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Advanced Cardiovascular Assessment for nurses | Assessing the Heart

by | Nov 14, 2023 | Nursing, Cardiac, Critical care, Emergency (ER), ICU, Nurse Practitioner, Nursing Assessment | 2 comments

Advanced Cardiovascular Assessment: Complete Nursing Cardiac Exam Guide

Nursing Cardiac Critical Care Emergency ICU Nurse Practitioner Nursing Assessment
William Kelly, MSN, FNP-C
William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
13 min read
Advanced cardiovascular assessment guide for nurses with heart assessment graphics

An advanced cardiovascular assessment helps nurses connect vital signs, history, auscultation, pulses, perfusion, JVP, and ECG findings into one clear picture of cardiac stability.

A strong cardiac exam is not just “S1/S2 noted.” It is a bedside pattern-recognition skill: What does the patient look like? Are they perfusing? Is the rhythm stable? Are there signs of fluid overload, valve disease, ischemia, shock, or vascular compromise?

In This Guide
  1. Why Cardiovascular Assessment Matters
  2. When to Perform a Cardiac Assessment
  3. Fast Bedside Cardiac Scan
  4. Cardiac History
  5. Vital Signs and Perfusion
  6. Cardiac Auscultation
  7. Point of Maximal Impulse
  8. Peripheral Pulses
  9. Bruits and Thrills
  10. Jugular Venous Pressure
  11. ECG and Telemetry Evaluation
  12. Red Flags and Escalation
  13. References

Why Cardiovascular Assessment Matters

The cardiovascular system drives oxygen delivery, perfusion, and hemodynamic stability. A careful assessment can help nurses recognize ischemia, dysrhythmias, heart failure, shock, vascular compromise, and complications before the patient crashes.

Cardiovascular disease remains the leading cause of death globally, so cardiac assessment is not “extra.” It is a core nursing skill across ER, ICU, med-surg, telemetry, perioperative, and outpatient settings.

The big idea: the best cardiac assessment combines what you see, hear, feel, measure, and trend — not one isolated finding.

When Should a Cardiovascular Assessment Be Done?

A basic cardiac assessment belongs in most focused and comprehensive exams. The depth depends on the setting, complaint, acuity, and baseline risk.

Twelve lead ECG machine icon for chest pain assessment
Chest Pain or Pressure
Assess vital signs, perfusion, heart sounds, lung sounds, pulses, and obtain ECG per protocol.
Pulmonary fluid icon for heart failure and shortness of breath
Shortness of Breath
Listen for crackles, check SpO2, assess work of breathing, JVP, edema, and cardiac rhythm.
Portable telemetry monitor icon
Unstable Vitals
New hypotension, tachycardia, bradycardia, syncope, or altered mental status needs a rapid hemodynamic assessment.
Doppler pulse icon for absent extremity pulse
Limb or Vascular Concern
Pain, pallor, pulselessness, paresthesia, paralysis, or poikilothermia should trigger urgent circulation checks.

Fast Bedside Cardiac Scan

Before the detailed exam, get a quick read of whether the patient looks stable. This is especially useful when a patient has chest pain, dyspnea, dizziness, syncope, palpitations, sepsis, trauma, or a concerning rhythm.

1
Look at the patient

General appearance, work of breathing, skin color, diaphoresis, anxiety, altered mentation, positioning, and visible distress all matter.

2
Check the numbers

Trend blood pressure, heart rate, respiratory rate, SpO2, temperature, and pain. One abnormal value matters less than the pattern.

3
Feel perfusion

Assess skin temperature, capillary refill, peripheral pulses, edema, and whether pulses are symmetrical.

4
Listen strategically

Auscultate heart and lungs. Listen for rhythm irregularity, murmurs, extra heart sounds, rubs, crackles, or new asymmetry.

5
Connect to the monitor

Review telemetry or obtain a 12-lead ECG when symptoms, vitals, or policy call for it.

Do Not Delay ECG for Acute Chest Pain

For patients with acute chest pain or symptoms concerning for ACS, a 12-lead ECG should be obtained and reviewed rapidly according to protocol. New STEMI, unstable rhythm, hypotension, syncope, or acute respiratory distress should trigger urgent escalation.

Cardiac History: What to Ask Before You Listen

The cardiac exam is only as useful as the clinical context around it. History helps you decide whether you are looking for ACS, heart failure, dysrhythmia, pulmonary embolism, medication effect, volume depletion, valvular disease, vascular disease, or something else entirely.

Symptoms: Chest pain/pressure, shortness of breath, palpitations, dizziness, syncope, orthopnea, edema, fatigue, diaphoresis, nausea, jaw/arm/back pain, or exercise intolerance.
PQRST/OPQRST: Onset, provoking factors, quality, radiation, severity, timing, associated symptoms, and what changed from baseline.
Risk factors: Known CAD, hypertension, hyperlipidemia, diabetes, smoking/vaping, CKD, family history, obesity, prior MI/stroke, pregnancy/postpartum state, and stimulant/cocaine use when clinically relevant.
Meds and devices: Antihypertensives, beta blockers, calcium channel blockers, nitrates, diuretics, anticoagulants, antiplatelets, antiarrhythmics, pacemaker/ICD, LVAD, or recent med changes.
Baseline: What is normal for this patient? Compare with prior vitals, prior ECGs, usual edema, usual oxygen need, and known murmur or rhythm history.

Vital Signs and Perfusion

Vital signs provide the quickest objective snapshot of cardiovascular status. The most useful finding is often the trend: rising heart rate, falling blood pressure, increasing oxygen need, or widening/narrowing pulse pressure can be more important than one isolated number.

Blood pressure cuff icon showing elevated blood pressure
Blood Pressure
Normal adult BP is <120/<80 mmHg. Stage 1 hypertension begins at 130–139 or 80–89; stage 2 begins at ≥140 or ≥90. Treat the patient, trend, and clinical context — not just the number.
Telemetry heart rate animation at 92 beats per minute
Heart Rate
Adult resting HR is commonly 60–100 bpm. Tachycardia can reflect pain, fever, dehydration, shock, arrhythmia, anxiety, hypoxia, PE, or ischemia; bradycardia may be baseline, medication-related, or pathologic.
Finger pulse oximeter icon
Pulse Oximetry
SpO2 reflects oxygen saturation, not perfusion by itself. Poor waveform, cold extremities, nail polish, dyshemoglobinemias, shock, or motion can affect readings.
Doppler checking a foot pulse
Peripheral Perfusion
Check skin temperature, color, capillary refill, edema, sensation, movement, and distal pulses. Compare both sides.

Blood Pressure Update

The old “140/90” cutoff is incomplete for current adult BP categories. In general adult classification, 130–139 systolic or 80–89 diastolic is Stage 1 hypertension; ≥140 systolic or ≥90 diastolic is Stage 2. Diagnosis and treatment decisions still require proper measurement, repeat readings, and clinical context.

Cardiac Auscultation

Auscultation means listening with a stethoscope. During cardiac auscultation, listen for rate, rhythm, S1/S2, extra sounds, murmurs, and rubs. Use the diaphragm for higher-pitched sounds and the bell for lower-pitched sounds such as S3/S4 when appropriate.

Five cardiac auscultation landmarks: aortic, pulmonic, Erb point, tricuspid, and mitral
The classic cardiac auscultation landmarks help you hear each valve area best: aortic, pulmonic, Erb point, tricuspid, and mitral/apex.
Where to listen
Aortic: Right 2nd intercostal space at the sternal border.
Pulmonic: Left 2nd intercostal space at the sternal border.
Erb point: Left 3rd intercostal space near the sternal border.
Tricuspid: Left lower sternal border.
Mitral / Apex: Left 5th intercostal space near the midclavicular line.
Heart sounds nurses should recognize
S1 and S2 normal heart sounds icon
S1 and S2
Normal “lub-dub.” S1 is closure of the mitral/tricuspid valves; S2 is closure of the aortic/pulmonic valves.
S3 and S4 extra heart sounds icon
S3 and S4
Extra low-pitched sounds. S3 can be physiologic in some young/pregnant patients but may suggest volume overload or heart failure in older adults. S4 suggests a stiff ventricle and is absent in atrial fibrillation.
Heart murmur icon
Murmurs
Murmurs are caused by turbulent flow. Document timing, location, intensity/grade, radiation, and changes with position or maneuvers when assessed.
Pericardial friction rub icon
Pericardial Rub
A scratchy, high-pitched sound that can occur with pericarditis, often best heard with the diaphragm while the patient leans forward.

Do Not Forget the Lungs

Lung sounds are part of the cardiac picture. Crackles may support fluid overload, heart failure, or pulmonary edema when paired with dyspnea, hypoxia, JVD, edema, hypertension, or weight gain.

Point of Maximal Impulse (PMI)

The PMI is the point on the chest wall where the cardiac impulse is felt most strongly. It is usually near the left 5th intercostal space at the midclavicular line, around the mitral/apical area.

Point of maximal impulse location at the left fifth intercostal space midclavicular line
The PMI is often near the mitral area. A displaced or sustained PMI can suggest ventricular enlargement or pressure/volume overload.
Position: Assess supine first; left lateral decubitus can make the apical impulse easier to palpate.
Location: A laterally displaced PMI can suggest cardiomegaly or left ventricular enlargement.
Size: A diffuse impulse can be abnormal and should be interpreted with the full clinical picture.
Amplitude/duration: A sustained or heaving impulse may suggest pressure overload or ventricular hypertrophy.

Peripheral Pulses

Peripheral pulses give bedside clues about circulation, rhythm regularity, arterial disease, and acute vascular compromise. Always compare side to side and document asymmetry clearly.

Peripheral pulse locations including carotid, brachial, radial, femoral, popliteal, posterior tibial, and dorsalis pedis
Common pulse points include carotid, brachial, radial, femoral, popliteal, posterior tibial, and dorsalis pedis.
Pulse grading
0
Absent

No palpable pulse. Confirm with Doppler when appropriate and escalate if this is new or associated with limb symptoms.

1+
Weak / diminished

Difficult to palpate, may be thready, and can suggest low flow, vasoconstriction, edema, or arterial disease.

2+
Expected / normal

Easily palpable and not unusually weak or bounding.

