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CARDIO NOTES Sources: MS by Brunner, MS by Black and Hawks, nsg review notes and racked-up notes han 3rd

d year pa kita..
Cardiovascular diseases one of the leading causes of death and disability ANATOMY AND PHYSIOLOGY (brief) Heart - 4 chambers - 3 layers of pericardium (out to in): epicardium, myocardium and endocardium - Valves: Atrioventricular valves (AV valves bicuspid/mitral and tricuspid valves) and Semilunar valves (aortic, pulmonic, and heart eps) *heart eps extra valve found in small proportion of population Arteries, Veins and Capillaries blood vessels - Layers (out to in): tunica adventitia, tunica media and tunica intima - Capillaries one cell-thick walls - Largest artery: Aorta - Largest vein: Vena cava *Veins carry 40-55% O2 NOT blood without O2! :) Coronary Circulation: LADA (Left Anterior Descending Artery) anterior wall of the heart LMCA (Left Main Coronary Artery) main branch of left coronary artery LCXA (Left Circumflex Artery) circles around the lateral left wall of the heart RCA (Right Coronary Artery) to inferior wall Posterior Descending Artery to posterior portion Electrical Conduction: Starts with the Sinoatrial (SA) node pacemaker; normal rate: 60-100bpm Impulses pass to Atrioventricular (AV) node 0.12-0.20 seconds delay Then to the Bundle of His, to the Purkinje fibers and to the whole ventricular walls ECG measures electrical activity of the heart.

- Either 12 or 15-lead ECG


Can ECG determine structural abnormalities? YES! If there is a defect, electrical activity in that part is abnormal! Cardiac Output = Stroke Volume x Heart rate Note: very high HR can decrease CO (ex: in Ventricular fibrillation or V-fib where the heart quivers instead of pumping properly) Carotid Arteries left and right - Internal and external carotid arteries - In stroke: Middle cerebral artery and internal carotid artery are commonly affected. External Jugular Vein vein that can be easily assessed (for JVD) Subclavian Vein can be used for cannulations (e.g. cardiac catheterization) Pulse Pressure = SBP DBP *if PP = < 20 cardiac tamponade * BP is changed by: > diameter and elasticity of blood vessels (hunahunaa daw an tubo nga guti ngan dako kun hain it mas makusog it awas?) > blood viscosity (the more viscous, the slower blood flow) > force of heart contractions > volume of blood SBP cardiac output; DBP resistance to blood flow Control: by epinephrine and norepinephrine ASSESSMENT Hx - Smoking - HPN - Obesity heart becomes overworked; increased risk of atherosclerosis - Sex - Activity - Family HX - DM - Age (*menopause 2x risk of MI) - Respiratory Probs (to determine presence of cor pulmonale or pulmonary hypertension) - Meds PE - Appearance - V/S including peripheral pulses

- Weight if increased to 3 lbs/ 24 hrs (fld retention) - Pulsus alternans beat to beat change in amplitude; indicates left heart failure - Pulsus paradoxus exaggerated decline of PP during inspiration; indicates cardiac tamponade and constrictive pericarditis - Kussmauls sign engorged jugular veins during breathing; not to be confused with Kussmauls respiration (deep respirations in an attempt to blow off CO2 e.g. in DKA patients) - Chest pain use COLDSPA questions *most dangerous type of chest pain: UNSTABLE ANGINA AND VARIANT ANGINA (occurs at rest) - Respiratory SOME DX EXAMS: ECG 2D-Echocardiogram (or simply, 2D-echo) sees heart structures Holter monitor with portable monitor Cardiac catheterization and Arteriography Stress test ECG + exertion (may treadmill iton) Radionucleide tests uses isotope to detect CA; CA cells glow indicating that they are hypermetabolic Pulse oximetry important nsg responsibility: remove nail polish; stroke patients: on unaffected side Hemodynamic Monitoring ex. CVP MRI contrarindications: metal implants and claustrophobic patients (e.g. psychiatric patients) Cardiac enzymes CPK-MB (increased 2-4 hrs after MI); Troponin I (increases 6-8 hrs after MI) DISORDERS: I. Congenital Disoders/Anomalies > 4 different classifications based on hemodynamics: - Increased pulmonary blood flow - Obstruction of blood flow leaving the heart - Mixed blood flow - Decreased pulmonary blood flow a. disorders with increased pulmonary blood flow left to right shunt, between 2 systems of great arteries 1. Ventricular Septal Defect (VSD) > opened septum between 2 ventricles

