 minutes Unstable: retrosternal pain that is worse, occurs at rest, lasts 15-20 minutes, does not have a consistent trigger, not relieved with nitroglycerin PE: patient will prefer to be upright, diaphoresis Etiology: ischemia from coronary artery disease. Stable → unstable → myocardial infarction. Epidemiology: age 40-75, males more likely Dx: normal CKMB & troponin, EKG (ST depression), nuclear stress test and perfusion imaging, coronary angiography Tx: GI cocktail (antacid, viscous lidocaine, donnatal (antispasmodic)) to rule out esophageal spasm. Nitroglycerin, antiplatelet (aspirin, clopidogrel), control hypertension (beta blocker, calcium channel blocker, diuretics, ACE inhibitor), slow atherosclerosis (statin), percutaneous coronary intervention (PCI-stent), coronary artery bypass graft (CABG)  Prinzmetal Angina (Variant Angina, Coronary Artery Vasospasm) Hx: retrosternal pain at rest or during early morning sleep hours (not activity induced). Pain radiates to neck, shoulder, jaw PE: normal Etiology: coronary artery vasospasm triggered by hyperventilation, cocaine, tobacco, amphetamines, high dose caffeine energy drinks, low magnesium. Etiology is unknown (theory is nitric oxide deficiency, which is a vasodilator). Epidemiology: Japanese (3x risk), over age 50 Dx: normal CKMB and troponin, EKG (transient ST elevation only during attack that resolves within minutes), ergonovine given during angiography induces vasospasm. Check magnesium lab. Tx: nitroglycerin, calcium channel blockers (nifidipine, amlodipine, verapamil, diltiazem), magnesium supplement (if low)  Venous Insufficiency Hx: achy, heavy, restless feeling in the legs. Symptoms improve with ambulation, elevation, compression PE: malleolar ulcers, pitting edema, hyperpigmentation, tortuous varicose veins Etiology: vein valves are damaged from increased back pressure or volume overload, blood pools in legs. Sedentary, pregnancy, prolonged standing Jmarchn, NIH)- CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=62387372 Epidemiology: pregnancy, obesity, jobs with prolonged standing (retail, food and beverage, cashier, flight attendant) Dx: Doppler ultrasound, magnetic resonance venography (MRV) Tx: surgery (stripping, sclerotherapy, laser). Prevent with compression Malleolar ulcer stockings, exercise Nini00; http://www.varizinforma.com/Photo.htm (.jpg), CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=22518530  Peripheral Artery Disease Hx: calf pain that improves with rest and worsens with activity (claudication), finger pain worse with cold PE: calf muscle atrophy, hairless legs, thick toenails, weak pulses (dorsalis pedis & anterior tibial in leg, radial and ulnar in arm), gangrene of digits (fingers and toes) Etiology: atherosclerosis reduces arterial flow to extremities. Smoking, diabetes, high cholesterol, sedentary James Heilman, MD, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=14572015 Dx: ankle-brachial index, Doppler ultrasound, magnetic resonance angiography (MRA) Tx: surgery (stent, endarterectomy, bypass, amputate if gangrene). Prevent with lifestyle modifications and diabetes/cholesterol Gangrene control. Jmarchn , CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=31200275  Peripheral Arterial Thromboembolism Hx: acute pain out of proportion (first finding), numbness and paralysis (later findings) PE: cold, pallor/cyanosis, limited range of motion (later finding) Etiology: occlusion → ischemia → infarction. Atrial fibrillation (most common cause), atherosclerosis, hypercoagulable state (Factor V Leiden, Protein C/S deficiency), surgery (air embolus), femur fracture (fat embolus), septic (bacterial embolus) James Heilman, MD, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=15335626 Dx: Doppler ultrasound (definitive), hypercoagulable labs (PT, PTT, Factor V Leiden, protein C/S) Tx: surgical (embolectomy, stents, bypass). Prevent with anticoagulant (warfarin, heparin), antiplatelet (aspirin, clopidogrel)  Peripheral Venous Thromboembolism Hx: family history of thromboembolism, hypercoagulable state, unilateral acute leg pain PE: unilateral leg edema, erythema, positive Homan sign (pain behind knee with forced dorsiflexion) Etiology: Virchow’s triad (hemostasis, vessel