NHA EKG Technician (CET) — All Questions

What is the inherent firing rate of the sinoatrial node in a healthy adult?

• a.20 to 40 beats per minute
• b.100 to 150 beats per minute
• c.60 to 100 beats per minute✓
• d.40 to 60 beats per minute

The SA node in the upper right atrium is the heart's primary pacemaker and fires 60 to 100 times per minute, which is why normal sinus rhythm is defined by that range. The AV junction fires at 40 to 60 as a backup, and the Purkinje network fires at 20 to 40 as the last resort. A rate of 100 to 150 is a tachycardia, not an inherent pacemaker rate.

A patient's SA node fails completely. Which structure normally takes over, and at what rate?

• a.The bundle branches at 100 to 120 beats per minute
• b.The atrial muscle at 20 to 40 beats per minute
• c.The AV junction at 40 to 60 beats per minute✓
• d.The Purkinje fibers at 60 to 100 beats per minute

The AV junction is the secondary pacemaker and assumes control at 40 to 60 beats per minute when the SA node fails, producing a junctional escape rhythm with absent or inverted P waves. The Purkinje network fires only at 20 to 40 and takes over if the junction also fails. Bundle branches conduct rather than pace at a fast rate, and general atrial muscle is not a designated escape pacemaker.

What is the inherent rate of the Purkinje fibers, and what does a rhythm at that rate look like?

• a.40 to 60 beats per minute with inverted P waves
• b.20 to 40 beats per minute with wide QRS and no P waves✓
• c.100 to 150 beats per minute with sawtooth waves
• d.60 to 100 beats per minute with narrow complexes

The Purkinje network is the heart's pacemaker of last resort at 20 to 40 beats per minute, and because the impulse starts below the AV junction it spreads slowly through muscle, giving a wide QRS with no P wave in front of it. The 40 to 60 range with inverted P waves describes a junctional escape rhythm, one level higher in the conduction system. The 60 to 100 range with narrow complexes belongs to the SA node, and sawtooth waves indicate atrial flutter rather than any escape pacemaker.

What is the correct order of the cardiac electrical conduction pathway?

• a.SA node, bundle of His, AV node, Purkinje fibers, bundle branches
• b.AV node, SA node, Purkinje fibers, bundle of His, bundle branches
• c.SA node, AV node, bundle of His, right and left bundle branches, Purkinje fibers✓
• d.Purkinje fibers, bundle branches, bundle of His, AV node, SA node

The impulse begins in the SA node, spreads across the atria to the AV node, passes through the bundle of His, splits into the right and left bundle branches, and ends in the Purkinje fibers that depolarize the ventricular muscle. Any sequence that starts at the AV node or the Purkinje fibers reverses normal physiology, and the bundle of His always lies below the AV node, never above it.

Why does the impulse pause briefly at the AV node, and how does that pause appear on the EKG?

• a.To let the atria finish emptying; it is the flat part of the PR interval✓
• b.To let the coronary arteries fill before contraction; it is the ST segment
• c.To let the ventricles repolarize completely; it is seen as the T wave
• d.To slow the SA node so that it cannot fire too quickly; it is the TP segment

The AV node delays the impulse about a tenth of a second so the atria can complete their contraction and top off ventricular filling before the ventricles fire, and that delay is the flat portion of the PR interval between the end of the P wave and the start of the QRS. The T wave represents ventricular repolarization, which happens after the ventricles have already contracted. The ST segment sits between ventricular depolarization and repolarization, and the AV node does not regulate the rate of the SA node.

What is depolarization?

• a.The closing of the atrioventricular valves in systole
• b.Electrical discharge of the cardiac cells before contraction✓
• c.The filling of the coronary arteries in diastole
• d.The relaxation of cardiac muscle as it returns to rest

Depolarization is the rapid electrical change across the cell membrane that triggers mechanical contraction, and it produces the P wave in the atria and the QRS complex in the ventricles. Electrical recovery and relaxation are repolarization, which is the opposite half of the cycle. Coronary filling and valve closure are mechanical events of the cardiac cycle, and an EKG does not record either of them.

A student asks why an EKG can look normal in a patient whose heart is not pumping effectively. What is the best explanation?

• a.The EKG measures blood pressure rather than electrical activity
• b.EKG machines are frequently inaccurate when cardiac output is low
• c.Electrical activity can occur without effective contraction✓
• d.The EKG records only atrial activity and not ventricular output

An EKG records only the electrical events of the heart, so an organized rhythm can appear on the monitor while the heart produces no pulse, a situation called pulseless electrical activity. This is exactly why the technician confirms the patient's condition rather than treating the monitor. The machine is not measuring pressure or output at all, so it is not a question of accuracy, and the tracing records both atrial and ventricular electrical activity.

What is the correct path of blood through the heart, starting with deoxygenated blood returning from the body?

• a.Right atrium, mitral valve, right ventricle, aorta, lungs, left atrium, tricuspid valve, left ventricle
• b.Right ventricle, right atrium, lungs, left ventricle, left atrium, aorta
• c.Right atrium, tricuspid valve, right ventricle, pulmonic valve, lungs, left atrium, mitral valve, left ventricle, aorta✓
• d.Left atrium, mitral valve, left ventricle, lungs, right atrium, tricuspid valve, right ventricle, aorta

Deoxygenated blood enters the right atrium from the venae cavae, passes the tricuspid valve into the right ventricle, leaves through the pulmonic valve to the lungs, returns oxygenated to the left atrium, crosses the mitral valve into the left ventricle, and exits through the aortic valve to the body. The mitral valve is always on the left and the tricuspid on the right, and blood always flows atrium to ventricle, never the reverse.

