What are the components of the cardiac conduction system?
- Sinoatrial (SA) node
- Atrioventricular (AV) junctional area
- Bundle branch system
What is the sinoatrial (SA) node?
- 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
What is the atrioventricular (AV) junctional area?
- 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
What is the bundle of His?
- 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
What are the Purkinjie fibers?
- 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
What are the valves of the heart?
- Atrioventricular valve
- Tricuspid valve
- Mitral valve
- Semilunar valve
- Pulmonic valve
- Aortic Valve
What is the atrioventricular valve?
- Separates atria from the ventricles
- Control blood flow btwn atria and ventricles
What is the tricuspid valve?
- Located btwn the right atrium and the right ventricle
- Has three leaflets
What is the mitral valve?
- Located bten the left atrium and left ventricle
- Has two leaflets
What are the leaflets of the AV valves?
- Connected to the papillary muscles by the chordae tendinae to prevent backflow
- S1, the first heart sound, is heard when AV valves close
What are the semilunar valves?
- 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
What is the pulmonic valve?
- Located btwn the right ventricle and the pulmonic artery
- Unoxygenated blood flows through this valve to the lungs
What is the aortic valve?
- 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
Right heart circulation- deoxygenated blood
Venous syatem -> right atrium -> right ventricle -> lungs for oxygenation via pulmonary artery
Left heart circulation- oxygenated blood
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
Right coronary artery
- R atrium, R ventricle, inferior L ventricle, posterior septum, SA node
Left coronary artery
- 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
Coronary vessel blood flow
- 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
What is the P wave?
A deflection representing atrial depolarization
What is the PR segment?
- 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
What is the PR interval?
- 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)
what is the QRS complex?
- 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
What is the QRS duration?
- 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)
What is the ST segment?
- 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
What is the T wave?
- 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
What is the U wave?
- 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
What is the QT interval?
- 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
What is artifact?
- 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
ECG rhythm analysis
- Determine heart rate
- Determine heart rhythm
- Analyze P waves
- Measure PR interval
- Measure QRS duration
- Interpret the rhythm
- Normal sinus rhythm (NSR)
- Sinus arrythmia
What is NSR?
- 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
What is sinus arrhythmia?
- 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
What are dysrhythmias?
- 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
What are tachydysrhythmias?
- 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
What are bradydysrhythmias?
- 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
What are premature complexes?
- 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
What is bigeminy?
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
What is trigeminy?
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
What is quadrigeminy?
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
What are escape complexes/rhythms?
- 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
Classification of dysrhythmias?
- 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
What is sinus tachycardia?
- 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
What is sinus bradycardia?
- 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
What is an atrial dysrhythmia?
- 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
What are premature atrial complexes?
- 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
What is supraventricular tachycardia?
- 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
What is atrial fibrillation?
- 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
What is atrial flutter?
- 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
What are junctional dysrhythmias?
- 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
What are ventricular dysrhythmias?
- 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