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Hypertension Etiology (ET) Systolic ≥140 or Diastolic ≥ 90 o Stage I systolic=140- 159; Diastolic is 90-99 o Stage II is systolic= ≥160; Diastolic ≥100. Hypertensive emergency - blood pressure > 180/120 mm Hg with evidence of end organ dysfunction Hypertensive urgency o blood pressure > 180/120 mm Hg without evidence of progressive end-organ dysfunction Can be primary or secondary. Has no specific identifiable causes, pathogeneses is multifactorial o Genetic predisposition, more prelevant with increased age and in blacks. o Environmental factors excessive salt intake and obesity o Exacerbated in males, smokers, blacks and sedentary lifestyle. Onset usually 20-55. Secondary Hypertension suspect those at early age or patient experiencing symptoms for the first time is >50 yo. causes of secondary hypertension include o renal any cause of chronic kidney disease renovascular hypertension o endocrine Cushing syndrome primary hyperaldosteronism hyperthyroidism hyperparathyroidism pheochromocytoma o obstructive sleep apnea (OSA) o coarctation of aorta o medications Course (CS) capacity of system increase renin, angiotensin and aldosterone secretion. Wall may dilate or tear, forming aneurysm, or forming MI Cardiovascular P are kidneys, 1 S/S Physical Findings (PF) Diagnostic testing (DT) Treatment (Tx) Cardiovascular brain, and retina. Poor control of HTN can lead to chronic renal failure, stroke due to hemorrhage, loss of vision, or CHF. Frequently asymptomatic in early stages. Initial symptoms are vague and nonspecific. o Fatigue, malaise, and at times morning headache o Elevated bp under various conditions is key sign of htn. Accelerated HTN- somnolence , confusion, visual disturbance, n/v Most Pt asymptomatic common complaint is nonspecific headache. In untreated HTN you see end organ damage like- HF, renal failure, stoke, dementia, aortic dissection, atherosclerosis, retinal hemorrhage, av nicking Loss of peripheral pulses w/ atherosclerosis. Systolic BP ≥ 140 or diastolic BP ≥ 90 on ≥2 separate occasions Once diagnosed diagnostic test are indicated to assess end-organ damage, id and additional risk factors , exclude secondary causes of htn and assist with medication choice. o EKG may show LVH or HF o CXR may show ventricular hypertrophy, but cxr not considered necessary in uncomplicated HTN. o or UA) may indicate renal dz or diabetes. o Lipid profile to assess atherosclerosis. Non-pharm Tx of essential htn should be stressed should include DASH diet, weight loss, exercise, stop smoking, limitation of Alc, limitation of sodium. Diabeic patients and those with renal dz = aggressive tx to achive BP < 130/80 For patients with prehypertension (120- 130/80-89) or HTN stage one = lifestyle modification. o If patient stage one patient is HTN after 3 months of lifestyle mod start antihypertensive medication. o Stage II Pt and Pt with diabetes (with systolic bp > 130 and diastolib >80 needs earlier pharm tx. The goal of HTN meds is to o o direct vasodilation =hydralazine inhibition of vasoconstriction. Block sns =alpha blocker Block ca activated smooth muscle contraction=ccb Block aldosterone=aldosterone 2 Cardiovascular antagonist= spirolactone Block renin angiotensin system= ACE inhibitors and ARB’s Diuretics plasma volume and chronically reduce peripheral resistance Recommended as initial tx for HTN. K suppliments may be needed for some patients. o Thiazides most conservative effective o Loop diuretic used only with renal dysfunction and when close electrolyte monitoring is assured. Βeffective in younger white patients. Angiotensin-Converting enzyme (ACE) inhibitors, also inhibit bradykikin degredation and stimulate synthesis of vasodilation prostaglandins= Initial drug choice for Htn pt’s with diabetes and the tx of choice for mild or moderate HTN, especially younger white pt, or when diuretics are insufficient. o Side effect= cough o ARB’s= interaction of angiotensin 2 on receptors. Calcium Channel blockers = peripheral vasodilation, preferable in blacks and