Which valve separates the right atrium from the right ventricle?

• a.Aortic valve
• b.Pulmonic valve
• c.Tricuspid valve✓
• d.Mitral valve

The tricuspid valve, named for its three cusps, lies between the right atrium and right ventricle and prevents backflow during ventricular systole. The mitral valve is the corresponding atrioventricular valve on the left side. The pulmonic and aortic valves are semilunar valves that guard the exits from the right and left ventricles.

When does blood flow into the coronary arteries to supply the heart muscle itself?

• a.During ventricular diastole, when the muscle is relaxed✓
• b.Only during atrial contraction, in late diastole
• c.During ventricular systole, when pressure is highest
• d.Continuously and equally through the cardiac cycle

The coronary arteries branch from the base of the aorta and fill mainly during diastole, because during systole the contracting myocardium squeezes the vessels running through it. This is one reason very fast heart rates, which shorten diastole most, can provoke ischemia. Atrial contraction contributes to ventricular filling rather than coronary perfusion, and coronary flow is distinctly phasic rather than constant.

How is cardiac output calculated?

• a.Heart rate divided by stroke volume
• b.Heart rate multiplied by stroke volume✓
• c.Stroke volume multiplied by blood pressure
• d.Systolic pressure minus diastolic pressure

Cardiac output equals heart rate times stroke volume, the amount of blood ejected by the left ventricle each beat, and it is normally about 4 to 8 liters per minute in an adult. Subtracting diastolic from systolic pressure gives pulse pressure. Dividing rate by stroke volume or multiplying stroke volume by blood pressure produces no meaningful physiologic measurement.

What happens during ventricular diastole?

• a.Blood is forced into the aorta and pulmonary artery
• b.The atrioventricular valves snap shut
• c.The ventricles relax and fill with blood✓
• d.The ventricles contract and eject blood

Diastole is the relaxation and filling phase, during which the atrioventricular valves are open and blood flows from the atria into the ventricles. Contraction and ejection define systole. The atrioventricular valves close at the start of systole, and blood enters the great vessels only when the ventricles contract.

A patient arrives with crushing chest pain radiating to the left jaw. The 12-lead shows ST segment elevation in leads II, III, and aVF. What does this pattern most likely represent?

• a.Benign early repolarization in a young adult
• b.Acute pericarditis with diffuse ST elevation
• c.Acute infarction of the inferior wall✓
• d.Left atrial enlargement with a notched P

ST segment elevation confined to a group of anatomically related leads is the classic sign of acute myocardial injury, and leads II, III, and aVF all look at the inferior wall of the left ventricle. Pericarditis is the answer worth taking seriously, because it also elevates the ST segment, but it typically does so diffusely across leads from several different territories rather than in one region. The technician does not diagnose either one, but must recognize the pattern and notify the nurse or physician immediately. Atrial enlargement changes the P wave rather than the ST segment.

How does stable angina differ from a myocardial infarction?

• a.Angina causes permanent muscle death, while an infarction is reversible
• b.Angina occurs only at rest, while an infarction occurs with exertion
• c.Angina shows ST elevation, while an infarction shows ST depression
• d.Angina is reversible ischemia; an infarction kills muscle✓

Angina is chest pain from a temporary oxygen shortage in the myocardium, typically brought on by exertion and relieved within minutes by rest or nitroglycerin, and it may show transient ST depression or T wave inversion. A myocardial infarction is a sustained occlusion that kills muscle tissue and often produces ST elevation and, later, pathologic Q waves. The answers that reverse the two have the relationship backward: it is the infarction that causes permanent damage, and it is stable angina, not infarction, that is predictably provoked by exertion.

A patient scheduled for an EKG has ankle swelling, shortness of breath when lying flat, and a history of congestive heart failure. What is happening physiologically?

• a.The SA node has stopped firing and an escape rhythm has taken over
• b.The conduction system has been interrupted below the AV node
• c.The heart cannot pump well, so blood backs up behind it✓
• d.The coronary arteries are completely blocked by a fresh clot

In congestive heart failure the weakened ventricle cannot move the volume delivered to it, so fluid backs up behind the failing side, producing pulmonary congestion and orthopnea on the left and dependent edema on the right. Complete coronary occlusion describes an acute infarction, which presents with pain over minutes to hours rather than chronic swelling. SA node failure produces an escape rhythm, and a conduction block changes the rhythm without by itself causing fluid overload.

Long-standing untreated hypertension most commonly produces which EKG-related change?

• a.Absent P waves with an irregularly irregular ventricular response
• b.Pacemaker spikes in front of every QRS complex on the tracing
• c.A QT interval shortened to less than 0.20 second at any rate
• d.Left ventricular hypertrophy with tall left-sided R waves✓

Chronic high blood pressure forces the left ventricle to work against increased resistance, so the muscle thickens and generates larger voltage, appearing as tall R waves in the left-sided leads and deep S waves in V1 and V2. Atrial fibrillation is a genuine long-term complication of hypertension, but absent P waves are not the change hypertension most commonly produces, and the question asks for the usual finding. A QT under 0.20 second is not a hypertensive finding, and pacemaker spikes come from an implanted device.