3+
Increased

More prominent than expected; may be seen with high-output states or other clinical conditions.

4+
Bounding

Very strong, may be visible or difficult to obliterate; interpret with fever, anemia, pregnancy, hyperthyroidism, anxiety, or vascular conditions in mind.

New Absent Pulse Is Urgent

If a limb pulse is newly absent or significantly weaker — especially with pain, pallor, coolness, numbness, weakness, or delayed capillary refill — notify the provider team immediately and assess circulation, motor function, and sensation. Use Doppler per policy.

Bruits and Thrills

A bruit is an abnormal vascular sound heard over an artery, often from turbulent blood flow. A thrill is a palpable vibration that also suggests turbulent flow. In the right context, they can point toward stenosis, aneurysm, valvular disease, or a functioning dialysis access.

AV fistula bruit and thrill icon
AV Fistula
A working AV fistula should have a bruit and thrill. Absence can suggest access dysfunction or clotting and should be escalated.
Turbulent blood flow murmur icon
Cardiac Thrill
A palpable thrill over the precordium can suggest a loud murmur or significant turbulent flow.
Scratchy rub icon
Bruit Locations
Carotid, abdominal, renal, femoral, or graft/fistula areas may be assessed depending on the patient and setting.
Doppler pulse assessment icon
Pair With Pulses
Bruits/thrills should be interpreted alongside pulses, perfusion, symptoms, and risk factors.

Jugular Venous Pressure and JVD

Jugular venous pressure estimates right atrial pressure by observing venous pulsation in the neck, preferably the right internal jugular vein. Elevated JVP/JVD can support volume overload, right-sided heart failure, pulmonary hypertension, tricuspid valve disease, constrictive pericarditis, or cardiac tamponade depending on the clinical picture.

Illustration of increased jugular venous pressure
Kussmaul Sign
JVP normally falls with inspiration. A paradoxical rise can occur with constrictive pericarditis, restrictive cardiomyopathy, severe right heart failure, or other impaired filling states.
Hepatojugular reflux liver pressure and JVP illustration
Hepatojugular Reflux
A sustained rise in JVP with firm right upper quadrant/abdominal pressure can support elevated right-sided filling pressures.
Position the patient: Place the head of bed around 30–45 degrees and adjust as needed until venous pulsations are visible.
Use the right side: The right internal jugular is preferred because it has a more direct path to the right atrium.
Measure vertically: Estimate the vertical height above the sternal angle, then add about 5 cm to estimate pressure above the right atrium.
Interpret carefully: JVP is technically difficult and should be interpreted with symptoms, lung sounds, edema, BP, kidney function, echo findings, and response to therapy.

JVP Measurement Clarified

The old shortcut “measurements >4 cm indicate JVD” can be confusing. Clinically, many references describe normal mean JVP around 6–8 cm H2O above the right atrium; at the bedside this is estimated by measuring venous height above the sternal angle and adding about 5 cm.

Animation showing Kussmaul sign with increased jugular venous pressure during inspiration
Kussmaul sign: JVP rises or fails to fall with inspiration.
Animation showing hepatojugular reflux with abdominal pressure increasing jugular venous pressure
Hepatojugular reflux: JVP rises with sustained abdominal pressure.

ECG and Telemetry Evaluation

ECG and telemetry are not separate from the physical assessment — they are part of the cardiac story. Symptoms plus vital signs plus rhythm data can rapidly change priorities.

Twelve lead ECG machine vector icon
12-Lead ECG
Best for suspected ischemia/infarction, chest pain, new arrhythmia, syncope, electrolyte concerns, and many medication/toxicity presentations.
Portable cardiac monitor vector icon
Telemetry
Useful for trend monitoring of rate, rhythm, ectopy, pauses, heart block, and response to interventions.
Rate: Is the patient too fast, too slow, or changing quickly? Match the rhythm to symptoms and perfusion.
Rhythm: Regular or irregular? Sinus, atrial fibrillation, flutter, SVT, VT, heart block, paced, or unclear?
Ischemia clues: ST elevation/depression, T-wave changes, new bundle branch block pattern, or reciprocal changes should be escalated per protocol.
Compare: Old ECGs are gold. A new change matters more than a chronic baseline abnormality.
Need a rhythm refresher? Review How to Read an ECG Rhythm Strip and Atrial Fibrillation with RVR for the most common bedside patterns.

Cardiac Assessment Red Flags

Assessment only helps if abnormal findings are acted on. Escalate per protocol when the patient has concerning symptoms, unstable vital signs, new rhythm changes, or signs of poor perfusion.

Escalate Immediately For

Chest pain with concerning features, new STEMI/ischemic ECG changes, hypotension with symptoms, acute dyspnea or pulmonary edema, syncope, sustained VT, symptomatic bradycardia, new absent pulse, acute neuro symptoms, severe tearing chest/back pain, or signs of shock.

Bedside Pearls

1
Trend beats snapshot. A HR of 112 may be less alarming than a HR climbing from 78 to 112 with falling BP.
2
Compare both sides. Pulse asymmetry, unilateral edema, or one cold limb can matter more than a single “normal” value.
3
Lungs are cardiac clues. Crackles, rising oxygen requirement, and orthopnea can support heart failure or pulmonary edema.
4
Do not chart vague abnormalities. Instead of “pulses weak,” document location, grade, side-to-side comparison, Doppler use, color, temperature, sensation, movement, and who was notified.

Wrapping It Up

Advanced cardiovascular assessment gives nurses a practical bedside framework for evaluating stability. Start with appearance and vital signs, then layer in history, auscultation, pulses, perfusion, JVP, lung sounds, and ECG findings.

The goal is not to perform every maneuver on every patient. The goal is to recognize patterns early, document clearly, and escalate quickly when the cardiac story does not make sense.

Related Clinical Guides

Advanced physical exam guide thumbnail
Assessment
Advanced Physical Exam Maneuvers
ECG rhythm strip guide thumbnail
ECG
How to Read an ECG Rhythm Strip
Atrial fibrillation with RVR guide thumbnail
Cardiac
Atrial Fibrillation with RVR
ER nursing hacks article thumbnail
ER
10 Nursing Hacks Every ER Nurse Should Know

References

Clinical Databases & Guidelines
  1. World Health Organization. Cardiovascular diseases. WHO.
  2. Malik MB, et al. Cardiac Exam. StatPearls. National Library of Medicine. NCBI Bookshelf.
  3. Ernstmeyer K, Christman E, eds. Chapter 9: Cardiovascular Assessment. Nursing Skills. National Library of Medicine. NCBI Bookshelf.
  4. Gopal S, Nagalli S. Jugular Venous Distention. StatPearls. National Library of Medicine. NCBI Bookshelf.
  5. Cook DJ. The Jugular Venous Pressure and Pulse Contour. Clinical Methods. National Library of Medicine. NCBI Bookshelf.
  6. American Heart Association. High blood pressure categories. American Heart Association.
  7. Gulati M, et al. 2021 AHA/ACC Guideline for the Evaluation and Diagnosis of Chest Pain. Circulation. AHA Journals.
Textbooks
  1. American Heart Association. 2020 Handbook of Emergency Cardiovascular Care for Healthcare Providers. American Heart Association; 2020.
  2. Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History Taking. 12th ed. Wolters Kluwer; 2017.
  3. Jarvis C. Physical Examination & Health Assessment. 8th ed. Saunders; 2019.

AFIB RVR on EKG: Management of Atrial Fibrillation

by | Apr 13, 2022 | Emergency (ER), Cardiac, Critical care, ECG, ICU, Med-Surg | 9 comments

AFIB with RVR: A Nurse's Guide to Recognizing & Managing Atrial Fibrillation

Emergency (ER) Cardiac Critical Care ECG ICU Med-Surg
William Kelly, MSN, FNP-C
William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
13 min read
AFIB RVR on the EKG — atrial fibrillation with rapid ventricular response

Atrial fibrillation (AFib) is the most common sustained arrhythmia you'll encounter as a nurse — and when it tips into rapid ventricular response (RVR), it can turn a stable patient into an unstable one fast. You'll see it on every unit: the ER, the floor, the ICU, and the cath lab recovery bay.

Most patients with AFib are surprisingly asymptomatic. But the ones in RVR — heart rates ripping past 100, 130, 150 beats per minute — can decompensate into hypotension, chest pain, and even cardiac arrest. Recognizing AFib on the monitor and knowing the first moves to make is a core nursing skill, because you're the one at the bedside when it happens.

This guide walks through what AFib is, why RVR develops, how to spot it on the ECG, and exactly how it's managed — from your initial interventions to rate control, rhythm control, and anticoagulation.

In This Guide
  1. What Is Atrial Fibrillation?
  2. Cardiac Conduction Review
  3. What Is AFib RVR?
  4. What Causes AFib?
  5. Nursing Assessment
  6. AFib on the ECG
  7. Initial Nursing Interventions
  8. Workup for AFib RVR
  9. Complications of AFib
  10. Treatment of AFib RVR
  11. Rate Control
  12. Rhythm Control
  13. Anticoagulation

What Is Atrial Fibrillation?

Atrial fibrillation (AF or AFib) is an irregularly irregular arrhythmia that usually develops in a structurally diseased heart. It happens when too many electrical impulses — most often firing from the muscle sleeves around the pulmonary veins — overwhelm the atria, causing them to fibrillate, or "quiver," instead of contracting in an organized way.

Remember the heart's four chambers: the left and right atria on top, and the left and right ventricles below. In AFib, the top chambers are stuck in a constant state of fibrillation rather than beating in rhythm.

During a normal heartbeat, the atria contract first and push blood down into the ventricles — the so-called "atrial kick" — and then the ventricles pump that blood out to the body. In AFib, the atria lose this kick entirely. The result is ineffective atrial filling and reduced cardiac output, and that drop becomes much more pronounced at rapid rates.

The big idea: AFib means the atria are quivering instead of contracting. You lose the atrial kick, cardiac output drops, and blood pools in the atria — which is why both low output and clot formation are the dangers we manage.

Cardiac Conduction Review

To understand AFib, it helps to quickly review how the heart's electrical system normally works. The heart has specialized electrical conduction tissue that generates and moves the signal through the heart in an organized sequence — and that organization is exactly what lets the heart fill and pump effectively.