elderly. Aliskiren, renin inhibitor- recently approved for mom tx or combo. Aldosterone receptor antagonist, like spirolactone are used for refractory HTN as addition. Secondary HTN- TX underlying cause Target BP o target blood pressure (BP) < 140/90 for most patients o target systolic blood pressure < 150 mm Hg recommended in older patients (age ≥ 60 years or age ≥ 80 years varies by guideline) o in patients with diabetes guidelines vary but targets range from < 130/80 mm Hg to < 140/90 mm Hg o in patients with chronic kidney disease, current guidelines recommend < 140/90 mm Hg, with multiple guidelines suggesting < 130/80 mm Hg if proteinuria or diabetes present; lower blood pressure targets associated with reduced risk of end-stage renal disease in patients with proteinuria o in patients with coronary artery disease reaching systolic blood pressure ≤ 130 mm Hg appears associated with reduced risk of heart failure and stroke but increased risk of hypotension . IV saline if volume depleted for Urgency and Emergency 3 Follow up Refer Cardiomyopathy Dilated Cardiomyopathy Cardiovascular Hyepertensive Urgency (no evidence of end organ damage) may be treated with any of o nicardipine 5 mg/hour orally, increase by 2 mg/hour every 15 minutes, maximum dose 15 mg/hour o captopril 25 mg orally 2-3 times daily o clonidine adults - initial dose 0.1-0.2 mg orally, then increase 0.05-0.2 mg every hour up to total dose 0.5-0.7 mg as needed children aged 1-17 years - initial dose 0.05-0.1 mg orally, repeat up to maximum 0.8 mg o labetalol dose options include initial dose 20-80 mg IV, then additional 40-80 mg dose (range 20-80 mg) at 10minute intervals until desired blood pressure achieved initial dose 0.5-2 mg IV infusion, adjust as required initial dose 200 mg oral, then additional 200-400 mg dose after 6-12 hours as needed Hypertensive emergency o admit to intensive care unit for IV medications o lower blood pressure by 10%-15% over first o For patients receiving lifestyle modification advice alone o follow-up at 3-6 month intervals o if higher BP, follow-up at 1-2 month intervals For patients on antihypertensive drug treatment o follow-up every 1-2 months depending on BP, until readings on 2 consecutive visits are below target o for symptomatic patients or those with severe hypertension, intolerance of antihypertensive drugs, or target organ damage, follow-up more frequently than 1-2 months o see patients every 3-6 months after target BP is reached Referral to a hypertension specialist considered in severe cases, or when secondary hypertension. Dz of heart muscle characterized by their presentation and pathophysiology. Dilated cardiomyopathy is a progressive disease of heart muscle that is characterized by ventricular chamber enlargement and contractile dysfunction with normal left ventricular (LV) wall thickness. 4 Etiology Course S/S PF DT Cardiovascular The right ventricle may also be dilated and dysfunctional. Dilated cardiomyopathy is the most frequent reason for heart transplantation Middle age men most affected Big and baggy not thick and strong. decreased contractile function without pressure overload, volume overload or coronary artery disease Associated with reduced strength of ventricular contraction, result in dilation of the left ventricle. Causes include o genetic abnormalities o Secondary to other cardiovascular disease: ischemia, hypertension, valvular disease, tachycardia induced o excessive alcohol consumption o postpartum state o Toxicity o Endocronopathies- Thyroid, Pheochromocytoma. o myocarditis o may be idiopathic Can lead to heart failure (cause of death in 70%), embolism, atrial flutter, atrial fibrillation dyspnea on exertion, fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, chest pain, systemic and pulmonary embolism. Left or biventricular chf Edema, increasing weight and abdominal girth increased. Tachypnea, tachycardia and hypertension, Hypoxia signs (clubbing, Cyanosis) small pulse pressure Coronary artery dz pulsus alternans typically seen with advanced myocardial disease jugular-venous distention (JVD) (heart failure) Pulmonary edema with crackles and or wheezes cardiomegaly S3 galllop murmurs aortic regurgitation, mitral regurgitation, less commonly tricuspid regurgitation, arrhythmias pulmonary rales (heart failure) hepatomegaly (heart failure) Goiter ascites peripheral edema (heart failure) Chest x-ray - massive cardiomegaly, pulmonary vascular congestion, interstitial pulmonary edema 5 TX FU/Referral Hypertrophic Cardiomyopathy Etiology Course S/S PF DT Cardiovascular EKG- S-T changes, , conduction abnormalities, ventricular ectopy Echo= excludes valvular lesions, you will see LVH dilation and dysfunction, low CO. Most useful study. Abstinence from alcohol is essential Underlying disease should be treated Congestive heart failure requires supportive treatment Refer to cardiology Massive hypertrophy , particularly of septum, sm left ventricle, systoloic anterior mitral motion, and diastolic dusfunction. Almost exclusively genetic Hypertrophic cardiomyopathy and elderly is a distinct form. Complications of HCM may include the following: Congestive heart failure Ventricular and supraventricular arrhythmias Infective mitral endocarditis A-fibrillation with mural thrombus formation Sudden death Sudden cardiac death (the most devastating presenting manifestation) usually occurs impatience younger than 30 years old. Dyspnea (the most common presenting symptom) Syncope and presyncope Angina Palpitations Orthopnea and paroxysmal nocturnal dyspnea (early signs of congestive heart failure [CHF]) CHF (relatively uncommon but sometimes seen) Dizziness Double apical impulse or triple apical impulse (less common) Normal first heart sound; second heart sound usually is normally split but is paradoxically split in some patients with severe outflow gradients; S3 gallop is common in children but signifies decompensated CHF in adults; S4 is frequently heard Jugular venous pulse revealing a prominent a wave Double carotid arterial pulse Apical precordial impulse that is displaced laterally and usually is abnormally forceful and enlarged Systolic ejection crescendo-decrescendo murmur Holosystolic murmur at the apex and axilla of mitral regurgitation Diastolic decrescendo murmur of aortic regurgitation (10% of patients) Echocardiography is the key to diagnosis MRI is also useful diagnostic tool 6 TX FU/Referral Restrictive Cardiomyopathy Etiology Course Chest radiograph is often not remarkable. EKG abnormalities include nonspecific ST and T-wave changes exaggerated septal Q waves and left ventricular hypertrophy. Initial tx is Beta blockers or CCB; Diasopyramide is usedfor its negative inotropic effects. Surgical or nonsurgical ablation of the hypertrophic septa may be required Dual chamber pacing implantable defibrillators or mitral valve replacement may be indicated. Cardiology consultation for diagnosis Restrictive cardiomyopathy is rare its principal abnormality is diastolic dysfunction—specifically, restricted ventricular filling, ventricles are stiff. Results from fibrosis or infiltration of the ventricle wall because of collagen defects diseases most commonly amylodoises, radiation post operative changes diabetes and endomyocardial fibrosis. Left ventricle is small or normal with mildly reduced function Complications of RCM may include the following; S/S PF DT Cardiovascular Thromboembolism Dysrhythmias Cardiac cirrhosis Progressive deterioration of cardiac function Patients may be more comfortable in the sitting position because of fluid in the abdomen or lungs. Weight loss and cardiac cachexia are not uncommon. Easy bruising, periorbital purpura, macroglossia, and other systemic findings, such as carpal tunnel syndrome, should advise the clinician to consider amyloidosis. Patients present with decreased exercise tolerance In advance dz patients developed right-sided congestive failure Pulmonary hypertension usually it’s present Heart sounds S1 and S2 are normal, with a normal S2 split. o A loud early diastolic filling sound (S3) may be present but is uncommon in amyloidosis Breath sounds are decreased due to pleural effusion, frequently bilateral, and large in amyloidosis. Crepitations or rales are rarely heard, even in advanced heart failure of amyloidosis. Echocardiogram is the key to diagnosis Chest x-ray may show a mild to moderately large cardiac silhouette. 