[A_B] Dwayne A Williams - Pance Prep Pearls V3 A_B (2019, Independently published) - libgen.li.pdf

T A B L E O F C O N Abbreviations 1 - C A R D I O V A S C U L A R SYSTEM T E N T S.6 7 2 - P U L M O N A R Y SYSTEM 100 3 - GASTROINTESTINAL S Y S T E M / N U T R I T I O N A L 155 4 - M U S C U L O S K E L E T A L SYSTEM 234 5 - EENT (EYES, EARS, NOSE, & T H R O A T ) DISORDERS 313 6 - REPRODUCTIVE...

T A B L E O F C O N Abbreviations 1 - C A R D I O V A S C U L A R SYSTEM T E N T S.6 7 2 - P U L M O N A R Y SYSTEM 100 3 - GASTROINTESTINAL S Y S T E M / N U T R I T I O N A L 155 4 - M U S C U L O S K E L E T A L SYSTEM 234 5 - EENT (EYES, EARS, NOSE, & T H R O A T ) DISORDERS 313 6 - REPRODUCTIVE SYSTEM (MALE AND FEMALE) 352 7-ENDOCRINE 409 8 - RENAL SYSTEM 454 9 - GENITOURINARY SYSTEM (MALE AND FEMALE)...483 1 0 - NEUROLOGIC SYSTEM 511 1 1 - PSYCHIATRY AND BEHAVIORAL DISORDERS 565 1 2 - DERMATOLOGIC SYSTEM 608 1 3 - INFECTIOUS DISEASES 655 1 4 - HEMATOLOGIC SYSTEM 717 1 5 - PEDIATRIC PEARLS 6 763 Chapter 1 - Cardjoyascular System CHAPTER 1 - CARDIOVASCULAR DISORDERS Cardiomyopathy Conduction disorders/dysrhythmias 8....14 Congenital heart d i s e a s e 33 Coronary artery disease 45 Heart failure 54 Hypertension 60 Hypotension 65 Lipid d i s o r d e r s 71 Traumatic, infectious, and inflammatory heart d i s e a s e s 74 Valvular disorders 81 Vascular disease 90 Chapter 1 - Cardiovascular System DILATED CARDIOMYOPATHY (DCMP Systolic dysfunction, l e a d i n g to a dilated, w e a k h e a r t. Most common type of Cardiomyopathy (95%). RISK FACTORS Most common 20-60 years of age, men. ETIOLOGIES I d i o p a t h i c m o s t c o m m o n c a u s e (may be familial). Infections: v i r a l m o s t c o m m o n (especially the e n t e r o v i r u s e s - C o x s a c k i e v i r u s B, Echovirus). postviral myocarditis, HIV, Lyme disease. Parvovirus B19, Chagas disease. Toxic: a l c o h o l a b u s e , cocaine, anthracyclines (eg, D o x o r u b i c i n ) , radiation. Pregnancy, autoimmune. Metabolic: eg, thyroid disorders, v i t a m i n B l ( t h i a m i n e ) deficiency. CLINICAL MANIFESTATIONS Systolic h e a r t failure: - Left-sided failure: L for Lung symptoms - dyspnea, fatigue. - Right-sided failure: peripheral edema, jugular venous distention, hepatomegaly, GI symptoms. - Embolic events, arrhythmias. Physical examination: S3 gallop h a l l m a r k (due to filling of a dilated ventricle). Mitral or tricuspid regurgitation. DIAGNOSTIC STUDIES E c h o c a r d i o g r a m : d i a g n o s t i c t e s t of c h o i c e - left v e n t r i c u l a r d i l a t i o n (large chamber), thin ventricular walls, d e c r e a s e d ejection fraction, ventricular hypokinesis. Similar findings to Systolic heart failure. Chest radiograph: c a r d i o m e g a l y , pulmonary edema, pleural effusion. ECG: may show sinus tachycardia or arrhythmias. MANAGEMENT S t a n d a r d systolic h e a r t failure t r e a t m e n t : Mortality r e d u c t i o n w i t h ACE i n h i b i t o r s , Beta b l o c k e r s (eg, Metoprolo!, Carvedilol), ARBs, Spironolactone. S y m p t o m c o n t r o l w i t h d i u r e t i c s , Digoxin. Automated implantable cardioverter/defibrillator if ejection fraction < 35-30%. Chapter 1 - Cardiovascular System STRESS (TAKOTSUBO) CARDIOMYOPATH Transient regional systolic dysfunction of the left ventricle t h a t can imitate Myocardial infarction, but is associated with the a b s e n c e of significant obstructive coronary artery d i s e a s e or e v i d e n c e of plaque rupture. Risk factors: p o s t m e n o p a u s a l w o m e n exposed to physical or emotional stress (eg, death of relative, catastrophic medical diagnoses, acute medical illness). PATHOPHYSIOLOGY Thought to be multifactorial, including catecholamine surge during physical or emotional stress, microvascular dysfunction, and coronary artery spasm. CLINICAL MANIFESTATIONS Similar to Acute coronary syndrome (ACS) - eg, substernal chest pain, dyspnea, syncope. DIAGNOSIS ECG: ST elevations (especially in the anterior leads similar to anterior MI). May have ST depressions. Cardiac enzymes: often positive. Coronary angiography: a b s e n c e of acute plaque rupture or obstructive coronary disease. On examinations, this is an "all the way question", meaning the diagnosis is considered in patients with ACS with no evidence of obstructive coronary disease on coronary angiography. Echocardiogram: transient regional left ventricular systolic dysfunction, especially apical left ventricular ballooning. Usually performed after ACS has been ruled out. A) Echocardiograph showing dilatation of the left ventricle in the acute phase. (B) Resolution of left ventricular function on repeat echocardiograph 6 days later. Photo credit: Tara C Gangadhar, Elisabeth Von der Lohe, Stephen G Sawada and Paul R Helft [CC BY 2.0 (https://creati vecomm ons.org/li censes/by/2.0] ] INITIAL MANAGEMENT Because the initial presentation of Takotsubo cardiomyopathy presents similar to ACS, patients a r e treated as ACS with Aspirin, Nitroglycerin, Beta blockers, Heparin, and coronary angiography to rule out obstructive coronary a r t e r y disease. SHORT-TERM MANAGEMENT Because Takotsubo cardiomyopathy is a transient condition, conservative a n d supportive care is t h e mainstay of t r e a t m e n t (eg, Beta blockers, ACE inhibitors for 3-6 m o n t h s with serial imaging t o assess for improvement). Anticoagulation in some with severe LV dysfunction (eg, EF left-sided failure symptoms. - Right-sided failure: eg, peripheral edema, jugular venous distention, hepatomegaly, ascites, GI symptoms. - Left-sided failure: L for Lung symptoms (eg, d y s p n e a m o s t c o m m o n c o m p l a i n t , fatigue). K u s s m a u l ' s sign: the lack of an inspiratory decline or i n c r e a s e in j u g u l a r v e n o u s p r e s s u r e w i t h inspiration. Signs of h e a r t failure. S3 may be heard. Pulmonary hypertension. DIAGNOSIS E c h o c a r d i o g r a m : d i a g n o s t i c t e s t of c h o i c e - n o n - d i l a t e d v e n t r i c l e s w i t h n o r m a l t h i c k n e s s (may be slightly thick), d i a s t o l i c dysfunction, m a r k e d d i l a t i o n of b o t h a t r i a. Systolic function generally preserved in early disease. Bright speckled myocardium in Amyloidosis. Chest radiograph: normal ventricular chamber size, enlarged atria. Pulmonary congestion. ECG: low voltage QRS, arrhythmias. Increased BNP. E n d o m y o c a r d i a l biopsy; definitive d i a g n o s i s (not used often). - Amyloidosis associated with apple-green birefringence with Congo-red staining. MANAGEMENT No specific treatment. Treat t h e underlying disorder (eg, chelation for Hemochromatosis, Glucocorticoids for Sarcoidosis). Gentle diuresis for symptoms, vasodilators. 10 Chapter 1 - Cardiovascular System HYPERTROPHIC CARDIOMYOPATH Autosomal dominant genetic disorder of inappropriate LV a n d / o r RV hypertrophy with diastolic dysfunction. Subaortic outflow obstruction due to asymmetrical septal hypertrophy and systolic anterior motion of the mitral valve. The obstruction w o r s e n s with Increased contractility (eg, exercise, Digoxin, beta agonists) a n d / o r Decreased LV volume (eg, dehydration, decreased venous return, Valsalva maneuver). CLINICAL MANIFESTATIONS Dyspnea m o s t c o m m o n symptom, fatigue, angina (chest pain), pre syncope, syncope, dizziness, arrhythmias. M a y b e asymptomatic initially. Sudden cardiac death, especially in adolescent or preadolescent children especially during t i m e s of e x t r e m e exertion usually due to Ventricular fibrillation. PHYSICAL EXAMINATION Harsh systolic murmur best heard at the left sternal border. Increased m u r m u r intensity with d e c r e a s e d v e n o u s return (eg, Valsalva, standing) or decreased afterload (eg, Amyl nitrate). Decreased m u r m u r intensity with increased v e n o u s return (eg, squatting, supine, leg raise) or increased afterload (eg, handgrip). Increased LV volume preserves outflow. May have loud S4, mitral regurgitation, S3, or pulsus bisferiens. DIAGNOSIS Echocardiography: a s y m m e t r i c ventricular wall thickness (especially septal) 1 5 m m or greater, systolic anterior motion of the mitral valve, & small LV chamber size. ECG: left ventricular hypertrophy, anterolateral & inferior pseudo q waves, enlarged atria. MANAGEMENT Focus on early detection, medical management, surgical management, a n d / o r ICD placement. Medical: Beta blockers first-line medical m a n a g e m e n t Alternatives include Calcium channel blockers & Disopyramide. Surgical: Myomectomy usually performed in young patients refractory to medical therapy. Alcohol septal ablation: an alternative to surgical myomectomy. Patients should a v o i d dehydration, e x t r e m e exertion, and exercise. Cautious u s e of Digoxin, Nitrates, and diuretics (Digoxin increases contractility; Nitrates & diuretics decrease LV volume). EXAM TIP Aortic stenosis fAS) VS. Hypertrophic obstructive cardiomyopathy (HOCM) Both: angina, syncope, systolic murmur. Both m u r m u r s go in the same direction with afterload maneuvers (eg, both increase with Amyl nitrate & both decrease with handgrip). HOCM: preload maneuvers t h a t decrease LV volume (eg, Valsalva, standing) will w o r s e n the m u r m u r of HOCM w h e r e a s these maneuvers will decrease the intensity of most other m u r m u r s (including AS). Increased LV v o l u m e (eg, squatting, leg raise) will d e c r e a s e t h e m u r m u r of HOCM w h e r e a s these m a n e u v e r s will increase the intensity AS. No carotid radiation. 11 Cardiomyopathy: disease of the heart muscle (myocardial tissue) with cardiac dysfunction NOT due to other heart diseases* DILATED CARDIOMYOPATHY (95%) RESTRICTIVE CARDIOMYOPATHY (i%) HYPERTROPHIC CARDIOMYOPATHY ( 4 % ) 1 SYSTOLIC DYSFUNCTION O ventricular DIASTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION due to impaired ventricular DEFINITION -Ventricular rigidity impedes ventricular dilation *$ "dilated, weak heart" relaxation/ffUing. filling (J.ventricularcompliance) SUBAORTIC OUTFLOW OBSTRUCTION: -hvpertrophled septum Preserved contractility early on in-disease. - svstolic anterior motion fSAM) of mitral valve & SAM is increased with: O jcontractility (exertion) & © |LV volume (eg, ^decreased venous return, dehydration). Idiopathic MC cause, autoimmune Inherited genetic disorder of inappropriate LV and/or Infiltrative diseases ETIOLOGIKS Viral myocarditis (eg, enteroviruses) - Amyloidosis most common (MC) cause RVhypertrophy (especially septal). Toxic: ETOH, cocaine, pregnancy -Sarcoidosis, Hemochromatosis XRT, doxorubicin, daunorubicin - Scleroderma, metastatic disease. Idiopathic Systolic heart failure symptoms RIGHT SIDED FAILURE more > left sided Dyspnea most common initial complaint (90%1. CLINICAL MANIFESTATIONS - Dyspnea, edema, increased JVD failure. Angina pectoris Embolic phenomena. Arrhythmias Dyspnea most common symptom. Arrhythmias AF: VT/VF (palpitations, svncope). Viral Myocarditis: viral prodrome ** signs Poorly tolerated tachyarrhythmias Sudden cardiac death: especially in of heart failure or chest pain, +cardiac adolescent/preadolescent children (especially enzymes, nonspecific ST-T changes. exertional) due to ventricular fibrillation. I. heart failure Kussmaul'ssign: t(VP with inspiration Harsh svstoHc crescendo-decrescendo murmur LLSB PHYSICAL -Pulmonary congestion: rales, tachycardia, - |murmur intensity: fvenous return (eg. squatting. cough, pleural effusion lying supine) because |LV volume preserves outflow. R-sided heart failure Handgrip (increased afterload). R heart failure Peripheral edema, fJVP, hepatic congestion. - Peripheral edema, |JVP, hepatic -tmurmur intensity: Jvenous return (Valsalva & congestion L-sided heart failure standing) & exertion - J.LV volume & ^contractility will.[cardiac output Amyl nitrate (decreases Crackles (rales). afterload). Usually no carotid radiation. Normal pulse, Loud Si. ± MR Echocardiogram: Echocardiogram: Echocardiogram most useful test DIAGNOSIS - O left ventricular dilation: - Ventricles nondilated with normal wall - Asymmetric wall thickness (septal), SAM mitral valve. thin ventricular walls thickness. - © Rejection fraction f_EF) ECG: - © Regional or global LV hypokinesia. - MARKED DILATION OF BOTH ATRIA - Left ventricular hypertrophy, septal q waves MANAGEMENT OCR: - Cardiomegaly, Pulmonary edema. Standard svstolic heart failure treatment -ACEI, Beta blockers, Na restriction -Symptom control: diuretics, digoxin. - Implantable defibrillator if EF S in V1 or R >7 mm in height in V1 LEFT VENTRICULAR HYPERTROPHY: Sokolow-Lvon criteria: S in V1 + R in V5 (or V6) >35 mm in men; >30 mm in women. Cornell Criteria: R in aVL + S in V3 >28 mm in men; >20 mm in women. 