Chapter 28, Part 1: Cardiology

Cardiology- the study of the heart and its function Cardiovascular disease (CVD)- disease affecting the heart, peripheral blood vessels, or both. Coronary heart disease (CHD)- a type of CVD; the single largest killer of Americans. Cardiovascular Anatomy Mediastinum Three tissue layers of the heart 1. Endocardium- the innermost layer 2. Myocardium- the muscular middle layer Epicardium- outer later of the heart 3. Pericardium- the protective sac surrounding the heart 4 Chambers of the heart 1. Atria- Superior Right & Left 2. Ventricle- Inferior Right & Left Heart Valves Mitral Valves o Mitral valve- between the left atrium and Ventricle o Tricuspid valve- between the right atrium and ventricle Semi-lunar Valves o Aortic valve- between the left ventricle and aorta o Pulmonary valve- between the right ventricle and pulmonary artery. Vessels o Arteries Pulmonary artery- takes O2 deficient blood to the lungs to get reoxygenated. Aorta o Veins Vena Cava- brings deoxygenated blood from the body back to the heart (right atrium) Superior Vena Cava Inferior Vena Cava Pulmonary Vein- takes Oxygenated blood back to the left artery o Coronary arteries- supply nutrients and O2 to the heart from the Aorta Left coronary artery- supplies the left ventricle, interventricular septum, part of the right ventricle, and the conduction system. Has 2 main branches: Anterior descending artery Circumflex artery Right coronary artery- supplies a portion of the right atrium and right ventricle and part of the conduction system. Has 2 major branches:

Posterior descending artery Marginal artery

Cardiac Physiology Cardiac Cycle o -Systole- part of the cardiac cycle when the heart is contracting, and the semi-lunar valves open o -Diastole- part of the cardiac cycle when the heart is relaxed and cardiac filling and profusion occur. Ejection fraction- each ventricle ejects about 2/3 of the blood it contains Stroke volume- the amount of blood ejected from the ventrical Preload- is the end-diastolic volume and influences the force of the next contraction because of the stretch it exerts (Starlings Law) Afterload- is the resistance against which the heart muscle ust pump. Cardiac output = Stroke Volume x Heart Rate. o Autonomic Control of the Heart Chronotrophic effect- rate of the heart Inotrophic effect- cardiac contractile force Dromotrophic effect- speed of impulse transmission in the heart. Atrophy- a decrease in cell size due to a decrease in workload. Dysplasia- a change in cell size, shape, or appearance caused by an external stressor. Usually leads to cancer. o Electrolytes- these are electrolytes that effect cardiac function. Sodium (Na+)- plays a major role in depolarizing the myocardium. Calcium (Ca++)- takes part in myocardial depolarization and myocardial contraction. Potassium (K+)- influences repolarization. Magnesium (Mg++) Chloride (Cl-) Electrophysiologyo Intercalated discs- connect cardiac muscle fibers and conduct electrical impulses quickly from one muscle fiber to the next. o Syncytium- group of cardiac muscles that physiologically function as a unit. Atrial Syncytium- contracts from superior to inferior, so that the atria express blood to the syncytium contracts from superior to inferior, so that the atria express blood to the ventricles. Ventricular Syncytium- contracts from inferior to superior, expelling blood from the ventricles into the aorta and pulmonary arteries.

o Cardiac Depolarization- the change from the resting potential to a relatively more positive charge inside the cell, Contraction. Resting potential- the normal electrical state of cardiac cells. Action potential- the stimulation of myocardial cells, as evidenced by a change in the membrane electrical charge, that subsequently spreads across the myocardium. o Cardiac Repolarization- the return to normal resting state. Relaxation o Cardiac Conduction System- how the heart transmits electrical impulses across the heart. Cardiac Conductive Cells- are specialized conductive fibers that transmit the depolarization potential through the heart very quickly. Cardiac Conductive Cells Must have: Excitability- the cells can respond to an electrical stimulus. Conductivity- the cells can take the electrical impulse form cell to cell. Automaticity (self-excitation)- each cell can depolarize without any outside impulse. Contractility- the cells have the ability to contract. This is the Normal path that the Cardiac Conductive Cells transmit there impulses: 1. SA Node- Pacemaker of the heart, located atop the Right Atrium. It initiates an electrical impulse that initiates depolarization (contraction) across the heart. 2. Internodal Atrial Pathways- take the electrical impulse across the atrium and depolarize the Atria. Bachmans Bundle is located in the Left Atrium and leads to the Bundle of Kent. 3. AV Node- is located @ the middle of the heart were the atria meets the ventricles and in the middle of the Septum (separates the right from left sides of the heart). The AV node receives the electrical impulse from the atrium and pauses the electrical impulse for a moment (.04-.08sec), before delivering the impulse to the Ventricles. 4. Bundle of His- is the Internodal pathway leaving the AV node. The Bundle of His receives the electrical impulse form the AV node and delivers it to the Right and Left Bundle Branches. 5. Right and Left Bundle Branches- Are a super fast electrical highway that deliver there electrical impulse to the Purkinje fibers. 6. Purkinje fibers- send the electrical impulse to the Ventricular Muscle fibers to be depolarized (contracted). o Each conduction system component has its own intrinsic rate of excitation.

