cardiac

• Sinoatrial (SA) node
• Atrioventricular (AV) junctional area
• Bundle branch system

• Natural pacemaker
• Located close to the surface of the right atrium near its junction with superior vena cava
• Primary pacemaker
• Rate 60-100 bpm
• Has greatest degree of automaticity
• Impulses move directly through atrial muscle and lead to atrial depolarization, which is reflected in a P wave on a ECG

• Consists of a transitional cell zone, the AV node, and the bundle of His
• Lies just beneath the R atrial endocardium, btwn the tricuspid valve and the ostium of the coronary sinus
• T-cells cause impulses to slow down or be delayed in the AV node before proceeding to the ventricles
• Delay is reflected in the PR segment on the ECG
• The slow conduction allows the atria to contract and the ventricles to fill
• Contraction is known as "atrial kick" and contributes to additional blood volume for a greater CO

• Connects with the distal portion of the AV node and continues through intraventricular septum
• Extends as a right bundle branch down the right side of intraventricular septum to the apex of the right ventricle
• On the left side, it extends as a left bundle branch, which further divides

• At ends of both R and L bundle branch systems are the Purkinjie fibers
• Interweaving network located on the endocardial surface of both ventricles, from apex to base
• Fibers then partially penetrate into the myocardium
• Makes up the bundle of Hiis, bundle branches and terminal Purkinjie fibers
• Responsible for rapid conduction of electrical impulses throughut the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction
• When SA and AV nodes fail, can initiate impulses at a rate of 20-40 bpm

• Atrioventricular valve
• Tricuspid valve
• Mitral valve
• Semilunar valve
• Pulmonic valve
• Aortic Valve

• Separates atria from the ventricles
• Control blood flow btwn atria and ventricles

• Located btwn the right atrium and the right ventricle
• Has three leaflets

• Located bten the left atrium and left ventricle
• Has two leaflets

• Connected to the papillary muscles by the chordae tendinae to prevent backflow
• S₁, the first heart sound, is heard when AV valves close

• Pulmonic valve
• Aortic valve
• Separate the cardiac chambers from the great vessels
• Control blood flow out of the cardiac chambers
• Each valve has three cusps that prevent backflow
• S₂, the second heart sound, is heard when the semilunar valves close

• Located btwn the right ventricle and the pulmonic artery
• Unoxygenated blood flows through this valve to the lungs

• Located btwn the left ventricle and the aorta
• Oxygenated blood is pumped from the heart through this valve into systemic circulation

• Blood flows from the body into the R atrium and from the lungs into the L atrium
• With atrial contraction, the blood is pumped from the atria into the ventricles
• With ventricular contraction, the blood is pumped from the R ventricle into the pulmonary artery and lungs, and from the L ventricle into the aorta and the arterial circulation

Venous syatem -> right atrium -> right ventricle -> lungs for oxygenation via pulmonary artery

Lungs via pulmonary veins -> left atrium -> left ventricle -> aorta -> systemic circulation for tissue perfusion

• Right main coronary artery
• Left main coronary artery
• 2 main branches-
• Circumflex coronary artery
• Left anterior descending coronary artery

• Supplies:
• R atrium, R ventricle, inferior L ventricle, posterior septum, SA node

• 2 main branches
• LAD: descends toward anterior wall and apex of L ventricle, supplies portions of L ventricle, ventricular septum, chordae tendinae, papillary muscle, to lesser extent R ventricle
• Circumflex: descends toward lateral wall of L ventricle and apex, supplies L atria, lateral and posterior surfaces of L ventricle, sometimes portions of intraventricular septum

• 75% of coronary blood flow occurs during diastole
• Need diastolic pressure of 60 to maintain adequate flow to the heart muscle
• Flow increases with activity and sympathetic stimulation