Which layer of the heart wall is the thick muscular layer responsible for contraction?

• a.Myocardium✓
• b.Epicardium
• c.Pericardium
• d.Endocardium

The myocardium is the middle, muscular layer whose contraction generates the pumping force, and it is the tissue damaged in a myocardial infarction. The endocardium is the thin inner lining in contact with the blood. The epicardium is the outer surface layer of the heart, and the pericardium is the surrounding sac.

Why is the left ventricle the thickest chamber of the heart?

• a.It must generate the pressure for the entire systemic circuit✓
• b.It holds a much larger volume of blood than the other chambers
• c.It houses the SA node and needs extra muscle for protection
• d.It receives all of the blood returning through the venae cavae

The left ventricle pumps against the high resistance of the systemic circuit, so its wall is roughly three times thicker than the right ventricle, which only has to move blood to the nearby low-pressure lungs. Both ventricles eject about the same volume with each beat, so chamber volume is not the reason for the difference. The SA node sits in the right atrium, and the venae cavae empty into the right atrium as well.

Which layer of the heart wall is continuous with the visceral layer of the pericardium?

• a.The endocardium, the smooth inner lining of the chambers
• b.The parietal pericardium, the sac's outer serous layer
• c.The fibrous pericardium, anchored to the diaphragm
• d.The epicardium, the outer layer of the heart wall✓

The visceral layer of the serous pericardium lies directly on the surface of the heart, and that same sheet is the epicardium, the outermost of the three heart wall layers. The endocardium is at the opposite end of the wall, lining the chambers and valves on the inside. The parietal serous layer is the sheet that faces the epicardium across the pericardial space rather than being part of the heart wall. The fibrous pericardium is the tough outer sac that anchors to the diaphragm and great vessels and is not a heart wall layer at all.

Depolarization leaving the sinoatrial node reaches the left atrium chiefly by way of which structure?

• a.Bachmann's bundle, an interatrial conduction tract✓
• b.The two divisions of the bundle of His
• c.The anterior internodal tract, ending at the AV node
• d.The coronary sinus, along the posterior wall

Bachmann's bundle is the interatrial band that carries the impulse from the right atrium across to the left atrium, which is why the P wave represents both atria depolarizing nearly together. The internodal tracts also leave the sinoatrial node, but they carry the impulse down the right atrium toward the AV node rather than across to the left atrium. The bundle of His sits below the AV node and serves the ventricles, so it plays no part in atrial spread. The coronary sinus is a venous channel, not a conduction pathway.

In the large majority of adults, the atrioventricular node is supplied by a branch of which artery?

• a.The left anterior descending artery, which feeds the septum
• b.The left circumflex artery, which supplies the lateral wall
• c.The right coronary artery, in most adult hearts✓
• d.The left main coronary artery, before it branches out

Most people have a right-dominant coronary circulation, and in those hearts the AV nodal artery branches from the right coronary artery. That anatomy explains why an inferior wall infarction so often comes with AV nodal block and a slow junctional rhythm. The circumflex supplies the AV node only in the minority of hearts that are left-dominant, which makes it a reasonable but less common answer. The left anterior descending artery supplies the anterior wall, the front of the septum, and much of the bundle branches, while the left main is only a short trunk that divides almost immediately.

The left anterior descending artery is the main blood supply to which regions?

• a.The lateral left ventricular wall and the left atrium
• b.The inferior left ventricular wall and the AV node
• c.The anterior left ventricular wall and the septum✓
• d.The right ventricle and the right atrial wall

The left anterior descending artery runs down the front of the heart in the anterior interventricular groove and feeds the anterior wall of the left ventricle plus the front two thirds of the interventricular septum. Because much of both bundle branches sits in that septum, a blockage there can produce a bundle branch block as well as anterior wall damage. The lateral wall and the left atrium belong mostly to the circumflex, and the inferior wall with the AV node belongs to the right coronary artery in most hearts. The right ventricle and right atrium are also right coronary territory.

At which moment in the cardiac cycle does the aortic valve open?

• a.When left ventricular pressure exceeds aortic pressure✓
• b.When the left atrium contracts to top off the ventricle
• c.When the ventricles relax and chamber pressure falls off
• d.At the same instant the mitral valve opens

A semilunar valve is pushed open by pressure from behind it, so the aortic valve opens only once the contracting left ventricle has built up a pressure higher than the pressure in the aorta. Atrial contraction adds the last portion of filling while the aortic valve is still shut, so that moment is far too early. Falling ventricular pressure during relaxation is what lets the aortic valve snap closed, which is the opposite event. The mitral valve opens during filling, when the aortic valve is closed, so the two cannot open together.

The absolute refractory period of the ventricles covers which portion of the tracing?

• a.The PR segment, while the impulse waits at the AV node
• b.The downslope of the T wave into the TP segment
• c.The QRS complex through the peak of the T wave✓
• d.The P wave, while the atria depolarize

Ventricular cells cannot be restimulated from the start of the QRS until roughly the peak of the T wave, no matter how strong the stimulus, and that span is the absolute refractory period. The downslope of the T wave is the relative refractory period, where a strong enough stimulus can capture partially recovered tissue. The PR segment reflects the delay at the AV node before the ventricles have depolarized at all. The P wave is atrial depolarization and says nothing about ventricular recovery.