0 Pathological Q waves? Q wave >1 box (in depth or width). STEP 6: EVALUATE ST SEGMENT 0 ST depression or elevation >1 mm in depth/height? STEP 7: EVALUATE T WAVES 0 Any T wave inversions (TWI); T wave flattening? Is the QT interval prolonged? 14 Chapter 1 - Cardiovascular System SUMMARY OF THE 12 LEADS AND THEIR RELATION TO THE Coronary Artery A n a t o m y Aortic Arch LEFT MAIN CORONARY ARTERY HEART The leads and their relation to the coronary arteries LEFT MAIN CORONARY ARTERY Left Ventricle Right Ventricle AREA OF INFARCTION ANTERIOR WALL - SEPTAL LEFT ANTERIOR DESCENDING ARTERY Q WANES/ ST ELEVATIONS VI through V4 VI & V2 V1-V4 Septal (VI A V2) Leads H, m, aVF ARTERY INVOLVED Left Anterior Descending ("LAD) Proximal LAD LATERAL WALL LaVL,V5,V6 Circumflex fCFX) ANTEROLATERAL I, aVL, V4 + V5 + V6 Mid LAD +/- CFX II, III, aVF Right Coronary Artery f RCA") ST DEPRESSIONS V1-V2 (really the reciprocal changes since there are no "posterior" leads on a standard 12 lead ECG) RCA, CFX INFERIOR "_._ _ POSTERIOR WALL QRS AXIS 1 D E T E R M I N A T I O N Axis: the general direction of t h e impulses through the heart. It is the summation of all the vectors. Vectors move t o w a r d s hypertrophy & away from infarction. N o r m a l QRS a x i s is -30° t o + 9 0 ° PERPENDICULAR QUADRANT METHOD 1180° > | 0° QUADRANT METHOD: If LAD (based on I and aVF) o check lead II. If QRS is predominantly negative in lead II 3ft&lt ** TrYegufar, rrionomorpic, ^may/considpr. z EXCEPTION TO SYMPTOMATIC/UNSTABLE BRADYARRHYTHMIA RULE? 1. 3rd Degree heart block: transcutaneous pacing usually first line followed by permanent pacemaker placement as definitive treatment. Calcium Channel Blockers Non-dihydropyridines* Diltiazem, Verapamil Amiodarom* O.IMfeconds r\im mtDsion Transcutanepus Pacing, S-B lockers: Metoprolol, Esmolol, Propranolol 9 d (ft regufar & n a r r o ^ M S ) * Beta B|ocKer f orOa|ciyf| ' leilfdck'efs i o § w Vagal Maneuvers: Hold breath & bear down or carotid massage (make sure no carotid bruits are present before performing) o o 3 STABLE NARROW-COMPLEX TACHYARRHYTHMIAS: 1. ATRIAL FLUTTER OR A. FIB: Beta blocker or Calcium Channel Blocker 1st line. 2. WOLFF-PARKINSON-WHITE fWPW): Procainamide preferred. Amiodarone. Avoid ABCD if wide complex (Adenosine, Beta blockers, CCBs, Digoxin). 3. SVT: Vagal maneuvers. Adenosine first-line medical management 4. Sinus arrhythmia: treat the underlying cause. 9 a o < (a o a < Chapter 1 - Cardiovascular System SINUS RHYTHMS I m p u l s e s originate at t h e SA (sinoatrial) node. NORMAL SINUS RHYTHM fNSRI Every P wave is followed by a QRS complex. P waves a r e positive/upright in leads I, II, aVF, & negative in aVR. Rate 60-100 bpm. SINUS ARRHYTHMIA Irregular rhythm originating from the sinus node. Normal variation of normal sinus rhythm (meets t h e r s a m e criteria except t h a t the rhythm is irregular). More commonly seen in children, young adults and patients with Sinus bradycardia. PHYSIOLOGY Beat to beat variations with respiration - rhythm increases w i t h inspiration and d e c r e a s e d w i t h expiration, reflecting changes in stroke volume during respiration. DIAGNOSIS ECG: normal-appearing P waves, beat to beat variation of the P-P interval (>.12 seconds), s h o r t e r intervals during inspiration (increased rate) and longer P-P intervals during expiration (decreased heart rate]. MANAGEMENT None n e e d e d in m o s t c a s e s (it is considered a normal variant). If symptomatic bradycardia occurs, Atropine is the first-line management. Transcutaneous pacing, Epinephrine, and Dopamine a r e second-line agents. 17 Chapter 1 - Cardiovascular System SINUS TACHYCARDL Increased h e a r t rate > 100 b p m originating from t h e sinus node. ETIOLOGIES Physiologic: n o r m a l r e s p o n s e to exercise, emotional stress. Normal in y o u n g children & infants. Pathologic: fever, hypovolemia, hypoxia, pain, infection, h e m o r r h a g e , hypoglycemia, anxiety, thyrotoxicosis, shock, s y m p a t h o m i m e t i c s (eg, d e c o n g e s t a n t s , cocaine). DIAGNOSIS ECG: regular, rapid r h y t h m (> 100 b p m ) , n o r m a l - a p p e a r i n g P w a v e with every P followed by a QRS complex. MANAGEMENT T r e a t t h e u n d e r l y i n g c a u s e (first-line t r e a t m e n t ). Beta blockers (eg, Metoprolol) u s e d in t h e m a n a g e m e n t of p e r s i s t e n t sinus tachycardia in t h e setting of Acute c o r o n a r y a r t e r y s y n d r o m e. SINUS BRADYCARDL Decreased h e a r t rate < 60 b p m originating from t h e sinus node. ETIOLOGIES Physiologic: y o u n g athletes, vasovagal reaction, increased intracranial p r e s s u r e , nausea, vomiting. Pathologic: Beta blockers, calcium channel blockers, digoxin, carotid massage, sinoatrial n o d e ischemia, g r a m negative sepsis, & hypothyroidism. DIAGNOSIS ECG: regular, s l o w , r h y t h m (< 6 0 b p m ) , n o r m a l - a p p e a r i n g P w a v e with every P followed by a QRS complex 4-t 3 ** ft m * MANAGEMENT Symptomatic or unstable: Atropine l^-line treatment. E p i n e p h r i n e or t r a n s c u t a n e o u s pacing if n o t r e s p o n s i v e to Atropine. A s y m p t o m a t i c : n o t r e a t m e n t n e e d e d if p h y s i o l o g i c. Observation o r cardiac consult m a y b e n e e d e d if pathologic. 18 25 Chapter 1 - Cardiovascular System SICK SINUS SYNDROME ( b r a d v - t a c h v s v n d r o m e Dysfunction of t h e s i n u s n o d e t h a t leads to a combination of s i n u s a r r e s t w i t h a l t e r n a t i n g p a r o x y s m s of atrial t a c h y a r r h y t h m i a s & b r a d y a r r h y t h m i a s. ETIOLOGIES Sinus n o d e fibrosis ( m o s t c o m m o n ) , o l d e r age, corrective cardiac surgery, medications, systemic diseases t h a t affect the h e a r t CLINICAL MANIFESTATIONS I n t e r m i t t e n t s y m p t o m s of b r a d y c a r d i a & o r tachycardia: eg, palpitations, lightheadedness, angina, d y s p n e a on exertion, presyncope, o r syncope. dizziness, T e l e m e t r y o r a m b u l a t o r y ECG m o n i t o r i n g m a y be n e e d e d to d o c u m e n t episodes. MANAGEMENT Stable: may n o t r e q u i r e u r g e n t t h e r a p y as t h e s y m p t o m s a r e often t r a n s i e n t Hemodynamically unstable: Atropine epinephrine. T r a n s c u t a n e o u s pacing. first-line if m e d i c a t i o n s are needed. Dopamine, Long-term: p e r m a n e n t p a c e m a k e r definitive. Addition of an a u t o m a t i c i m p l a n t a b l e c a r d i o v e r t e r defibrillator if a l t e r n a t i n g b e t w e e n tachycardia a n d b r a d y c a r d i a. 19 T R I O V E N T R I C U L A R C O N D U C T I O N BLOCKS AV BLOCK: interruption of the normal impulse from the SA node to the AV node (AV node dysfunction). PR I n t e r v a l (PR1) m o s t helpful in d e t e r m i n i n g t h e p r e s e n c e of AV c o n d u c t i o n blocks. FIRST-DEGREE AV B L O C5 AV node dysfunction leading to delayed but conducted impulses. ETIOLOGIES Often a n o r m a l v a r i a n t (individuals with high vagal tone without structural h e a r t disease). Intrinsic AV node disease, acute myocardial infarction (eg, inferior wall MI), electrolyte disturbances (eg, hyperkalemia), AV nodal blocking drugs (eg, Digoxin, Beta-blockers & Calcium channel blockers), myocarditis due to Lyme, cardiac surgery. CLINICAL MANIFESTATIONS Asymptomatic in most cases. If symptomatic, it is due to bradycardia-related decreased perfusion - fatigue, dizziness, dyspnea, chest pain, syncope, or in severe cases (hypotension or altered mental status). DIAGNOSIS ECG: all atrial impulses are delayed b u t conducted to the ventricles = p r o l o n g e d PR i n t e r v a l (> 0.20 seconds) + all P^vaves a r e followed b y QRS c o m p l e x e s. MANAGEMENT A s y m p t o m a t i c : n o t r e a t m e n t , observation. Cardiac consult in some cases. S y m p t o m a t i c : A t r o p i n e first-line, epinephrine. Pacemaker definitive if persistently symptomatic & severe (PRI > 0.30 seconds). SECOND DEGREE AV BLOCK 2 n d = not all of the atrial impulses are conducted to the ventricles. This leads to some P waves that are not followed by QRS complexes ('dropped QRS'). M O B I T Z I - WENCKEBACH M O B I T Z I - WENCKEBACH PROGRESSIVE P R I LENGTHENING >^> d r o p p e d QRS. Shortened R-R interval MANAGEMENT Symptomatic ^ A t r o p i n e. Epinephrine, ± pacemaker. Asymptomatic ^observation. ± Cardiac consult. MOBITZ II MOBITZ II; block commonly in the bundle of HIS. CONSTANT/PROLONGED P R I => d r o p p e d QRS. MANAGEMENT: A t r o p i n e o r t e m p o r a r y pacing. Progression to 3 rd degree AV block common so p e r m a n e n t pacemaker is the definitive t r e a t m e n t 20 Chapter 1 - Cardiovascular System MOBITZ I SECOND DEGREE AV BLOCK ( W e n c k e b a c h ) Interruption of electrical impulse at the AV node resulting in occasional non-conducted impulses. PATHOPHYSIOLOGY: AV node dysfunction (commonly above the bundle of HIS). ETIOLOGIES Often a normal variant (individuals with high vagal tone without structural heart disease). Inferior wall MI (AV node ischemia), AV nodal blocking agents (eg, Beta blockers, Digoxin, Calcium channel blockers), myocarditis due to Lyme, hyperkalemia, cardiac surgery. CLINICAL MANIFESTATIONS Asymptomatic in most cases. Bradycardia-related decreased perfusion - eg, fatigue, dizziness, dyspnea, chest pain, syncope, or in severe cases (hypotension or altered mental status). DIAGNOSIS ECG: progressive lengthening of t h e PR interval until an occasional non-conducted atrial impulse (dropped QRS complex). MANAGEMENT Asymptomatic: n o treatment, observation. Cardiac consult in some cases. Symptomatic: Atropine first-line. Epinephrine. Pacemaker definitive if persistent. MOBITZ II SECOND DEGREE AV BLOC" Interruption of electrical impulse at the AV node resulting in occasional non-conducted impulses. PATHOPHYSIOLOGY: AV node dysfunction (commonly at the bundle of HIS). ETIOLOGIES Rarely s e e n i n patients without structural heart d i s e a s e (eg, myocardial ischemia, myocardial fibrosis, myocarditis (eg, Lyme disease), endocarditis. Iatrogenic - AV nodal blockers, post-catheter ablation, post-cardiac surgery. CLINICAL MANIFESTATIONS Asymptomatic in most cases. Symptomatic: due to bradycardia-related decreased perfusion - fatigue, dizziness, dyspnea, chest pain, syncope, o r in severe cases, hypotension o r altered mental status. DIAGNOSIS ECG: constant PR interval before & after the non-conducted atrial beat (dropped QRS complexes). If ischemia is suspected based on clinical picture, cardiac biomarkers, chest radiograph, and electrolytes should be ordered. MANAGEMENT Initial: t r a n s c u t a n e o u s pacing o r Atropine for s y m p t o m a t i c bradycardia with p e r m a n e n t pacemaker long-term management. These patients often do not respond to Atropine. Definitive: p e r m a n e n t p a c e m a k e r required in m a n y patients because it often progresses to third degree AV block and is associated with complications of hypotension, and cardiac arrest. 21 Chapter 1 - Cardiovascular System THIRD DEGREE AV BLOC AV dissociation = no atrial impulses reach the ventricles, so the atrial activity is independent of the ventricular activity. This leads to an escape rhythm from below the block. ETIOLOGIES Myocardial ischemia (inferior wall MI), AV nodal blocking a g e n t s (eg, Beta-blockers, Digoxin, Calcium channel blockers), endocarditis, myocarditis due to Lyme, cardiac surgery. Increased vagal tone, hypothyroidism, hyperkalemia, myocarditis. CLINICAL MANIFESTATIONS M a y b e asymptomatic. If symptomatic, it is due to b r a d y c a r d i a - r e l a t e d decreased perfusion especially during exertion (eg, fatigue, dyspnea, dizziness, chest pain, syncope) or in severe cases, hypotension or altered mental status. DIAGNOSIS ECG: shows regular P-P intervals & regular R-R intervals but they are n o t related to each other. 