> with RV hypertrophy and pulmonary hypertension >more common in boys > idiopathic > with easy fatigability (poor oxygenation) > harsh loud pansystolic murmur > thrills >dx: echocardiography and MRI >mgt: if hole is small: closes spontaneously. If > 3mm hole, open heart surgery (usually done before age 2 to prevent pulmonary hypertension) >complication: endocarditis 2. Atrial Septal Defect (ASD) > hole in between atria > common in girls > foramen ovale did not close > 2 types: a. ASD I / Osteum Primum hole is distal to center b. ASD II/ Osteum Secondum hole is proximal to center > assessment: harsh systolic murmur in pulmonic area > dx: 2d-echo, cardiac catheterization >mgt: elective surgery done within 1-3 yrs * can cause emboli during pregnancy if left undiagnosed! 3. Atrioventricular Canal Defect (AVCD) > or endocardial cushion defect > incomplete fusion of the septum of the heart at the junction of the atria and ventricles > mgt: pulmonary artery bonding narrowing pulmonary artery to equalize pressure between the left and right sides of the heart 4. Patent Ductus Arteriosus (PDA) > DA fails to close > O2-rich blood back to lungs > increases pressure on the left side > with RV hypertrophy >dx: 2d-echo >mgt: - Ibuprofen inhibits release of prostaglandins to close the PDA - IV indomethacin *prostaglandins maintains the PDA - cardiac catheterization - ductal ligation (major surgery) b. Disorders with Obstruction to blood flow caused by valve or vessel that is narrowed 1. Pulmonary Stenosis

> narrowed pulmonary valve > ventricular hypertrophy occurs > lesser blood for oxygenation > assessment: mild right sided heart failure, cyanosis, systolic ejection murmur, thrills > mgt: balloon angioplasty thru cardiac catheterization 2. Aortic Stenosis > narrowed aortic valve > backpressure to pulmonary vein > congestion to LV > causes pulmonary edema > decreases CO > assessment: faint pulses (decreased CO), hypotension, tachycardia, chest pain, sometimes sudden death > mgt: stabilization by beta-blocker and calcium channel blockers, balloon valvuloplasty 3. Coarctation of the Aorta > narrowed lumen of aorta due to constricting band > one of the causes of CHF > 2 locations: a. Preductal between subclavian artery and ductus arteriosus b. Postductal after ductus arteriosus > assessment: headache (increased BP on upper side and decreased BP on lower side), vertigo, dizziness, N&V, absence of palpable femoral pulses, faint brachial pulse >mgt: balloon catheterization, interventional cardiography, surgery to repair the defect, diuretic therapy to prevent CHF *girls need repair before childbearing age to be able to adjust to the increased blood volume c. Disorders with Mixed blood flow mixing of blood from pulmonary and systemic circulation; with compromised oxygenation 1. Transposition of Great Arteries > switching of places of the great arteries (aorta and pulmonary artery) > incompatible with life unless the child has ASD, VSD or PDA > with murmurs > mgt: prostaglandin therapy (to open DA) Balloon catheterization (to increase diameter of the septal defect) Surgery (1 week to 3 months to switch back to normal positions) 2. Total Anomalous Pulmonary Venous Return > pulmonary veins are attached to superior vena cava > often with patent foramen ovale

> found in patients without spleen >mgt: surgery and prostaglandin therapy 3. Truncus Arteriosus > fused aorta and pulmonary artery > accompanied by VSD > assessment: cyanosis, musmurs (VSD) >mgt: restructuring by surgery 4. Hypoplastic Left Heart Syndrome (HLHS) > atresia of the mirtal and aortic valve > nonfunctional LV > increased pressure on the right side > RV hypertrophy > with PDA >mgt: prostaglandin therapy and heart transplant d. Disorders with decreased pulmonary blood flow obstruction to pulmonary blood flow that would increase the pressure on the right side 1. Tricuspid Atresia > closed tricuspid valve > with open foramen ovale >extreme cyanosis, tachycardia >mgt: prostaglandin therapy Glenn Shunt Baffle restructuring of the right side of the heart 2. Tetralogy of Fallot > 4 anomalies in one a. Pulmonary Stenosis b. VSD c. Dextroposition of Aorta (or Overriding Aorta) d. RV hypertrophy > abnormal chromosome 22 (long arm) > with polycythemia vera (compensation to provide adequate blood to tissues deprived of O2) >severe dyspnea, clubbing of fingers > with hypoxic episodes >squatting and knee-chest position are the relieving factors (traps blood in lower extremities and thus resting the heart) > mgt: surgery, O2, beta-blockers, Blalock-Taussig procedure (creating a shunt between aortic and pulmonic artery), Brock procedure (full repair) II. Structural Cardiac Disorders 1. Mitral Valve disease stenosis, regurgitation and prolapse > stenosis result from acute rheumatic fever (Grp A Betahemolytic Streptococci - can increase pressure on the left atrium