injury, hypercoagulable) causes thromboembolus. Risk factors include cancer, smoking, oral contraceptives, hormone replacement therapy, pregnancy, Lupus, orthopedic surgery, long flight Dx: elevated D-dimer (screen), Doppler ultrasound (definitive), CT pulmonary angiogram (if concern for pulmonary embolus) James Heilman, MD, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=9444797 Tx: heparin or fondaparinux (initial) followed by dabigatran (Pradaxa), rivaroxaban (Xarelto), edoxaban (Savaysa), apixaban (Eliquis), or warfarin (Coumadin). If unresponsive, thrombolytic (tPA, alteplase, reteplase), embolectomy (catheter or surgical). Monitor for progression to pulmonary embolus (cough, tachycardia). Prevent with compression stockings and frequent ambulation.  Congenital Heart Diseases Non-cyanotic Cyanotic Oxygenated blood Deoxygenated blood from right heart is shunted to from left heart is left heart and body shunted to right heart 5Ts and 1-5 mnemonic and lungs 1: Truncus arteriosus (vessels join to make 1) Atrial septal defect 2: Transposition of great vessels (2 major vessels switched) Ventricular septal defect 3: Tricuspid atresia (3=tri) Patent ductus arteriosus 4: Tetralogy of Fallot (4 defects) Coarctation of the aorta 5: Total anomalous pulmonary vascular return (5 words) (Also, Hypoplastic left heart)  Atrial Septal Defect Hx: fatigue with feeding, dyspnea on exertion, syncope PE: wide fixed S2 split (sound of aortic and pulmonic valves closing). Crescendo-decrescendo systolic murmur over left sternal border 2nd intercostal Etiology: non-cyanotic, interatrial septum defect. Oxygenated pulmonary venous return in left atrium shunted to right atrium (instead of left ventricle). Dx: echocardiogram Tx: surgical repair Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Ventricular Septal Defect Hx: fatigue with feeding, dyspnea on exertion PE: harsh, holosystolic murmur at the left lower sternal border with a thrill Etiology: non-cyanotic, intraventricular septum defect. Oxygenated left ventricular blood mixes with deoxygenated right ventricular blood. Epidemiology: most common non cyanotic heart lesion. 1:200 births. Dx: echocardiogram Tx: surgical repair Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Patent Ductus Arteriosus Hx: premature infant, fatigue with feeding, hoarse cry PE: displaced point of maximal impulse (PMI), thrill over suprasternal notch, bounding peripheral pulses, harsh continuous machinery murmur over left sternal border Etiology: non cyanotic, failure to close duct between descending aorta and pulmonary artery (normally closes in 1-3 days). Oxygenated blood from aorta mixes with deoxygenated blood in pulmonary artery. Rubella during pregnancy, maternal amphetamine/EtOH/phenytoin use Epidemiology: 10% of congenital heart defects Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=33041254 Dx: echocardiogram + bubble test (high velocity jets in pulmonary artery) Tx: close ductus arteriosus with indomethacin in neonate, surgical ligation past infancy  Coarctation of the Aorta Hx: respiratory distress 1-3 days after birth (when ductus arteriosus closes) PE: tachypnea, tachycardia, brachial systolic blood pressure Frank Gaillard - https://radiopaedia.org/cases/6279, CC BY-SA 3.0, https://commons.wikimedia.org/w/index higher than femoral, brachial-femoral pulse delay, left.php?curid=90326382 infraclavicular systolic murmur, suprasternal notch pulsation Rib notching Etiology: ductus arteriosus shunts oxygenated blood past stenotic aortic segment with post-stenotic dilation. When ductus arteriosus closes, minimal oxygenated blood is circulated. Associated with bicuspid aortic valve and ventricular septal defect. Epidemiology: 1:2000 births, Turner’s syndrome Dx: chest x-ray (rib notching; enlarged collateral vessels overlying the ribs), echocardiogram, aortic angiography Tx: maintain patent ductus arteriosus (prostaglandin), (PDA, oPen, Prostaglandin), surgery Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Truncus Arteriosus Hx: fatigue when feeding/crying, failure to thrive PE: tachypnea, cyanosis Etiology: Cyanotic. Single arterial trunk from left ventricle and right ventricle via single semilunar valve straddles ventral septal defect. Atrial septal