5 atients are often bradycardic. t*_4 MANAGEMENT Acute or symptomatic: placement transcutaneous pacing often followed by p e r m a n e n t Definitive: p e r m a n e n t pacemaker p l a c e m e n t ST 1 HEART BLOCKS DEGREE: - REVIEW Prolonged PRI, every P followed by QRS (all conducted) 2 nd degree = dropped QRS (some NOT conducted) MOBITZ 1: Progressive lengthening PRI - dropped QRS MOBITZ 2: Same length (may be prolonged) + Occasional dropped QRS 3RD DEGREE AV Dissociation (NONE are conducted) 22 pacemaker TRIAL DYSRHYTHMIAS ATRIAL FLUTTEi 1 irritable atrial focus firing at a fast rate (atrial rate usually around 300 beats/min). Similar to Atrial fibrillation, there is an increased risk of atrial thrombus formation that can lead to cerebral & / o r s y s t e m i c embolization (eg, stroke). It may occur alone or be an interval rhythm between sinus tachycardia and atrial fibrillation. CLINICAL MANIFESTATIONS Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain. Unstable: are due to hypoperfusion and can include refractory chest pain, h y p o t e n s i o n (eg, systolic BP in double digits) or altered mental status. DIAGNOSIS ECG: flutter ("sawtooth" atrial w a v e s usually around 300 beats per minute (250-350 normal e P waves. The flutter waves a r e identical (1 ectopic atrial focus). MANAGEMENT Stable: Vagal maneuvers. Rate control with Beta blockers (eg, Metoprolol, Atenolol or Esmolol) OR non-dihydropyridine Calcium channel blockers (eg, Diltiazem, Verapamil). Unstable: direct current (synchronized) cardioversion. Anticoagulation: similar criteria (eg, CHA2DS2-VASc) for nonvalvular atrial fibrillation in patients at risk for embolization. Reversion to normal sinus rhythm: - Radiofrequency catheter ablation (definitive management). - Direct current cardioversion. - Class IA, IC, or III antiarrhythmics (eg, Ibutilide). 23 Chapter 1 - Cardiovascular System ATRIAL FIBRILLATION fAF Multiple i r r i t a b l e a t r i a l foci fire at fast rates. Similar to Atrial flutter, there is an i n c r e a s e d r i s k of a t r i a l t h r o m b u s f o r m a t i o n t h a t c a n l e a d t o c e r e b r a l & / o r s y s t e m i c e m b o l i z a t i o n (eg, stroke). Atrial fibrillation is the most common chronic arrhythmia. Most patients are asymptomatic. ETIOLOGIES Cardiac disease, ischemia, pulmonary disease, infection, cardiomyopathies, electrolyte imbalances, idiopathic, endocrine or neurologic disorders (eg, thyroid disorders), increasing age, genetics, hemodynamic stress, medications, drug or alcohol use. Men > women; Whites > blacks. TYPES - Paroxysmal: self-terminating within 7 days (usually 7 days. Requires termination (medical or electrical). - Permanent: persistent AF >1 year (refractory to cardioversion or cardioversion never tried). - Lone: paroxysmal, persistent or p e r m a n e n t without evidence of heart disease. CLINICAL MANIFESTATIONS Symptomatic: palpitations, dizziness, fatigue, & dyspnea. U n s t a b l e : are due to hypoperfusion and can include h y p o t e n s i o n (eg, systolic BP in double digits), a l t e r e d m e n t a l s t a t u s , & r e f r a c t o r y chest pain. DIAGNOSIS ECG: Ashman's p h e n o m e n o n (seen here on 2 nd & 8th beat) Irregularly irregular rhythm with fibrillatory w a v e s (no discrete P waves). Often atrial rate >250 beats per minute. The AV nodal refractory period determines the ventricular rate. ± Ashman's phenomenon: occasional aberrantly conducted beats (wide QRS) after short R-R cycles. Cardiac monitoring: a Holter monitor or telemetry can be used if Atrial fibrillation is not seen on an ECG but is suspected. MANAGEMENT Stable: Rate control with Beta b l o c k e r s (eg, Metoprolol, Atenolol, or Esmolol) OR non-dihydropyridine Calcium c h a n n e l b l o c k e r s (eg, Diltiazem, V e r a p a m i l ). Digoxin may be used when Beta blockers or calcium channel blockers are contraindicated (eg, CHF or severe hypotension). Unstable: Direct c u r r e n t (synchronized) cardioversion. Long-term: Rate control usually preferred over rhythm control for long-term management. Direct current (synchronized cardioversion) or pharmacologic cardioversion. Radiofrequency catheter ablation or surgical "MAZE" procedure. Anticoagulation: similar criteria (eg, CHA2DS2-VASc) for nonvalvular atrial fibrillation in patients at risk for embolization. 24 Chapter 1 - Cardiovascular System CARDIOVERSION Direct current (synchronized cardioversion) or pharmacologic cardioversion. Cardioversion is most successful when performed within 7 days after the onset of Atrial fibrillation. Echocardiogram is n e e d e d prior to cardioversion to ensure there are no atrial clots. AF greater than 4 8 hours undergoing elective cardioversion, anticoagulation for at least 3 w e e k s before cardioversion or a transesophageal echocardiography guided approach with abbreviated anticoagulation. AF < 4 8 hours undergoing elective cardioversion, anticoagulation prior is recommended. Anticoagulation m u s t b e continued for 4 w e e k s after cardioversion. With effective anticoagulation the stroke risk is decreased 3-fold after 4 weeks of anticoagulation. CANDIDATES FOR ANTICOAGULATION WITH NONVALVULAR AF CHA2DS2-VASc score for nonvalvular Atrial fibrillation assess patients' risk for embolization. Chronic oral anticoagulation (eg. Warfarin or Novel oral anticoagulants) is r e c o m m e n d e d for m o d e r a t e t o high risk (score of 2 or greater). The use of anticoagulant therapy has been shown to reduce embolic risk by 70%. ANTICOAGULATION RISK STRATIFICATION IN NONVALVULAR ATRIAL FIBRILLATION CHA7DS7- VASc CRITERIA POINTS RECOMMENDED T H E R A P Y Congestive Heart Failure > 2 = Moderate to high risk: chronic oral anticoagulation recommended. Hypertension &ge > 75y 1 = low risk: Diabetes Mellitus Based on clinical judgment, consideration of risk to S21 Stroke, TIA, thrombus benefit assessment & discussion with patient Vascular disease (prior MI, Anticoagulation may be recommended in some cases. aortic plaque, peripheral arterial disease") 0 = very low risk: Age 65 - 74y No anticoagulation needed. Sex (female] May be recommended in some (based on clinical MAXIMUM SCORE judgment & consideration of risk to benefit ratio). ANTICOAGULANT AGENTS: 1. Non-vitamin K antagonist oral anticoagulants fNOAC): usually now preferred over Warfarin in most cases due to similar or lower rates of major bleeding as well as lower risk of ischemic stroke, convenience of not having to check the INR, & less drug interactions. - Dabigatran: direct thrombin inhibitor (binds & inhibits thrombin). - Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors. 2. Warfarin: Indications: may be preferred in some of the following patients - some with severe chronic kidney disease, contraindications to the NOAC (eg, HIV patients on protease inhibitor-based therapy, on CP450-inducing antiepileptic medications such as Carbamazepine, Phenytoin etc), patients already on Warfarin who prefer not to change, cost issues (Warfarin is less expensive). Warfarin usually bridged with heparin until Warfarin is therapeutic. Monitoring: International Normalized Ratio (INR) goal of 2-3. Prothrombin Time (PT). 3. Dual antiplatelet therapy: (ex. Aspirin + Clopidogrel). Anticoagulant monotherapy is superior to dual antiplatelet therapy. Dual antiplatelet therapy may be reserved for patients w h o cannot be treated with anticoagulation (for reasons OTHER than bleeding risk). 25 Chapter 1 - Cardiovascular System PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) Any tachyarrhythmia originating above the ventricles (either an atrial or atrioventricular nodal source). SVT is an umbrella term when a more specific t e r m cannot be applied to a tachyarrhythmia originating above the ventricles. PATHOPHYSIOLOGY: reentry circuits AV n o d e re-entrant tachycardia: two pathways (1 normal and 1 accessory pathway both within the AV n o d e ). Most c o m m o n type. AV reciprocating tachycardia: t w o pathways (1 normal and 1 accessory pathway outside of the AV node) - eg, Wolff-Parkins on-White (WPW) & Lown-Ganong-Levine syndrome (LGL). CLINICAL MANIFESTATIONS Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain. Unstable: hypoperfusion can cause hypotension (eg, systolic BP in double digits), altered mental status, & refractory chest pain. ECG Orthodromic (95%): regular, narrow-complex tachycardia (no discernable P w a v e s due to the rapid rate) - "If you can't tell if the b u m p is a P or a T, then it must be SVT!" Antidromic f5%1: regular, w i d e - c o m p l e x tachycardia (mimics ventricular tachycardia). Heart rate >100 bpm. Rhythm usually regular with narrow QRS complexes. P waves hard to discern due to the rapid rate. MANAGEMENT Stable (regular, narrow complex"): Vagal maneuvers. - AV nodal blockers - A d e n o s i n e first-line medical m a n a g e m e n t. - Second-line: Calcium channel blockers (eg, Diltiazem); Beta blockers (eg, Metoprolol); Digoxin. Stable (wide complex): antiarrhythmics (eg, Amiodarone). Procainamide if WPW suspected. Unstable: direct current (synchronized) cardioversion. Definitive: radiofrequency catheter ablation. WANDERING ATRIAI MAKER fWAPl & MULTIFOCAL ATRIAL TACHYCARDIA fMATl WANDERING ATRIAL PACEMAKER: Multiple ectopic atrial foci generate impulses that are conducted to the ventricles. ECG: heart rate < 1 0 0 b p m & £ 3 P w a v e morphologies. MULTIFOCAL ATRIAL TACHYCARDIA: Same as wandering atrial pacemaker except the heart rate is >100 bpm. ECG: heart rate > 1 0 0 b p m & S3 P w a v e morphologies. MAT classically associated with s e v e r e COPD (chronic obstructive pulmonary disease). Difficult to treat: Calcium channel blocker (eg, Verapamil) or (3-blocker used if LV function is preserved. 26 X Chapter 1 - Cardiovascular System WOLFF-PARKINSON-WHITE fWPWI Preexcitation syndrome that is a type of AV reciprocating tachycardia (AVRT). PATHOPHYSIOLOGY Accessory pathway (Bundle of Kent) outside of the AV node "preexcites" t h e ventricles (directly connects the atria & ventricles, bypassing the AV node), leading to a delta w a v e (slurred, wide QRS). CLINICAL MANIFESTATIONS Most patients are asymptomatic b u t they are prone to the development of tachyarrhythmias. Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain. Unstable: are due to hypoperfusion and can include h y p o t e n s i o n (eg, systolic BP in double digits), altered mental status, & refractory chest pain. ECG: 3 components "WPW" ^ a v e - delta w a v e (slurred QRS upstroke) £R interval that is short Mflde QRS complexes (> 0.12 seconds) iTnTT Delta waves (arrows) MANAGEMENT Stable (wide c o m p l e x ! tachycardia: Antiarrhythmics - Procainamide preferred. Amiodarone. Avoid AV nodal blocking agents ABCD if w i d e QRS c o m p l e x e s (Adenosine, Beta blockers. Calcium channel blockers, Digoxin) because they can lead to preferential conduction d o w n t h e Bundle of Kent, worsening the tachycardia. Unstable: Direct current (synchronized) cardioversion. Definitive: Radiofrequency catheter ablation definitive m a n a g e m e n t - electrically destroys the abnormal pathway. May be indicated if patients experience recurrent, symptomatic episodes. V JUNCTIONAL DYSRHYTHMIAS AV node/junction becomes the dominant pacemaker of the heart in AV junctional rhythms. Etiologies: sinus disease, coronary artery disease, most common rhythm seen with Digitalis toxicity, Myocarditis. May be seen in patients without structural heart disease. ECG: Regular rhythm. P w a v e s inverted (negative) if p r e s e n t in leads w h e r e they a r e normally positive (I, II, aVF) or are n o t seen. Classically associated with a n a r r o w QRS (± wide). Junctional Rhythm: heart rate is usually 40-60 bpm (reflecting the intrinsic rate of the AV junction). Accelerated Junctional: h e a r t rate 60-100 bpm. lunctional Tachycardia: h e a r t rate > 1 0 0 b p m. Junctional rhythm with inverted P waves Junctional rhythm with absent P waves *w*» Hinimnwimiiwii imoiii 27 Chapter 1 - Cardiovascular System VENTRICULAR DYSRHYTHMIAS P R E M A T U R E VENTRICULAR COMPLEXES fPVC] J i.jK --U- v us -i'V.