- can cause pulmonary congestion (backflow) and a-fib (hypertrophy of the atrium) - can create mural thrombi due to blood stasis in LA - loud first heart sound hard valves > regurgitation failure of the valves to close - some of the blood regurgitates back to LA - can decrease CO - PND (paroxysmal nocturnal dyspnea) and orthopnea occurs - blowing pitch murmur - splitting of 2nd heart sound (due to increased blood vol. in LV, there is a delay in closure in pulmonic valve) >prolapse - regurgitant murmur or midsystolic click - mgt: prevent beta-hemolytic strep infection (RF and RHD), beta blockers, aspirin to prevent thrombi formation 2. Aortic Valve Disease stenosis and regurgitation - leads to increased LV pressure - congenital or degenerative - leads to LSHF * aortic regurgitation vs mitral regurgitation AR diastolic event, there is compensatory dilation due to vol. overload in LV MR systolic event -with angina pectoris, syncope, LV enlargement, Water Hammer Pulse or Corrigans pulse (sudden sharp pulse then collapse of diastolic pulse), diastolic murmurs -mgt: prophylactic meds, digitalis, diuretics, avoid vigorous physical activity, valve replacement 3. Tricuspid Valve Disease -manifestaions: pulsations in the jugular veins, peripheral edema, weight loss, murmur increases with inspiration, hepatic congestion - mgt: diurteics, digitalis, surgery for severely stenotic leaflets 4. Pulmonic Valve disease - high-pitched murmur - can decrease CO - with pumonic stenosis -leads to RSHF -mgt: V/S q1-4 hrs, auscultate chest, emotional support, stress importance of follow-up exams, prevent edema, valve reconstruction, Anuloplasty, Balloon valvuloplasty 5. Cardiomyopathy - disorders of the myocardium - heart walls are replaced by fibrotic tissue - heart enlarges - 3 types: a. Dilated LV and RV dilate

- most common - there is myocardial degeneration to fibrotic tissue replacement consequently decreases contractility and ultimately leads to clot formation (blood pooling) and heart failure (low CO) b. Hypertrophic - thickening of interventricular septum leading to decreased size of the chamber of the heart -mgt: rest, O2, beta blockers, no inotropics and nitrates, no alcohol; anticoagulants, prophylactic meds c. Restrictive deposition of eosinophilic CHONs in the heart muscles - result of an autoimmune or allergic reaction - heart loses its ability to expand (axa ngani restrictive! ;) ) - common cause: amyloidosis -can decrease resistance to LV filling leading to low CO and then failure -mgt: Na restriction, pacemaker, diuretics, and vasodilators to prevent heart failure; myotomy ( surgical incision or resection of a portion of interventricular septum) and heart transplant 3 types of Cardiac Surgery: a. Reparative b. Reconstructive c. Substitutional Heart Transplantation 2 types: a. Orthotropic b. Heterotropic III. Infectious Diseases of the Heart 1. Pericarditis - inflammation of the pericardium - causes: >may be idiopathic > local infection > disorders of connective tissue > allergic reaction > neoplastic > trauma > radiation therapy -clin. Manifestations: > pain (like MI) aggravated by breathing > pericardial friction rub > signs of infection > tachycardia -complications:

Cardiac Tamponade compression Becks triad: Increased CVP with neck vein distention Muffled heart sounds Pulsus paradoxus Intervention: emergency pericardiocentesis 2. Myocarditis - inflammation in the muscles of the heart -causes: > viral, fungal, or parasitic infection > immunosuppression >allergic reaction - hallmark: Pulsus alternans - with gallop rhythm - murmurs -dyspnea - tachycardia - chest pain - intervention; bed rest, O2, monitor for digitalis toxicity -complications: mural thrombi formation and cardiomyopathy 3. Infective Endocarditis - infection of the inner lining of the heart secondary to bacterial contamination -causes: > prolonged IV therapy > invasive surgical procedure > structural defects of the heart > previous dental extraction - 3 main classifications: a. Acute most fatal -Staphylococcus aureus -with high fever b. Subacute Streptococcus viridans -with low-grade fever c. Chronic in IV drug users - manifestations: > loud regurgitant murmurs > petechiae > splinter hemorrhage > Roths spots white/yellow center surrounded by a bright red, irregular halo seen in oplthalmoscope > Oslers nodes painful, erythematous nodules >Janeways lesions flat, small, nontender red spots on palms and soles Dukes Criteria for IE

Major Criteria Positive blood culture Vegetations seen in echocardiogram Minor Criteria Predisposition Fever Vascular phenomenon Microbiologic evidence 4. Rheumatic Fever/Rheumatic Heart Disease (RF/RHD) - caused by Grp A beta-hemolytic Streptococci - autoimmune disease - mitral and aortic valves are destroyed as a result of an autoantibody reaction - interventions: eradicate infection by Penicillin IV or PO or Erythromycin if allergic to Pen; digitalis, diuretics, promote comfort Jones Criteria of Diagnosis Major Criteria Carditis Painful migratory polyarthritis Chorea Erythema marginatum Subcutaneous nodules Minor Criteria Elevated ESR Positive culture Elevated anti-streptolysin O titer (ASO) IV. Functional Disorders 1. Coronary Artery Disease (CAD) - major risk factor of MI - risk factors: > age >heredity > smoking > gender more on men > HPN > elevated serum cholesterol level (240 mg/dL) > sedentary lifestyle > obesity > DM ( >126 mg/dL) > stress > elevated homocysteine levels

> menopause 2x risk S&S (near MI): N&V Chest pain Cold clammy skin Female MI shows atypical presentation (epigastric pain) Complications of MI: Dysrhythmias Heart failure and pulmonary edema Pulmonary embolism Recurrent MI Complications caused by myocardial necrosis Ventricular rupture Ventricular aneurysm Dresslers syndrome (late pericarditis) Pericarditis Patterns of Angina: Stable angina triggered by predictable degree of exertion or emotion Unstable angina triggered by unpredictable degree of exertion or emotion Variant or Prinzmetals angina occurs during rest Nocturnal angina during sleep (REM stage) Angina decubitus occurs when the client reclines and lessens when he sits or stand up Intractable angina unresponsive to intervention Postinfarction angina - after MI, when residual ischemia may cause episodes of angina Meds to treat acute attack in angina: Opiate analgesics reduce pain, decrease HR, decrease demand for O2 Vasodilators Beta-adrenergic blockers decrease workload of the heart, decrease myocardial O2 demand, decrease no. of angina attacks Ca-channel blockers dilate coronary arteries, increase O2 supply to myocardium Anriplatelet agents prevent clot formation Dx: ECG ST segment changes (>1mm) *starts in toddlerhood. :(

* cows milk has 24g of fat while breastmilk has 4.2g of fat *max dose of Captopril: 3 doses * low fat diet: step1 - <1500 mg fat ; step2 - <1200mg fat *nitroglycerin use: Store in dark glass container Replace every 4-6 months Take when pain starts and rest Bring the supply with you If there is no relief, get medical help Max dose: 3 tabs - Treatment of CAD: Lifestyle changes Angioplasty Morphine SO4 pain and improves microcirculation Anticoagulant Anti-lipidemic meds Beta blockers Calcium channel blockers Low-dose aspirin therapy (80mg as maintenance) Nitrates muscle relaxant (vasodilation) 2. Coronary Heart Disease - high LDL and low HDL - TC = HDL + LDL + TRIG - N.V. = <240 mg/dL 3. Hypertension - elevated BP - diagnosed after 3 consecutive BP takings (6 months interval and BP is 140/90 and above) - 2 types: essential/primary HPN and secondary HPN - dx: BP, U/A (+)CHON, BUN and CREA, blood sugar levels - silent killer >:) - S&S: > asymptomatic > headache >blurred vision > possible kidney damage -mgt: >antihypertensives First-line: hydrochlorothiazides (diuretics) Next: ACE inhibitors, beta-blockers, and Ca-channel blockers >weigh everyday >I&O > low fat, low Na diet (NOT Na-restricted diet) > lifestyle changes * weight loss of 7kg = decreased risk of dying from metabolic d/o by 20%