1. SA/Atrial rate- 60-100bpm 2. AV rate- 40-60bpm 3. Ventricle rate- 20-40bpm Electrocardiographic Monitoring Electrocardiogram (ECG/EKG)- the graphic recording of the hearts electrical activity. It may be displayed either on paper or on an oscilloscope. ECG Leads Bipolar (limb)- leads I, II, III Augmented (unipolar)- aVR, aVL, aVF Precordial- V1, V2, V3, V4, V5, V6 Einthovens Triangle- formed by leads I, II, III ECG Paper 1 small box = .04sec 1 large box = .20sec ECG Components P Wave- Atrial depolarization. QRS Complex- ventricular depolarization T Wave- ventricular repolarization U Wave- maybe associated w/ electrolyte abnormalities or may be normal. ECG Time Intervals w/normal ranges P-R Interval- .12 - .20sec QRS Interval- .08 - .12sec S-T Segment 1. Ischemia- lack of O2 2. Injury 3. Necrosis- cell death, infarction QT Interval- .33 - .42sec, prolonged QT interval .44< ECG Periods Refractory period- the period of time when myocardial cells have not yet completely repolarized and cannot be stimulated again. Absolute refractory period the period of the cardiac cycle when stimulation will not produce any depolarization whatsoever. Relative refractory period the period of the cardiac cycle when a sufficiently strong stimulus may produce depolarization Overview of ECG lead groupings Leads Portion of the heart examined I and aVL II, III, and aVF aVR V1 and V2 High Lateral left side of the heart in a vertical plane Inferior (diaphragmatic) side of the heart Right side of the heart in a vertical plane Septal wall/right ventricle

V3 and V4

Intraventricular septum and the Anterior wall of the left ventricle V5 and V6 Anterior and Low Lateral wall of the left ventricle INTERPRETATION OF RHYTHM STRIPS: Analyzing RATE six second method, count complexes in a six second interval and x by 10. Analyzing RHYTHM measure the R-R interval, is it constant or do they vary? Analyzing P Waves - are the P waves present?, regular?, do they look alike?, is there one P for each QRS?, are they upright or inverted Analyzing P-R interval normal 0.12-0.20 sec. any deviation is abnormal Analyzing QRS complex do they look alike? Normal is 0.04-0.12 any deviation is abnormal DYSRHYTHMIAS: Dysrhythmia any deviation from normal electrical rhythm of the heart Arrhythmia the absence of cardiac electrical activity BRADY 0-60bpm Normal 60-100bpm Tachy 100+ Causes of dysrhythmias: - MI, ischemia, necrosis - Autonomic nervous system imbalance - Distention of heart chambers ( especially in the atria, secondary to CHF) - Blood gas abnormalities, including hypoxia and abnormal pH - Electrolyte imbalance - Trauma to myocardium - Drug effects/toxicity - Electrocution - Hypothermia - CNS damages - Idiopathic events - Normal occurrences Ectopic Foci heart cells other than the pacemaker cells automatically depolarizing, producing ectopic beats (abnormal beats). PVCs and PACs are examples of ectopic beats. Reentry may cause isolated premature beats (tachydysrhythmias). It occurs when ischemia or another disease process alters two branches of a conduction pathway, slowing conduction in one branch and causing a unidirectional block in the other. DYSRHYTHMIAS ORIGINATING IN THE SA NODE Sinus Bradycardia- results from slowing of the SA node Etiology: may result from- increased parasympathetic tone, intrinsic disease of SA node, drug effects, normal in healthy athletes Rules of interpretation/lead II monitoring: Rate- less than 60 Rhythm- regular Pacemaker site- SA node P wave- upright and normal in morphology QRS complex- normal (0.04-0.12 sec)