Diagram of the cardiac conduction system: SA node, AV node, Bundle of His, bundle branches, and Purkinje fibers
The cardiac conduction system — from the SA node down through the Purkinje fibers.

The heart's natural pacemaker is the sinus (SA) node, located in the right atrium. It fires the "normal" impulse, which spreads across both atria and then reaches the AV node. The AV node deliberately slows conduction down to allow time for the ventricles to fill — this brief pause is what the PR interval represents on the EKG.

From the AV node, the impulse travels through the Bundle of His, splits down the left and right bundle branches, runs through the Purkinje fibers, and finally reaches the ventricles — producing a heartbeat.

In AFib, that orderly process breaks down. Rapid, chaotic firing originates in the atria — usually where the pulmonary veins meet the left atrium — causing both atria to quiver and eliminating the atrial kick. The AV node does its best to filter this storm of impulses, but it can only slow things down so much. When too many impulses slip through to the ventricles, you get very fast heart rates — what we call AFib with RVR.

What Is AFib RVR?

AFib RVR — rapid ventricular response — occurs when those frequent atrial impulses overwhelm the AV node's ability to filter them. Too many signals conduct through to the ventricles, driving the ventricular rate above 100 bpm, and often far higher.

Patients at these fast rates are frequently symptomatic and can become hypotensive as cardiac output falls. They'll usually need IV medications to slow the rate, and if they're unstable, electrical cardioversion (more on that below).

Stable vs. Unstable

RVR itself isn't automatically a crisis — but a patient who is hypotensive, has chest pain, altered mental status, or signs of shock because of the rate is unstable and follows the ACLS tachycardia pathway. Always tie the rhythm back to how the patient looks.

What Causes AFib?

AFib usually develops in a predisposed heart and is often set off by a reversible trigger. Thinking in those two buckets — the chronic substrate underneath, and the acute trigger on top — helps you anticipate which patients are at risk and what to look for.

Chronic Conditions That Predispose the Heart
Atrial enlargement
Atrial Enlargement
CHF, cardiomyopathy, COPD, OSA, and obesity all stretch and remodel the atria.
Valvular heart disease
Valvular Heart Disease
Rheumatic disease, aortic stenosis, and valve replacements raise the risk.
Ischemic heart disease
Ischemic Heart Disease
Coronary artery disease and prior MIs leave scarred, irritable tissue.
Hyperthyroidism
Hyperthyroidism
A low TSH raises sympathetic tone and predisposes to arrhythmias.
Reversible Triggers That Set It Off
Cardiac surgery
Surgical Procedures
Common after CABG or transplant, usually within the first 2 weeks post-op.
Pulmonary embolism
Pulmonary Embolism
A PE strains the right atrium and raises pulmonary vascular resistance.
Alcohol
Alcohol
Binge drinking triggers "Holiday Heart" — seen in up to 60% of binge drinkers.
Stimulant drugs
Stimulant Drugs
Cocaine and amphetamines spike sympathetic tone and provoke arrhythmias.
Low magnesium
Hypomagnesemia
Low magnesium (often <1.5) can precipitate AFib — always check and replace.
Medications
Medications
Certain drugs, including theophylline, can trigger AFib in susceptible patients.

What about caffeine?

Caffeine is often blamed for ectopy and AFib, but the evidence doesn't actually support it as a reliable trigger. It's worth noting in the history, but don't assume the morning coffee caused the rhythm.

Nursing Assessment of AFib RVR

Up to 44% of patients with AFib are completely asymptomatic. Symptoms become more likely at faster rates, and patients with heart failure are the ones most likely to become hemodynamically unstable — think dropping blood pressure and a potential code situation.

Common Symptoms
Fatigue
Fatigue
The most common complaint patients report.
Dyspnea
Dyspnea
Shortness of breath, especially with exertion.
Palpitations
Palpitations
Fluttering, skipping, or a pounding sensation in the chest.
Dizziness
Dizziness
Lightheadedness from reduced cardiac output.
Chest pain
Chest Pain
Pressure or discomfort — always work this up.
Syncope
Syncope
Loss of consciousness — a red-flag, unstable sign.
Physical Exam
Inspection
Inspection
  • Pallor or flushing
  • Diaphoresis
  • May appear tachypneic
Vital signs
Vital Signs
  • BP: May be low at fast rates with poor output
  • HR: Often >100 (RVR), frequently irregular
  • RR: Normal or increased
  • SpO₂: Usually normal
Auscultation
Auscultation
  • Lungs: Usually clear; crackles if CHF is present
  • Heart: Rapid, irregularly irregular rhythm

Identifying AFib RVR on the ECG

This is the skill that matters most at the bedside. AFib has a few hallmark features that, once you know them, make it recognizable at a glance on the monitor or 12-lead.

Annotated ECG strip showing atrial fibrillation: absent P waves, fibrillatory baseline, and irregularly irregular R-R intervals
AFib on the rhythm strip — no discernible P waves, a fibrillatory baseline, and an irregularly irregular rhythm.
No visible P waves. Instead of organized atrial depolarization, you'll see a chaotic fibrillatory baseline — rapid "twitches" firing 350–600 times per minute.
Narrow QRS complex. The QRS stays narrow unless there's an underlying conduction delay like a bundle branch block.
Irregularly irregular R-R intervals. The spacing between beats constantly changes with no repeating pattern — this is the signature finding.
Obscured T waves. The fibrillatory baseline can bury the T waves, and T-wave flattening is common.

AFib can occur at any rate, but anything faster than 100 bpm is considered RVR. Without rate-controlling medications, untreated rates commonly run between 110 and 170 bpm.

Initial Nursing Interventions

When your patient is in AFib RVR, these are your first moves. They're also exactly what the provider will expect you to have started before they arrive at the bedside.

1
STAT 12-Lead EKG
  • Any patient with cardiac symptoms needs an EKG.
  • New AFib should be confirmed with a 12-lead.
  • At very fast rates, keep them on the monitor to capture another tracing once the rate improves or they convert.
2
Cardiac Monitoring
  • Place any symptomatic patient on the cardiac monitor.
  • Patients with known AFib at controlled rates don't always require continuous monitoring.
3
Oxygen Support

If the patient is significantly hypoxic or tachypneic, apply 2–4 L/min via nasal cannula to keep SpO₂ >90%.

4
IV Access
  • Start two peripheral IVs — at least 22g, ideally one 20g or larger. RVR patients often need a Cardizem drip and IV heparin in separate lines.
  • If PE or embolic stroke is a concern, place an 18–20g in the AC.
  • Draw a blue-top while you're in there — PT/INR, PTT, and a D-dimer may be ordered.

Unstable? Think ACLS

Any unstable tachyarrhythmia follows the ACLS tachycardia algorithm. If the patient has low BP or impending arrest, get the defibrillation pads on and prepare for synchronized cardioversion.

Workup for AFib RVR

The workup depends on whether the patient has new-onset or chronic AFib, and whether they're in RVR. Patients with known AFib and controlled rates usually need no specific testing — they're typically already on rate-control meds and an anticoagulant. New AFib or RVR warrants a broader workup.

12-lead ECG
12-Lead ECG
Confirms AFib and screens for other findings like a STEMI.
Basic labs
Basic Labs
CBC, CMP, and a magnesium level are commonly drawn.
Additional labs
Additional Labs
Coags (PT/INR, PTT), a BNP if heart failure is suspected, a digoxin level if applicable, and a D-dimer.
Chest x-ray
Chest X-Ray
Obtain for any cardiac or pulmonary complaints.
CT angiography
CTA Chest
If PE is suspected. Can detect atrial thrombi too, though not sensitively.
CT head
CT Head
For any altered mental status or stroke-like symptoms.

Complications of AFib

So why do we care so much about AFib? Because untreated, it carries three serious consequences — and understanding them is what makes the treatment plan make sense.

Hemodynamic instability
Hemodynamic Instability
Lost atrial kick plus a rapid rate drops cardiac output — leading to hypotension, hypoxemia, and potentially cardiac arrest.
Worsened heart failure
Worsened CHF
Patients with low-EF heart failure already have a weak heart; the output drop hits them hardest and can tip them into instability.
Blood clots
Blood Clots
Quivering atria cause blood stasis — one leg of Virchow's triad — raising the risk of stroke and PE.

Where the clots go

A right atrial thrombus can embolize to the lungs as a pulmonary embolism. A left atrial thrombus can travel to the brain and cause an embolic stroke. Both can be devastating — which is exactly why anticoagulation matters so much.

Treatment of AFib RVR

Treatment is individualized to the patient's symptoms, stability, and quality of life — and it's ultimately directed by the provider and cardiology team. It rests on three pillars, and a given patient may need one, two, or all three:

1 · Rate Control Slow the ventricular response without necessarily converting the rhythm

Rate control uses medications to slow conduction through the AV node, bringing the ventricular rate down. Common agents include metoprolol, diltiazem, digoxin, esmolol, amiodarone, and magnesium. For acute RVR, the two workhorses are:

Diltiazem
IV DiltiazemCardizem · calcium channel blocker
The more common first-line choice for AFib RVR. 0.25 mg/kg bolus (~20 mg) pushed over 2 minutes. A repeat 0.35 mg/kg bolus can follow in 15 minutes if rate control is inadequate, then transition to a titratable Cardizem drip.
Metoprolol
IV MetoprololLopressor · beta blocker
Especially useful if the patient takes a beta blocker at home and may have missed doses. 2.5–5 mg IV q5min ×3, each pushed over 2 minutes with close rhythm and BP monitoring. Use caution in asthma/COPD exacerbation.

The hypotension paradox

Patients with significant LV heart failure and RVR can sometimes improve their blood pressure with rate control, since slowing the rate restores filling time. A low dose of metoprolol or diltiazem may still be reasonable even with borderline hypotension — but always confirm with the provider first.

2 · Rhythm Control Convert and maintain the patient in normal sinus rhythm

Rhythm control is achieved with medications or electrical cardioversion. Unstable patients are cardioverted; otherwise a cardiologist may start an antiarrhythmic. Many elderly, minimally symptomatic patients won't pursue rhythm control at all — it's a cardiology decision.