7 FU/Referral Endomyocardial biopsy may be necessary to differentiate restrictive disease from other forms of cardiomyopathies or pericarditis. No specific treatmen The mainstays of medical treatment include diuretics, vasodilators, and angiotensin-converting enzyme inhibitors (ACEs) as indicated, as well as anticoagulation (if not contraindicated) Cardiology Conduction Disorders Atrial Fibrillation TX Etiology Course S/S PF DT Tx Cardiovascular Atrial fibrillation is the most common chronic arrhythmia Incidents and prevalence increases with age Called holiday heart when caused by excessive alcohol use or withdrawal. Hemodynamic stress Atrial ischemia Alcohol and drug abuse Endocrine disorders Genetic factors Advanced aging Non-cardiovascular respiratory causes Can lead stroke and MI. Patients may present with palpitations, angina, fatigue or other symptoms of heart failure. Patients may be completely asymptomatic paroxysmal, persistent, or permanent Patients with decompensated congestive heart failure (CHF) Patients with hypotension Patients with uncontrolled angina/ischemia Absence of P ways replaced by a regular leaves Irregular ventricular rate Heart rate typically will be from 110 240 beats per minutes. EKG Acute atrial fib depends on the presentation and includes electronic cardioversion , treatment of underlying disease, and control of rate. o Cardioversion if <48 hours o Agents used for rate control in acute aphid include Diltiazem Metopolol Digoxin- rarely mono tx Amiodarone (mainly for patients who are intolerant of or unresponsive to other 8 Follow up/ Referral A-Flutter ET Cardiovascular agents) o Anticoagulation is indicated as follows Patients with newly diagnosed AF and those awaiting electrical cardioversion can be started on intravenous (IV) heparin or low-molecular-weight heparin (LMWH) Concomitantly, patients can be started on warfarin in an inpatient setting while awaiting a therapeutic INR value (2-3) Oral direct thrombin inhibitors may present an alternative to warfarin in a higher-risk population with nonvalvular AF Treatment of chronic atrial fib includes control of rate and prevention of thromboembolism o Appropriate antithrombotic regimen should be balanced between the risk of stroke and the risk of bleeding. Warfarin- targer 2-3 Alternatives if above can not be used adding clopidogrel to aspirin may be considered o Agents used for rate control include Beta blockers Nondihydropyridine calcium channel blockers Digoxin Amiodarone o Agents used for rhythm control include Flecanide Propafenone Dofetilide Amiodarone Sotalol Cardiology A cardiac arrhythmia characterized by atrial rates of 242-400 beats per minute. Usually occurs in patience with chronic obstructive pulmonary disease, CHF, atrial septal defect or coronary artery disease. Associated with a variety of cardiac disorders Conditions also associated with a flutter o Hypoxia o COPD o Pulmonary embolism o Hyperthyroid o Pheochromocytoma o Diabetes o Electrolyte imbalance 9 Course S/S PF DT TX Follow up/Referral Atrioventricular Block Cardiovascular o Alcohol consumption o Obesity o Digitalis toxicity Any prolonged atrial arrhythmia can cause a tachycardiainduced cardiomyopathy Palpitations, fatigue or poor exercise tolerance, mild dyspnea, presyncope. Less common symptoms o Angina, profound dyspnea, or syncope. o Tachycardia may or may not be present, depending on the degree of AV block associated with the atrial flutter activity The heart rate is often approximately 100-150 beats/min because of a 2:1 AV block The pulse may be regular or slightly irregular Hypotension is possible, but normal blood pressure is more commonly observed Saw tooth pattern in EKG ECG – This is an essential diagnostic modality for this condition General treatment goals for symptomatic atrial flutter are similar