Clinical significance: Decreased HR can cause decreased cardiac output, hypotension, angina, or CNS symptoms Treatment: Unnecessary unless hypotension or ventricular irritability is present. If tx. Is required, 0.5 mg bolus of atropine sulfate. Repeat every 35 min. until satisfactory rate or have given 0.04 mg/kg of the drug. If atropine fails consider transcutaneous cardiac pacing (TCP). Sinus Tachycardia- results from an increased rate of the SA node discharge Etiology: may result from: exercise, fever, anxiety, hypovolemia, anemia, pump failure, increased sympathetic tone, hypoxia, hyperthyroidism Rules of interpretation/lead II monitoring: o Rate- greater than 100 o Rhythm- regular o Pacemaker site- SA node o P wave- upright and normal in morphology o P-R interval- normal o QRS complex- normal Clinical significance: If <140 cardiac output may fall because ventricular filling time is inadequate. Treatment is directed at the underlying cause. Hypovolemia, fever, hypoxia, or other causes should be corrected. Sinus Dysrhythmia- often results from a variation of the R-R interval Etiology: often a normal finding and is sometimes related to the respiratory cycle and changes in intrathoracic pressure. Rules of interpretation/lead II monitoring: o Rate- 60-100 o Rhythm- irregular o Pacemaker site- SA node o P wave- upright and normal morphology o QRS complex- normal Clinical significance: normal, particularly in the young and the aged. Treatment: typically, none required Sinus Arrest- occurs when the sinus node fails to discharge, resulting in short periods of cardiac standstill Etiology: can result from: ischemia of SA node, digitalis toxicity, excessive vagal tone, degenerative fibrotic disease Rules of interpretation/lead II monitoring: Rate- normal to slow, depending on frequency and duration of the arrest Rhythm- irregular Pacemaker site- SA node P wave- upright and normal morphology P-R interval- normal QRS complex- normal Clinical significance: frequent episodes may result in syncope and other problems

Treatment: If pt. in extreme bradycardia or symptomatic, 0.5 mg bolus of atropine sulfate. Repeat every 3-5 min until satisfactory rate or 0.04 mg/kg of the drug. Consider TCP. DYSRHYTHMIAS ORIGINATING IN THE ATRIA Wandering Atrial Pacemaker- the passive transfer of pacemaker sites from the sinus node to other latent pacemaker sites in the atria and AV junction. Often more than one pacemaker site will present, causing variations in RR intervals and P wave morphology. Etiology: can result from: variant of sinus dysrhythmia, normal phenomenon in the very young or aged, ischemic heart disease, atrial dilation Rules of interpretation/lead II monitoring: Rate- usually normal Rhythm- slightly irregular Pacemaker site- varies among SA node, atrial tissue, and AV junction P wave- morphology changes from beat to beat, may disappear entirely P-R interval- varies,<0.12 sec, normal, or .0.20 sec. QRS complex- normal Clinical significance- usually no detrimental effects, can be a precursor of other atrial dysrhythmias such as a-fib. Treatment: asymptomatic=observation, symptomatic=consider adenosine or verapamil. Multifocal Atrial Tachycardia- seen in acutely ill pts, significant pulmonary disease is seen in about 60% of these pts. Etiology: can result from: pulmonary disease, metabolic disorders, ischemic heart disease, recent surgery Rules of interpretation/lead II monitoring: Rate- >100 Rhythm- irregular Pacemaker site- ectopic sites in atria P waves- organized, discrete nonsinus P waves with at least 3 different forms P-R intervals- varies QRS complex- may be < 0.12 sec, normal, > 0.20 sec, depending on AV nodes refractory status when impulse reaches it Clinical significance: frequently these pts are acutely ill, may indicate serious underlying illness. Treatment: tx of underlying illness usually resolves the dysrhythmia Premature Atrial Contractions- results from a single electrical impulse originating in the atria outside the SA node Etiology: can result from: use of caffeine/tobacco/alcohol, sympathomimetic drugs, ischemia heart disease, hypoxia, digitalis toxicity, idiopathic