Chemical cardioversion
Chemical Cardioversionantiarrhythmic medications
IV amiodarone, or an oral antiarrhythmic such as amiodarone, sotalol, or dofetilide, started under cardiology guidance.
Electrical cardioversion
Electrical Cardioversionsynchronized shock
Unstable patients undergo synchronized cardioversion. Remember to press SYNC; the typical starting dose is 50–100 J, and the patient needs sedation and pain control (e.g., IV fentanyl).
Ablation
Radiofrequency Ablationdefinitive procedure
Often considered in younger, frequently symptomatic patients — the triggering atrial tissue is ablated to prevent recurrence.
3 · Anticoagulation Prevent thrombus formation, stroke, and PE

Anticoagulation is almost always used in AFib unless there's active bleeding or a high bleeding risk. In the hospital, this usually means:

Heparin drip
Heparin Driptitratable IV anticoagulation
Ordered per facility protocol, often with an initial bolus. PTT is checked periodically and the drip adjusted. Its big advantage: quickly reversible if bleeding develops.
Lovenox
SubQ Lovenoxenoxaparin · LMWH
An alternative at 1 mg/kg SubQ BID.

Before discharge, patients are transitioned to an oral anticoagulant — typically a DOAC such as Eliquis, Xarelto, or Pradaxa (warfarin is used less often now due to monitoring and dietary demands). The CHA₂DS₂-VASc score helps gauge stroke risk and guide the decision, weighing factors like age, sex, heart failure, hypertension, prior stroke/TIA, vascular disease, and diabetes.

Clinical Pearls

1
There's no one-size-fits-all. Workup and treatment hinge on the patient's symptoms and overall picture — let their stability guide you.
2
Master rate control and anticoagulation. Get comfortable with IV Cardizem (and titrating a drip) and IV Lopressor — these are your bread and butter.
3
Unstable means shock. Synchronized cardioversion, 50–100 J, press SYNC, and don't forget sedation and pain control.
ECG Rhythm Master course

Want to master every rhythm?

My complete video course ECG Rhythm Master is built specifically for nurses. With it you'll:

  • Identify every cardiac rhythm inside and out
  • Understand the pathophysiology behind each arrhythmia
  • Manage arrhythmias like an expert nurse
  • Get proficient with pacing, defibrillation, and synchronized cardioversion
Check Out the Course →

Related Guides

STEMI and NSTEMI guide
STEMI & NSTEMI: A Nurse's Comprehensive Guide
Advanced cardiovascular assessment
Advanced Cardiovascular Assessment for Nurses
Pulmonary embolism guide
Pulmonary Embolism: A Nurse's Reference Guide

Blood Pressure Crash Course for nurses

by | Mar 3, 2022 | New Nurse, Cardiac, Critical care, Emergency (ER), Med-Surg, Procedures & Skills | 5 comments

Home› Cardiac & ECG› Blood Pressure Crash Course
Cardiac Med-Surg ER New Nurse

Blood Pressure: A Crash Course for Nurses

William Kelly, MSN, FNP-C
William Kelly, MSN, FNP-C
Updated June 2026
12 min read
How to take a manual blood pressure

Blood pressure is one of the five vital signs, and knowing what's normal, what's not, and how we manage each is core to bedside nursing. In the hospital, vitals are usually checked every 4 hours, and you'll run into both high and low readings constantly.

Low blood pressure is often the more worrisome of the two, and you may want to call an RRT if it's significantly low, especially when the patient is altered or symptomatic. High blood pressure is common and usually not an emergency unless it's very high, where the goal is to bring it down slowly rather than too fast.

In This Guide
  1. What Is Blood Pressure?
  2. "Normal" Blood Pressure
  3. How to Measure It
  4. Mean Arterial Pressure (MAP)
  5. Hypertension
  6. Treating Hypertension
  7. Hypotension
  8. Treating Hypotension

What Is Blood Pressure?

Blood pressure isn't the pressure of your blood — it's the pressure within your vascular system. When we talk about systemic blood pressure, we mean the pressure inside the arteries, which rises with each heartbeat and falls in between.

Systole versus diastole
Systole is the pressure during the heartbeat; diastole is the resting pressure between beats.

The pressure in the arteries while the heart contracts is the systolic pressure (the top number). When the heart relaxes between beats, the pressure settles to its baseline — the diastolic pressure (the bottom number). Systolic is always higher than diastolic, and diastolic should never read 0. Both are measured in millimeters of mercury (mmHg).

"Normal" Blood Pressure

A normal systolic runs roughly 100–120 mmHg and a normal diastolic 60–80 mmHg. The old "gold standard" of 120/80 is now framed as an upper limit — you want to be at or below 120/80.

"Good" Is Relative

In the ER, anything under 160/90 is often considered fine and won't need meds in the moment. But 160/90 as someone's everyday home pressure is genuinely high and should be treated. Context matters as much as the number.

How to Measure Blood Pressure

We check blood pressure everywhere — the hospital, the clinic, and just about every patient encounter. Machines do most of the work now, but they aren't perfect, and knowing how to do it yourself is an essential nursing skill. There are three main methods:

Manual Blood PressureSphygmomanometer + stethoscope

Place the stethoscope over the brachial artery and the cuff on the bicep. Pump the cuff to about 160–180 mmHg (higher if the BP is very high), then slowly release while you auscultate. The first Korotkoff sound is the systolic; the point where the sounds disappear is the diastolic.

Palpating a Pressure

While a cuff inflates or deflates, you can palpate the radial artery. When the pulse disappears, that's your systolic. There's no way to get a diastolic by palpation.

Automated Blood PressureDinamap or bedside monitor

A machine essentially performs a manual BP on its own using oscillometry. A sensor detects tiny oscillations from your pulse — when the pulse vanishes, that's the systolic; when it returns, that's the diastolic.

Arterial LineMost accurate, ICU

An a-line measures pressure directly from inside the artery via a sensor, rather than indirectly like the methods above. It's the most accurate option and gives real-time changes, which is why it's common in the ICU for strict monitoring.

What Is the "MAP"?

Once you've been at the bedside a while, you'll hear about the MAP. While systolic gets most of the attention, the MAP is often the number that actually matters. MAP stands for Mean Arterial Pressure — the average pressure in the arteries across one cardiac cycle.

Mean arterial pressure equation
MAP ≈ (SBP + 2 × DBP) ÷ 3.

Don't reach for a calculator, though — the bedside monitor calculates MAP for you, as does most EMRs, and there are quick online calculators if you need one. MAP is a great marker of tissue perfusion: keeping it above 65 mmHg generally provides enough pressure to perfuse the organs and prevent anoxic injury. In the ICU especially, providers care far more about MAP than systolic when the pressure is low.

Hypertension

Hypertension — high blood pressure — is often dismissed as "no big deal," but it's a genuine silent killer. Over time it strains the heart, vasculature, and kidneys, raising the risk of heart disease, stroke, and kidney failure. It's called silent because it's usually asymptomatic, which doesn't make it any less dangerous in the long run.

Blood pressure level categories
Blood pressure categories at a glance.

The current ACC/AHA (2017) guideline classifies blood pressure into four categories:

Normal
< 120 / 80 mmHg
Elevated
120–129 / < 80 mmHg
Stage 1 HTN
130–139 / 80–89 mmHg
Stage 2 HTN
≥ 140 / 90 mmHg

Hypertension can be chronic or acute, and it's always worth asking about symptoms like chest pain, shortness of breath, or headache. Here are the three forms you'll hear about most:

Primary HypertensionFormerly "essential" HTN

Chronic high blood pressure with no single clear cause, thought to involve genetics, diet, and lifestyle. This is what most people with HTN are diagnosed with. Risk factors include:

  • Older age
  • Obesity
  • Family history of HTN
  • Black race
  • High-sodium diet
  • Excessive alcohol
  • Sedentary lifestyle
Hypertensive Urgency> 180 / 120 mmHg, no organ damage

A very high pressure (> 180/120 mmHg) without evidence of organ damage — no concerning symptoms or lab abnormalities — but the patient is at risk for organ damage or stroke.

Hypertensive Emergency> 180 / 120 mmHg WITH organ damage

The same very high pressure (> 180/120 mmHg) but now there is evidence of end-organ damage. Look for at least one of:

  • Chest pain or shortness of breath
  • Pulmonary edema
  • Severe headache, seizures, or confusion
  • Elevated troponin
  • Acute kidney injury (rising creatinine)

Treating Hypertension

Treatment is often not aggressive — usually slow, gradual adjustments to an outpatient regimen. If the patient is symptomatic, BP meds should be given. And because pressures run higher in urgent and emergency settings ("white coat hypertension" is common), home readings matter for the real picture.

Common Oral Antihypertensives

ACE inhibitors Lisinopril ARBs Losartan Calcium channel blockers Amlodipine Beta-blockers Metoprolol Diuretics HCTZ Central alpha-2 agonists Clonidine

IV Options (hospital / urgency)

IV Hydralazine Hydralazine Calcium channel blockers CardizemNicardipine Beta/alpha blocker Labetalol Beta-blocker Metoprolol (Lopressor)

Never Drop the Pressure Too Fast

Lowering blood pressure too quickly can cause ischemic damage, because a body used to chronically high pressure relies on it for perfusion. In severe cases, the goal is to lower the MAP by 10–20% in the first hour, then another 5–15% over the next day — often less than 180/120 in the first hour and under 160/110 by 24 hours.

Always Ask About Symptoms

With any abnormal blood pressure (or heart rate), ask the patient how they feel. Screen for chest pain, shortness of breath, dizziness, palpitations, headache, and numbness or tingling. Symptoms change the urgency.

Hypotension

Hypotension is when the blood pressure is too low — technically anything under 100/60 mmHg, though it's often not treated as true hypotension until below 90/50 mmHg. Patients who are small and thin may simply run borderline-low at baseline.

Trend Before You Worry

Worried about a low BP? Trend it across this visit and previous ones. If it's 92/48 but they always run there and feel fine, that's reassuring. A new drop is far more concerning than a stable baseline.