>exercise = 30 mins, 3-4 times a week (HR must be 150% of resting HR) >DASH diet *low fat (Mediterranean diet) 4. Myocardial Infarction (MI) - affected artery: LADA - danger zone: 24-48 hrs after MI - most common complication: fibrillation (prolonged loss of blood flow plus sudden return) - S&S: > dyspnea > hypotension >substernal pain Tx: Thrombolytic drugs Lidocaine (class I antidysrhythmic) O2 Morphine SO4 Bypass surgery *follow-up: 10 days after discharge *resume work? 8-10 weeks after *resume sex? After walking 2 flights of stairs Mgt for treatment of MI (think of ABCDE and MONA) A aspirin and anti-anginal therapy B beta-blocking therapy and BP control C cigarettes and cholesterol control D - diet and diabetes E education and exercise M morphine SO4 O O2 therapy N Nitrates A Aspirin 5. Congestive Heart Failure (CHF) - unable to pump - LSHF or RSHF - LSHF - more on pulmonary manifestations (PND, orthopnea, rales, hemoptysis, dyspnea, etc.) - RSHF back to venous circulation (edema, ascites, hepatic congestion, JVD, etc.) - PMI 6th-7th ICS left of MCL (cardiomegaly) Normal PMI: 5th ICS at MCL -Mgt: > Fowlers position

> bed rest (cardiomegaly hypermetabolic state) >I&O >abdominal girth > skin care in edematous areas - DONT MASSAGE!! - turn to side - antibedsore mattress - use banana leaves for cooling effect > observe for arrhythmia >O2 hypersaturate the blood with O2 even at low HR > diuretics > watch out for DVT > monitor for digitalis toxicity *digoxin decreases HR and increases strength of contractions - monitor K levels - take HR (apical) - not given if HR is < 45 bpm - increase intake of K-rich foods V. Arrhythmias / Dysrhythmias - abnormal rhythms Normal sinus rhythm normal heart rhythm that starts in the SA node (60-100 bpm) -disturbances in 3 major mechanisms: a. Automaticity generating a heart rhythm b. Conduction speed the impulses travels through SA, AV and Purkinje Fibers c. Reentry of Impulses cardiac tissues is depolarized multiple times by the same impulse Ectopic pacemaker other cardiac cells originating the impulse other than the SA node ECG interpretation steps: 1. Calculate the HR either: a. Count the no. of R waves in 6-inch strip of ECG tracing (6 secs) x 10 = rate/min. b. Count the no. of large squares between R waves. Find an R wave crossing a large square. Count the no. of large squares until the next R wave. 2. Measure the regularity of R waves (ventricular rhythm) - <0.12 s bet. Beats normal - >0.12 s bet. Beats abnormal 3. Examine the P waves - normal: P wave then the QRS -abnormal: absence or in abnormal position (ectopic pacemaker) 4. Measure the PR interval - normal: 0.12-0.20 s

-abnormal: prolonged or reduced (defect in conduction system between atria and ventricles) 5. Measure duration of QRS complex - abnormal: >0.12 s (interventricular conduction defect occurs) 6. Examine the ST segment - normal: isoelectric not elevated or depressed -abnormal abnormality in the onset of recovery of ventricular muscle usually because of injury (acute MI) 7. Examine the T wave - normal: upright and 1/3 the height of the QRS complex - abnormal: inverted interference to normal repolarization Tall hyperkalemia Normal values: P wave - <0.11 s PR interval 0.12-0.20 s QRS complex 0.04-0.11 s QT interval male: 0.42 s; female: 0.43 s REMEMBER: P wave atrial depolarization QRS complex ventricular depolarization T wave Ventricular repolarization A. SA NODE DYSRHYTHMIAS a. Disturbances in Automaticity 1. Sinus Tachycardia - >100 bpm - P wave and QRS normal - increased SNS stimulation and decreased vagal stimulation 2. Sinus Bradycardia - <60 bpm - P wave and QRS normal - increased vagal tone 3. Sinus Dysrhythmia - phasic changes in the automaticity in the SA node, causing it to fire at varying speeds - irregular PP interval 4. Sick Sinus Syndrome - persistent sinus bradycardia, sinus arrest or pauses, combination of SA and AV node conduction disturbances and alternating paroxysms of rapid atrial tachycardias b. Disturbances in Conduction 1. SA Arrest - neither the atria nor the ventricles are stimulated - pause of rhythm - PQRST will be missing for one or more cycles 2. Sinus Exit Block