A premature ventricular beat lands on the downslope of the preceding T wave. Why is that timing dangerous?

• a.The ventricles have fully recovered, so the beat lands with extra force
• b.Recovery is uneven, so the beat can trigger fibrillation✓
• c.The T wave is where the atria repolarize, so atrial filling is lost
• d.The AV node is refractory then, so the beat cannot reach the ventricles

The downslope of the T wave is the relative refractory period, when some ventricular cells have recovered and others have not, and a stimulus arriving into that patchwork can start a chaotic reentrant rhythm such as ventricular tachycardia or ventricular fibrillation. This is the R on T phenomenon, and it is a finding a technician reports promptly rather than interprets. Full recovery of the ventricles happens later, after the T wave has ended, so the idea of a merely forceful beat misses the hazard. Atrial repolarization is buried inside the QRS complex, not in the T wave, and a ventricular beat by definition arises below the AV node and does reach the ventricles.

Rapid depolarization of a working ventricular muscle cell is produced mainly by which ion movement?

• a.Potassium moving out of the cell through slow channels
• b.Calcium entering slowly and sustaining the plateau phase
• c.Chloride shifting inward to balance the membrane charge
• d.Sodium rushing into the cell through fast channels✓

A working ventricular cell rests near negative 90 millivolts, and when threshold is reached the fast sodium channels open and sodium floods in, driving the steep upstroke that the QRS complex represents. Calcium is a genuinely tempting answer because slow calcium entry does maintain the plateau that keeps the cell contracting, and calcium rather than sodium drives the upstroke in pacemaker cells, but it is not what produces the rapid upstroke in working myocardium. Potassium leaving the cell is repolarization, the recovery phase seen as the T wave. Chloride shifts are not the driver of the cardiac action potential upstroke.

A technician obtains a 12-lead on a dialysis patient and sees tall, narrow, peaked T waves in most leads. Which electrolyte problem is classically associated with that pattern, and what is the technician's role?

• a.High potassium; reported to the nurse without interpreting the tracing✓
• b.Low potassium; reported to the nurse without interpreting the tracing
• c.Low calcium; reported to the nurse without interpreting the tracing
• d.High calcium; reported to the nurse without interpreting the tracing

Tall, narrow, peaked T waves are the classic tracing change described with an elevated potassium level, and a patient on dialysis is exactly the person in whom it is expected. A low potassium level does the opposite: it flattens the T wave and brings out a U wave. A low calcium level lengthens the QT interval and a high calcium level shortens it, and neither one peaks the T wave. The technician's role is the same whichever finding is on the tracing: acquire it, report it promptly to the nurse or provider, and leave the diagnosis and any explanation to the patient to the licensed staff.

Which electrolyte abnormality is classically associated with a prolonged QT interval?

• a.A high potassium level, which first peaks the T waves
• b.A high calcium level, which shortens the ST segment
• c.A low calcium level, lengthening the ST segment✓
• d.A high sodium level, which lifts the QRS amplitude

A low serum calcium level stretches out the ST segment, and because the QT interval is measured from the start of the QRS to the end of the T wave, that stretch shows up as a prolonged QT. An elevated calcium level does the reverse and shortens the ST segment and the QT, which is why it is a tempting near miss. An elevated potassium level is tied to tall peaked T waves and, at higher levels, a widening QRS rather than QT prolongation. Sodium levels have no classic QT signature, and in every case the technician reports the tracing and leaves the interpretation to the provider.

A provider performs carotid sinus massage during monitoring. The resulting vagal stimulation has which effect?

• a.It speeds the sinus rate and shortens conduction through the AV node
• b.It increases the force of ventricular contraction without changing rate
• c.It blocks conduction in the right and left bundle branches
• d.It slows the sinus rate and delays AV nodal conduction✓

Pressure on the carotid sinus stimulates baroreceptors, which raise parasympathetic outflow through the vagus nerve to the sinoatrial and atrioventricular nodes; the sinus rate falls and conduction through the AV node slows, often lengthening the PR interval or briefly unmasking atrial activity. Speeding the rate and shortening AV conduction is the sympathetic response, the opposite of what the vagus does. Vagal fibers have little effect on ventricular contractile force, so a pure inotropic change does not fit. The bundle branches are not under meaningful vagal control, so a maneuver like this does not create bundle branch block.

Preload is best described as which of the following?

• a.The resistance the ventricle must overcome to eject blood
• b.The share of ventricular volume ejected with each beat
• c.The contractile strength at a given fiber length
• d.The volume stretching the ventricle at end-diastole✓

Preload is the degree of stretch on the ventricular muscle just before it contracts, which in practice means the volume in the ventricle at the end of diastole. Within limits, more stretch yields a stronger contraction, the Frank-Starling relationship. Resistance to ejection is afterload, the closest and most commonly confused answer, and it is raised by conditions such as hypertension or aortic stenosis. Contractile strength independent of stretch is contractility, and the fraction of volume ejected is ejection fraction; both are separate measures.

Ejection fraction expresses which relationship?

• a.The volume of blood the left ventricle pumps in one minute
• b.The number of milliliters ejected by a single heartbeat
• c.The pressure the ventricle generates while it is contracting
• d.The share of end-diastolic volume the ventricle ejects each beat✓

Ejection fraction is stroke volume divided by end-diastolic volume, expressed as a percentage; a ventricle holding 120 milliliters at the end of filling and ejecting 66 milliliters has an ejection fraction of 55 percent. Volume pumped per minute is cardiac output, a different quantity built from rate and stroke volume. Milliliters ejected per beat is stroke volume itself, the numerator of the fraction rather than the fraction. Pressure generated during contraction is a measure of force, not of the proportion of the chamber emptied.