Rules of interpretation/leads II monitoring: Rate- depends on underlying rhythm Rhythm- depends on underlying rhythm, usually regular except for the PAC Pacemaker site- ectopic focus in the atrium P wave- the P wave of the PAC differs from the P wave of the underlying rhythm. Occurs early or may be hidden P-R interval- usually normal QRS complex- usually normal Clinical significance: minimal significance. Frequent PACs may indicate organic heart disease Treatment: none, if symptomatic 02, IV Paroxysmal Supraventricular Tachycardia- (PSVT) occurs when rapid atrial depolarization overrides the SA node Etiology: may be precipitated by stress, overexertion, smoking or caffeine. Frequently associated with atherosclerotic cardiovascular disease and rheumatic heart disease. Rules of interpretation/lead II monitoring: Rate- 150-250 Rhythm- regular except at the onset and termination Pacemaker site- in the atria, outside the SA node P wave- is often buried in the preceding T wave, may be impossible to see P-R interval- usually normal, however can vary with the location of the pacemaker QRS complex- normal Clinical significance: pts often sense PSVT as palpitations. Rapid rates can cause a marked reduction in cardiac output Treatment: 1. vagal maneuvers. 2. Adenosine (Adenocard) 6 mg rapid IV bolus over 1-3 sec. If pt does not convert after 1-2 min. administer second bolus of 12 mg over 1-3 sec. If this fails and BP is normal, then look at width of QRS, if narrow medical direction may request verapamil 2.5-5.0 mg may be repeated once in 15-30 minutes if needed. Verapamil is contraindicated in hx of brady, hypotension, CHF. 3. Electrical therapy. If rate >150 or if pt is hemodynamically unstable. Use synchronized cardioversion. Sedate with 5-10 mg Valium (diazepam) or Versed (midazolam) Start at 100 joules repeat as per protocols. Atrial Flutter- results from a rapid atrial reentry circuit and an AV node that physiologically cannot conduct all impulses through to the ventricles. Etiology: may occur in normal hearts. Usually associated with organic disease. Atrial dilation, which occurs in CHF is a cause of atrial flutter Rules of interpretation/lead II monitoring: Rate- 250-350

Rhythm- atrial regular, ventricle regular, but can be irregular if the block is variable Pacemaker site- in the atria outside the SA node P wave- flutter waves are present, sawtooth or picket fence pattern P-R interval- usually constant but may vary QRS complex- normal Clinical significance: atrial flutter with normal ventricular rates generally well tolerated, rapid ventricular rates may compromise cardiac output and result in symptoms. Treatment: Synchronized cardioversion in unstable pts-those with rates >150 and associated chest pain, dyspnea, decreased level of consciousness, or hypotension. Drug therapy- diltiazem (Cardizem) Atrial Fibrillation- results from multiple areas of reentry within the atria or from multiple ectopic foci bombarding the AV node Etiology: may be chronic and is often associated with underlying heart disease such as rheumatic heart disease, atherosclerotic heart disease, CHF Rules of interpretation/lead II monitoring: Rate- 350-750 can not be counted Rhythm- irregularly irregular Pacemaker site- numerous ectopic foci in the atria P wave- none discernible P-R interval- none QRS complex- normal Clinical significance: the atria fails to contract and the so-called atrial kick is lost, reducing cardiac output 20-25% Treatment: same as a-flutter DYSRHYTHMIAS ORIGINATING WITHIN THE AV JUNCTION (AV BLOCKS) AV blocks- seen in lead II P-R Interval R-R Interval 1 > .20 sec 2 Type I varies varies 2Type II constant constant 3 varies constant First-Degree AV Block- is a delay in conduction at the level of the AV node rather than an actual block Etiology: can occur in a healthy heart. However, ischemia at the AV junction is the most common cause Rules of interpretation/lead II monitor: o Rate- depends on underlying rhythm o Rhythm- usually regular o Pacemaker site- SA node or atria o P wave- normal o P-R interval- >0.20 sec.