to those for atrial fibrillation and include the following Control of the ventricular rate o Ventricular rate control achieved with drugs that block the AV node. IV calcium channel blockers (eg, verapamil and diltiazem) or beta blockers can be used, followed by initiation of oral agents o The success rate of electrical cardioversion is higher than 95% o Pharm cardioversion tx Dofetilide and Ibutilide Restoration of sinus rhythm o RFA is often used as first-line therapy to achieve permanent restoration of sinus rhythm o The main difference between atrial fibrillation and atrial flutter is that most cases of atrial flutter can be cured with radiofrequency ablation (RFA) Prevention of recurrent episodes or reduction of their frequency or duration Prevention of thromboembolic complications o Anticoagulation tx Minimization of adverse effects from therapy Cardiology Atrioventricular (AV) block occurs when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized First-degree AV block o atrial-ventricular (AV) conduction delayed 10 ET Course Cardiovascular o PR interval prolonged, greater than 0.2 seconds o >65 most affected Second degree AV block o Mobitz I (Wenckeback) bradyarrhythmia with progressive prolongation in PR interval until P wave not conducted o Mobitz II almost always due to organic disease involving the infra-nodal conduction system. bradyarrhythmia sudden interruption of atrioventricular (AV) conduction with constant PR interval Third degree Block o bradyarrhythmia o complete absence of conduction between atria and ventricles o atrioventricular dissociation First degree and Mobiz I may occur in o normal individuals with heightened vagel tone o may also occur as a drug effect especially digitalis calcium channel blockers beta blockers or sympatholytic agents Clonidine Methyldopa o Organic disease o Disturbances also occur transiently or chronically due to ischemia, infarction, inflammatory process, fibrosis, calcification or infiltration. Mobitz II o degenerative change in His-Purkinje system o MI o calcific valvular stenosis Third Degree o Idiopathic o myocardial infarction o postsurgical valve replacement correction of congenital heart disease heart transplant o carotid sinus hypersensitivity o metallic metabolic abnormalities First Degree block no clinical consequences Mobiz I Syncope 11 S/S PF DT Tx Cardiovascular Progression to third-degree block uncommon. Mobitz II to can lead to complete heart block. Third Degree Heart Block Ventricular tachycardia asystole heart failure syncope First-degree AV block Usually asymptomatic Mobiz I Often asymptomatic Syncope or presyncope Dizziness Mobitz II Syncope or presyncope Dizziness fatigue and weakness Third degree Block syncope or presyncope dizziness palpitations Stokes-Adams syncopal attacks angina dyspnea edema First-degree AV block Normal physical exam Mobiz I Pulse ≤ 60 p/min Mobitz II pulse ≤ 60 May have a regular irregular heartbeat fixed PR intervals before and after blocked beats on electrocardiogram Third degree Block Pulse <50 complete absence of relationship between p waves and QRS. EKG First-degree AV block Usually no treatment necessary. Mobiz I Usually no treatment needed Atropine in emergency situations Mobitz II Cardiac pacemaker Atropine IV if symptomatic epinephrine infusion maybe use after atropine 12 FU/ Referral Bundle Brach Block ET Course S/S PF DT TX Cardiovascular dopamine Third degree Block immediate cardiac pacemaker if symptomatic Atropine is a temporizing measure while awaiting a transcutaneous pacemaker. First-degree AV block No screening indicated Mobiz I No screening indicated Mobitz II Cardiology Third degree Block Cardiology, Routine checks every 6-12 months Bundle branch block is a condition in which there's a delay or obstruction along the pathway that electrical impulses travel to make your heart beat. The delay or blockage may occur on the pathway that sends electrical impulses to the left or the right side of your heart. Bundle branch block sometimes makes it harder for your heart to pump blood efficiently through your