Before reaching the Purkinje network, the left bundle branch divides into which structures?

• a.The anterior and posterior internodal tracts
• b.The two divisions of the bundle of His
• c.The left anterior and left posterior fascicles✓
• d.The septal and marginal branches of the AV junction

The left bundle branch splits into a left anterior fascicle and a left posterior fascicle, which spread the impulse over the left ventricle before handing it to the Purkinje fibers; loss of one of them produces a hemiblock rather than a full bundle branch block. The internodal tracts are atrial pathways between the sinoatrial and atrioventricular nodes and never enter the ventricles. The bundle of His is the trunk that divides into the right and left bundle branches, so it sits above the split rather than being the product of it. The AV junction has no septal or marginal branches; those names belong to coronary arteries.

In an adult with normal anatomy, the apex of the heart sits at which location?

• a.In the second intercostal space at the right sternal border
• b.Just beneath the manubrium at the level of the second rib
• c.In the fifth intercostal space at the right midclavicular line
• d.In the fifth intercostal space, left midclavicular line✓

The heart lies in the mediastinum with about two thirds of its mass left of the midline, and the apex points down, forward, and to the left, landing at the fifth intercostal space in the left midclavicular line. That is the point of maximal impulse, and it is also the landmark for the V4 electrode. The mirror-image description on the right side is the same landmark on the wrong side of the chest, which is the trap in this item. The second intercostal space at the right sternal border marks the aortic area, and the region beneath the manubrium holds the great vessels rather than the apex.

Venous blood that has already perfused the myocardium returns to the circulation through which route?

• a.The pulmonary veins, which carry it to the left atrium
• b.The superior vena cava, with blood from the head and arms
• c.The coronary sinus, emptying into the right atrium✓
• d.The inferior vena cava, with blood from the abdomen and legs

The cardiac veins collect blood that has passed through the myocardium and drain into the coronary sinus, which lies in the posterior atrioventricular groove and empties directly into the right atrium. The venae cavae also deliver deoxygenated blood to the right atrium, but they carry blood returning from the body at large rather than from the heart muscle itself. The pulmonary veins carry oxygenated blood from the lungs into the left atrium, the opposite kind of blood and the wrong chamber. Coronary arterial filling, by contrast, occurs mainly during diastole.

While the sinoatrial node is functioning normally, why do the lower pacemaker sites not fire at their own intrinsic rates?

• a.Their pacemaker cells lose automaticity once a person reaches adulthood
• b.The AV node blocks retrograde impulses from traveling back down
• c.They fire only when the sympathetic nervous system stimulates them
• d.The faster sinus impulses reach and discharge them before they self-fire✓

Every latent pacemaker is drifting toward threshold, but the sinoatrial node reaches threshold first and its impulse arrives and depolarizes those sites before they can get there on their own; this is overdrive suppression, and it is why an escape rhythm appears only when the sinus node slows or fails. The lower sites keep their automaticity throughout life, which is exactly what makes an escape rhythm possible. Blocking impulses from returning upward does not explain why the lower sites stay quiet, since the issue is the downward impulse that keeps resetting them. Sympathetic stimulation modifies the rate of these sites but is not what starts them.

Automaticity refers to which property of cardiac cells?

• a.The ability to pass an impulse along to neighboring cells
• b.The ability to generate an impulse without outside stimulation✓
• c.The ability to respond to an electrical stimulus by depolarizing
• d.The ability to shorten and produce mechanical force

Automaticity is the capacity of certain cardiac cells to reach threshold and fire on their own, without any nerve or outside signal, and it is the property that lets the sinoatrial node, the AV junction, and the ventricles each serve as a pacemaker. Passing the impulse to neighboring cells is conductivity, the property that carries the wave through the myocardium once it has started. Responding to a stimulus by depolarizing is excitability, which is easily confused with automaticity because both describe an electrical response, but excitability requires a stimulus while automaticity does not. Shortening to produce force is contractility, the mechanical rather than electrical property.

In the classic three-stage model of a coronary event, which waveform change is linked to each stage?

• a.Ischemia produces pathologic Q waves, injury inverts the T wave, and infarction elevates the ST segment
• b.Ischemia produces T wave inversion, injury produces ST segment elevation, and infarction produces pathologic Q waves✓
• c.Ischemia produces ST segment elevation, injury produces a tall R wave, and infarction inverts the T wave
• d.Ischemia widens the QRS complex, injury depresses the ST segment, and infarction shortens the PR interval

The three stages are taught in the order the muscle is damaged. Muscle that is short of blood but not yet damaged repolarizes abnormally, which shows on the tracing as T wave inversion, often deep and symmetric. Muscle that is acutely damaged but still alive produces ST segment elevation in the leads sitting over that wall, and it is that finding which drives emergency treatment. Muscle that has died no longer conducts, so leads over it record pathologic Q waves. Pairing necrosis with T wave inversion or with a tall R wave reverses the sequence, and QRS widening with PR shortening belongs to conduction disorders rather than to this model.

A 12-lead shows Q waves at least 0.04 second wide in three neighboring leads. What does a pathologic Q wave indicate?