o QRS complex- usually < 0.12 sec Clinical significance: usually no danger in itself. May precede a more advanced block Treatment: no treatment, unless rate drops significantly Type I Second-Degree AV Block- an intermittent block at the level of the AV node Etiology: ischemia at the AV junction most common cause Rules of interpretation/lead II monitor: o Rate- atrial rate is unaffected, the ventricular rate may be normal or slowed o Rhythm- atrial is regular, ventricular is irregular because of the nonconducted beat o Pacemaker site- SA node or atria o P waves- normal, some P waves are not followed by QRS o P-R interval- becomes progressively longer until the QRS is dropped, the cycle then repeats. (P-R interval varies)(R-R interval varies) o QRS complex- usually < 0.12 sec Clinical significance: can cause syncope and angina. This block often occurs after an inferior wall MI Treatment: Avoid drugs that slow AV conduction (lidocaine, procainamide). If rate falls and pt. becomes symptomatic give 0.5 mg atropine IV, repeat every 3-5 min until obtained satisfactory rate or have given 0.04 mg/kg. If it fails consider TCP. Type II Second-Degree AV Block- an intermittent block characterized by P waves that are not conducted to the ventricles Etiology: usually associated with acute MI and septal necrosis Rules of interpretation/lead II monitor: Rate- Atrial rate is unaffected, ventricular rate is usually bradycardic Rhythm- regular or irregular depending upon whether the conduction ratio is constant or varied Pacemaker site- SA node or atria P wave- normal, some not followed by QRS P-R interval- constant for conducted beats, may be >0.12 sec. (P-R interval constant, R-R interval constant) QRS complex- may be normal, often > 0.12 sec Clinical significance: can compromise cardiac output causing syncope and angina. Treatment: Atropine will not work on these pts these pts need a pacemaker. (as per instructor) Third-Degree AV Block- complete block, the absence of conduction between the atria and the ventricles resulting from complete electrical block at or below the AV node.

Etiology: can result from acute MI, digitalis toxicity or degeneration of the conductive system as occurs in the elderly. Rules of interpretation/lead II monitor: Rate- Atrial rate is unaffected, ventricular rate 40-60 if the escape pacemaker is Junctional, < 40 if the escape pacemaker is lower in the vein. Rhythm- both Atrial and ventricular rhythms are usually regular Pacemaker site- SA node and AV junction or ventricle P wave- normal. They show no relationship to the QRS, often falling within the T wave and QRS. P-R interval- no relationship between the P and R waves. (P-R interval varies, R-R interval constant) QRS complex- > 0.12 sec. if pacemaker is ventricular; < 0.12 sec. if pacemaker is Junctional Clinical significance: can severely compromise cardiac output because of decreased heart rate and loss of coordination Atrial kick. Treatment: Atropine will not work. Give high flow O2 and put on TCP. DYSRHYTHMIAS SUSTAINED OR ORIGINATING IN THE AV JUNCTION Junctional rhythms usually progress to some other rhythm by the time we get to the patient. AV junction parameters: Inverted P wave P-R interval < 0.12 sec. Normal QRS complex duration DYSRHYTHMIAS ORIGINATING IN THE VENTRICLES Common ECG features: QRS complex > 0.12 sec. Absent P waves Types: Ventricular escape complexes and rhythms (p 1263) Accelerated idioventricular rhythm (p 1263) Premature Ventricular Contraction- (PVC) a single ectopic impulse arising from an irritable focus in either ventricle that occurs earlier than the next expected beat. PVCs occur in patterns: Bigeminy-every other beat is a PVC, Trigeminy-every third beat is a PCV, Quadrigeminy-every fourth is a PVC. Repetitive PVCs are two consecutive PVCs without a normal complex in between. Etiology: myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic, acid-base disturbance, electrolyte imbalances, normal variant. Rules of interpretation/lead II monitor: o Rate- depends on underlying rhythm and rate of PVCs o Rhythm- interrupts regularity of underlying rhythm; occasionally irregular o Pacemaker site- ventricle o P wave- none; however, a normal sinus P wave sometimes appears before a PVC. o P-R interval- none