Remember, a MAP under 65 mmHg puts the patient at risk for tissue ischemia and organ damage. In the hospital, low blood pressure is often a serious sign. Common causes include:

Sepsis
Persistent hypotension despite a 30 mL/kg fluid bolus. Needs pressors, a central line, IV antibiotics, and the ICU.
Anaphylaxis
Distributive shock from a severe allergy — massive vasodilation and swelling. Treat with epinephrine, steroids, and antihistamines.
Hemorrhage
Enough blood loss drops the pressure. These patients need STAT blood, often uncrossmatched O negative.
Cardiogenic Shock
The heart can't keep up with demand — seen in severe CHF or bradyarrhythmias.
Medications
BP meds at the wrong dose (or toxic levels) can over-shoot. Others, like amiodarone, list hypotension as a side effect.
Adrenal Insufficiency
A history of adrenal insufficiency often calls for stress-dose steroids to hold the pressure up.
Severe Dehydration
Has to be severe before pressure drops — think DKA, diabetes insipidus, or anything causing major fluid loss.

Treating Hypotension

Treatment always means addressing the underlying cause, but it generally starts with two steps:

1
Fluid Boluses

IV fluids to increase the circulating volume.

2
Vasopressors

If fluids don't hold the pressure (or it drops again afterward), pressors constrict the vessels — usually in the ICU.

From there, match the treatment to the cause:

Blood for blood loss.
Antibiotics and fluids for sepsis.
Steroids for adrenal crisis.
Steroids and antihistamines (plus epinephrine) for anaphylaxis.

Wrapping Up

1Double-check the pressure. If a reading doesn't fit the patient, recheck it manually — the provider will likely ask you to anyway.
2Always ask about symptoms. Chest pain, shortness of breath, dizziness, headache, palpitations, syncope — symptoms decide how urgent a number really is.
3Trend the pressures. Don't over-react to a high reading in an asymptomatic patient, and never correct it too fast. Look at the history.
4Worry more about low than high. A truly low pressure (or low MAP) threatens perfusion right now — escalate early.

Check Out Related Articles

CardiacAdvanced Cardiovascular Assessment for Nurses
CardiacAFib RVR on EKG: Managing Atrial Fibrillation
Critical CarePulmonary Embolism: Nurse's Reference Guide
ECGVTACH + VFIB: A Nurse's Guide to Ventricular Arrhythmias

References

  1. Basil, J., & Bloch, M. J. (2022). Overview of hypertension in adults. In T. W. Post (Ed.), UpToDate. uptodate.com
  2. Gaieski, D. F., & Mikkelsen, M. E. (2022). Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock. In T. W. Post (Ed.), UpToDate. uptodate.com
  3. Calder, S. A. (2012). Shock. In B. B. Hammond & P. G. Zimmerman (Eds.), Sheehy's Manual of Emergency Care (7th ed., pp. 213–221). Elsevier.
  4. Roe, D. M. (2015). Cardiac emergencies. In B. A. Tscheschlog & A. Jauch (Eds.), Emergency Nursing Made Incredibly Easy! (2nd ed., pp. 97–197). Lippincott Williams & Wilkins.
  5. Whelton, P. K., et al. (2018). 2017 ACC/AHA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Hypertension, 71(6).

Pulmonary Embolism: Nurse’s Reference Guide

by | Feb 10, 2022 | Emergency (ER), Cardiac, Critical care, HemOnc, ICU, Med-Surg, Pulmonary | 14 comments

Pulmonary Embolism: A Nurse's Reference Guide

Emergency (ER) Respiratory Critical Care
William Kelly, MSN, FNP-C
William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
14 min read
Pulmonary embolism: a nurse's reference guide

A pulmonary embolism (PE) is a blood clot that lodges in the pulmonary vasculature of the lungs. Sometimes it's asymptomatic, often it causes mild-to-moderate symptoms, and other times patients go straight into cardiac or respiratory arrest.

No matter the presentation, pulmonary embolisms can be deadly. This guide walks through the causes, assessment, diagnosis, treatment, and monitoring you need to know to care for these patients at the bedside.

In This Guide
  1. What Is a PE?
  2. Causes & Virchow's Triad
  3. Nursing Assessment
  4. Nursing Interventions
  5. Diagnosis of a PE
  6. Treatment
  7. Patient Monitoring
  8. References

What Is a Pulmonary Embolism?

A pulmonary embolism is a blood clot that lodges within the lungs. They can be large or small, single or many at once. The larger and more numerous the clots, the more dangerous — a PE can put significant strain on the heart and even cause cardiac arrest.

Hs & Ts. Remember that a Thrombus is one of the Hs and Ts to think about when a patient is coding. PEs are also highly associated with deep vein thrombosis (DVT) — and VTE (venous thromboembolism) is the umbrella term for any clot, including DVTs and PEs.

Causes of a PE: Virchow's Triad

Many things can cause a PE, but it all traces back to Virchow's Triad — for a clot to form, at least one of three conditions must be present. The more a patient has, the higher their risk (though a small percentage clot with none of these).

Stasis of blood
Stasis of Blood
Anything that makes blood "sit still": immobility, hospitalization, varicose veins, atrial fibrillation, heart failure, or elderly age (>65).
Endothelial injury
Endothelial Injury
Damage to vessels: recent surgery (especially orthopedic), trauma, chemotherapy, implanted devices, central lines, inflammation, or sepsis.
Hypercoagulable state
Hypercoagulable State
Increased clotting tendency: malignancy, estrogen (birth control), pregnancy, inherited mutations (Factor V Leiden), severe liver disease, smoking, or obesity.
Virchow's triad: stasis, endothelial injury, and hypercoagulable state
Virchow's Triad — the three drivers of clot formation.

Nursing Assessment

Patients with a PE usually present with shortness of breath. An area of the lung can still take in oxygen but can't exchange it for carbon dioxide at the clot site, creating a ventilation-perfusion (V/Q) mismatch.

Symptoms
Dyspnea
Dyspnea
Shortness of breath — with exertion or at rest. The most common symptom.
Chest pain
Chest Pain
Usually pleuritic — worse with deep breaths or coughing.
Cough
Cough
Usually non-productive, but may have pink frothy or bloody sputum.
Syncope
Syncope
Syncope with chest pain and SOB is suspicious for PE.
Signs of DVT
Signs of DVT
Extremity erythema, edema, or pain — clues to the clot's origin.

Hemoptysis Is Overrated

Coughing up blood (hemoptysis) is not nearly as common a PE symptom as your nursing textbook may have suggested. Many patients are asymptomatic or have vague symptoms — and some go straight into cardiac arrest, especially with very large PEs.

Physical exam
Inspection
Inspection
Respiratory distress — tachypnea, increased work of breathing, accessory muscle use — plus cough, pallor, and diaphoresis. Tachypnea is usually the first thing you'll notice.
Vital signs
Vital Signs
Temp may be low-grade; BP normal, high (pain), or low (severe); HR tachycardic (>100); RR increased; SpO₂ normal or low.
Auscultation
Auscultation
Lungs often normal, may be diminished; crackles if pulmonary infarct or acute CHF; possible pleural friction rub. Heart tachycardic.
Pleuritic pain pattern
Pleuritic Breathing
Pleuritic chest pain limits full breaths, so patients compensate with frequent shallow breathing — driving the respiratory rate up.
Quick tip: if a patient has chest pain or SOB and recently had surgery or is pregnant, always think PE. Very large PEs can cause hemodynamic compromise including hypotension and shock.

Nursing Interventions

1
Cardiac Monitoring

Place all chest-pain/SOB patients on a monitor. PEs often cause sinus tachycardia that doesn't fully resolve with fluids, plus arrhythmias like atrial fibrillation, bradycardia, RBBB, PVCs, and VTach/VFib.

2
STAT EKG

Obtain an EKG within 10 minutes of arrival — primarily to rule out STEMI/ischemia. Large PEs can cause right heart strain; in <10% of patients you may see a right heart strain pattern or the classic S1Q3T3.

3
Oxygen Support

If hypoxic or tachypneic, apply 2–4 L/min NC; titrate to SpO₂ >90%. Escalate to a non-rebreather, then BiPAP or intubation if needed.

4
IV Access & Labs

Start a large-bore peripheral IV (18–20g) in the AC — these patients will likely need a CTA, and high-pressure dye requires a big line. Draw a blue top (D-dimer, PT/INR) while you're in there.

S1Q3T3 pattern of right heart strain on EKG
The S1Q3T3 pattern — a classic (if uncommon) sign of right heart strain.

Diagnosis of a PE

Wells' criteria
Wells' Criteriaclinical risk stratification
A clinical tool that assigns points to estimate PE risk:
  • Signs of DVT — 3 points
  • PE the #1 likely diagnosis — 3 points
  • HR >100 bpm — 1.5 points
  • Immobilization ×3 days — 1.5 points
  • Surgery within 4 weeks — 1.5 points
  • Previous PE/DVT — 1.5 points
  • Hemoptysis — 1 point
  • Malignancy (treated within 6 mo or palliative) — 1 point
Low risk: 0–1 · Moderate: 2–6 · High: >6. A score of ≤4 with a negative D-dimer can effectively rule out a PE.
D-dimer
D-Dimersensitive, not specific
A byproduct of fibrin that rises whenever there's a clot — useful to minimize radiation in low-to-moderate suspicion. A negative D-dimer (below threshold, ~230 depending on the lab) reliably rules out a clot when suspicion is low to moderate. But it's not specific: bruising, pregnancy, heart disease, and infection all raise it, so a positive result usually forces a CTA. In high-likelihood patients, a D-dimer can miss a PE up to 15% of the time.
Other lab work
Other Lab Worktroponin, BNP, renal, coags
Order a troponin for chest pain/SOB (may be mildly elevated, or high if the PE causes an MI). A BNP if heart-failure signs are present. Check renal function before a CTA — a GFR >30 is usually adequate for dye. Coagulation studies may be done inpatient to find genetic clotting predispositions.
ABG
ABGif significant distress
Obtained if the patient is in significant respiratory distress or has AMS. A PE causing distress typically shows: PaO₂ low (<80), PCO₂ low (<35), pH alkalotic (>7.45), and HCO₃ possibly low (<22) — see ABG interpretation.
Chest X-ray
Chest X-rayrules out mimics
Almost always ordered — it rules out pneumothorax or pneumonia, but won't show the PE itself. It may reveal nonspecific atelectasis or effusions, or be completely normal.
CT pulmonary angiography
CTA (CT Pulmonary Angiography)the definitive test
Radiopaque dye is injected to visualize the pulmonary vasculature on CT, letting the radiologist directly see the embolism. Avoid contrast if GFR <30 (facility-dependent). If dye can't be given (low GFR or anaphylaxis), the alternative is a V/Q scan.
CT pulmonary angiography showing pulmonary emboli
CT pulmonary angiography directly visualizes the clot.
V/Q scan
V/Q Scannuclear medicine alternative
Uses radioisotopes with X-rays to detect ventilation/perfusion mismatches. Less definitive than a CTA — it gives probabilities (e.g., "very low probability"). The CXR should be clear, since significant consolidation or effusions make the scan unreliable.