• a.Muscle that is short of blood but intact, so the Q waves clear once the chest pain is treated
• b.Muscle that has died and no longer conducts, a change that usually stays on the tracing for the rest of the patient's life✓
• c.Coronary spasm that shows up during an episode of pain and disappears between the episodes
• d.A normal septal finding that is expected in all twelve leads of a healthy adult heart

A Q wave is called pathologic when it is at least 0.04 second wide, which is one small box at 25 mm/sec, or deeper than about one third of the R wave that follows it. Dead myocardium is electrically silent, so an electrode over that area records depolarization traveling away from it and writes a deep initial downward deflection. Because scar does not recover, these Q waves generally persist for years, which is why they mark an old infarction as well as a new one and cannot be used to judge how recent the event was. Reversible ischemia and coronary spasm change the ST segment and T wave rather than carving a permanent Q wave. Small narrow Q waves are normal in a few leads, but not in all twelve.

Leads V1 and V2 sit directly over which part of the heart?

• a.The septum between the two ventricles✓
• b.The lateral wall of the left ventricle
• c.The inferior surface of the heart
• d.The posterior wall of the left ventricle

V1 sits in the fourth intercostal space at the right sternal border and V2 in the fourth intercostal space at the left sternal border, so both electrodes face the interventricular septum from the front. Changes limited to this pair are described as septal. The lateral wall is viewed from leads I, aVL, V5, and V6, and the inferior surface from II, III, and aVF, all of which sit well away from the sternum. The posterior wall has no electrode directly over it on a standard 12-lead and is inferred from mirror-image changes or recorded with added posterior leads.

Occlusion of the left circumflex artery most often produces changes in which group of leads?

• a.Leads II, III, and aVF, the inferior lead group
• b.Leads V1 through V4, the anteroseptal lead group
• c.Leads V1 and V2 alone, the septal lead pair
• d.Leads I, aVL, V5, and V6, the lateral group✓

In most people the left circumflex artery runs in the groove between the left atrium and left ventricle and supplies the lateral wall, so injury in its territory appears in the leads that face that wall: I and aVL high on the left side and V5 and V6 on the left chest. The inferior group is supplied by the right coronary artery in the large majority of adults. The anterior and septal leads follow the left anterior descending artery and its septal branches. Because the circumflex also supplies part of the posterior wall in many people, a technician may be asked to add posterior leads when the lateral leads are abnormal.

A patient with chest pain has tall R waves with flat ST depression in V1 and V2, plus ST elevation in II, III, and aVF. What should the technician anticipate next?

• a.Reversed arm electrodes, so the whole tracing is discarded and repeated once the limb leads are swapped back
• b.A possible posterior wall infarction, and a request for the posterior leads V7, V8, and V9 across the left side of the back✓
• c.Right ventricular involvement, checked by moving the V4 electrode across to the right side of the chest
• d.Anterior wall ischemia, checked by running the same 12-lead again after the patient has rested

No electrode on a standard 12-lead faces the posterior wall, so posterior injury is read as a mirror image in the leads on the opposite side of the chest: the ST elevation appears as ST depression in V1 and V2 and the deep Q wave appears as a tall R wave. Posterior leads placed across the left side of the back give a direct view and confirm the finding. Right ventricular involvement is a real possibility with an inferior pattern and is checked with a right-sided chest lead, but it does not explain tall R waves in V1 and V2. Reversed arm electrodes distort the limb leads and leave the chest leads alone, so they cannot produce this picture. The technician reports the tracing at once and lets the provider decide which extra leads to order.

A patient describes chest discomfort that wakes her at about the same hour most nights and passes within a few minutes. A tracing captured during one episode showed ST elevation that had resolved by the time she reached the clinic. Which pattern does this fit?

• a.Stable angina, because the discomfort is predictable and brief
• b.Variant angina, from coronary spasm rather than from exertion✓
• c.Unstable angina, because the pattern has recently changed
• d.An evolving infarction, because the ST segment was elevated

Variant angina, also called Prinzmetal angina, comes from spasm of a coronary artery rather than from a fixed narrowing, so it strikes at rest and often at the same hour of the night, and the ST elevation it produces is transient and gone once the spasm relaxes. Unstable angina is the answer worth weighing, because it also occurs at rest and represents a change in pattern, but it usually shows ST depression or T wave inversion rather than elevation that comes and goes with the episode. Stable angina is provoked by exertion and relieved by rest, which does not fit discomfort that wakes a sleeping patient. An evolving infarction leaves ST elevation that persists and then evolves over hours rather than resolving in minutes. The technician records and reports what was captured and does not label the pattern on the tracing.

A tracing shows ST elevation in II, III, and aVF together with ST depression in I and aVL. How is the depression in I and aVL best described?

• a.A second blocked vessel supplying the high lateral wall, separate from the artery causing the elevation
• b.A reciprocal change, the same injury current recorded by leads that face the heart from the opposite side✓
• c.Digitalis effect, which drags the ST segment down into a sagging curve in the limb leads
• d.An artifact created by poor contact between the left arm electrode and the skin

An injured wall pushes the ST segment up in the leads sitting over it, and leads aimed at the heart from the far side record that same current heading away from them, which writes ST depression. Because I and aVL look at the heart from the high left side and II, III, and aVF look at it from below, those two groups are reciprocal to one another. A separate blockage is a real possibility when depression is deep or widespread, but the mirror pattern is expected with any inferior injury and does not by itself mean two vessels. Digitalis produces its sagging depression without ST elevation elsewhere, and a loose electrode would degrade the baseline rather than shift the ST segment in a matched pair of leads.