defect mixes oxygenated and deoxygenated blood Epidemiology: rare, 1:10000 births Dx: echocardiogram Tx: maintain patent ductus arteriosus (prostaglandin), (PDA, oPen, Prostaglandin), surgery Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Transposition of the Great Vessels Hx: cyanosis when feeding/crying, failure to thrive PE: cyanosis within hours of birth, high pitched, Madhero88, CC BY-SA 3.0, https://commons.wikimedia.org/w /index.php?curid=9773889 blowing, decrescendo diastolic apical murmur Egg on String Etiology: Cyanotic. Aorta arises from right ventricle and pulmonary artery arises from left ventricle. Some oxygenated blood from atrial septal defect mixes with deoxygenated blood going to body. Epidemiology: 1:3000 births, 70% males, diabetic mothers Dx: chest x-ray (egg on string), echocardiogram Tx: maintain patent ductus arteriosus (prostaglandin), (PDA, oPen, Prostaglandin), surgery Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Tricuspid Atresia Hx: cyanosis when feeding/crying, failure to thrive PE: cyanosis, jugular venous pulsations and distention, finger clubbing (at least 3 months old) Etiology: Cyanotic. Absent tricuspid valve, no connection between right atrium and right ventricle. Deoxygenated blood in right atrium shunts to the oxygenated left atrium. Left ventricle pumps mixed blood to lungs via ventricular septal defect and body via aorta Epidemiology: associated with transposition of great vessels Dx: echocardiogram Tx: surgery Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Tetralogy of Fallot Hx: cyanosis (Tet spells) when crying, exercise, stress, infection, or dehydration James Heilman, MD - CC BY-SA 3.0, https://commons.wikimedia.o rg/w/index.php?curid=15376 PE: cleft lip/palate, hypospadias, systolic thrill and harsh 351 ejection murmur along left sternal border, digit clubbing Boot shaped heart (older child) Etiology: Cyanotic. Right ventricle outflow obstruction, ventricular septal defect + aorta dextroposition + right ventricular hypertrophy. Maternal rubella, EtOH use Epidemiology: 1:2500 births. Most common cyanotic congenital heart disease. Associated with Down Syndrome Dx: chest x-ray (boot shaped heart), echocardiogram Tx: surgery Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Total Anomalous Pulmonary Vascular Return Hx: cyanosis within 3 days of birth (coincides with ductus arteriosus closure) PE: tachypnea, tachycardia, cyanosis Etiology: Cyanotic. Oxygenated pulmonary veins drain into the deoxygenated superior vena cava (instead of the left atrium). Associated with patent foramen ovale (connects left and right atrium), atrial septal defects, and pulmonary veins that do not connect to the left atrium Epidemiology: 6.8 per 100,000 Dx: echocardiogram Tx: surgery Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Hypoplastic Left Heart Syndrome Hx: symptoms begin within 3 days of birth (coincides with ductus arteriosus closure) PE: cyanosis, respiratory distress, weak pulses, loud single S2, tachycardia Etiology: Cyanotic. Hypoplastic left ventricle, hypoplastic ascending aorta, aortic and mitral valves are absent, hypoplastic, or stenotic. Can also include patent foramen ovale (connects left and right atrium), atrial septal defects, enlarged patent ductus arteriosus. Mix oxygenated and deoxygenated blood in right atrium. Epidemiology: 1:4000 births Dx: echocardiogram Tx: maintain patent ductus arteriosus (prostaglandin), (PDA, oPen, Prostaglandin), emergent heart transplant Centers for Disease Control and Prevention, CC0, https://commons.wikimedia.org/w/index.php?curid=29525840  Heart Sounds & Valvular Disorders Heart sounds Aortic stenosis & regurgitation Mitral stenosis & regurgitation Mitral valve prolapse Pulmonic stenosis & regurgitation Tricuspid stenosis & regurgitation  Heart Sounds Normal Heartbeat S1 – Systole: ventricles contract (Systole= Squeeze) – Tricuspid and mitral valves close S2 – Diastole: ventricles fill – Aortic and pulmonic valves close Preload: amount of blood in ventricles prior to systole – Increased with inhalation, squat (murmurs usually louder) – Decreased with exhalation, stand, valsalva (murmurs usually softer) Afterload: systemic pressure left ventricle must overcome to push blood through