A deflection representing atrial depolarization

• The isoelectric line from the end of the P wave to the beginning of the QRS complex, when the impulse is traveling through the AV node, where it is delayed
• It then travels through the ventricular conduction system to the Purkinjie fibers

• Measured from the beginning of the P wave to the end of the PR segment
• Represents the time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to the Purkinjie fibers
• Normally measures from 0.12 to 0.20 sec (5 small blocks)

• Represents ventricular depolarization
• Q wave is the first negative deflection
• It's small and it represents septal depolarization
• When Q wave is abnormally present it represents myocardial necrosis (cell death)
• The R wave is the first positive deflection-may be small, large, or absent
• The S wave is a negative deflection following the R wave

• Represents the time required for depolarization of both ventricles
• Measured from the beginning of QRS complex to the J point (the junction where the QRS complex ends and the ST segment begins)
• Normally measures from 0.04-0.10 sec (up to three small blocks)

• Normally an isoelectric line and represents early ventricular repolarization
• Occurs from the J point to the beginning of the T wave
• Length varies with changes in HR, administration of meds, and electrolyte disturbances
• Normally not elevated more than 1mm or depressed more than 0.5mm from baseline
• Its amplitude is measured at a point 1.5 - 2mm after the J point
• ST elevation or depression can be caused by myocardial injury, ischemia or infarction, conduction abnormalities, or the administration of meds

• Follows the ST segment and represents ventricular repolarization
• Usually positive, rounded, and slightly asymmetric
• If an ectopic stimulus excites the ventricles it may cause ventricular irritability, lethal dysrhythmias, possible cardiac arrest in the vulnerable heart-known as the R-on-T phenomenon
• Waves may become tall and peaked, inverted (negative), or flat as a result of myocardial ischemia, potassium or calcium imbalances, meds, or ANS effects

• When present, follows the T wave and may result from slow repolarization of ventricular Purkinjie fibers
• Of the same polarity as the T wave, although it is generally smaller
• Abnormal wave may suggest an electrolyte abnormality (particularly hypokalemia) or other disturbance
• Correct ID is important so that it is not mistaken for a P wave

• Represents the total time required for ventricular depolarization and repolarization
• Is meaured from the beginning of the QRS complex to the end of the T wave
• Interval varies with age, gender, and changes in HR, lengthening with slower HR and shortening with faster rates
• May be prolonged by certain meds, electrolyte disturbences, Prinzmetal's angina, or subarachnoid hemorrhage
• Prolonged QT may lead to unique type of ventricular tachycardia called torsades de pointes

• Interference seen on the monitor or rhythm strip, which may look like a wandering or fuzzy baseline
• May be caused by pt mvmnt, loose or defective electrodes, improper grounding, faulty ECG equip, such as broken wires or cables
• Some artifact can mimic lethal dysrhythmias like v tach or v fib
• Assess pt to differentiate artifact from lethal rhythms

• Determine heart rate
• Determine heart rhythm
• Analyze P waves
• Measure PR interval
• Measure QRS duration
• Interpret the rhythm

• Normal sinus rhythm (NSR)
• Sinus arrythmia

• Rate: a/v rates of 60-100bpm
• Rhythm: a/v rhythms regular
• P waves: present, consistent configuration, one P wave before each QRS complex
• PR interval: 0.12-0.20 sec and constant
• QRS duration: 0.04-0.10 sec and constant

• Variant of NSR
• All the characteristics of NSR except for its irregularity
• Rate: a/v rates btwn 60-100bpm
• Rhythm: a/v rhythms are irregular, with shortest PP or RR interval varying at least 0.12sec from the longest PP or RR interval
• P waves: one P wave before ea QRS complex, consistent configuration
• PR interval: normal, constant
• QRS duration: normal, constant

• Any disorder of the heartbeat
• Result from:
• A disturbance in the relationship btwn electrical conductivity and the mechanical response of the myocardium
• A disturbance in impulse formation (either from an abnormal rate or from an ectopic focus)
• A disturbance in impulse conduction (delays and blocks)
• The combination of several mechanisms