A patient who had an anterior myocardial infarction one month ago has deep Q waves in V3 and V4, ST segments back at the baseline, and shallow T wave inversion. Which description fits the tracing?

• a.An acute injury pattern that began within the past hour and is still developing
• b.A placement error, since V3 and V4 were set one interspace too high on the chest
• c.An evolved infarction, because the Q waves persist after the ST segment has returned to baseline✓
• d.A resolved infarction with a normal tracing, since the injured muscle has healed completely

A coronary event evolves in a fairly consistent order: tall T waves and ST elevation come first, Q waves appear over hours to days, and the ST segment settles back to the baseline over the following days to weeks while the T waves stay inverted for a while. Q waves are the part that does not fade, so a tracing with Q waves, a flat ST segment, and residual T wave inversion fits an event that happened some time ago. Acute injury would still show ST elevation, which this tracing does not. Calling the tracing normal ignores the Q waves, which record scar that will remain, and electrodes placed an interspace too high alter R wave progression rather than carving deep Q waves in a patient with a known infarction.

A technician finishes a 12-lead on a patient with chest pain and sees 2 mm of flat ST depression across V4, V5, and V6. What is the correct action?

• a.Tell the patient the tracing shows a partly blocked coronary artery
• b.Repeat the tracing after the patient has rested for thirty minutes
• c.Write lateral wall ischemia in the interpretation field of the report
• d.Report the finding to the nurse or provider without delay✓

ST depression and T wave inversion suggest that muscle is short of blood, a finding that can change quickly, so the tracing goes to a licensed clinician right away rather than waiting in a queue. The technician acquires, recognizes, and reports; naming a wall and a diagnosis on the report is interpretation and sits outside the certified technician's scope. Explaining the tracing to the patient is outside that scope as well, and it can frighten a patient over a finding the provider may read differently. Waiting half an hour to repeat the tracing delays care for a patient who may be infarcting.

A patient reports sharp chest pain that eases on leaning forward. The 12-lead shows ST elevation in nearly every lead with PR segment depression and no reciprocal depression. Which condition is classically linked to that pattern?

• a.An extensive anterior infarction that has spread across several coronary territories
• b.Left ventricular hypertrophy from years of poorly treated high blood pressure
• c.A high potassium level in a patient whose kidney function has fallen off
• d.Acute pericarditis, an inflammation of the sac that surrounds the heart✓

Inflammation of the pericardium touches the surface of the heart in every direction, so the ST elevation is spread across leads from many different angles instead of clustering in one arterial territory, and because no single wall is injured there is no mirror-image depression opposite it. Depression of the PR segment and pain that eases when the patient sits up and leans forward fit the same picture. An infarction follows the path of one artery, so its elevation is grouped and usually has reciprocal depression somewhere. Hypertrophy raises voltage and shifts the ST segment in the leads with the tallest complexes, and a high potassium level shows peaked T waves. The technician recognizes the pattern, reports it promptly, and leaves the diagnosis to the provider.

Which P wave change is classically associated with enlargement of the right atrium?

• a.A wide, notched P wave lasting longer than 0.12 second in lead II
• b.A P wave that changes its shape from one beat to the next in lead II
• c.A P wave inverted in lead II ahead of a narrow QRS
• d.A tall, peaked P wave of 2.5 mm or more in lead II✓

The first half of the P wave is written by the right atrium and the second half by the left. When the right atrium is enlarged its portion grows taller rather than longer, producing a pointed P wave of at least 2.5 mm in the inferior leads, a shape often reported with lung disease that raises pressure on the right side of the heart. A wide, notched P wave beyond 0.12 second reflects the left atrium taking extra time to depolarize and is the classic left-sided finding, which makes it the closest competitor here. A P wave inverted in lead II points to an impulse starting near the AV junction and traveling backward through the atria, and a P wave that keeps changing shape points to a pacemaker site that keeps moving.

Every complex on a finished 12-lead looks unusually small and is hard to measure. What should the technician check first?

• a.Whether the patient's body build accounts for the small complexes
• b.Whether the gain is set at 10 mm/mV rather than at half standard✓
• c.Whether the paper speed was left at 50 mm/sec instead of 25 mm/sec
• d.Whether the limb electrodes were placed on the torso

The standardization mark printed at the start of the tracing should stand 10 mm tall, which is the 10 mm/mV setting; if the machine was switched to half standard, every complex is recorded at half its true height and a normal heart appears to have low voltage. Checking that mark takes seconds and is done before anything is reported. Paper speed changes how wide the complexes look, not how tall, so 50 mm/sec would stretch the tracing rather than shrink it. A heavy chest wall, air trapping in the lungs, and fluid around the heart are genuine causes of small complexes, but they are considered after the machine settings have been ruled out, and torso limb placement alters the tracing without shrinking every lead uniformly.

A hypothermic patient's tracing shows a distinct positive deflection at the junction between the QRS complex and the ST segment. What is that deflection called?