Treatment of a PE

For a hemodynamically stable patient, treatment is admission, parenteral anticoagulation, then transition to oral anticoagulation. Patients with significant hemodynamic compromise may need reperfusion therapy.

Parenteral anticoagulation
Parenteral Anticoagulationheparin drip
Usually IV unfractionated heparin as a titratable drip guided by PTT (checked ~every 6 hours per protocol): a bolus IV, then a slow drip. SQ Lovenox 1 mg/kg BID is an alternative. Anticoagulants don't dissolve the existing clot — they prevent new clots and stabilize the existing one from breaking off and embolizing further.

Why Heparin Over Lovenox?

IV heparin is often preferred because it's more easily titrated and stopped quickly — useful if bleeding occurs or a procedure is needed while inpatient.

Oral anticoagulation
Oral Anticoagulationlong-term therapy
Stable patients may start directly on an oral agent (Eliquis, Coumadin) and go home, depending on the provider. Most need at least 3 months of therapy (the clot typically reabsorbs in ~6 weeks). Some need lifelong anticoagulation (genetic clotting disorders, atrial fibrillation). Not started in very recent surgery, hemorrhagic stroke, or active bleeding.
IVC filter
IVC Filtercatches clots
An inferior vena cava filter "catches" clots before they reach the right atrium. Used for patients who can't be anticoagulated or who get repeat PEs despite therapy. Can be temporary or permanent.
Thrombolytics
Thrombolyticsfor unstable patients
In hemodynamically unstable patients, thrombolytics dissolve the clot — like TPA in a stroke, but for a PE. There are many contraindications and a real bleeding risk.
Procedural removal
Procedural Removalembolectomy
An embolectomy can be performed when thrombolytics fail or are contraindicated, if the facility is capable. Options include ultrasound-assisted thrombolysis, rheolytic/rotational/suction embolectomy, thrombus fragmentation, and surgical embolectomy. Most facilities have thrombolytics but not all of these.

Saddle PE

A saddle PE is a very large clot at the bifurcation of the main pulmonary artery. Rare, but likely to cause significant hemodynamic compromise and cardiopulmonary arrest.

Patient Monitoring

Monitoring mainly consists of watching vital signs and supporting the patient through treatment.

Cardiac rhythm
Cardiac Rhythm
Continuous monitoring for tachycardia and arrhythmias — sinus tach that doesn't fully resolve with fluids is common.
Oxygenation
Oxygenation
Track SpO₂ and work of breathing; escalate support (NC → NRB → BiPAP → intubation) as needed.
Anticoagulation labs
Anticoagulation Labs
On a heparin drip, follow PTT (usually every 6 hours per protocol) and titrate accordingly.
Hemodynamics
Hemodynamics
Watch for hypotension and shock — signs a large PE is straining the right heart.
Bottom line: pulmonary embolisms are serious and potentially deadly. Knowing how to assess, anticoagulate, and monitor these patients — and when to escalate to reperfusion therapy — is essential bedside care.

Clinical Pearls

1
Surgery or pregnancy + chest pain/SOB = think PE. These are major Virchow's Triad red flags; a high index of suspicion saves lives.
2
Place a large-bore AC IV early. A CTA needs high-pressure dye injection, so an 18–20g AC line saves time when the patient heads to CT.
3
D-dimer rules out, it doesn't rule in. Use it for low-to-moderate suspicion; a positive result usually means a CTA is coming.
4
Anticoagulation stabilizes, it doesn't dissolve. Heparin prevents new and propagating clots — thrombolytics are what actually break down the clot in unstable patients.

Related Guides

Respiratory assessment and lung sounds
Respiratory
Lung Auscultation & Respiratory Assessment
Advanced cardiovascular assessment
Assessment
Advanced Cardiovascular Assessment
AFib RVR management
Cardiac
AFib RVR: Managing Atrial Fibrillation
Blood pressure crash course
Assessment
Blood Pressure Crash Course

References

Clinical Databases & Guidelines
  1. Thompson BT, Kabrhel C. Overview of acute pulmonary embolism in adults. UpToDate.
  2. Thompson BT, Kabrhel C, Pena C. Clinical presentation, evaluation, and diagnosis of suspected acute PE. UpToDate.
  3. Tapson VF, Weinberg AS. Treatment, prognosis, and follow-up of acute PE in adults. UpToDate.
  4. Haag A, et al. Pulmonary embolism. WikEM.
  5. Sharma R. Pulmonary embolism. Radiopaedia.org.

VTACH + VFIB | A Nurse’s Guide to Ventricular Arrhythmias

by | Aug 19, 2021 | ECG, Cardiac, Critical care, Emergency (ER), ICU | 3 comments

VTACH & VFIB: A Nurse's Guide to Ventricular Arrhythmias

Cardiac ECG Emergency (ER) Critical Care
William Kelly, MSN, FNP-C
William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
11 min read
A nurse's guide to ventricular arrhythmias: VFIB and VTACH

Ventricular arrhythmias like VTACH and VFIB occur in and out of the hospital — the difference is that outside it, no one is on the monitor, so instead of catching the arrhythmia you find the patient unresponsive.

VTACH and VFIB are huge deals, and these rhythms are deadly. Knowing how to recognize them is essential for any nurse in the inpatient or ER setting.

In This Guide
  1. What Is a Ventricular Arrhythmia?
  2. What Causes Them?
  3. Identifying VTACH
  4. Monomorphic VTACH
  5. Polymorphic VTACH & Torsades
  6. QT Prolongation
  7. Identifying VFIB
  8. VFIB & VTACH Management
  9. Reversible Hs & Ts
  10. References

What Is a Ventricular Arrhythmia?

Ventricular arrhythmias are those originating from the ventricles. Since the ventricles pump blood to the lungs and throughout the body, ventricular arrhythmias are often deadly.

When we talk about them, we're primarily talking about VTACH (ventricular tachycardia) or VFIB (ventricular fibrillation). Ventricular escape rhythm is a backup rhythm for very slow heart rates and isn't covered here.

VTACH
VTACH
A fast rhythm originating in the ventricles. May or may not perfuse — the patient may have a pulse, or may be pulseless and in cardiac arrest.
VFIB
VFIB
Chaotic, disorganized firing of all the ventricular cells. Never perfuses — it is always a CODE BLUE and degenerates into asystole unless reversed.

What Causes Ventricular Arrhythmias?

Ventricular arrhythmias are usually caused by coronary artery disease (CAD). Any lack of blood flow (i.e. a heart attack) deprives ventricular cells of oxygen. When the cardiac myocytes become hypoxic, they become irritable and prone to firing when they shouldn't, which leads to PVCs, VTACH, and even VFIB.

Coronary artery disease / MI — the most common cause; hypoxic myocytes become irritable.
Severe electrolyte abnormalities — especially low magnesium, potassium, or calcium.
QT prolongation from medications.
Aortic stenosis or dissection.
Blunt chest trauma.
Genetic or inherited syndromes.

Identifying VTACH

VTACH is a tachycardic rhythm originating within the ventricles. This produces very fast heart rates which may or may not be perfusing — meaning the patient may not have a pulse.

If they do have a pulse, the patient may be asymptomatic, but more likely will experience:

Chest pain
Chest Pain
From the strain of the very fast, poorly perfusing rhythm.
Shortness of breath
Shortness of Breath
Reduced cardiac output from impaired ventricular filling.
Dizziness
Dizziness
Lightheadedness from falling cardiac output.
Syncope
Syncope
Loss of consciousness if perfusion drops far enough.

If VTACH is pulseless, the patient will go unresponsive and be a CODE BLUE. VTACH is essentially a "run" of PVCs that just doesn't stop. There are different types based on morphology (how it looks): Monomorphic and Polymorphic VTACH.

Monomorphic VTACH

EKG rhythm strip showing monomorphic ventricular tachycardia
Monomorphic VTACH — a regular, wide-complex tachycardia.

Monomorphic VTACH originates from the same ventricular focus. The same cells act as the pacemaker, and the rest of the heart follows their lead.

Regular R-R interval.
HR 100–330 bpm (often near 200).
Wide QRS (>140 ms, or 3.5 small boxes).
AV dissociation: P waves are absent in about 40% of cases, but in the rest you may see them with no relation to the QRS — superimposed P waves marching through the VTACH.
AV dissociation in monomorphic VTACH with superimposed P waves, fusion, and capture beats
AV dissociation with visible superimposed P waves, plus occasional fusion and capture beats.

The morphology of monomorphic VTACH looks different depending on whether it arises from the left or the right ventricle. Knowing which doesn't change management, so just be aware that there can be more than one general "look."

Different morphologies of monomorphic VTACH depending on the ventricle of origin
Monomorphic VTACH morphology varies with the ventricle of origin.

Polymorphic VTACH & Torsades de Pointes

Polymorphic VTACH / Torsades de Pointes with a twisting ribbon-like appearance
Torsades de Pointes — a polymorphic VTACH with a twisting, ribbon-like appearance.

Polymorphic VTACH originates from multiple different ventricular foci. Different regions of cells fire impulses, leading to an irregular, deadly rhythm.

Irregular rhythm.
Wide but differing QRS morphologies.
No distinguishable P waves.

The most common polymorphic VTACH is Torsades de Pointes — literally "twisting of the points." It creates a ribbon-like effect that looks like it's twisting in on itself, usually caused by a prolonged QT interval from electrolyte abnormalities or medications. Torsades is unstable and often degenerates into VFIB.