• HR > 100bpm
• Major concern in adult pt with coronary artery disease (CAD)
• Coronary artery blood flow occurs mostly during diastole when the aortic valve is closed and is determined by diastolic time and BP in the root of the aorta
• They shorten the time and therefore the coronary perfusion time (the amount of time available for blood to flow through the coronary arteries to the myocardium)
• Initially increases CO and BP; however, a continued rise in HR decreases the ventricular filling time because of a shortened diiastole , decreasing the stroke volume. Consequently, CO and BP will begin to decrease, reducing aortic pressure and therefore coronary perfusion pressure
• Increase the work of the heart, increasing myocardial oxygen demand
• Pt may have: palpitations, chest discomfort, restlessness/anxiety, pale/cool skin, syncope from hypotension
• This may lead to heart failure
• Presenting symptoms are: dyspnea, lung crackles, distended neck veins, fatigue, and weakness

• HR < 60bpm
• Myocardial oxygen demand is reduced from the slow HR, which can be beneficial
• Coronary perfusion time may be adequate because of prolonged diastole, which is desireable
• Coronary perfusion pressure may decrease if HR is too slow to provide adequate CO and BP; this is a serious consequence
• Pt may tolerate this well if BP is adequate
• If BP not adequate, symptomatic bradydysrhythmias may lead to myocardial ischemia or infarction, dysrhythmias, hypotension, and HF

• Early rhythm complexes
• Occur when cardiac cell/cell group, other than SA node, becomes irritable and fires an impulse before the next sinus impulse is produced
• The ectopic focus (abnormal focus) may be generated by atrial, junctional, or ventricular tissue
• After the premature complex,there is a pause prior to the next normal complex, creating an irregularity in the rhythm
• Pt may/may not feel palpitations or a skipping of the heartbeat
• If premature complexes, esp ventricular, become more frequent, the pt may experience symptoms of decreased CO

When normal complexes and premature complexes occur alternately in a repetitive two-beat pattern, with a pause after each premature complex so that complexes occur in pairs

A repeated thee-beat pattern, usually occuring as two sequential normal complexes followed by a premature complex and a pause, with same pattern repeating itself in triplets

A repeated four-beat pattern, usually occuring as three sequential normal complexes followed by a premature complex and a pause, with same pattern repeating itself in a four-beat pattern

• Occur when SA node fails to discharge or is blocked or when a sinus impulse fails to depolarize the ventricles because of an AV nodal block
• Serve as secondary or escape pacemaker and are seen just after a pause
• May originate from AV junctional or ventricular tissue
• They stop when the SA or AV node can function normally
• If pauses are followed by escape beats or rhythms, pts may feel light-headed, dizzy, or faint during the pause

• Classified according to site of origin
• Sites include SA node, atrial tissue, AV node, junctional tissue, and ventricular tissue
• May be caused by a disturbance in impulse formation or by conduction delays or blocks

• SNS stimulation or vagal inhibition results in an increased rate of SA node discharge, which increases HR
• SA node discharge > 100bpm
• Sinus tach initially increases CO and BP
• Continued increases in HR decrease cardiac perfusion time, diastlic filling time, and coronary perfusion pressure while increasing myocardial oxygen demand
• Drugs such as catecholamines, atropine, caffeine, alcohol, nicotine, aminophylline, and thyroid meds may increase HR
• Sinus tach may be a compensatory response to decreased CO or BP as occurs with hypovolemic shock, MI, infection, and HF
• Assess for fatigue, weakness, SOB, orthopnea, neck vein distention, decreased oxygen saturation, and
• decreased BP
• Assess for restlessness and anxiety from decreased cerebral perfusion
• Assess for decreased urine output from impaired renal perfusion
• ECG pattern may show T-wave inversion or ST-segment elevation or depression in response to myocardial ischemia