• a.A delta wave from an accessory conduction pathway
• b.A U wave that follows the T wave in hypokalemia
• c.An Osborn wave at the J point of the complex✓
• d.A pathologic Q wave from an old infarction

The point where the QRS complex ends and the ST segment begins is called the J point, and in a cold patient an extra rounded hump appears there, named the Osborn wave after the physician who described it. It usually keeps company with a slow rate, lengthened intervals, and a wandering baseline from shivering, so the technician warms and steadies the patient before repeating the tracing. A delta wave sits at the start of the QRS as a slurred upstroke rather than at its end, and it shortens the PR interval. A U wave arrives after the T wave, well past the J point, and is linked to a low potassium level.

A rhythm strip shows a narrow vertical spike immediately before each wide QRS complex, and every spike is followed by a complex. What does this most likely represent?

• a.A ventricular pacemaker that is capturing, which the technician documents on the tracing before it goes to the provider✓
• b.Interference at 60 cycles per second from an electrical device close to the patient's bed
• c.A premature ventricular complex arising from an irritable focus below the AV junction
• d.Muscle tremor artifact from a patient who is shivering throughout the recording

An implanted pacemaker fires a brief pulse that the machine records as a thin vertical line, and when that line is followed each time by a QRS complex the pacemaker is capturing, meaning the ventricle answers every stimulus. The complex is wide because the impulse starts in the ventricle and spreads through muscle rather than down the normal conduction pathway. Noting the device is part of the record, since a provider reading the tracing without that note may mistake the paced complexes for a ventricular rhythm. Sixty-cycle interference lays a steady fine ripple over the entire tracing rather than a single spike tied to each beat, muscle tremor produces an irregular fuzzy baseline, and a premature ventricular complex is early and occasional rather than present ahead of every beat.

A patient who takes digoxin has a 12-lead with scooped, downsloping ST depression in the lateral leads and a short QT interval. What does that pattern most likely represent?

• a.Ischemia of the inner layer of the lateral wall of the left ventricle
• b.Digoxin toxicity, which means the technician holds the patient's next dose
• c.The expected digoxin effect, which is reported and not interpreted✓
• d.A low potassium level producing a U wave after each T wave

Digoxin at ordinary doses changes repolarization, and the classic footprint is a sagging, scooped ST depression with a shortened QT interval, seen most easily in the leads with tall R waves. This is a drug effect rather than a sign of poisoning, and it can appear in a patient whose blood level is entirely normal, so the technician notes the finding and the medication and lets the provider read it. True toxicity announces itself with rhythm disturbances rather than with the scooped ST segment, and holding a dose is a decision for a licensed clinician, not the technician. Subendocardial ischemia usually depresses the ST segment in a flat or downsloping line without shortening the QT interval, and a low potassium level adds a U wave after the T wave instead.

Which item in a patient's history is a non-modifiable risk factor for coronary artery disease?

• a.Type 2 diabetes that is controlled with an oral medication
• b.A father who had a myocardial infarction at age forty-six✓
• c.An LDL cholesterol level above the patient's treatment goal
• d.Cigarette smoking of about half a pack on most days

Risk factors are sorted by whether treatment or behavior can change them. Age, sex, and inherited tendency cannot be changed, so a close blood relative who had an early coronary event stays on the list for life and is weighed more heavily when the relative was young. Diabetes is the trap in this set, because the diagnosis is permanent while the risk it carries is very much modifiable through glucose control, which is why it is grouped with the treatable factors. Cholesterol and smoking are the textbook modifiable factors, since both respond to treatment or to stopping. A technician does not counsel the patient about these findings but does record an accurate history.

A 74-year-old woman with long-standing diabetes is short of breath and nauseated and denies any chest pain. The provider orders a 12-lead. What is the best reason for that order?

• a.Diabetes alters the shape of the QRS complex, so a baseline tracing is needed
• b.Nausea on its own is the most common first symptom of a coronary event
• c.Older adults, women, and people with diabetes often infarct without chest pain✓
• d.Shortness of breath points away from the heart, and the tracing documents that

The crushing substernal pain that textbooks describe is the typical presentation, not the only one. Older adults, women, and people who have had diabetes for years frequently present instead with shortness of breath, fatigue, nausea, sweating, or pain in the back, jaw, or upper abdomen, and long-standing diabetes can blunt the nerve signals that would otherwise produce pain at all. That is why a tracing is obtained on this patient rather than waiting for a symptom she may never report. Nausea alone is not the most common opening symptom of a coronary event, shortness of breath does not steer suspicion away from the heart, and diabetes does not reshape the QRS complex.

A patient scheduled for a routine 12-lead has an implanted cardioverter-defibrillator under the skin of the left upper chest. How should the technician proceed?

• a.Cancel the study, because current from the EKG machine can damage an implanted device
• b.Acquire the tracing as ordered, shifting an electrode slightly if one lands on the generator, and note the device on the record✓
• c.Move all six chest electrodes to the right side of the chest to keep them clear of the device
• d.Wait until the device has been turned off in the clinic and then record the tracing

A 12-lead machine only listens; it sends no current into the patient, so recording a tracing is safe for someone with an implanted defibrillator or pacemaker. The electrode positions do not change, although one that would sit directly over the hard bulge of the generator can be moved a small distance so it lies flat on skin and makes clean contact. The presence of the device belongs on the record, because pacing spikes and the wide complexes that follow them are easy to misread when the reader does not know a device is there. Mirroring the chest leads to the right side records an entirely different set of views and would misrepresent the patient, and asking for the device to be deactivated exposes the patient to risk for no benefit.