*}.1 >^f-U Unifocal (one morphology) Multifocal (>1 morphology) Bigeminy (every other beat is a PVC) Couplet (two PVCs in a row] - PVC: p r e m a t u r e beat originating from the ventricle => wide, bizarre QRS occurring earlier than expected. With a PVC, the T w a v e is in the o p p o s i t e direction of the QRS usually. Associated with a compensatory p a u s e = overall rhythm is unchanged (AV node prevents retrograde conduction]. MANAGEMENT - No t r e a t m e n t usually n e e d e d (common finding on ECG). - Most ventricular arrhythmias occur after a PVC. VENTRICULAR TACHYCARDIA Defined as 3 or more consecutive PVCs at a rate >100 beats p e r minute (usually between 120-300]. CLASSIFICATION Sustained VT = duration at least 30 seconds. Non-sustained if > 30 seconds. Monomorphic (same QRS morphology) or Polymorphic. Torsades d e p o i n t e s : a variant of polymorphic VT (waxing and waning QRS amplitude on ECG) ETIOLOGIES: Underlying h e a r t disease: ischemic heart d i s e a s e m o s t c o m m o n (eg, post MI), structural heart defects, cardiomyopathies. Prolonged QT interval, electrolyte abnormalities (eg, Hypomagnesemia, hypokalemia, hypocalcemia), Digoxin toxicity. CLINICAL MANIFESTATIONS Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain. Unstable: a r e due to hypoperfusion and can include h y p o t e n s i o n (eg, systolic BP in double digits), altered m e n t a l status, & refractory chest pain. ECG Regular, w i d e c o m p l e x tachycardia with no discernable P waves. MANAGEMENT OF ACUTE TACHYARRHYTHMIAS Antiarrhythmics (Amiodarone, Lidocaine, Procainamide). Stable s u s t a i n e d VT Direct current (Synchronized) cardioversion. U n s t a b l e VT w i t h a n u l s e - Defibrillation (Unsynchronized cardioversion) + VT ( n o p u l s e ) CPR (treat similar to Ventricular Fibrillation). IV Magnesium. Correct electrolyte abnormalities. Torsades de pointes 28 Chapter 1 - Cardiovascular System TORSADES DEPOINTES A variant of polymorphic Ventricular tachycardia (waxing and waning cyclic alterations of the QRS amplitude on ECG). PATHOPHYSIOLOGY Prolonged repolarization and early afterdepolarization + triggered activity. ETIOLOGIES Prolonged QT interval, electrolyte abnormalities (eg, Hypomagnesemia, hypokalemia, hypocalcemia), females > males. Congenital long QT syndrome. Medications: Digoxin, class IA antiarrhythmics (eg, Quinidine, Procainamide, Disopyramide), class III antiarrhythmics (Sotalol, Ibutilide), antibiotics (eg, Macrolides), antipsychotics, antidepressants, & antiemetics. CLINICAL MANIFESTATIONS Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain. DIAGNOSIS ECG: polymorphic Ventricular tachycardia (cyclic alterations of t h e QRS amplitude o n ECG around the isoelectric line) aka sinusoidal waveform. Labs: rule out Hypomagnesemia and hypokalemia. MANAGEMENT IV Magnesium sulfate first-line (suppresses early afterdepolarizations, terminating t h e arrhythmia). Magnesium is effective in both terminating and preventing r e c u r r e n t TdP. Correct electrolyte abnormalities. Discontinue all QT prolonging drugs. Isoproterenol and transvenous overdrive pacing may be used in refractory cases. VENTRICULAR FIBRILLATION A type of cardiac death associated with ineffective ventricular contraction. ETIOLOGIES Underlying h e a r t disease: ischemic heart d i s e a s e m o s t c o m m o n (eg, post MI), structural h e a r t defects, cardiomyopathies, sustained Ventricular tachycardia. CLINICAL MANIFESTATIONS Unresponsive, p u l s e l e s s patient, syncope. ECG Erratic pattern of electrical im pulses, no P waves. ffH +ffjstt$ Tn ft** Tr rtr tut «2 SJ~ \i It" BltttiH TTTt 5 : ^ -^N*- Tp fir H1 fikr-fr t*J IT H ffi ±32ttbr:UliUI Co ars e v ent ric ula.rfi )n lation Fin e ventr cular fib rillatio xt MANAGEMENT Unsynchronized cardioversion (Defibrillation) + CPR (initiate ACLS) 29 Chapter 1 - Cardiovascular System PULSELESS ELECTRICAL ACTIVITY Organized rhythm s e e n on a monitor but patient has n o palpable pulse (electrical activity is not coupled with mechanical contraction). MANAGEMENT: CPR + epinephrine + checks for "shockable" rhythm e v e r y 2 minutes. ASYSTOLE fVentricular standstill! MANAGEMENT: treated the same as PEA *-L^k y ^ _k-i- EARLY REPOLARIZATION ABNORMALITIES Usually a normal variant May be seen in thin, healthy males; African-American males. 2 EARLY REPOLARIZATION ABNORMALITIES Diffuse CONCAVE ST elevations >2 mm with large T. waves (especially precordial). Tall QRS voltage. Fishhook (slurring/notching) at the J point. LVH w i t h Left V e n t r i c u l a r STRAIN Often seen in patients with left ventricular hypertrophy (LVH) who also suffer from ischemic disease. The coronary artery supply is "strained" trying to supply the excess hypertrophic cardiac muscle. BRUGADA SYNDROME ST ELEVATIONS VI - V3 (often downsloplng) BRUGADA SYNDROME ECG PATTERNS Right bundle branch block (RBB) pattern (often incomplete). ST elevation V1-V3 (often downsloping pattern). T wave inversions V1&V2, ±S wave in lateral leads. 30 Chapter 1 - Cardiovascular System NTI-ARRHYTHMIC CLASS I NA+ CHANNEL BLOCKERS Class IA: Procainamide Quinidine Disopyramide AGENTS Decrease sodium conduction (especially depolarized cells). Affect phase 4 of depolarization (by blocking Na+ channel opening, they reduce SA node automaticity & cause membrane stabilization). MO A: decrease conduction velocity, prolong repolarization & refractory period. Prolong action potential & increase excitation threshold. Ind: atrial AND ventricular arrhythmias (eg, SVT, reentrant tachycardias, VT especially if resistant to other meds). Wolff-Parkinson White. S/E: Torsades de pointes, hypotension, tachycardia, tinnitus. Caution if kidney dz. Procainamide & Quinidine associated with drug-induced lupus-like syndrome. Quinidine may enhance Digoxin toxicity. Class IB: Lidocaine Tocainide MOA: decreases conduction velocity & shortens repolarization, shortens action potential (affects ischemic as well as depolarized ventricular tissue most useful in abnormal tissue as seen post MI) Indications: Stable VT (alternative). CI: narrow complex supraventricular tachycardia Class 1C: Flecainide Propafenone, Encainide MOA: decreases conduction velocity significantly (TQRS prolongation). Affects ventricular tissue in healthy cells. No effect on action potential duration. Indi ventricular tachycardia (used as last line management). CLASS II BETA-BLOCKERS Antagonizes beta adrenergic receptors to different degrees by decreasing slope of phase 4 (decreased calcium currents - decreased SA & AV node conduction) Ind: rate control of atrial flutter, atrial fibrillation, PSVT, ventricular tachycardias. Post MI. S/E: Bradycardia, AVblocks,hypotension, CNS (fatigue, depression, sexual dysfunction) may mask the symptoms of hypoglycemia. CI: sinus bradycardia, 2 n d /3 r d heart block, shock, CHF. Caution: Diabetes mellitus, peripheral vascular disease. Nonselectives may cause bronchospasm in patients with asthma & COPD. Glucagon is antidote for Beta-blocker toxicity. Atenolol, Metoprplol, Esmolol. insplpntwp fRi R>V ' Propranolol, Sotalol Nonselective «& 81 ?: Labetalol, Carvedilol CLASS HI K+CHANNEL BLOCKERS Amiodarone 'Ibutilide Dofetilide Sotalol Ca+ICHANNEL BLOCKERS Verapamil Diltiazem Class V (Other) Blocks K+ efflux during phase 3 "=> action potential prolongation & prolongation of effective refractory period, QT interval prolongation. Amiodarone (Class 111 but possess characteristics of class 1 through IV) Ind: atrial AND ventricular arrhythmias; refractory SVT. S/E of Amiodarone: pulmonary fibrosis, thyroid disorders (contains iodine so can cause hyperthyroidism/hypothyroidism), corneal deposits (>6mos use), hepatotoxicity, blue-green skin discoloration, hypotension. Monitor TFTs, PFTs & LFTs in patients on long-term Amiodarone. Slows SA node & AV node conduction (decreases L-type Ca*2 channels => decreased conduction speed, f PR interval, prolonged refractory period). Ind: atrial arrhythmias: atrial flutter, atrial fibrillation, PSVT S/E: peripheral edema, bradycardia, AV blocks. Antimuscarinic S/E with Verapamil (constipation, dizziness, flushing). Digoxin (cardiac glycoside). Ind; A fib, heart failure MQA: inhibit ATP-ase ^ positive inotrope, negative chronotrope/dromotrope Mets play in J3 fi for t h e Championship (Useful mnemonic to help r e m e m b e r the classes). Also Note: Class I and III used primarily for rhythm control. Class II & IV primarily for rate control 31 Chapter I - Cardiovascular System ADENOSINE INDICATIONS Paroxysmal supraventricular tachycardia (PSVT): s l o w s AV n o d e conduction time and blocks AV nodal reentry pathways. Short half-life (< 10 seconds) so followed by 5-10 cc IV saline flush. Pharmacologic cardiac stress testing: activates adenosine receptors (Al & A2), producing vasodilation of normal coronary arteries (excluding diseased coronary arteries). This leads to a shunting effect to mimic increased demand. Adenosine is usually used with thallium-201 stress testing. ADVERSE EFFECTS Common & short-lived: chest discomfort, dyspnea, flushing, lightheadedness, headache. Serious: bronchospasm, hypertension, arrhythmias, and myocardial infarction. CAUTIONS/CONTRAINDICATIONS Use in patients with second and third degree h e a r t block (without a pacemaker), WPW, wide complex tachycardias. Clinically active bronchospastic disorders (severe asthma/COPD), acute Myocardial ischemia. AMIODARONE MECHANISM OF ACTION Class HI antiarrhythmic (K+ channel blocker) with class I through IV properties. Prolongs the action potential. INDICATIONS Most c o m m o n l y u s e d for stable w i d e - c o m p l e x tachycardias but useful for both atrial and ventricular arrhythmias, including refractory SVT. ADVERSE EFFECTS IV use: h y p o t e n s i o n m o s t common, bradycardia, heart block, vasodilatation, polymorphic VT, phlebitis. Long-term use: corneal deposition with > 6 month use (most common side effect), thyroid disorders: hypo- or hyperthyroidism (contains iodine), pulmonary fibrosis, increased LFTs, blue-green discoloration of the skin. Monitor PFTs, TFTs, and LFTs for adverse effects. CAUTION Procainamide and Amiodarone are not generally used together. Amiodarone is a cytochrome p 4 5 0 inhibitor. CONTRAINDICATIONS Second or third-degree heart block who do not have pacemakers, WPW with concurrent A fib. 32 Chapter 1 - Cardiovascular Svstem N O R M A L FETAL CIRCULATION FETAL CARDIAC PHYSIOLOGY FETAL CIRCULATION USES RIGHT TO LEFT SHUNTS. T h e f e t u s r e c e i v e s i t s n u t r i e n t s & o x y g e n from t h e p l a c e n t a (not the fetal lungs). The oxygenated & nutrient-rich blood goes from the placenta to the right atrium. There a r e 2 right to left shunts that bypass the nonfunctioning fetal lungs: w h i c h s h u n t s about 2 / 3 of the blood from t h e r i g h t a t r i u m d i r e c t l y i n t o t h e left a t r i u m. The remaining 1 / 3 passes into the right ventricle. Most of the remaining 1 / 3 goes through the right ventricle and gets pumped into the pulmonary artery. FORAMEN OVALE: 2. DUCTUS ARTERIOSUS: s h u n t s b l o o d from t h e p u l m o n a r y a r t e r y d i r e c t l y i n t o t h e a o r t a (systemic circulation), bypassing the fetal lungs. Note: as a baby takes its first breath, left side pressure becomes > right side pressure, promoting closure of these openings. 4 ) Mixed Hood travels to the head and body, and back to the placenta via the aorta. The ductus arteriosus connects the aorta with the pulmonary artery, further shunting blood away from the lungs and into the aorta. The forameh ovale allows oxygenated blood in the right atrium to reach the left atrium. (1J Oxygenated blood from placenta enters ^ ^rightatrium via Inferior vena cava. * UmbBcat cord (contains umbilical artery and umbilical vein) Inferior vera cava The ductus venosus shunts oxygenated blood from the placenta away from the semifunctional liver and toward the heart. arrives ©1 ) viBlaood umbilical vein. By QpenStax College [CC BY 3.0 (http://creativecommons.Org/lfcenses/by/3.0)], via Wikimedla Commons CLINICAL CORRELATION P r o s t a g l a n d i n s k e e p t h e d u c t u s a r t e r i o s u s p a t e n t [prostaglandins are vasodilators). 1. To close a p a t e n t d u c t u s a r t e r i o s u s , a p r o s t a g l a n d i n i n h i b i t o r is given (eg, IV i n d o m e t h a c i n or Ibuprofen). MC used in p r e t e r m infants or within the 1 s t 10-14 days of life. 2. To k e e p t h e d u c t u s a r t e r i o s u s o p e n , a d m i n i s t e r p r o s t a g l a n d i n s. In severe cyanotic diseases (eg, severe coarctation of the aorta, tetralogy of Fallot or transposition of the great vessels), a p a t e n t ductus arteriosus allows for mixing of t h e blood to improve cyanosis. P r o s t a g l a n d i n E l a n a l o g s (eg, Alprostadil) maintains the ductus arteriosus open, reducing the cyanosis and improves circulation until surgical correction can be performed. 