QT Prolongation

The QT interval measured on an EKG
Measuring the QT interval.

QT prolongation is the main driver of Torsades, defined as a QT interval >440 ms in men and >460 ms in women. Dangerous ventricular arrhythmias are unlikely until >500 ms. It's caused by:

Electrolyte abnormalities
Electrolyte Abnormalities
Hypomagnesemia, hypokalemia, and hypocalcemia.
Medications
Medications
Antipsychotics, certain antibiotics, and antiemetics.
Ischemia
Ischemia
Reduced coronary blood flow.
Congenital or acquired disorders
Congenital / Acquired
Inherited long-QT syndromes and other acquired disorders.

Identifying VFIB

VFIB is similar to polymorphic VTACH but on a much wider scale. Essentially all of the ventricular cells are irritable, producing a disorganized, chaotic arrhythmia that does not perfuse the body and is a CODE BLUE. It will degenerate into asystole unless rapidly reversed.

VFIB is usually caused by CAD, with active or previous myocardial infarction being a primary cause, along with the other causes of ventricular arrhythmias — severe electrolyte abnormalities, hypoxia, or trauma (see the Hs & Ts below).

Irregular — completely chaotic.
No organized pattern. Either coarse (>3 mm amplitude) or fine (<3 mm amplitude) fibrillation.
EKG rhythm strip showing ventricular fibrillation
VFIB — chaotic, disorganized, no identifiable complexes.

VFIB & VTACH Management

Now that we can identify these rhythms — what do we actually do? First, know that you will not be dealing with this alone. These are true emergencies: a Code Blue or RRT should be called, and other nurses and providers will arrive to help. Management is covered extensively in ACLS, which should always be followed. Here are the 5 basic steps in the hospital setting.

1
Check for a Pulse / Breathing

If you see a ventricular arrhythmia on the monitor, assess your patient first — go (preferably run) to the room and check responsiveness. If unresponsive, immediately check a carotid pulse and breathing at the same time. In true VFIB the patient is always unresponsive and pulseless. VTACH is hit or miss; if pulseless, it's treated just like VFIB.

2
Call an RRT or Code Blue

If the patient is pulseless, call for help and call a Code Blue. If they have a pulse but are in VTACH, call an RRT — it's still emergent and they can go down at any minute. This is the in-hospital equivalent of activating the emergency response system in BLS.

3
Start CPR If Needed

If the patient is pulseless, immediately start compressions as you call for help. Per ACLS, compress at a rate of 100–120 bpm, at least 2 inches or ⅓ the depth of the chest, at 30 compressions for every 2 breaths until the patient is intubated, then continuously.

4
Give Life-Saving Treatment

Defibrillation is the goal with unstable or pulseless ventricular arrhythmias because it can restore a perfusing rhythm — and each minute of delay drops the chance of success. Epinephrine 1 mg IV every 3–5 minutes is given in pulseless codes. Antiarrhythmics like amiodarone (sometimes lidocaine) can chemically convert the rhythm.

5
Reverse Any Known Causes (Hs & Ts)

ACLS teaches the Hs and Ts — an acronym to brainstorm reversible causes of these arrhythmias (as well as asystole or PEA). Once a potential cause is found, it should actively be reversed. See the full list below.

Pulseless = Defibrillate

Time is muscle — and brain. For pulseless VTACH and VFIB, high-quality CPR plus early defibrillation is what restores a perfusing rhythm. Don't wait.

ECG Rhythm Master course

Master Every Rhythm with ECG Rhythm Master

A complete video course built for nurses — go far deeper on ventricular arrhythmias, their pathophysiology, and how to manage them like an expert.

  • Identify all cardiac rhythms inside and out
  • Understand the pathophysiology behind arrhythmias
  • Get hands-on with defibrillation, synchronized cardioversion & pacing
Check Out the Course

Reversible Hs & Ts

Use this acronym to brainstorm and reverse the causes of cardiac arrest:

Hypovolemia
Hypovolemia
From hemorrhage or shock, though it must be severe to cause arrest.
Hypoxia
Hypoxia
From pulmonary embolism or respiratory failure.
Hydrogen ions / acidosis
Hydrogen Ions (Acidosis)
From severe DKA or respiratory failure.
Hyperkalemia
Hyperkalemia
Usually secondary to severe ESRD or AKI.
Hypokalemia
Hypokalemia
From severe GI losses, diuretics, or decreased intake.
Hypothermia
Hypothermia
From environmental exposure, hypoglycemia, or severe sepsis.
Tension pneumothorax
Tension Pneumothorax
Usually from penetrating trauma or spontaneous.
Cardiac tamponade
Tamponade (Cardiac)
From chest trauma, MI, or pericarditis.
Toxins
Toxins
Overdoses of opioids, benzos, TCAs, beta-blockers, or CCBs.
Thrombosis
Thrombosis
Large pulmonary embolism or myocardial thrombosis / infarction.

Clinical Pearls

1
Assess the patient, not the monitor. Any ventricular arrhythmia on the screen means going to the bedside and checking a pulse and breathing first.
2
Pulseless VTACH is treated like VFIB. CPR plus early defibrillation is the priority.
3
Torsades means think QT. A twisting polymorphic VTACH points to a prolonged QT — check magnesium, potassium, and the med list.
4
Always work the Hs & Ts. Reversing the underlying cause is often what brings the patient back for good.

Related Guides

How to read an EKG rhythm strip
ECG
How to Read an ECG Rhythm Strip
STEMI and NSTEMI guide
Cardiac
STEMI & NSTEMI: A Nurse's Guide
Vagal maneuvers for SVT
Cardiac
Vagal Maneuvers: Stop SVT
Cardiac lab interpretation
Labs
Cardiac Lab Interpretation & Troponin

References

Clinical Databases & Guidelines
  1. Pozner CN, Post TW. Advanced cardiac life support (ACLS) in adults. UpToDate.
  2. Prutkin JM. ECG tutorial: Ventricular arrhythmias. UpToDate.
  3. Ganz LI, Buxton A. Sustained monomorphic ventricular tachycardia: clinical manifestations, diagnosis, and evaluation. UpToDate.
  4. Burns E. Polymorphic VT and Torsades de Pointes (TdP). LITFL ECG Library.
  5. Burns E. Ventricular Fibrillation (VF). LITFL ECG Library.
Textbooks
  1. Dubin D. Rapid Interpretation of EKG's (6th ed.). Cover Pub. Co.
  2. Grauer K. ECG Pocket Brain: Expanded Version (6th ed.). KG/EKG Press.

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

by | Jun 16, 2021 | Cardiac, Critical care, ECG, Emergency (ER), ICU, Med-Surg, Popular | 9 comments

STEMI & NSTEMI: A Nurse's Guide to Reading & Managing Heart Attacks

Cardiac ECG Emergency ICU Critical Care Med-Surg
William Kelly, MSN, FNP-C
William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
15 min read
STEMI and NSTEMI: a nurse's guide to reading and managing heart attacks

A STEMI — ST-Segment Elevation Myocardial Infarction — is the most dangerous type of heart attack, and recognizing it fast on the 12-lead can save your patient's heart muscle and their life.

An NSTEMI (Non-STEMI) is still a heart attack, but without ST elevation on the ECG. Ruling out a STEMI is the whole reason 12-leads get ordered, and the sooner one is caught, the better the outcome. Providers should lay eyes on every ECG quickly, but that doesn't always happen on time. The faster a STEMI is identified, the more heart tissue survives — and that recognition often starts with the nurse.

In This Guide
  1. Coronary Artery Anatomy
  2. Acute Coronary Syndrome
  3. Ischemia & Infarction on the ECG
  4. ST-Segment Depression
  5. ST-Segment Elevation
  6. Q Waves
  7. LBBB or Ventricular Paced
  8. STEMI Progression
  9. STEMI Location
  10. Acute Management of STEMI
  11. NSTEMI Management

Coronary Artery Anatomy

The coronary arteries lie on the surface of the heart (the epicardium) and deliver the blood and oxygen that keep the myocardium perfused and beating. The three main vessels are the left anterior descending (LAD), the circumflex (Cx), and the right coronary artery (RCA). Knowing what each one feeds tells you which wall is in trouble when you see changes on the ECG.

Right Coronary Artery (RCA)
Right atrium and ventricle, the inferior/posterior LV (~85%), the SA node (~60%), and the AV node (~85–90%).
Left anterior descending artery
Left Anterior Descending (LAD)
Anterior wall and part of the lateral LV, plus the anterior two-thirds of the interventricular septum.
Circumflex artery
Circumflex (Cx)
Left atrium and the lateral LV; the SA node (~40%) and AV node (~10–15%) in some people.
Posterior descending artery
Posterior Descending (PDA)
Branches off the RCA (most people) or the Cx. Whichever supplies it is the "dominant" coronary artery.

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is the umbrella term for any condition that drops blood flow to the heart — ischemia. Prolonged ischemia leads to infarction, the death of heart tissue, which releases troponin into the bloodstream.

Most cardiac ischemia is caused by atherosclerosis — plaque buildup in the coronary arteries from factors like diet, obesity, sedentary lifestyle, hyperlipidemia, smoking, and genetics. When that plaque ruptures, it spills its contents, triggers local inflammation and a coagulation cascade, and the resulting clot can completely occlude the artery, causing infarction.

Coronary plaque rupture leading to clot formation and arterial occlusion
Plaque rupture triggering clot formation and occlusion.
STEMI vs NSTEMI in one line: a STEMI is a full-thickness (transmural) infarction with ST elevation in contiguous leads; an NSTEMI is a smaller, usually subendocardial infarction with a rising troponin but no ST elevation.

An NSTEMI often shows nonspecific changes — T-wave inversion or ST depression in contiguous leads, with or without inversion — and the ECG can even be completely normal. Troponin is elevated, confirming cell death. A STEMI, by contrast, shows ST elevation in at least 2 contiguous leads, and where that elevation appears tells you which wall is infarcting and which artery is occluded.

Want the lab side of this picture? See Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP).

Ischemia & Infarction on the ECG

The ST-segment sits right after the QRS and before the T wave. It represents early ventricular repolarization and should rest at the isoelectric line. Use the TP segment as your baseline, or the PR segment if the TP is hard to see.