o QRS complex- > 0.12 sec and bizarre in morphology Clinical significance: Pts often sense PVCs as skipped beats. PVCs are classified as malignant or benign. Treatment: If no hx of cardiac disease and no symptoms then no treatment needed. If pt has a prior hx of cardiac disease or has symptoms then O2 and IV line. May use lidocaine 1.0-1.5 mg/kg. give additional lidocaine bolus of 0.5-0.75 mg/kg every 5-10 min. if necessary, until total of 3.0 mg/kg. Venticular Tachycardia- consists of three or more ventricular complexes in succession at a rate of 100 beats per minute or more. Etiology: myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic, acid-base disturbances, electrolyte imbalances Rules of interpretation/lead II monitor: o Rate- 100-125 o Rhythm- usually regular, can be slightly irregular o Pacemaker site- ventricle o P wave- if present not associated with the QRS complex. (usually no P wave) o P-R interval- none o QRS complex- > 0.12 sec. and bizarre in morphology Clinical significance: usually results in poor stroke volume, which, coupled with the rapid ventriular rate, may severely compromise cardiac output and coronary artery profusion. Treatment: If pt is perfusing, as evidenced by the presence of a pulse, administer O2, IV. Lidocaine 1.0-1.5 mg/kg. Additional dose 0.5-0.75 mg/kg until total of 3.0 mg/kg. If this fails give procainamide 20-30 mg/min to max of 17 mg/kg. If this fails consider amiodarone (Cordarone) 150-300 mg IV. Use synchronized cardioversion if pt becomes unstable, as evidenced by chest pain, dyspnea, or systolic BP < 90 mm/kg. Torsade de Pointes- is a polymorphic ventricular tachycardia that differs in appearance and cause from V-tach in general. Commonly caused by the use of certain antidysrhythmic drugs, quinidine (Quinidex), procainamide (Pronestyl), disopyramide (Norpace), flecanide (Tambocor), sotolol (Betapace), and amiodarone (Cordarone). The morphology of the QRS varies from beat to beat (hence the term torsade de pointes, twisting on a point). The QRS complexes are wide and change in size over the span of several complexes. Attempting treatment of torsade de pointes with antidysrhythmic usually used for Vtach can have disastrous consequences. Treatment is 1-2 grams of magnesium sulfate placed in 100 ml of D5W and administered over 1-2 minutes. Ventricular Fibrillation- a chaotic ventricular rhythm usually resulting from the presence of many reentry circuits within the ventricles. Etiology: results from advanced coronary artery disease. Rules of interpretation/lead II monitor:

o Rate- no organized rhythm o Rhythm- no organized rhythm o Pacemaker site- numerous ectopic foci throughout the ventricles o P wave- usually absent o P-R interval- absent o QRS complex- absent Clinical significance: a lethal dysrhythmia, cardiac arrest Treatment: CPR-shock-meds (protocol) Asystole- absence of all cardiac electrical activity Etiology: MI, ischemia, necrosis Rules of interpretation/lead II monitor: o Rate- no electrical activity o Rhythm- no electrical activity o Pacemaker site- no electrical activity o P wave- absent o P-R interval- absent o QRS complex- absent Clinical significance: cardiac arrest Treatment: CPR, airway, O2, meds. If in any doubt about rhythm- attempt defibrillation. Artificial Pacemaker Rhythm- patients with implanted pacemaker. Usually placed in the right ventricle, but can be anywhere in the heart. Rules of interpretation/lead II monitor: o Rate-depends on pacemaker o Rhythm- regular if pacing constantly, irregular if pacing on demand o P wave- none produced by ventricular pacemakers. o P-R interval- varies o QRS complex- associated with pacemaker are usually > 0.12 sec. and bizarre in morphology. Problems with pacemakers: run away- results in a rapid discharge rate. Demand pacemakers can fail to shut down. Considerations for management: Treat bradydysrhythmias, asystole, and V-fib from pacemaker failure as in any other patient. May need defibrillation or external pacing Pulseless Electrical Activity- electrical complexes are present, but with no accompanying mechanical contractions of the heart. Causes of PEA: hypovolemia, cardiac tamponade, tension pneumothorax, hypoxemia, acidosis, massive pulmonary embolism, ventricular wall rupture. Treatment: use PEA with PEA patients (Pacing, Epi, Atropine) Aberrant conduction- is a single supraventricular beat conducted through the ventricles in a delayed manner.

Bundle branch block- is a disorder in which all Supraventricular beats are conducted through the ventricles in a delayed manner. Wolff-Parkinson-White syndrome- a reentry problem. Short P-R interval (<0.12 sec), long QRS duration (> 0.12 sec)