33 PEDIATRIC FUNCTIONAL MURMURS I n n o c e n t (functional, physiologic! m u r m u r s : non-pathologic, "functioning" m u r m u r s caused by blood moving through the chambers. Innocent m u r m u r s tend to be soft, not associated with symptoms, position-dependent, often occurs during systole & seen in up to 4 0 % of children at some point in their lives. Systolic m u r m u r s may be innocent or pathologic. Diastolic murmurs are almost always pathological. STILL MURMURS Most c o m m o n i n n o c e n t (physiologic) m u r m u r. Usually heard from 2 months of age until preadolescence. Pathophysiology: thought to be due to the vibration of the valve leaflets. PHYSICAL EXAMINATION Musical, v i b r a t o r y , noisy, t w a n g i n g , low-pitched early to mid-systolic ejection m u r m u r that is best h e a r d in the inferior aspect of the left l o w e r s t e r n a l b o r d e r & a p e x. Minimal to no radiation (may radiate to the carotids). Diminishes with standing o r Valsalva. Accentuated in the supine position and hyperdynamic states (eg, fever, anxiety). CERVICAL VENOUS HUM 2 nd most common innocent m u r m u r (after Still's) & m o s t c o m m o n c o n t i n u o u s benign murmur. Most commonly seen between 2-8 years of life. PATHOPHYSIOLOGY Due to turbulent blood flow from blood returning to the heart at the junction between the jugular vein and the superior vena cava. PHYSICAL EXAMINATION Soft, whirling, low-pitched c o n t i n u o u s m u r m u r , best heard in the right sternal border and right infraclavicular area in the upright position. The m u r m u r does not radiate. Increased intensity: sitting or upright position with the head extended. D e c r e a s e d m u r m u r i n t e n s i t y : s u p i n e , j u g u l a r c o m p r e s s i o n , & r o t a t i o n o r flexion of t h e h e a d , Valsalva. P U L M O N A R Y EJECTION MURMU Usually heard in older children and adolescents. It is best heard in mid systole and in the left second intercostal space (or superior aspect of the left lower sternal border). Due to blood flowing across the pulmonary valve into the pulmonary artery. Commonly heard in in older children & adolescents. Best heard in mid-systole in the s e c o n d left i n t e r c o s t a l s p a c e (or superior aspect of the left lower sternal border). Harsh in quality. 34 Chapter 1 - Cardiovascular System PATENT FORAMEN OVALE Covered b u t not sealed open communication between the right and left atria; however, a PFO is not considered an ASD because no septal tissue is missing (it is due to failed septal fusion). CLINICAL MANIFESTATIONS Most a r e asymptomatic Strokes from paradoxical embolism, cryptogenic stroke (stroke with no other underlying cause), decompression sickness, migraine, and acute limb ischemia secondary to emboli. DIAGNOSIS Echocardiogram: best t e s t t o m a k e the diagnosis. Transthoracic echocardiogram is usually performed first b u t Transesophageal echocardiogram is more sensitive. MANAGEMENT Percutaneous device closure, surgical PFO closure. Cryptogenic stroke: antiplatelet or anticoagulants. TRIAL SEPTAL DEFECT Abnormal opening in the atrial septum between the right and left atrium. Pathophysiology: allows for a left to right shunt (non cyan otic). Types: ostium s e c u n d u m m o s t c o m m o n type (80%), ostium primum (associated with mitral valve abnormalities), sinus venosus, coronary sinus. CLINICAL MANIFESTATIONS Most patients are asymptomatic or minimally symptomatic in childhood. Symptoms often initially occur in the third decade of life or later. Infants & voung children: recurrent respiratory infection, failure to thrive, exertional dyspnea. Adolescents & young adults: exertional dyspnea, easy fatigability, palpitations, atrial arrhythmias, syncope, heart failure. May develop paradoxical emboli (stroke from venous clots) or dysrhythmias later in life. PHYSICAL EXAMINATION Systolic ejection crescendo-decrescendo flow m u r m u r at the pulmonic area (left u p p e r sternal border). Wide, fixed split S2 that d o e s n o t vary w i t h respirations, loud SI and hyperdynamic right ventricle. DIAGNOSIS Echocardiogram: b e s t t e s t to m a k e the diagnosis. ECG: incomplete RBBB. Crochetage sign (notching of the peak of the R wave in the inferior leads). CXR: cardiomegaly & increased cardiovascular markings. Cardiac catheterization: definitive b u t rarely needed. MANAGEMENT Small ASD < 5 m m m a y b e observed (most small ASD spontaneously close in the first year if life). Surgical correction: if > 1cm or symptomatic (usually between 2-4 years of age). Percutaneous transcatheter closure vs. surgical intervention. 35 Chapter 1 - Cardiovascular System PATENT DUCTUS ARTERIOSUS Persistent communication between the descending thoracic aorta and main pulmonary artery after birth. Usually associated with a left to right shunt (noncyanotic). Risk factors: prematurity, female (2 times more common), fetal hypoxia. PATHOPHYSIOLOGY Continued prostaglandin E l production & low arterial oxygen content promotes patency. CLINICAL MANIFESTATIONS Most a r e asymptomatic. Infants may develop poor feeding, weight loss, frequent lower respiratory tract infections, pulmonary congestion, infective endocarditis. Eisenmenger syndrome: pulmonary hypertension & cyanotic h e a r t disease occurring when a left-toright shunt switches and becomes a right-to-left shunt (cyanotic). Patients may develop cyanotic^ lower extremities (cyanosis and clubbing of the feet). PHYSICAL EXAMINATION Continuous machine-like or "to and fro" murmur l o u d e s t at the pulmonic area (left upper sternal border). Wide pulse pressures (bounding peripheral pulses), loud S2. DIAGNOSIS Echocardiogram: b e s t initial test. ECG: LVH, left atrial enlargement. CXR: normal or cardiomegaly. Cardiac catheterization: definitive but usually not necessary. MANAGEMENT NSAlDs first-line medical prostaglandin synthesis. treatment (eg, IV Indomethacin, Ibuprofen). NSAIDs inhibit Surgical correction (eg, percutaneous catheter occlusion or surgical ligation) if no closure with Indomethacin. Best if done before 1-3 years of age. 36 f Chapter 1 - Cardiovascular System COARCTATION OF THE AORT. Congenital narrowing of the aortic l u m e n at the distal arch or descending aorta. 2 times m o r e common in males. Often associated with bicuspid aortic valve (70%), mitral valve defects, p a t e n t ductus arteriosus, and Turner syndrome. PATHOPHYSIOLOGY Narrowing of the aorta most commonly a t the insertion of the ductus arteriosus distal to the origin of the left subclavian vein results in hypertension in the arteries proximal to the lesion (eg, primary arteries supplying the u p p e r extremities) with relative hypotension in t h e lower extremities. Over time, the body compensates by developing collaterals around the coarctation (eg, intercostal arteries). TYPES Post-ductal (adult type) - narrowing occurs distal to the ductus arteriosum. Pre-ductal (infantile type) - narrowing occurs proximal to ductus arteriosum. CLINICAL MANIFESTATIONS May range from asymptomatic to heart failure or shock after birth with closure of the patent ductus arteriosus. Bilateral claudication, dyspnea on exertion, syncope. Neonatal presentation: failure to thrive in infants, poor feeding 1-2 weeks after birth. PHYSICAL EXAMINATION ^ Upper extremity systolic hypertension with l o w e r extremity h y p o t e n s i o n a n d / o r d i m i n i s h e d or delayed l o w e r extremity p u l s e s (eg, femoral & dorsalis pedis pulses). Systolic m u r m u r radiating to t h e back, scapula or chest. DIAGNOSIS Echocardiography: confirmatory t e s t (narrowing of the aorta). CXR: posterior rib notching (due to increased intercostal artery collateral flow), 3 sign (narrowed aorta looks like the notch of the n u m b e r 3). ECG: left ventricular hypertrophy Angiography: gold standard MANAGEMENT Corrective surgery or transcatheter-based intervention (eg, balloon angioplasty with or without stent placement), preferably in early childhood. Prostaglandin E l (eg, Alprostadil) preoperatively to stabilize t h e condition - maintains a patent ductus arteriosus, reducing symptoms & improves lower extremity blood flow. 37 Chapter 1 - Cardiovascular System TETRALOGY OF FALLOT Constellation of 1) RV outflow obstruction 2) Right ventricular hypertrophy (RVH) 3) large unrestrictive VSD and 4) overriding aorta. Most c o m m o n cyanotic congenital heart d i s e a s e (associated with a right-to-left shunt). Risk factors: genetic & environmental factors. Associated with chromosome 22 deletion. CLINICAL MANIFESTATIONS Infancy: c y a n o s i s m o s t c o m m o n presentation (blue baby syndrome). Older children: exertional dyspnea, cyanosis t h a t worsens with age. Tet spells - paroxysms of c y a n o s i s relieved w i t h squatting (squatting decreases right-to-left shunting, improving oxygenation). In infants, Tet spells are relieved with putting the knees to the chest. PHYSICAL EXAMINATION Harsh systolic m u r m u r at left mid to u p p e r sternal border (VSD), right ventricular heave (RVH) U digital clubbing, cyanosis. DIAGNOSIS Echocardiogram: test of choice. CXR: boot-shaped heart (prominent right ventricle). ECG: RVH, right atrial e n l a r g e m e n t MANAGEMENT Surgical repair performed ideally in the first 4-12 months of life. Prostaglandin infusion prior to surgery to maintain a patent ductus arteriosus (improves circulation). Prophylaxis for bacterial endocarditis 38 Chapter 1 - Cardiovascular System TRANSPOSITION OF THE GREAT ARTERIES (TOGA Discordance between the aorta and pulmonary trunk (the aorta arises from the right ventricle and t h e pulmonary t r u n k arises from the left ventricle). Most common cyanotic heart disease presenting in the neonatal period (dextro). TYPES Dextro-TGA: m o s t c o m m o n. The aorta arises from the right ventricle & t h e p u l m o n a r y artery from the left ventricle, leading to t w o parallel circuits. The systemic circuit sends systemic deoxygenated blood back to the systemic circulation. The pulmonary circuit sends oxygenated pulmonary venous blood back to the lungs. Prior to surgical correction, survival is d e p e n d e n t upon the p r e s e n c e of shunts b e t w e e n the right and left circulations (eg, patent ductus arteriosus, ASD, VSD). Levo-TGA: is usually a cyan otic. The right atrium (RA) sends blood to the morphologic left ventricle (LV), which is on the right side physically. This morphologic LV sends blood to pulmonary system. The left atrium (LA) sends blood to morphologic right ventricle (RV) located on the left side; The morphologic right ventricle sends blood to the systemic circulation. CLINICAL MANIFESTATIONS Severe cyanosis & tachypnea within the first 3 0 days of life n o t affected by exertion or the use of oxygen. DIAGNOSIS Echocardiogram: primary m e a n s of diagnosis. Electrocardiography: may be normal or show right axis deviation or right ventricular hypertrophy. Chest radiography: "egg on a string" appearance - t h e h e a r t a p p e a r s as an egg on its side with the narrowed, atrophic thymus of the superior mediastinum appearing as the string. Mildly increased pulmonary vascular congestion, & mild cardiomegaly. Cardiac catheterization: gold standard but rarely used to make the diagnosis b u t may be used in therapeutic treatment (eg, balloon atrial septostomy). MANAGEMENT Arterial switch operation. Prostaglandin E l analog to maintain a p a t e n t ductus arteriosus & balloon atrial septostomy may be needed for t e m p o r a r y intercirculatory mixing prior to definitive surgical repair. Without treatment, 9 0 % die by 1 year. 5 year survival rate after surgery >80%. 39 o PATENT DUCTUS AIUI-RJOSUS I COARCTATION OF AORTA TETRALOGY OF FALLOT ! ATRIAL SEPTAL DEFECT Hole in atrial septum [opening Congenital narrowing of descending Communication between descending MC cyanotic congenital heart disease DEFINITION between right & left atrium). thoracic aorta. Male:female2:l thoracic aorta & pulmonary artery Right to Left (Cyanotic)* Left to Right (Noncyanotic) Left to Right (Noncyanotic) SHUNT Noncyanotic usually © RV outflow obstruction T L V afterload with SNS activity & RAAS Prematurity, perinatal distress & ETIOLOGIES Ostium secundum MC* (80%) pulmonary artery stenosis activation n»l m o s t c o m m o n cause of R-sided failure is L-sided failure. Pulmonary d i s e a s e (COPD, Pulmonary hypertension). Mitral stenosis. 