ST segment on the ECG
The ST-Segment
Should sit flat on the isoelectric line; deviation up or down is the key MI clue.
J point on the ECG
The J-Point
Where the QRS meets the ST segment — the reference point for measuring elevation or depression.

ST-Segment Depression

ST depression most often signals cardiac ischemia, and it can appear as a reciprocal change in an acute MI. It can also reflect strain, digitalis effect, hypokalemia, hypomagnesemia, or be rate-related — but those tend to be diffuse rather than localized to 2 contiguous leads.

It's defined as ≥0.5 mm (½ small box) below the isoelectric line, measured 80 ms (2 small boxes) after the J-point. Horizontal and down-sloping depression are more specific for ischemia; up-sloping is less concerning but can still indicate it.

Up-sloping, horizontal, and down-sloping ST-segment depression types
Up-sloping, horizontal, and down-sloping ST depression.

Don't Miss De Winter T Waves

In about 2% of acute LAD occlusions there's no obvious ST elevation. Instead you'll see up-sloping ST depression at the J-point with tall, symmetric T waves in the precordial leads (V1–V6). Treat it like a STEMI equivalent.

ST-Segment Elevation

ST elevation usually means myocardial infarction when it appears in at least 2 contiguous leads. Other causes exist — coronary vasospasm, pericarditis, benign early repolarization, LBBB, LV hypertrophy, ventricular aneurysm, Brugada, paced rhythms, raised ICP, blunt chest trauma, and hypothermia — so context matters.

It's defined as ≥1 mm (1 small box) above the isoelectric line at the J-point. Leads V2–V3 have higher thresholds: >1.5 mm in women, >2 mm in men ≥40, and >2.5 mm in men <40.

Concave Elevation
Less ominous; can reflect benign early repolarization, especially when diffuse.
Convex "Tombstoning"
Convex-upward elevation is almost always a large MI — a true red flag.
Concave versus convex ST-segment elevation morphology
Concave vs convex ("tombstone") ST elevation.

Q Waves

A Q wave is the initial negative deflection of the QRS complex, reflecting septal depolarization. Small Q waves are normal in many leads. Pathologic Q waves point to underlying pathology — usually a current or prior MI.

They're defined as >40 ms wide (1 small box) and >2 mm deep (2 small boxes). Any Q wave in V1–V3 is considered pathologic. Q waves can appear hours to days after an infarct begins and may persist for years.

Pathologic Q wave on the ECG
Pathologic Q wave.

LBBB or Ventricular Paced Rhythm

Spotting ST changes is tricky in a left bundle branch block (LBBB) or a ventricular paced rhythm, because both normally carry some ST elevation and discordant T waves. To suspect ischemia or infarction in these patients, look for the Sgarbossa-type findings:

Concordant ST elevation >1 mm in a lead with a positive QRS complex.
ST depression >1 mm in V1, V2, or V3.

New LBBB + Chest Pain = Concern

A new LBBB morphology with acute chest pain or shortness of breath should make you highly suspicious of an acute MI, even without classic ST elevation.

New to rhythm strips? Start with How to Read an EKG Rhythm Strip.

STEMI Progression

A STEMI tends to evolve through a recognizable sequence on the ECG. Knowing the stages helps you place where your patient is in the timeline.

1
Hyperacute T Waves

Tall, peaked, symmetric T waves in ≥2 contiguous leads. These last only minutes to about an hour.

2
ST Elevation

Elevation appears at the J-point in ≥2 contiguous leads, initially concave, then becoming convex/rounded upward.

3
Tombstone Pattern

The ST segment merges with the T wave until they're indistinguishable. Reciprocal ST depression may show in opposite leads.

4
Resolution & Q Waves

The ST segment drifts back to baseline over a week or so. Q waves develop over hours to days and deepen over time, followed by T-wave inversion that may be temporary.

Typical ECG progression of a STEMI over time
The typical ECG evolution of a STEMI.

STEMI Location

STEMIs are classified by where they sit — which leads are affected on the ECG. Contiguous leads are simply leads that look at the same anatomical region of the heart.

Anteroseptal
V1, V2
Anteroapical
V3, V4
Anterolateral
V5, V6
Lateral
I, aVL
Inferior
II, III, aVF
12-lead ECG map showing which leads correspond to each region of the heart
Which leads look at each region of the heart.

The precordial and lateral leads often light up together, since the infarct area isn't always precise. Here's an inferior wall STEMI as an example:

Inferior wall STEMI with ST elevation in II, III, aVF and reciprocal lateral changes
Inferior wall MI: ST elevation in II, III, and aVF with reciprocal changes in the lateral leads.

Acute Management of STEMI

STEMIs are true emergencies. The patient is at high risk for conduction disturbances, arrhythmias, and cardiac arrest, and every minute of delay means more dead heart cells and worse outcomes.

12-Lead Within 10 Minutes

Any patient with significant cardiac symptoms — chest pain or SOB — needs a 12-lead ECG within 10 minutes. Women, older adults, and diabetics may have atypical or even "silent" MIs with no chest pain at all.

A lot happens fast. Activate a code STEMI (or your facility's equivalent) to alert the interventional cardiologist and cath team immediately. Then work the bedside basics:

1
Monitor & Access

Place the patient on the monitor, get vitals, establish two IVs (ideally 18g), and apply defibrillation pads.

2
Labs

Draw and send labs including troponin and PT/PTT.

3
Stabilize

Address any abnormal vitals, and manage arrhythmias per ACLS guidelines.

Medications
Aspirinantiplatelet
324 mg chewed and swallowed. A 300 mg rectal suppository is an option if the patient can't take it by mouth.
P2Y12 Inhibitorclopidogrel · ticagrelor
A receptor blocker such as Plavix or Brilinta is given in addition to aspirin for dual antiplatelet therapy.
Nitroglycerinvasodilator
0.4 mg SL × 3, q5min for persistent chest discomfort, hypertension, or signs of heart failure. An IV nitro drip can be used for ongoing symptoms.

When NOT to Give Nitro

Avoid nitroglycerin with recent PDE5 inhibitor use (Viagra/Cialis within 24–48 hours), hypotension, severe aortic stenosis, or a suspected right ventricular infarct (can accompany inferior wall MIs). In these patients nitro can cause severe hypotension.

Anticoagulationheparin · enoxaparin
An unfractionated heparin drip is commonly used; Lovenox is another option.
High-Intensity Statinatorvastatin
Atorvastatin 80 mg PO ASAP, ideally before PCI. If the patient is already on a statin, increase to 80 mg.

Be Cautious with Morphine

Morphine 2–4 mg slow IVP q5–15min can be used for refractory chest pain or anxiety, but research links it to higher mortality in STEMI — likely because it blunts the antiplatelet effect of P2Y12 inhibitors. Reserve it for pain that can't be controlled otherwise.

Oxygen is given only to keep SpO2 >90% (routine oxygen in non-hypoxic patients isn't beneficial). If the patient has left heart failure, treat with nitro, a loop diuretic like Lasix, and consider BiPAP. Beta-blockers are started within 24 hours unless contraindicated (bradycardia, heart failure, severe reactive airway disease), usually after PCI.

STEMI medications quick reference for nurses
STEMI medication quick reference.
Reperfusion is the priority. Primary PCI in the cath lab (angiography + stent) is the preferred method and should happen ASAP. Fibrinolytics are the alternative when PCI isn't available within ~120 minutes, as long as symptoms began <12 hours ago and there are no bleeding contraindications.

NSTEMI Management

As the name says, an NSTEMI has no ST elevation on the ECG — but it's still a heart attack, marked by an elevated and rising troponin. The ECG may be normal or show nonspecific T-wave changes or ST depression in contiguous leads.

Medication management mirrors a STEMI, with two key differences: NSTEMI patients do not receive fibrinolytics and are not rushed emergently to the cath lab. Instead, medical therapy is maximized, the patient is monitored, and troponins are trended (typically every 6–8 hours). They may or may not get a cardiac cath during the admission.

STEMIs and NSTEMIs are high-stakes events every nurse will encounter. Recognizing a STEMI on the ECG is the first and most important step.

Clinical Pearls

1
Location maps to artery. Inferior (II, III, aVF) → usually RCA; anterior/septal (V1–V4) → LAD; lateral (I, aVL, V5–V6) → Cx or LAD. The leads tell you the vessel.
2
Inferior STEMI? Think right ventricle. A right-sided infarct makes the patient preload-dependent — hold the nitro and be ready with fluids if they drop their pressure.
3
New LBBB with chest pain is a STEMI until proven otherwise. Look for the Sgarbossa findings rather than waiting for textbook elevation.
4
Time is muscle. 12-lead within 10 minutes, activate the cath team early, and aim for the fastest possible reperfusion.
ECG Rhythm Master course

Master the ECG, Code STEMI Included

Want to go deeper? ECG Rhythm Master is a complete video course built for nurses, covering rhythms, pathophysiology, and emergency procedures in real depth.

  • Identify every cardiac rhythm with confidence
  • Understand why and how arrhythmias happen
  • Manage emergencies — pacing, defibrillation, synchronized cardioversion
  • Bonus guides including a Code STEMI EKG reference
Check Out the Course →

Related Guides

Cardiac lab interpretation guide
Cardiac
Cardiac Lab Interpretation: Troponin, CK, CK-MB & BNP
EKG rhythm strip guide
ECG
How to Read an EKG Rhythm Strip
Vagal maneuvers for SVT guide
Cardiac
Vagal Maneuvers: How to Stop Your Patient's SVT
Adverse drug reactions guide
Meds
Adverse Drug Reactions Nurses Need to Know

References

Clinical Databases & Guidelines
  1. Reeder, G., & Kennedy, H. Overview of the acute management of ST-elevation myocardial infarction. UpToDate.
  2. ECG tutorial: Myocardial ischemia and infarction. UpToDate.
  3. American Heart Association. ACLS Algorithms.
Textbooks
  1. Aehlert, B. ECGs Made Easy (6th ed.).
  2. Davis, K. EKGs for the Nurse Practitioner and Physician Assistant.
Attribution
  1. "Coronary Blood Vessels" by OpenStax College, licensed under CC BY 3.0; changes were made.