aortic valve – Increased in hypertension, aortic stenosis, handgrip (squeezes arterioles and increases peripheral vascular resistance)  SYSTOLIC DIASTOLIC Ventricles squeeze blood to body/lungs Ventricles relax and fill S1 S2 S3 S4 S1 A/P Open T/M Open T/M Closed A/P Closed Aortic Stenosis Aortic Regurgitation Mitral Regurgitation Mitral Stenosis Pulmonic Stenosis Pulmonic Regurgitation Tricuspid Regurgitation Tricuspid Stenosis Diastolic: Diameter of circle made with your AR MS PR TS (arms parts) Extra Beats S3 (“Ken-tuck-y”): Volume overload. Blood from atrium splashing into blood in an already full ventricle. Can be normal. Congestive heart failure, pregnancy. S4 (“Tenn-e-see”): Atria contract and force blood into rigid ventricle. Always pathologic. Severe aortic stenosis, hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, late congestive failure.  Murmurs 1. Determine Location 2. Systole or Diastole? RIGHT LEFT Aortic Stenosis Aortic Regurgitation 2nd IC AS P 2nd IC Pulmonic Stenosis AR 3rd IC Pulmonic Regurgitation (SS over DS) Systolic stenosis top 2 valves T 5th IC Diastolic stenosis in bottom 2 valves M Apex Tricuspid Regurgitation Tricuspid Stenosis Mitral Regurgitation Medical gallery of Blausen Medical 2014;. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - CC BY 3.0, Mitral Stenosis https://commons.wikimedia.org/w/index.php?curid=30111376  Valvular Stenosis Valve is narrowed Normal Blood has smaller area to flow through Blood builds up in previous chamber Mild Enlarges previous chamber Moderate Severe  Valvular Regurgitation (Insufficiency) Normal Prolapse Valve is floppy and does not seal Annulus is widened so valves cannot touch to seal Blood flows into next chamber Chordae Annulus Rupture Dilation Blood flows back to previous chamber Enlarges previous chamber and next chamber  Aortic Stenosis and Aortic Regurgitation Murmur: Aortic Stenosis: systolic, crescendo-decrescendo, radiates to carotids, over 2nd right intercostal space, narrow pulse pressure (systolic minus diastolic 40) (ventricle is overly full and requires more pressure to pump) Etiology: Aortic Stenosis: calcification, rheumatic heart disease. Most common valve disorder over age 65 Aortic Regurgitation: aortic root dilation, idiopathic, hypertension Dx: echocardiogram (left ventricular hypertrophy) Tx: Aortic Stenosis: balloon valvuloplasty, replacement (severe) Aortic Regurgitation: replacement (severe) Wapcaplet, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253  Mitral Stenosis and Mitral Regurgitation Murmur: Mitral Stenosis: diastolic, opening snap, rumble at left lateral apex Mitral Regurgitation: systolic, high pitched, blowing, at apex, radiates to axilla Etiology: Mitral Stenosis: rheumatic heart disease. Leads to pulmonary hypertension Mitral Regurgitation: papillary muscle or chordae rupture from myocardial infarction, mitral valve prolapse (see next slide) Dx: echocardiogram (left atrial hypertrophy) Tx: Mitral Stenosis: balloon valvuloplasty, replacement (severe) Mitral Regurgitation: replacement (severe) Wapcaplet, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253  Mitral Valve Prolapse (MVP) Hx: mostly asymptomatic. If severe, (4 Ps): Pain, Palpitation, Panic Attack, SyncoPe. PE: systolic, high pitched, mid-systolic click blowing over apex. Louder with valsalva and standing (decreases preload), softer with squatting (increases preload) Exception to rule (murmurs usually softer with decreased preload) because increased preload stretches the ventricles and pulls the valves taught, reducing the snapping sound. Etiology: benign floppy mitral valve. Autosomal dominant, Marfan syndrome Epidemiology: most common valve abnormality. Younger female (at diagnosis), 4% of population Dx: echocardiogram Tx: increase preload (beta blocker), valve replacement if severe Patrick J. Lynch, medical illustrator, CC BY 2.5, https://commons.wikimedia.org/w/index.php?curid=1495998  Tricuspid Stenosis and Tricuspid Regurgitation Murmur: Tricuspid Stenosis: diastolic, opening snap, left sternal border 4th intercostal Tricuspid Regurgitation: systolic, high pitched, left sternal border 4th intercostal Etiology: rare, rheumatic, congenital (Ebstein anomaly; valve shifted downwards into