2. SYSTOLIC vs. DIASTOLIC HSSTOflSR I ejection fraction. ±SagaIlop. Systolic m o s t c o m m o n form of heart failure. - Etiologies: p o s t Myocardial infarction, Dilated cardiomyopathy, Myocarditis. THWffBWffl p r e s e r v e d ejection fraction (normal/fEF), ± $± gallop = forced atrial contraction into a stiff ventricle. Associated with normal cardiac size. - Etiologies: Hypertension, Left ventricular Hypertrophy, elderly, valvular heart disease, Cardiomyopathies (hypertrophic, restrictive), Constrictive pericarditis. DIASTOLIC FAILURE SYSTOLIC FAILURE DIASTOUCHaVfr HeAtfr - Preserved - decreased ejection fraction (EF is ejection fraction (EF) n o r m a l / i n c r e a s ed) weak - thick ventricular walls - thin ventricular walls - small LV chamber - © S4 on auscultation - dilated LV chamber to- © S3 on auscultation 3. HIGH O U T P U T v. L O W O U T P U T High output: t h e metabolic d e m a n d s of t h e b o d y exceeds n o r m a l cardiac function. - thyrotoxicosis, w e t beriberi, s e v e r e anemia, AV shunting, Paget's disease of t h e bone. Low o u t p u t : i n h e r e n t p r o b l e m of myocardial contraction, ischemia, chronic h y p e r t e n s i o n. 4. ACUTE V. CHRONIC Acute: largely systolic (ex. h y p e r t e n s i v e crisis, acute MI, papillary muscle r u p t u r e ). Chronic: typically seen in p a t i e n t s with dilated c a r d i o m y o p a t h y or valvular disease. PATHOPHYSIOLOGY OF HEART FAILURE Initial insult leads to tafterload, fpreload &/or ^contractility. The injured h e a r t tries makes shortt e r m compensations that, over time, promote cardiovascular deterioration. Compensations include: O Sympathetic nervous system activation © Myocyte hypertrophy/remodeling © RAAS activation: fluid overload, ventricular remodeling/hypertrophy ^ CHF 54 Chapter 1 - Cardiovascular System CLINICAL MANIFESTATIONS Left-sided Heart failure Increased pulmonary venous pressure from fluid backing up into the lungs (L for Lungs and JLsided). Dyspnea m o s t c o m m o n symptom. Includes exertional, orthopnea, paroxysmal nocturnal dyspnea. Fatigue. Chronic, nonproductive cough or productive with pink, frothy sputum. Physical examination: Pulmonary e d e m a & congestion: rales (fluid in the alveoli), rhonchi, wheezing. Tachypnea (rapid, shallow breathing). Cheyne-Stokes breathing - deeper, faster breathing with gradual decrease & periods of apnea, cyanosis. S3 gallop w i t h Systolic heart failure. S 4 gallop w i t h Diastolic heart failure. Dusky pale skin, diaphoresis, cool extremities NEW YORK HEART ASSOCIATION FUNCTIONAL CLASS Class I - No symptoms, no limitation during ordinary physical activity. Class II - Mild symptoms (dyspnea &/or angina), slight limitation during ordinary activity. Class III - Symptoms cause marked limitation in activity (even with minimal exertion) comfortable only at rest. Class IV - Symptoms even while at rest, severe limitations & inability to carry out physical activity. Right-sided Heart failure Increased systemic venous pressure from fluid backing up into the roads (R for R-sided and 3 Roads = inferior vena cava, superior vena cava, & hepatic circulation). IVC: peripheral edema: pitting edema of the legs, cyanosis. SVC: jugular v e n o u s distention due to increased jugular venous pressure. GI & hepatic congestion: anorexia, nausea, vomiting, hepatojugular reflux (increased JVP with liver palpation), hepatosplenomegaly. DIAGNOSIS Heart failure Echocardiogram: diagnostic test of choice in the outpatient setting t o m a k e t h e diagnosis of Heart failure. It measures ejection fraction, assesses ventricular function, & may reveal t h e cause. Ejection fraction m o s t important determinant of prognosis (EF 1 0 0 = CHF is likely. N-terminal pro-BNP may also be used. Cardiac enzymes to r / o MI. 55 Chapter 1 - Cardiovascular System LONG -TERM MANAGEMENT OF HEART FAILURE Initial management: ACEI (& diuretic for symptoms). ACEI > beta blockers best 2 druffsfor | mortality. DRTO/INTBRVENTION COMMENTS Na restriction 1 8 0 mmHg a n d / o r DBP > 1 2 0 m m H g w i t h o u t e v i d e n c e of end organ damage. CLINICAL MANIFESTATIONS General: headache (most common), dyspnea, chest pain, focal neurologic deficits, altered mental status, delirium, seizures, nausea, vomiting. MANAGEMENT Gradual reduction of m e a n arterial pressure b y n o m o r e than 2 5 % over 2 4 - 4 8 h o u r s w i t h oral medications (eg, Clonidine, Captopril, Labetalol, Nicardipine, Furosemide). Treatment goals a r e blood p r e s s u r e < 1 6 0 / 1 0 0 mmHg. Clonidine Captopril Furosemide Labetalol Nicardipine ORAL DRUGS USED FOR HYPERTENSIVE URGENCIES Mechanism of Action :: Adverse Effects Centrally acting a-z adrenergic agonist Headache, tachycardia, nausea, (short-term use only) vomiting sedation, fatigue dry mouth, rebound hypertension if discontinued abruptly - (mimics Pheochromocytoma). ACE Inhibitor Angioedema, Acute kidney injury. Loop diuretic Electrolyte abnormalities, alkalosis. a i p i p 2 blocker CI in severe asthma/COPD, AV heart block, congestive heart failure. Calcium channel blocker Reflex tachycardia, headache, nausea 63 Chapter 1 - Cardiovascular System HYPERTENSIVE EMERGENC SBP > 1 8 0 mmHg a n d / o r DBP > 1 2 0 mmHg with e v i d e n c e of end organ damage. CLINICAL MANIFESTATIONS General: headache (most common), dyspnea, chest pain, focal neurologic deficits, altered mental status, delirium, seizures, nausea, vomiting. Neurologic: encephalopathy, stroke (hemorrhagic or ischemic), seizure. Cardiac: Acute coronary syndrome, Aortic dissection, Acute heart failure (pulmonary edema). Workup includes CXR, ECG, cardiac enzymes, BNP. Renal: Acute kidney injury, proteinuria, hematuria (glomerulonephritis). Retinal: malignant Hypertension, severe (Grade IV) retinopathy. MANAGEMENT IV blood p r e s s u r e reduction agents. For most hypertensive emergencies, m e a n arterial p r e s s u r e should b e reduced gradually by about 1 0 - 2 0 % in the first hour and by an additional 5-15% o v e r t h e n e x t 2 3 hours. The 3 main exceptions are as follows: Acute phase of an ischemic stroke: blood pressure is usually not lowered u n l e s s i t i s s 1 8 5 / 1 1 0 m m H g in patients who are candidates for reperfusion treatment OR > 2 2 0 / 1 2 0 mmHg in patients who are not candidates for reperfusion. Acute aortic dissection: systolic blood pressure is rapidly lowered to a goal of 100-120 mmHg within 20 minutes. Intracerebral hypertension: t r e a t m e n t depends on different factors. EMERGENCY NEUROLOGIC HTN ENCEPHALOPATHY FIRST LINE Nicardipine or Clevidipine Labetalol, Fenoldopam Sodium Nitroprusside NOTES Must r / o stroke. HTN encephalopathy often presents with confusion, headache, nausea & vomiting. Symptoms improve with lowering of BP. Nitroprusside, Nitroglycerin & Hydralazine may increase intracranial pressure. HEMORRHAGIC STROKE Nicardipine or Labetalol Benefits vs. risks of lowering blood pressure must be weighed in hemorrhagic strokes. ISCHEMIC STROKE Nicardipine or Labetalol Avoid cerebral hypoperfusion if ischemic. Reduce blood pressure ONLY if BP is: £220/120 (nota thrombolytic candidate). >185/110 (if a thrombolytic candidate]. Decreases shearing forces. Beta blocker tx target: systolic BP 100-120mmHg & pulse 65 years. ETIOLOGIES Impaired autonomic function a n d / o r decreased intravascular volume. Medications: includes antihypertensives (eg, Alpha blockers, Nitroglycerin, ACE inhibitors), diuretics, narcotics, antipsychotics, antidepressants, and alcohol consumption Neurologic: include diabetic neuropathy, Parkinson disease, polyneuropathies etc. Hypovolemia (eg, Loop diuretics, hemorrhage or vomiting). CLINICAL MANIFESTATIONS Due to cerebral hypoperfusion - dizziness, lightheadedness, palpitations, blurred vision, darkening of visual fields, a n d / o r syncope. WORKUP Blood pressure measurement Tilt t a b l e t e s t : blood pressure reduction at a 60-degree angle. Labs (eg, hematocrit, electrolytes, BUN, creatine, glucose) to evaluate for anemia or dehydration. MANAGEMENT Initial management: c o n s e r v a t i v e initial m a n a g e m e n t of c h o i c e - i n c r e a s i n g s a l t a n d fluid i n t a k e , gradual positional changes, compression stockings or abdominal binder, exercise, and " discontinuation of offending medications. Caffeine may be helpful. F l u d r o c o r t i s o n e is t h e first-line m e d i c a l m a n a g e m e n t if persistent symptoms despite nonpharmacologic measures. Midodrine (alpha-1 agonist) or Droxidopa (pressor agent) may be used in patients if additional therapy is needed or if the patient is unable to take Fludrocortisone. Avoiding the flat position, sleeping with the head of the bed raised 30-45 degrees if refractory to medical therapy. REFLEX-MEDIATED SYNCOPE Neurally-mediated syncope. VASOVAGAL SYNCOPE Due to vasovagal hypotension (self-limited systemic hypotension associated with bradycardia a n d / o r peripheral venodilation/vasodilation). Most c o m m o n c a u s e of s y n c o p e , especially without a p p a r e n t neurologic or cardiovascular disease. Triggers: blood phobia, emotional stress/fear, pain, trauma. Manifestations: p r o d r o m a l p h a s e (eg, dizziness, lightheadedness, epigastric pain, palpitations, blurred vision, darkening of visual fields) followed by syncope followed by a postdromal phase. CAROTID SINUS SYNCOPE Syncope with minor stimulation of the carotid sinus ( e g shaving, putting on neckties, wearing a tight collar, head turning, or applying minor pressure to the carotids). SITUATIONAL SYNCOPE Triggers include defecation, micturition, coughing/sneezing, post-prandial, or trigger points. 65 Chapter I - Cardiovascular System CIRCULATORY SHOC Inadequate organ perfusion & t i s s u e oxygenation t o meet the body's oxygenation requirements. Often associated w i t h hypotension (but not always). S h o c k i s d e t e r m i n e d by EITHER: 1. Low cardiac output OR 2. Low s y s t e m i c vascular r e s i s t a n c e (SVR). SVR = the resistance to blood flow through the circulatory system (determined by peripheral blood vessels). Peripheral vasoconstriction increases SVR. Vasodilation decreases SVR. 4 MAIN TYPES OF SHOCK 1. HYPOVOLEMIC ' loss of blood or fluid v o l u m e (eg, hemorrhage). primary myocardial dysfunction "^reduced cardiac output (eg, MI). 2. CARDIOGENIC 3. OBSTRUCTIVE extrinsic or intrinsic obstruction to circulation (eg, pericardial tamponade). maldistribution of blood flow from essential organs to nonessential organs 4. DISTRIBUTIVE (eg, septic or neurogenic shock). PATHOPHYSIOLOGY OF SHOCK 1. Inadequate t i s s u e perfusion: inability to meet t h e body's metabolic oxygen requirements >=> metabolic acidosis & organ dysfunction. 2. Autonomic n e r v o u s s y s t e m activation: in an attempt to improve systemic O2 delivery. - Sympathetic nervous system activation: causes vasoconstriction (|SVR) & |contractility (to |C0). tNorepinephrine, dopamine & Cortisol release. The |SVR helps to maintain cerebral & cardiac perfusion by causing vasoconstriction of splanchnic, musculoskeletal & renal blood flow. - RAAS activation: water & sodium retention (|urine output to minimize renal water & salt loss). Also causes vasoconstriction to help maintain cardiac output 3. Systemic effects of shock: - ATP depletion => ion p u m p dysfunction leading to cellular dysfunction, cell swelling & d e a t h / - Metabolic acidosis: d u e to lack of oxygen => cells resort to anaerobic metabolism, producing lactic acid as a byproduct. Order lactate levels as p a r t of workup. - Multiorgan Dysfunction Syndrome (MODS): physiologic consequences of shock on organ systems. Includes l u n g kidney, heart, & brain dysfunction as well as DIC (disseminated intravascular coagulation). - Multisvstemic Organ Failure (MSOF): organ failure if the conditions persist. CLINICAL MANIFESTATIONS OF SHOCK 1. Generally acutely ill, altered mental status, decreased peripheral pulses, tachycardia, skin usually cool and mottled (may be warm and flushed in distributive shock), systolic blood pressure 70%. 66 Chapter 1 - Cardiovascular System HYPOVOLEMIC SH0C1 Loss OF BLOOD OR FLUID VOLUME due to h e m o r r h a g e or fluid loss. ETIOLOGIES Hemorrhagic: eg, GI bleed, AAA rupture, massive hemoptysis, trauma, ectopic postpartum hemorrhage. pregnancy, Non-blood fluid loss: GI: vomiting, bowel obstruction, pancreatitis; severe burns, diabetic ketoacidosis (causes osmotic diuresis in response to hyperglycemia). PATHOPHYSIOLOGY Loss of blood or fluid volume => t h e a r t r a t e * vasoconstriction (|SVR), hypotension,.