• Excessive vagal stimulation (PNS) to heart causes decreased rate of sinus node discharge
• This stimulus slows HR and decreases speed of conduction through heart
• Sinus node discharge < 60bpm
• Increases coronary perfusion timeMay decrease coronary perrfusion pressure
• Myocardial oxygen demand is decreased
• Excessive vagal stimulation may result from carotid sinus massage, vomiting, suctioning, valsalva maneuvers, occular pressure, or pain
• Sinus brady may also result from hypoxia, inferior wall MI, admin of drugs such as beta-blockers, calcium channel blockers, and digitalis
• Assess pt for syncope, dizziness/weakness, confusion, hypotension, diaphoresis, SOB, ventricular ectopy (superficial beats), anginal pain

• The focus of impulse generation shifts away from the sinus node to the atrial tissue, which acts as an ectopic pacemaker for one or more beats
• The shift changes the direction of atrial depolarization, resulting in a P wave shape that differs from normal P waves
• Most common are premature atrial complexes, supraventricular tachycardia, atrial flutter, and atrial fibrillation

• Occurs when atrial tissue becomes irritable
• This ectopic focus fires an impulse before the next sinus impulse is due
• The premature P wave may not always be visible because it can be hidden in the preceeding T wave
• A PAC is usually followed by a pause
• Causes of atrial irritability iclude stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, drugs such as catecholamines, sympathomimetics, amphetamines, digitalis, or anesthetic agents
• PACs can also result from myocardial ischemia, hypermetabolic states, electrolyte imbalance or atrial stretch

• Involves rapid stimulation of atrial tissue at a rate of 100-280bpm
• P waves may not be visible because they are imbedded in the preceeding T wave
• Usually due to a re-entry mechanism in which one impulse circulates repeatedly throughout the atrial pathway, restimulating the atrial tissue at a rapid rate
• Assess for palpitations, CP, weakness, fatigue, SOB, nervousness, anxiety, hypotension, syncope
• Cardiovascular deterioration may occur if the rate does not sustain adequate BP

• The most common dysrhythmia
• Multiple rapid impulses from many atrail foci depolarize the atria in a totally disorganized manner at a rate of 350-600 times per minute
• Results in a chaotic rhythm with no clear P waves, no atrial contractions, loss of atrial kick, and an irregular ventricular response
• Often the ventricles beat with a rapid rate in response to the num,erous atrial impulses
• Heart dilation and blood pooling in the atria can lead to thrombus formation
• Rapid and irregular ventricular rate decreases ventricular filling and reduces CO, futher impairing the heart's perfusion ability
• Because of loss of atrial kick, pt is at greater risk fo inadequate CO
• Assess pt for fatigue, weakness, SOB, distended neck veins, dizziness, decreased exercise tolerance, anxiety, syncope, palpitations, chest discomfort/pain, hypotension

• Rapid atrial depolarization occuring at a rate of 250-350 times per min
• The AV node blocks the number of impulses that reach the ventricles as a protective mechanism
• May be caused by rheumatic or ischemic heart disease, HF, AV valve disease, pre-excitation syndromes, septal defects, pulmonary emboli, thyrotoxicosis, alcoholism, or pericarditis
• Assess pt for palpitations, weakness, fatigue, SOB, nervousness, anxiety, syncope, angina, evidence of HF, shock

• Nodal cells in the AV junctional area can generate electrical impulses and are therefore secondary or latent pacemaker cells
• Hane a slower rate of dicscharge, usually 40 to 60bpm, and are usually suppressed
• Rhythms are most commonly temporary, and pts usually remain stable

• Ventricles have the fewest nodal cells and are the slowest pacemaker
• Irritable ventricular cells may generate electrical impulses and fire prematurely
• The impulse originates in and depolarizes one ventricle first and then spreads to depolarize the other, the resulting QRS complex is wide, measuring > 0.12sec