circulatory system. Left bundle branch block heart disease congestive heart failure cardiomyopathy high blood pressure Right bundle branch block Congenital MI Myocarditis hypertension scar tissue that develops after surgery pulmonary embolism Can lead to a sudden onset cardiac death if person have MI and then develop Bundle branch block. may need pacemaker. Syncope presyncope bradycardia Atherosclerosis, cardiomyopathy ischemic heart disease, Htn. EKG No specific treatment, treat underlying condition Some people may benefit from the pacemaker 13 FU/ Referral Paroxysmal Supraventricular tachycardia (PSVT) Cardiology PSVT is the most common paroxysmal tachycardia and usually occurs in persons without structural problems. episodic condition with an abrupt onset and termination o supraventricular arrhythmia which may include(1) atrioventricular nodal reciprocating tachycardia (AVNRT) atrioventricular reciprocating tachycardia (AVRT) atrial tachycardia ET triggered by a reentry mechanism. This may be induced by premature atrial or ventricular ectopic beats. Other triggers include hyperthyroidism and stimulants, including caffeine, drugs, and alcohol. It is usually a narrow-complex tachycardia that has a regular, rapid rhythm usually bening. Tachycardia may induce ischemia May precipitate heart failure or hypotension during acute MI. Usually asymptomatic palpitations fatigue lightheadedness chest pain dyspnea presyncope syncope o pulse > 140-250 beats/minute during acute episode of paroxysmal supraventricular tachycardia(1) o pulse > 100 beats/minute with sinus tachycardia EKG Mechanical measures to interrupt a cute PSVT include Valsalva maneuver, coughing, breath holding, stretching, putting the head between the knees, applying Coldwater to face and unilateral carotid sinus massage Synchronize shock Adenosine Verapamil Cardiology form of ventricular tachycardia characterized by "twisting of the peaks" morphology on electrocardiogram (QRS complex rotation around an isoelectric baseline) often associated with a prolonged QT/QTC interval Drugs that prolong QT o Disopyramide Course S/S PF DT Tx FU/referral Torsades de Pointes ET Cardiovascular 14 Course S/S PF DT TX FU/ Referral Ventricular Tachycardia ET Course S/S PF Cardiovascular o Dofetilide o Ibutilide o Procainamide o Quinidine o Sotalol Prolongation of QT interval can be congenital Sudden cardiac death Recurrent episodes of palpitations, dizziness, and syncope; 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 o Rapid pulse, low or normal blood pressure, or transient or prolonged loss of consciousness. o This could be preceded by bradycardia or premature ventricular contractions o Pallor and diaphoresis may be noted, especially with a sustained episode EKG Magnesium Sulfate None 3 or more beats of ventricular origin (wide QRS) at rate 100-200 for wide QRS tachycardia in adult, consider ventricular tachycardia until proven otherwise oronary artery disease cardiomyopathy electrolyte abnormalities myocardial ischemia hypoxemia acidosis idiopathic syncope heart failure angina ventricular fibrillation Palpitation Light-headedness Syncope Chest pain Anxiety tachycardia (regular rhythm with pulse > 120), hypotension Tachypnea Signs of diminished perfusion, including a diminished level of consciousness, pallor, and diaphoresis 15 DT TX Follow up Ventricular Flutter Etiology Course S/S PF DT TX Follow up Wolff-Parkinson-White syndrome ET Cardiovascular High jugular venous pressure Abnormal splitting of S2 EKG no treatment if asymptomatic if unstable - O2, IV access, consider sedation (unless hemodynamically unstable, for example, hypotension, pulmonary edema or unconscious), cardiovert 50 joules (unsynchronized if hemodynamically unstable to avoid delay, consider precordial thump if hemodynamically stable), cardiovert 100 joules, cardiovert 200 joules, cardiovert up to 360 joules, if recurrent add lidocaine and cardiovert at previously successful energy level then add procainamide or bretylium if stable - O2, IV access, lidocaine, procainamide, cardiovert No driving