[cardiac output. Body's response to hypovolemia: - rapid: peripheral vasoconstriction, fcardiac activity. - sustained: arterial vasoconstriction, Na*/water retention, f Cortisol. CLINICAL MANIFESTATIONS Loss of volume => | h e a r t rate (tachycardia), hypotension, J.CO (oliguria or anuria), vasoconstriction (f SVR) => pale cool dry skin/extremities, s l o w capillary refill > 2 seconds, j s k i n turgor, dry m u c o u s membranes, AMS. Usually does not cause profound respiratory distress. CLASSES OF HEMORRHAGIC SHOCK < 15% blood loss Pulse usually normal, systolic blood pressure (SBP) usually normal. 15 - 30% blood loss Tachycardia (pulse >100). SBP usually >100mmHg. 30 - 40% blood loss Tachycardia, decreased systolic blood pressure (40% blood loss Tachycardia, decreased SBP, lethargy, no urine output DIAGNOSIS Hallmarfa Vasoconstriction (tSVR), hypotension, J,CO & d e c r e a s e d p u l m o n a r y capillary pressure. - CBC: t H g b / H c t = dehydration (hemoconcentration). J,Hgb/Hct is late sign in hemorrhagic shock. - Decreased CVP (central venous pressure)/PCWP (pulmonary capillary wedge pressure). MANAGEMENT 1. ABCDE's, Insert 2 large bore IV lines or a central line. 2. Volume resuscitation: crystalloids (Normal Saline or Lactated Ringer's) often given 3-4 liters to restore blood volume. Monitor urine output to assess success of resuscitation. 3. Control the source of h e m o r r h a g e to prevent further sequelae. ± Packed RBC blood transfusion if severe hemorrhage: (O-negative or cross-matched). 4. Prevention of hypothermia, t r e a t any coagulopathies. 67 Chapter 1 - Cardiovascular System CARDIOGENIC SHOC PRIMARY CARDIAC/MYQCARDIAL DYSFUNCTION inadequate tissue perfusion => J,CO (cardiac output) w i t h fsystemic vascular resistance (SVR). Often systolic in nature. Cardiogenic often produces increased respiratory effort/distress w h e r e a s hypovolemic does not. ETIOLOGIES Cardiac d i s e a s e : myocardial infarction, disease, cardiomyopathy, arrhythmias. myocarditis, valve dysfunction, congenital heart PATHOPHYSIOLOGY J.CO & evidence of tissue hypoxia in the presence of adequate intravascular volume. Sustained hypotension in the presence of ^ p u l m o n a r y c a p i l l a r y w e d g e p r e s s u r e (>15mmHg). V a s o c o n s t r i c t i o n (fSVR), h y p o t e n s i o n J.CO & T p u l m o n a r y c a p i l l a r y w e d g e p r e s s u r e. MANAGEMENT 1. Oxygen, isotonic fluids (avoid a g g r e s s i v e IV fluid t r e a t m e n t - u s e s m a l l e r a m o u n t s of fluid). NOTE CARDIOGENIC SHOCK IS THE ONLY SHOCK IN WHICH LARGE AMOUNTS OF FLUIDS AREN'T GIVEN. 2. I n o t r o p i c s u p p o r t : drugs to increase myocardial contractility & cardiac output: - Dobutamine (positive inotrope), Epinephrine (positive inotrope & vasoconstrictor). - Amrinone may be used if refractory (Amrinone is a phosphodiesterase-3 inhibitor that is a positive inotrope). - Intraaortic balloon p u m p s u p p o r t 3. T r e a t t h e u n d e r l y i n g c a u s e : ex. Ml: early angioplasty or thrombolytics. O B S T R U C T I V E SHOC OBSTRUCTION OF BLOOD FLOW DUE TO PHYSICAL OBSTRUCTION OF HEART OR GREAT VESSELS. Intrinsic or extrinsic (texternal pressure on the heart decreases the heart's ability to p u m p blood). ETIOLOGIES: 1. Massive p u l m o n a r y e m b o l i s m : obstruction to pulmonary artery blood flow. Cyanosis, tachycardia, hypotension, VQ mismatch, hemoptysis. ECG: S1Q3T3, sinus tachycardia. ABG: Pa02 60mmHg. ± IV hydrocortisone. ANAPHYLACTIC SHOCK: I g E - m e d i a t e d s e v e r e s y s t e m i c h y p e r s e n s i t i v i t y r e a c t i o n. History of incest bite/stings, food or drug allergy, recent IV c o n t r a s t Symptoms usually begin within 60 minutes of exposure. PHYSICAL EXAM: pruritus, hives, angioedema => respiratory distress, stridor, sensation of "lump in throat", hoarseness (life threatening laryngeal edema). MANAGEMENT: E p i n e p h r i n e 1 s t l i n e (0.3mg IM of 1:1000 repeat q5-10min as needed). If cardiovascular collapse, give Epinephrine l m g IV (1:10,000). A i r w a y m a n a g e m e n t , a n t i h i s t a m i n e s (Diphenhydramine 25-50mg IV blocks Hi, Ranitidine IV blocks H2), IV fluids. O b s e r v e p a t i e n t for 4 - 6 h o u r s because up to 2 0 % of patients have a biphasic phenomenon (return of symptoms 3-4 hours after the initial reaction). 3. i?fantTiTna3Tf%lIllII|fl: d u e to a c u t e s p i n a l c o r d injury, regional anesthesia. PATHOPHYSIOLOGY: autonomic sympathetic blockade unopposed "["vagal tone. «=> b r a d y c a r d i a & h y p o t e n s i o n. Loss of sympathetic tone => warm, dry skin. CLINICAL: w a r m skin, normal or |HR, J.SVR, hypovolemia, WIDE p u l s e p r e s s u r e. Management: fluids, pressors + / - corticosteroids. ENDOCRINE SHOCI j: e g A d r e n a l insufficiency ( A d d i s o n i a n crisis). M a n a g e m e n t : H y d r o c o r t i s o n e lOOmg IV (often unresponsive to fluids & pressors). 69 -J o HYPOVOLEMIC CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE 4 types (below) 1. SEPTIC Early (warm) 2. NEUROGENIC 3. ANAPHYLACTIC PATHOPHYSIOLOGY ETIOLOGIES LOSS OF BLOOD OR FLUID Hemorrhage! GI bleed, AAA VOLUME *>|PVR & |HR rupture etc. to maintain CO. Fluid loss: GI: vomiting, diarrhea, pancreatitis, severe burns etc. PRIMARY MYOCARDIAL Myocardial Infarction ABAQBkWiK ^ heart Myocarditis unable to maintain CO Valvular disease Cardiomyopathies Arrhythmias EXTRINSIC OR INTRINSIC Pericardial tamponade OBSTRUCTION of heart Massive Pulmonary Embolism or great vessels Tension Pneumothorax Aortic dissection MALDISTRIBUTION OF BLOOD Septic & VASODILA TION with Neurogenic shunting of blood away Anaphylactic from vital to non vital Hypoadrenal organs Severe host immune Bacteria response Vasodilation Sympathetic blockade => unopposed vagal tone on vessels => vasodilation IgE mediated systemic HSN reaction with histamine release 7.5% risk for having a h e a r t attack or stroke within 10 years. 3. People >21 years of age with LDL levels >190 mg/dL. 4. Any patient with any form of clinical atherosclerotic cardiovascular disease. 5. Patients Statins, Bile acid sequestrants. l o w e r elevated triglycerides => Fibrates, Niacin. i n c r e a s e HDL => Niacin, Fibrates. Statins, Fibrates 71 Chapter 1 - Cardiovascular System HMG-COA REDUCTASE INHIBITORS fSTATIN! Simvastatin Pravastatin Lovastatin Atorvastatin Rosuvastatin Mechanism of action: Inhibit the rate-limiting step in hepatic cholesterol synthesis via inhibition of the enzyme HMG-CoA reductase. Increase LDL receptors, promoting LDL clearance. Reduce triglycerides. Indications: Best drug to decrease LDL levels. Statins have been shown to decrease cardiovascular complications. Adverse effects: Muscle damage (eg myalgias, myositis, Rhabdomyolysis). Statins may also cause increased liver function tests, hepatitis (most common), gastrointestinal symptoms, Diabetes mellitus. Considerations: Atorvastatin, Rosuvastatin can be taken any time of the day, most of the others are taken in the evening LFTs order prior to the initiation of statin therapy. Drug interactions: Drugs that inhibit the CP450 system (eg Erythromycin, Diltiazem, -azoles) may increase drug levels. Contraindications: Active hepatic disease, persistent elevated LFTs, pregnancy, & breastfeeding. Mechanism of action: increases HDL (delays HDL clearance). Decreases hepatic production of LDL & its precursor VLDL. Decreases triglycerides. Indications: Best drug to increase HDL levels. Adverse effects: Increased prostaglandins (eg flushing, warm sensation, pruritus, headache). Pretreatment of 30 minutes with NSAIDs or Aspirin can be given to counter flushing. Dry skin, hyperuricemia (may precipitate gout), hyperglycemia, hepatotoxicity. GI symptoms (nausea, vomiting, dyspepsia) - GI symptoms reduced if taken with meals. Contraindications: Active Peptic ulcer disease, active liver disease, arterial bleeding. Mechanism of action: Inhibit triglyceride synthesis, increase the activity of lipoprotein lipase (stimulating catabolism of triglyceride-rich lipoproteins), increase HDL synthesis & decrease LDL synthesis. Indications: best drugs to decrease triglycerides. Adverse effects: headache, dizziness, GI symptoms, increased liver function tests, increased gallstones. They are also associated with myalgias & myositis (especially with concomitant statin use). The only fibrate FDA approved to be used in combination with a Statin is Fenofibric acid. Contraindications: Active hepatobiliary disease, severe renal disease, breastfeeding Gemfibrozil + Repaglinide. 72 Chapter^^^ardiovascularSystem Mechanism of action: Bile acid sequestrant (binds bile acids in the intestine, blocking enterohepatic reabsorption of bile acids), reduces cholesterol pool, lowers intrahepatic cholesterol. Because the liver has to make new bile acids, it increases its LDL receptors, decreasing LDL levels. Indications: Often used in combination with a Statin to reduce LDL levels, mild to moderate increases in HDL. Safe in pregnancy (not systemically absorbed). Cholestyramine used to treat pruritus associated with biliary obstruction. Adverse effects: GI side effects (nausea, vomiting, bloating crampy abdominal pain), increased LFTs. Increased triglyceride levels. Osteoporosis with long-term use. Interactions: May impair absorption other medications (eg, antibiotics, Digoxin, Warfarin, fat-soluble vitamins) so these medications should be taken 1 hour before or 4 hours after BAS. Contraindications; Severe hypertriglyceridemia, complete biliary obstruction. Mechanism of action: Inhibits intestinal cholesterol absorption. Indications: Often used in combination with a Statin to reduce LDL levels. Adverse effects: Headache, diarrhea, increased LFTs (especially with Statin use). 73 Chapter 1 - Cardiovascular System INFECTIVE ENDOCARDITIS Infection of the endothelium/valves 2n to colonization (eg, during transient/persistent bacteremia). Mitral valve m o s t c o m m o n valve involved (M>A>T>P). Exception is IV drug u s e - tricuspid valve most c o m m o n in IV drug users. Risk factors: increased age, rheumatic heart disease, IV drug use, immunosuppression, prosthetic heart valves, congenital heart disease. TYPES Acute bacterial endocarditis: Infection of normal valves with a virulent organism (eg, S. aureus). Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organism (eg S. viridans). IV drug-related endocarditis: Most commonly d u e to S. aureus (especially MRSA). Pseudomonas, Candida. Prosthetic valve endocarditis: Early (within 6 0 days): Staphylococcus epidermis m o s t common. Late (after 60 days) resembles native valve endocarditis. ORGANISMS Staphylococcus aureus: Most common cause of ACUTE infective endocarditis (rapidly progressive). Affects normal valves. Also common in patients with IV drug u s e (especially MRSA). Streptococcus viridans Most common cause of SUBACUTE infective endocarditis. Affects damaged valves. Part of the oral flora (associated with poor dentition or dental procedures). Staphylococcus epidermis: Most common organism in early prosthetic valve endocarditis (especially within 60 days of the procedure). Enterococcus: Seen especially in men >50 years with a recent history of gastrointestinal or genitourinary procedure. HACEK organisms (Haemophilus aphrophilus, Actinobacillus, £ardiobacterium hominis, Eikenella corrodens, Kingella kingae) are gram- negative organisms that a r e hard to culture. Suspect these organisms in patients with endocarditis & negative b l o o d cultures. Streptococcus bovis: Especially in patients with colon cancer or ulcerative colitis. CLINICAL MANIFESTATIONS Generalized constitutional symptoms: persistent fever m o s t common, malaise, fatigue, anorexia etc. New o n s e t of a m u r m u r or worsening of an existing murmur. Osier nodes: painful or tender raised violaceous nodules on the pads of the digits and the palms (may be seen on the t h e n a r or hypothenar eminence). Janeway lesions: p a i n l e s s erythematous macules on the palms & soles. Splinter h e m o r r h a g e s (linear reddish-brown lesions under the nail bed), petechiae (skin or mucous membranes). Roth spots: retinal hemorrhages with central clearing. Splenomegaly, septic arterial or pulmonary emboli, glomerulonephritis 74 Chapter 1 - Cardiovascular System DIAGNOSTIC STUDIES Blood c u l t u r e s : (before antibiotic initiation). 