ventricle) Dx: echocardiogram (right atrial hypertrophy) Tx: Tricuspid Stenosis: balloon valvuloplasty, replacement (severe) Tricuspid Regurgitation: diuretics, replacement (severe) Wapcaplet, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253  Pulmonic Stenosis and Pulmonic Regurgitation Murmur: Pulmonic Stenosis: systolic, thrill, crescendo-decrescendo, at left sternal border 2nd intercostal. Wide S2 split (aortic and pulmonic). Pulmonic Regurgitation: diastolic, high-pitched, decrescendo, at left sternal border 2nd intercostal space (also called Graham Steel murmur) Etiology: Pulmonic Stenosis: congenital heart disease Pulmonic Regurgitation: pulmonary hypertension pressure pushes back on valve Dx: echocardiogram (right ventricular hypertrophy) Tx: Pulmonic Stenosis: balloon valvuloplasty, replacement (severe) Pulmonic Regurgitation: replacement (severe) Wapcaplet, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=830253  Cardiac & Vessel Disorders Cardiomyopathies Rheumatic heart disease Hypertrophic Bacterial endocarditis Congestive heart failure Acute pericarditis Cor pulmonale Pericardial effusion Restrictive Cardiac tamponade Myocarditis Abdominal aortic aneurysm Aortic dissection Superficial thrombophlebitis  Hypertrophic Obstructive Cardiomyopathy Hx: family history of sudden cardiac death, syncope, palpitations, dyspnea PE: double carotid pulse, displaced point of maximal impulse (PMI), systolic crescendo- decrescendo murmur on left sternal border that radiates to suprasternal notch. Murmur gets softer with increased preload, louder with decreased preload. Exception to rule (murmurs usually softer with decreased preload) because increased preload opens ventricular space, moving hypertrophied septum away from aortic opening Etiology: autosomal dominant mutation causes left ventricular hypertrophy and outflow obstruction → diastolic dysfunction → ventricular arrhythmia → sudden death Epidemiology: most common cause of sudden death in young athletes Dx: EKG (ST abnormal, long PR), echocardiogram (increased velocity across left ventricle outflow, diastolic dysfunction, left ventricle thicker than 15mm) Tx: avoid strenuous activity/sports, beta blocker (increases preload), antiarrhythmic (amiodarone, disopyramide), surgery Npatchett, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=43733288 RIGHT SIDED HEART FAILURE LEFT SIDED HEART FAILURE Right side pumps deoxygenated blood to lungs Left side pumps oxygenated blood to body When it fails, blood backs up into the body When it fails, blood backs up into the lungs First symptom is peripheral edema (but may have First symptoms are pulmonary (cough, chronic pulmonary symptoms from smoking) dyspnea, orthopnea) Caused by smoking Caused by alcoholism  Congestive Heart Failure (CHF) Hx: dyspnea on exertion → orthopnea (dyspnea when lying flat) → dyspnea at rest. Polyuria (fluid retention), frothy blood tinged sputum X-ray findings PE: Cheyne-Stokes respirations, dusky skin, thready pulse, ascites (from cirrhosis), regurgitation murmur, lungs (rales), cardiac (S3, displaced point of maximal impulse) Etiology: LEFT SIDE, DILATED CARDIOMYOPATHY. Systolic (weak dilated myocardium cannot eject). Cirrhosis → portal venous hypertension → fluid back up/retention → cardiac dilation/failure → pulmonary edema. Alcoholism (#1), postpartum (fluid overload), uncontrolled hypertension, myocarditis Mikael Häggström, CC0, https://commons.wikimedia.org/w/index.php?curid=61614661 Decompensation caused by ADMIT-Now (Arrhythmia, Drinking, Medication non-compliance, Infarction/Illness, Thyroid disease, Na/NSAIDS (cause fluid retention)) Normal Epidemiology: most common cardiomyopathy CHF Dx: elevated BNP (B-type natriuretic peptide), chest x-ray (meniscus sign, Kerley lines, cardiomegaly), echocardiogram (left ventricular hypertrophy, thin walls, decreased output) Tx: Stage A: lifestyle modification, ACE inhibitor Stage B: add beta blocker Stage C: add diuretics, salt restriction, defibrillator, pacemaker Stage D: transplant vs. hospice, positive inotropes (e.g., digoxin, norepinephrine), left assist device Decompensation: (LMNOP) Lasix, Morphine, Nitroglycerin, Oxygen, Position http://www.scientificanimations.com/wiki-images/, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=63766023  