for six months Life-threatening ventricular tachyarrhythmia Associated with coronary artery disease Can lead to cardiac arrest Palpitations Fatigue or poor exercise tolerance Mild dyspnea Presyncope The heart rate is often approximately 150 beats/min The pulse may be regular or slightly irregular Hypotension is possible, but normal blood pressure is more commonly observed EKG o immediate nonsynchronized direct current (DC) shock if loss of consciousness o lidocaine may be useful in post-myocardial infarction setting to suppress symptomatic ventricular arrhythmias(1) o consider placement of implantable cardioverterdefibrillator Cardiology o beta blockers o amiodarone may be indicated for patients with history of acute sustained ventricular arrhythmias congenital condition involving abnormal conductive tissue between the atria and the ventricles that provides a pathway for a reentrant tachycardia circuit wide QRS (> 0.12 second) with initial slurring (delta wave), sinus rhythm, short PR (< 0.12 second) accelerated conduction due to accessory atrioventricular (AV) pathway, leading to ventricular preexcitation congenital phenomena that are related to a failure of insulating tissue maturation within the AV ring—even 16 Course S/S PF though their manifestations are often detected in later years, making them appear to be acquired Risk of recurrence after a single episode of supraventricular tachycardia (SVT) is uncertain Once identified and appropriately treated, WPW syndrome is associated with an excellent prognosis, including the potential for permanent cure through RF catheter ablation palpitations anxiety light-headedness chest pain pounding sensation in the neck and chest dyspnea Normal cardiac examination findings in the vast majority of cases During tachycardic episodes, the patient may be cool, diaphoretic, and hypotensive Crackles in the lungs from pulmonary vascular congestion In many young patients, only minimal symptoms (eg, palpitations, weakness, mild dizziness) despite exceedingly fast heart rates pulse uniformly rapid, often > 220 beats/minute Follow Up/Refer "frog sign" is presence of prominent jugular venous pulsations (cannon a-waves) due to atrial contraction against closed tricuspid valve occasionally expiratory splitting of S2 ECG diagnosis o short PR interval o delta wave - initial slurring of QRS o wide QRS complex f atrial fibrillation - lidocaine, procainamide, DC shock after Versed digoxin and verapamil are contraindicated with refractory period < 300 milliseconds(1) if unresponsive to vagal maneuver - drug of choice is adenosine (Adenocard) IV 6 mg radiofrequency catheter ablation Cardiology Heart failure DT TX Cardiovascular Inability of the heart to deliver sufficient oxygenated blood to meet the needs of tissues and organs heart failure with reduced ejection fraction o ejection fraction ≤ 40% o Also called systolic heart failure. o Absolute/relative impaired myocardial contractility with decreased ejection fracture 17 ET Course S/S Cardiovascular heart failure with preserved ejection fraction o typically ejection fraction ≥ 50% o Also called diastolic heart failure o Normal myocardial contractility and ejection fraction with impaired relaxation and feeling. o coronary artery disease (resulting in myocardial infarction and ischemic cardiomyopathy) causes about two-thirds of systolic heart failure o systemic hypertension o valvular heart disease including aortic stenosis, aortic regurgitation, mitral regurgitation o severe renal failure o constrictive pericarditis o dilated cardiomyopathy genetic causes viral infection (recognized or unrecognized) alcohol use disorder (alcoholic cardiomyopathy) chemotherapy (doxorubicin or trastuzumab) o hypertrophic cardiomyopathy o restrictive cardiomyopathy o infiltrative disorders (cardiac sarcoidosis, hemochromatosis, amyloidosis) o peripartum cardiomyopathy o myocarditis o infectious endocarditis o arrhythmia o tachycardia-induced heart failure o beriberi o HIV infection o muscular dystrophy o causes of right ventricular failure most common cause is left