3 s e t s a t l e a s t 1 h o u r a p a r t if the patient is stable. ECG: at regular intervals to assess for new conduction abnormalities (prone to arrhythmias). Echocardiogram: obtain TTE first; consider TEE if TTE is nondiagnostic or increased suspicion. T r a n s e s o p h a g e a l e c h o c a r d i o g r a m (TEE) m u c h m o r e s e n s i t i v e t h a n TTE (>90% v 50% in NVE) (82%v 3 6 % in PVE) so maybe used in patients with suspected Prosthetic valve endocarditis. Labs: CBC: leukocytosis, anemia (normochromic, normocytic); tESR/Rheumatoid Factor. MODIFIED DUKE CRITERIA MINOR MAIOR SUSTAINED BACTEREMIA 2 © blood cultures by Predisposing condition organism known to cause endocarditis. abnormal valves, IVDA, indwelling catheters, etc Fever (>38° C /100.4°F). Vascular & embolic phenomena: Janeway lesions, ENDOCARDIAL INVOLVEMENT: documented by septic arterial or pulmonary emboli, ICH. either: Immunologic phenomena: - © echocardiogram: (vegetation, abscess, - Osier's nodes, Roth spots, © Rheumatoid factor valve perforation, prosthetic dehiscence) - Acute glomerulonephritis © Blood culture not meeting major criteria. - clearly established new valvular regurgitation © echocardiogram not meeting major criteria (aortic or mitral regurgitation) (eg, worsening of existing murmur). Clinical criteria for infective endocarditis: 2 major OR 1 major + 3 minor OR 5 minor (80% accuracy) INDICATIONS FOR SURGERY Refractory CHF; persistent or refractory infection, invasive infection, prosthetic valve, recurrent systemic emboli, fungal infections. MANAGEMENT OF INFECTIVE ENDOCARDITIS: suggested F.mniric t h e r a p y : NATIVE VALVE A n t i - s t a p h y l o c o c c a l p e n i c i l l i n (eg, Nafcillin, Oxacillin) p l u s e i t h e r Ceftriaxone o r G e n t a m i c i n. Vancomycin suspected. PROSTHETIC VALVE FUNGAL substituted if Penicillin allergy or MRSA V a n c o m y c i n + G e n t a m i c i n + Rifampin Amphotericin B ( t r e a t 6-8 weeks). Patients often n e e d surgical intervention for fungal cases Penicillin & Vancomycin have great gram-positive coverage Gentamicin & Ceftriaxone have great gram-negative coverage In acute Endocarditis, antibiotics a r e started promptly after culture data is o b t a i n e d In subacute Endocarditis, if t h e patient is h e m o d y n a m i c a l l y stable, antibiotics m a y b e d e l a y e d in o r d e r to p r o p e r l y o b t a i n b l o o d c u l t u r e data, especially if prior t r e a t m e n t with antibiotics. Adjust t h e a n t i b i o t i c r e g i m e n b a s e d on o r g a n i s m , c u l t u r e & s e n s i t i v i t i e s. F e v e r m a y p e r s i s t u p t o 1 w e e k after a p p r o p r i a t e a n t i b i o t i c t h e r a p y h a s b e e n i n i t i a t e d. D u r a t i o n o f t h e r a p y u s u a l l y 4 - 6 w e e k s (with aminoglycosides used only for t h e first 2 weeks). 75 Cardiac conditions Procedures Regimens Chapter 1 - Cardiovascular System ENDOCARDITIS PROPHYLAXIS INDICATIONS 1. Prosthetic (artificial) heart valves. 2. Heart repairs using prosthetic material (not including stents). 3. Prior history of endocarditis. 4. Congenital heart disease. 5. Cardiac valvulopathy in a transplanted heart. 1. Dental: involving manipulation of gums, roots of the teeth, oral mucosa perforation. 2. Respiratory; surgery on respiratory mucosa, rigid bronchoscopy. 3. Procedures involving infected skin/musculoskeletal tissues (including abscess incision & drainage). Amoxicillin 2g 30-60 minutes before the procedures listed above. Clindamycin 6 0 0 m g if penicillin allergic Macrolides or Cephalexin are other options. NOTE prophylaxis is no longer routinely recommended for gastrointestinal or genitourinary procedures. NOTE prophylaxis no longer routinely recommended for most types of valvular heart disease (including mitral valve prolapse, bicuspid aortic valve, acquired mitral or aortic valve disease, hypertrophic cardiomyopathy). Good o r a l h y g i e n e r e c o m m e n d e d t o r e d u c e t e m p o r a r y e p i s o d e s of b a c t e r e m i a. LIBMAN-SACKS ENDOCARDITIS Nonbacterial thrombotic endocarditis (marantic endocarditis) is a noninfectious endocarditis due to sterile platelet thrombi deposition on the affected valve. It most commonly affects the mitral and aortic valves. ETIOLOGIES Can be seen with malignancy, systemic lupus erythematosus, antiphospholipid antibody syndrome, rheumatic fever and other inflammatory conditions. CLINICAL MANIFESTATIONS Most patients are asymptomatic and are usually afebrile. Symptoms are usually due to emboli to the skin, kidney, extremities, and spleen. MANAGEMENT Manage the SLE. May need anticoagulation. 76 Chapter 1 - Cardiovascular System CUTE PERICARDITIS Inflammation of the pericardium, the outer layer of the heart. Fibrinous or serofibrinous: eg, post MI, infectious. Serous: autoimmunity (eg, SLE, RA). ETIOLOGIES 2 m o s t c o m m o n causes are idiopathic & viral (especially Coxsackievirus & Echovirus), neoplastic. Dressier syndrome (post MI pericarditis + fever + pleural effusion) Autoimmune, uremia, bacterial, radiation, medications. CLINICAL MANIFESTATIONS Chest pain: sudden onset of pleuritic (sharp, worse with inspiration), persistent, postural ( w o r s e w h e n supine & improved w i t h sitting forward). Pain may radiate to the shoulder, back, neck, arm, or epigastric area. Pericardial friction rub: best h e a r d a t end expiration while upright and leaning forward. 3 components. DIAGNOSTIC STUDIES ECG: diagnostic test of choice - diffuse ST elevations in the precordial leads w i t h associated PR d e p r e s s i o n s in those leads (aVRassociated with the opposite - PR elevations and ST depressions). May have cardiac enzyme positivity. Echocardiogram: useful to evaluate for an associated pericardial effusion a n d / o r signs of cardiac tamponade. MANAGEMENT Anti-inflammatory meds: NSAIDs or Aspirin first-line x 7-14 days (symptoms usually subside in 1-2 days). Colchicine second-line. Dressier syndrome: Aspirin or Colchicine (avoid NSAIDS because they can interfere with myocardial scar formation). 77 Chapter 1 - Cardiovascular System PERICARDIAL EFFUSION Accumulation of fluid in the pericardial space. Normally, about 5-15 ml of fluid is in the pericardial space. ETIOLOGIES Same causes of acute Pericarditis (eg, viral, idiopathic, immune, malignancy - lung cancer most common, b r e a s t second most common, aortic dissection, uremia). CLINICAL MANIFESTATIONS Chest pain (if associated with acute Pericarditis), dyspnea, fatigue. Physical examination: d e c r e a s e d (muffled) heart s o u n d s (due to fluid). DIAGNOSIS E c h o c a r d i o g r a m : t e s t of c h o i c e increased fluid in the pericardial space. ECG: electrical alternans (alternating amplitudes of the QRS complexes) in large effusions. Low QRS voltage. Chest radiograph: not used in the diagnosis. Findings may include appearance of the heart as a "water bottle" (not sensitive or specific). MANAGEMENT Treat the underlying cause (eg, acute Pericarditis). Serial echocardiography if necessary. Large effusions may need pericardiocentesis for symptomatic relief. 78 Chapter 1 - Cardiovascular System CARDIAC TAMPONADE Pericardial effusion causing significant p r e s s u r e on the heart, impeding cardiac filling, leading to decreased cardiac output and shock (medical emergency). The rate of accumulation of fluid is m o r e critical than the volume. A rapid accumulation of as little as 150ml of fluid can cause tamponade, while as much as 1 liter can slowly accumulate if the pericardium is compliant Usually starts on the right side because the right walls are thinner. Etiologies: complication of acute Pericarditis or trauma. Malignancy is the most common nontraumatic cause of Tamponade. CLINICAL MANIFESTATIONS Beck's triad: distant (muffled) heart sounds, increased JVP, and systemic hypotension. Pulsus paradoxus: exaggerated (>10 mmHg) decrease in systolic blood pressure with inspiration. Dyspnea, fatigue, peripheral edema, shock, reflex tachycardia, cool extremities. DIAGNOSTIC STUDIES Echocardiogram: pericardial effusion + diastolic collapse of cardiac chambers. ECG: signs of pericardial effusion (low voltage QRS complexes, electrical alternans). Chest radiograph: may show an enlarged cardiac silhouette. Right heart catheterization: equalization of pressures in diastole. MANAGEMENT Pericardiocentesis (immediate) to remove the pressure. Volume resuscitation and pressor support if needed. Pericardial window drainage if recurrent. CONSTRICTIVE PERICARDITIS Loss of pericardial elasticity (thickening, fibrosis & calcification) leading to restriction of ventricular diastolic filling. Pathophysiology: fibrosis limits ventricular filling, decreasing stroke volume a n d cardiac output. Etiologies: any cause of acute Pericarditis. In the US, idiopathic and viral are the most common causes. Worldwide, Tuberculosis is the leading cause. CLINICAL MANIFESTATIONS Dyspnea most common symptom, fatigue, orthopnea. Right-sided h e a r t failure signs: increased jugular v e n o u s distention, peripheral edema, nausea, vomiting, increased hepatojugular reflex, Kussmaul's sign (the lack of a n inspiratory decline o r increase in jugular vein p r e s s u r e with inspiration). Pericardial knock: high pitched diastolic sound similar to S3 (sudden cessation of ventricular filling). DIAGNOSTIC STUDIES Chest radiograph: pericardial calcification may be seen especially on lateral view, clear lung fields. Normal or slightly increased heart size, Square root sign on cardiac catheterization. Echocardiography: pericardial thickening a n d / o r calcification. Also used to rule out Restrictive cardiomyopathy. "Square root" sign - early diastolic dip followed by a plateau of diastasis. CT scan or MRI: more sensitive than echocardiography - pericardial thickening or calcification. MANAGEMENT Diuretics for symptom relief as well as reduction of edema and venous pressure. Pericardiectomy definitive management. 79 o ACUTE PERICARDITIS DEFINITION Inflammation of the pericardium. PERICARDIAL DISEASES PERICARDIAL EFFUSION PERICARDIAL TAMPONADE Tfluidin pericardial space. CONSTRICTIVE PERICARDITIS Pericardial effusion "=> pressure on Fibrotic, calcified pericardium the heart* limits ventricular limits ventricular diastolic filling diastolic filling & icardlac output Same as pericarditis. Same as pericarditis 2 most common causes are idiopathic Same as acute pericarditis. [probably postviral) & viral (esp Enteroviruses: Coxsackievirus & May be traumatic. Chronic inflammation Echovtruses). Neoplastic, autoimmune (SLE, RA) Inflammatory, vascular etc [ Dressler's syndrome: post MI o i 5 P's of pericarditis: Dyspnea MCsx* Distant (muffled) heart sounds* BECK'S TRIAD* CLINICAL 0 Distant heart sounds (effusion) R-SIDED FAILURE SX*: MANIFESTATIONS : 'Chest Pain -Pleuritic (sharp pain worse with ±sx of pericarditis. OyVP Qugular venous pressure) - Peripheral edema i inspiration)* © Systemic HYPOtension -yvp I -Postural (pain worse supine, - Hepatic congestion, N/V O relieved with sitting forward).* - Persistent chest Pain Pulsus paradoxus - drop >10mmHa PERICARDIAL KNOCK* 3rd heart of systolic BP with inspiration sound from sudden cessation of 5' Pericardial Friction Rub [pulses disappear with inspiration). ventricular filling o ETIOLOGIES DIAGNOSIS MANAGEMENT ECG: \ 'ECG: -Diffuse ST elevations* (concave up) - Low voltage QRS complex* in precordial leads with PR -Electric Alternans depressions In same leads* «* T 1 wave inversions => resolution. -aVR: ST depression & PR elevation. ECHOCARDIOGRAM: ECHOCARDIOGRAM: - ^pericardial fluid. -Normal (± pericardial effusion). Used mainly to r/o tamponade. - No hemodynamic compromise. ASPIRIN OR NSAlDstx of choice* Treat underlying cause 1 Colchicine 2nd line Steroids If refractory (sx > 48h) Pericardial window if recurrent 'Dressler's svndrome: j Aspirin or Colchicine - Kussmaul's sign: t/VP c inspiration. Pulsus paradoxus Kussmaul's siqn ECG: -Low voltage QRS complexes* - Electric Alternans 5? ECHOCARDIOGRAM: ECHOCARDIOGRAM: -PERICARDIAL THICKENING* & - -fpericardial fluid + diastolic calcification* collapse of cardiac chambers* hemodynamic compromise. PERICARDECTOMY* PERICARDIOCENTESIS* Chapter 1 - Cardiovascular System THE 5 GOLDEN RULES TO CONQUER MURMURS RULE! -QUALITY OF THE MURMUR HARSH/RUMBLE SOUNDS = think STENOSIS: AS. MS: abnormal forward flow ofblood through [stenotic) valve that should be open. Stenotic lesions lead to pressure overload. Regurgitation leads to volume overload. BLOWING sound - think REGURGITATION: AR, MR: abnormal backflow ofblood (regurgitation) through an incompletely closed valve. Regurgitation leads to volume overload. RU