Cor Pulmonale (Right sided heart failure) Hx: fatigue, dyspnea, cough/hemoptysis (from smoking), history of smoking or lung disease PE: jugular venous distention, hepatojugular reflux, hepatomegaly, pitting leg edema, cyanosis, finger clubbing, wheezing, cardiac (S3, displaced point of maximal impulse) Etiology: RIGHT SIDE, DILATED CARDIOMYOPATHY. Chronic lung scarring → pulmonary hypertension → decreased right ventricular output → venous backup → ascites. COPD (most common), interstitial lung disease Pitting Edema James Heilman, MD, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=11787530 Epidemiology: 7% of heart disease Dx: elevated BNP, echocardiogram (right ventricular hypertrophy and dilation, decreased output), chest x-ray (pulmonary artery enlargement, cardiomegaly) Tx: oxygen, diuretics reduce ventricular filling volume (hydrochlorothiazide, furosemide), calcium channel blockers reduce afterload (nifidipine, diltiazem), prostacyclin analogues and PDE5 inhibitors cause pulmonary vasodilation (epoprostenol, treprostinil, bosentan, sildenafil), increase contractility-adjunctive only (theophylline, digitalis) Dilation Yale Rosen CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31128151  Restrictive Cardiomyopathy Hx: exercise intolerance, angina, syncope PE: Kussmaul sign (jugular venous distention with inspiration, blood backs up since heart can’t fill), weak pulse, ascites, leg pitting edema, hepatomegaly, S4 (atrial blood being forced into stiff ventricles) Etiology: rigid ventricles cannot dilate and fill during diastole. Idiopathic, radiation, scleroderma, sarcoidosis, hemochromatosis, amyloidosis, metastatic cancer Epidemiology: least common cardiomyopathy Dx: EKG (low voltage, atrial fibrillation is common), echocardiogram (non-dilating, normally contracting myocardium), cardiac cath (reduced ventricular filling volumes) Tx: increase filling time, relax ventricles, decrease afterload (carvedilol, diltiazem, verapamil), nitrates reduce preload (nitroglycerin), diuretics reduce preload (hydrochlorothiazide, furosemide), vasodilators reduce filling pressure (hydralazine), inotropes increase contractility (digoxin-use with caution-may cause arrhythmia), if atrial fibrillation (warfarin, heparin), pacemaker, cardiac transplant  Rheumatic Fever/Heart Disease Hx: recent strep throat, polyarthritis, malaise Erythema Marginatum PE: fever, arthritis (red, swollen joints), carditis (murmur, pericardial friction rub), chorea (involuntary movements, milkmaid hand, dysphasia, dyskinesia), erythema marginatum (serpiginous), subcutaneous nodules (painless, bony prominences) Etiology: autoimmune reaction to untreated group A Streptococcal pharyngitis. Acute (myocarditis, vegetation), Chronic (valvular fibrosis) Adsie CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=100819255 Epidemiology: countries without antibiotic access Myocarditis Dx: throat culture, anti-streptolysin (ASO) antibody titer, EKG (long PR), JONES criteria (Joints, arditis, Nodules, Erythema marginatum, Sydenham chorea), echocardiogram Tx: bed rest, prednisone, chorea (valproic acid), penicillin G benzathine for 4 weeks. Resolve: nodules (2 weeks), erythema marginatum (3 weeks), polyarthritis (4 weeks), chorea (3 years) CDC/Dr. Edwin P. Ewing, Jr., PHIL ID# 847, Public Domain, https://commons.wikimedia.org/w/index.php?curid=825655  Bacterial Infective Endocarditis Hx: history of rheumatic fever, congenital heart disease, heart surgery, valvular Valvular Vegetations stenosis/regurgitation, recent dental surgery, IV drug use. Fever, chills, night sweats, weight loss, malaise, cough PE: petechiae, Janeway lesion (non painful erythematous macules on palms/soles), Osler Nodes (painful; Ouch!, erythematous macules on palms/soles), splinter hemorrhage (nails), Roth Spots (Retinal hemorrhage), cardiac (new murmur) Etiology: endocardial infection causes valvular vegetation and emboli. Mitral and aortic valves most common (aortic stenosis and mitral valve prolapse are BruceBlaus, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=57340203 common), tricuspid valve (IV drug users; first to get systemic infection from body) Splinter Hemorrhage Native valve: Streptococcus viridans (dental procedures), Streptococcus bovis (colon cancer) Prosthetic valve: Staphylococcus (aureus, epidermis) (during implantation) IV drug users: Pseudomonas, fungal Dx: blood culture, transesophageal echocardiogram (valvular vegetation) Tx: IV antibiotics (e.g., vancomycin, gentamicin, rifampin) Splarka, Public Domain, https://commons.wikimedia.org/w/index.php?curid=11254973  Pericarditis→ Pericardial Effusion→ Cardiac Tamponade Hx (all three): retrosternal angina radiates to shoulder, neck, arm. Worse with cough, inspiration, and lying flat, better sitting forward Effusion: + syncope, anxiety, confusion Pericarditis Tamponade: + restlessness, sense of doom PE (all three): pericardial friction rub/knock, Kussmaul sign (jugular venous distention (JVD) with inspiration), ascites, pulsus paradoxus (systolic and diastolic pressure drop >10mmHg during inspiration due to decreased left ventricular filling and decreased stroke volume). Effusion: + hepatojugular reflex, Ewart sign (dull to percussion below left scapula) NIH, Public Domain, https://commons.wikimedia.org/w/index.php?curid=29590112 Tamponade: + Beck triad (hypotension, muffled heart sounds, constant JVD) Effusion https://www.sc Etiology: pericarditis (inflammation) → pericardial effusion (fluid between myocardium and pericardium) ientificanimati ons.com, CC → cardiac tamponade (EMERGENT prevents contraction). Idiopathic, viral, bacterial, Lupus, BY-SA 4.0, https://commo ns.wikimedia. org/w/index.p Rheumatoid, Dressler syndrome (2-3 weeks post myocardial infarction), penetrating trauma (tamponade) hp?curid=726 74453 Dx: elevated ESR and CRP, +/- troponin, EKG (ST elevation + PR depression all leads) Pericarditis: echocardiogram (thick pericardium) Tamponade Effusion: echocardiogram (swinging heart sloshing in fluid), pericardiocentesis Tamponade: echocardiogram (diastolic collapse), chest x-ray (water bottle heart), EKG (Low QRS), pericardiocentesis Tx: Pericarditis: NSAIDs only (if vitals stable) Effusion: NSAIDs + pericardiocentesis Tamponade: urgent pericardiocentesis, pericardial window, or pericardiostomy  Myocarditis Hx: acute heart failure with no history of heart disease. Chest pain, fever, dyspnea, recent 1-2 weeks of flu- like symptoms PE: tachycardia, mitral regurgitation murmur Etiology: idiopathic (50%), viral (Coxsackie B, influenza, Epstein Barr, HIV, Parvovirus), bacterial (streptococci, diphtheria, tuberculosis, staphylococci, mycoplasma), fungal (aspergillus, candida), other (postpartum, syphilis, Lyme, parasitic, sarcoidosis, insect venom, heavy metals, chemotherapy, cocaine, amphetamines) Acute phase (first 2 weeks): myocyte infection and inflammation Chronic phase (after 2 weeks): autoimmune destruction of infected myocytes Epidemiology: young adult men, immunocompromised, pregnant, neonate Dx: CBC (eosinophilia), elevated ESR, CRP and CK, elevated troponin (50%), usually normal CK-MB. EKG (right bundle branch block, ventricular arrhythmia), endomyocardial biopsy (if chronic and unknown cause) Tx: self resolve (weeks to months), 33% develop dilated cardiomyopathy, 20% mortality in first year. Diuretics (furosemide), vasodilator (nitroglycerin), ACE inhibitor or ARB  Abdominal Aortic Aneurysm Hx: family history, other aneurysms, isolated groin pain, referred lumbar pain PE: pulsatile abdominal mass, abdominal bruit, systolic pressure in thigh less than arm (vessel becomes larger, pressure drops). If rupture, signs of hemorrhagic shock. Etiology: degenerative weakened ballooning aorta. COPD, hypertension, Marfan BruceBlaus - CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=47113849 Epidemiology: Caucasian, males, over age 65, smoker Dx: 1 x ultrasound screen (male, age 65 smoker), CT scan Tx: monitor with ultrasound/CT every 6 months (less than 4.5 cm), control hypertension (beta blocker), surgery (greater than 5 cm) Bakerstmd, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=38183427  Aortic Dissection Hx: acute, severe, ripping, mid-scapular pain PE: altered mental status, muffled heart sounds, interarm blood pressure difference >20mmHg (depends on dissection location relative to left/right subclavian artery-aortic junctions, hematoma can compress), wide pulse pressure (>100/