ventricular failure (rightsided failure usually late in course) mitral stenosis pulmonary arterial hypertension (may be due to chronic obstructive pulmonary disease, pulmonary embolism) right-sided infective endocarditis right ventricular infarction o high output cardiac failure - anemia, thyrotoxicosis, arteriovenous fistula, Paget disease of bone Can lead to cardiac arrhythmias, salt and water retention and and organ damage. Exertional dyspnea and/or dyspnea at rest Orthopnea Acute pulmonary edema Chest pain/pressure and palpitations Tachycardia Fatigue and weakness 18 PF DT TX Cardiovascular Nocturia and oliguria Anorexia, weight loss, nausea Exophthalmos and/or visible pulsation of eyes Distention of neck veins Weak, rapid, and thready pulse Rales, wheezing S3 gallop and/or pulsus alternans Increased intensity of P2 heart sound Hepatojugular reflux Ascites, hepatomegaly, and/or anasarca Central or peripheral cyanosis, pallor Rails heard over lungs JVD Hepatomegaly Edema S3 , S4, Gallup, cardiomegaly, pulsus alterans Cyanosis Echocardiogram is diagnostic standard for identifying heart failure BNP o guideline-directed medical therapy for symptomatic heart failure with reduced ejection fraction angiotensin-converting enzyme (ACE) inhibitors (or angiotensin receptor blockers [ARBs]) recommended for all patients o ACE inhibitors appear to reduce mortality and rates of myocardial infarction and hospital admission in patients with left ventricular dysfunction or symptomatic heart failure o ARBs reduce heart failure hospitalization and possibly mortality o ARBs may have similar clinical outcomes compared with ACE inhibitors, but may be better tolerated beta blockers recommended for all patients o beta blockers (bisoprolol, carvedilol, or sustained-release metoprolol succinate) reduce mortality in stable patients with class II and III heart failure and possibly class IV heart failure loop diuretics for all volume overload, NYHA class IIIV patients o such as furosemide (Lasix) 20-40 mg/day in 1-2 doses initially, maximum 600 mg/day o diuretics may reduce risk of death and worsening heart failure and improve exercise capacity hydralazine plus isosorbide dinitrate for persistently symptomatic, NYHA class III-IV, African-American patients o addition of isosorbide dinitrate plus hydralazine 19 Follow up/referral Cardiovascular (BiDil) to standard heart failure therapy reduces mortality in black patients with advanced heart failure aldosterone antagonist for NYHA class II-IV patients with serum creatinine < 2.5 mg/dL (221 mcmol/L) in men or < 2 mg/dL (177 mcmol/L) in women and potassium < 5 mEq/dL o monitor for hyperkalemia and impaired renal function o aldosterone blockers (eplerenone [Inspra] or spironolactone [generic, Aldactone]) reduce allcause mortality and hospitalizations in patients with left ventricular dysfunction and heart failure or postmyocardial infarction including patients with mild symptoms o other medications commonly used in heart failure digoxin may be considered for patients with heart failure and reduced ejection fraction and persistent or severe symptoms on guideline-directed medical therapy o digoxin reduces hospitalization and clinical deterioration in symptomatic patients with systolic heart failure aspirin o aspirin 75-100 mg/day (or clopidogrel 75 mg/day) recommended if established coronary artery disease but not suggested if no coronary artery disease o aspirin may increase hospitalization rates in patients with heart failure anticoagulant therapy o in patients with atrial fibrillation, chronic anticoagulant therapy recommended if additional risk factor for cardioembolic stroke and reasonable if no additional risk factor for cardioembolic stroke, in absence of contraindications o anticoagulation not recommended in patients without atrial fibrillation, prior thromboembolic event, or cardioembolic source o warfarin reduces risk for ischemic stroke but increases risk for major bleeding compared to aspirin in patients with ejection fraction ≤ 35% and in sinus rhythm Cardiology 20 Cardiovascular 21