- conduction delay occurs between the SA node and the atrial muscle - patterns of pauses B. ATRIAL DYSRHYTHMIAS a. Disturbances in Automaticity 1. Premature Atrial Contractions (PACs) - early beats arising from ectopic foci - enhanced automaticity of atrial muscle -P waves are premature and often differ in appearance and shape b. Reentry of Impulses 1. Paroxysmal Atrial Tachycardia (PAT) - sudden rapid firing from ectopic atrial pacemaker - 150-200 bpm 2. Atrial Fibrillation (A-fib or AF) - most common supraventricular dysrhythmia - chaotic P wave, not one clear P wave, Irregular RR interval - 400-700 bpm - blood pools in the quivering atria 3. Atrial Flutter - saw-toothed atrial formations (saw-toothed P waves) - 220-350 bpm - may have 3 P waves for every QRS complex (3:1) C. ATRIOVENTRICULAR JUCNTIONAL DYSRHYTHMIAS a. Disturbances in Automaticity 1. Premature Junctional Contractions (PJCs) - single, early firing of junctional ectopic focus - no P wave 2. Paroxysmal Junctional Tachycardia (PJT) - > 60 bpm junctional rhythm b. Disturbances in Impulse Conduction 1. First-degree AV block - prolonged PR interval (>0.20 s) - regular rhythm 2. Second-degree AV block - some impulses are conducted, some are blocked - 2 types: > Mobitz Type I (Wenckebach phenomenon) abnormally long refractory period at the AV node; initial prolongation then missing QRS > Mobitz Type II P wave not conducted, dropped QRS complex; may progress to third-degree heart block

3. Third-degree AV block - AV dissociation - complete heart block - complete dissociation of impulse bet. Atria and ventricles

- tissues allow electrical conduction between atria and ventricles at sites other than the AV node (shortcut??) - ex: Wolff-Parkinson-White Syndrome (WPW Syndrome) c. Disturbances in Conduction 1.Ventricular Asystole - cardiac standstill - no electrical activity, no palpable pulse, no CO, no rhythm 2. Pulseless Electrical Activity (PEA) - formerly Electromechanical Dissociation (EMD) - with electrical activity but no pulse -caused by cardiac tamponade and shock 3. Sudden Cardiac Death - cardiac arrest - abrupt loss of heart function GOOD LUCK HA ATON TANAN, HESSONITES!! KAYA NATIN TO! :D \m/ Simplify complicated things and never try to complicate simple things. -PhiL :)

c. Interventricular Impulse Conduction Abnormalities 1. Bundle Branch Block - left or right bundle branch block - conduction impaired in bundle branches (distal to bundle of His) - wide (>0.20s) or notched QRS complex D. VENTRICULAR DYSRHYTMIAS - more serious and life-threatening - causes greater hemodynamic compromise - wide and bizarre QRS complexes a. Disturbances in Automaticity 1. Premature Ventricular Contractions (PVCs) - firing of an irritable pacemaker in the ventricles - wide and bizarre QRS complex (>0.12s) - trigeminy: 1 normal QRS and 2 abnormal QRS - bigeminy: 1 normal and 1 abnormal QRS 2. Ventricular Tachycardia - three or more series of PVCs with no normal beats in between - no P waves and PR interval absent -100-220 bpm - monomorphic one focal site - polymorphic multiple foci 3. Torsades de Pointes -literally means twisting of points - QRS complexes constantly changing or twisting around an isoelectric line - 150-300 bpm - tx of choice: MgSO4 b. Reentry of Impulses 1. Ventricular Fibrillation (V-fib or VF) - extremely rapid, erratic impulse formation and conduction - primary cause of sudden cardiac death - impossible to identify P waves 2. Preexcitation Syndromes - accessory connections between atrium an ventricle are result of anomalous embryonic development of myocardial tissue bridging the fibrous tissues that separates the 2 chambers