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Cardiorespiratory Look-Alikes and Special Patients

Which heart failure, syncope risk, chest pain mimics, lead reversal, IO and crush fluids, oxygen targets, non-cardiac edema, neck bleeds, and patients with special physiology or equipment

Reviewed by Alex G, BSN, RN, CEN, CCRN, CMC, NREMT-P · Checked against current sources October 2026

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Heart failure: which side, and is it the heart?

PicturePoints to
Crackles, orthopnea, pink frothy sputum, S3 (extra sound just after S2)Left failure: fluid backs into the lungs
JVD, pitting edema, big tender liver, ascites, clear lungsRight failure: systemic congestion; commonest cause is left failure
Wheeze plus JVD, crackles, edema, CHF, diuretics or missed dialysis"Cardiac asthma" (pulmonary edema): CPAP and nitro
Wheeze, prolonged expiration, shark-fin EtCO₂, asthma or COPD historyBronchospasm: see asthma-copd

Young hearts that collapse

ConditionClueParamedic action
Obstructive HCMExertional syncope; murmur louder with Valsalva or standing; LVH with deep T inversionsHypotension: supine, legs up, fluid bolus; no nitro or other vasodilators; pads on
Commotio cordisBlow to the chest (baseball) then instant collapse in a normal heartVF: CPR and shock now; survival about 40% if within 3 min, 5% after

Syncope: who is low risk

Chest pain look-alikes and the 12-lead

Aspirin, nitro and STEMI destinations: acs-stemi, prehospital-stroke-stemi.
FindingDo
Tender chest wall but ischemic story or ST depressionTreat as possible ACS: tenderness does not exclude ischemia
Low ACS likelihood, likely non-cardiac (blunt chest trauma)Defer aspirin and nitro; treat pain; keep monitoring
Lead I all negative (P, QRS, T), aVR upright, normal chest leadsArm leads reversed: fix electrodes and repeat before reading
First ECG not diagnostic, symptoms continueSerial 12-leads

Infection, clots and veins

ConditionClueAction
Infective endocarditisIV drug use or prosthetic valve, weeks of fever, new murmur, painful fingertip nodules, strokeTreat sepsis or stroke; 12-lead (heart block); report the suspicion
Acute limb ischemiaSudden pain, pale, cold, pulseless, numb, weak leg; often a clot from the heart (atrial fibrillation)Note onset time; analgesia; urgent vascular-capable hospital
SVC syndromeCancer or central line; face and arm swelling, fixed neck veins, worse lying flatHead up, oxygen; watch for stridor

Access and fluids: shock and crush

Oxygen targets by patient

PatientTarget
Most patients94-98%
Hypercapnic risk: COPD, morbid obesity, CF, chest wall or neuromuscular disease88-92% (asthma-copd)
Pulmonary fibrosis or other ILD94-98% or the highest reachable
SpO₂ below 85%, no hypercapnic riskReservoir mask 15 L/min, then step down
Known low baseline (Glenn, cyanotic heart)The documented baseline

Pulmonary edema that is not heart failure

CauseClueCare
Negative-pressure edemaPink frothy sputum and crackles minutes after choking or laryngospasmOxygen, CPAP or PEEP; diuretics are of doubtful value; usually clears in 12-24 h
EVALIVaping (informal THC cartridges); cough, dyspnea plus vomiting, diarrhea, feverAsk about vaping; oxygen, NIV if severe; can worsen within 48 h
Missed dialysisAnuric, overloadedCPAP, nitro; only dialysis removes the fluid

Neck, airway and chest air

ProblemClueDo
Post-tonsillectomy bleedWithin 14 days of surgerySit upright with suction ready, or on the side to keep blood out of the airway; IV; no probing; ENT-capable ED
Thyroid surgery hematomaNeck swelling, trouble swallowing, anxiety, fast breathing, stridor (late)Head up, high-flow oxygen, call ahead so surgery and airway teams wait
Bronchial foreign bodyCough began in dental work or eating; one-sided wheezeAlbuterol relief does not exclude it; imaging and bronchoscopy
PneumomediastinumChest pain, neck crepitus, Hamman crunch after breath-held inhalation or strainingOxygen, comfort, transport; no positive pressure unless failing
CF hemoptysisBright blood during an exacerbationBleeding side down, suction, oxygen, no cough suppressant; CF center

Special physiology and equipment

Trach and vent troubleshooting: vent-liberation, rsi-airway.
PatientKey pointDo
PAH on IV or SC prostacyclinPump stopped: rebound pulmonary hypertension, RV failure, syncopeRestart with the backup pump; avoid hypoxia and hypotension; small boluses only; no nitro; PH center
Glenn (awaiting Fontan)SpO₂ runs low (one ICU survey: post-op targets mostly 76-85%); the child's own baseline is what countsUse the documented baseline; treat a fall below it; avoid needless positive pressure; cardiac center
Home ventilator failingPower or battery lost, falling SpO₂Bag-valve to the trach; DOPE; bring the go-bag; transport
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In depth

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Heart failure patterns and the fluid question

Left ventricular failure raises pulmonary venous pressure, so the lungs fill: dyspnea, orthopnea, crackles, sometimes wheeze from swollen small airways, and blood-tinged frothy sputum. Right failure backs blood into the systemic veins: raised jugular venous pressure, pitting edema of the feet and ankles, a large and sometimes pulsatile liver, and ascites. Merck names left failure as the commonest cause of right failure; cor pulmonale is right failure caused by lung disease. A patient with right-sided signs and clear lungs is not a CPAP-and-nitro patient and may need careful fluid.

Third and fourth heart sounds both occur in heart failure. By classic teaching the S3 falls just after S2 in early diastole, as blood rushes into a full ventricle (the "Ken-tuck-y" cadence), and in an adult it supports decompensated failure; the S4 falls just before S1, from atrial contraction into a stiff ventricle ("Ten-nes-see"), as in hypertension or ischemia.

NASEMSO sorts respiratory distress by cause. Fluid overload is suggested by JVD, rales, peripheral edema and a history of CHF, diuretics, dialysis noncompliance or hypertension; bronchospasm by wheeze, a shark-fin capnogram, a prolonged expiratory phase and an asthma or COPD history. CHF tends to give a lower EtCO₂ than COPD. When the two coexist, NASEMSO allows bronchodilators in line with NIV. Its shock guideline adds the safety rule: if the patient worsens after fluid, or rales or hepatomegaly develop, think cardiogenic shock and withhold further fluid. A modest blood pressure in a known heart failure patient is not on its own a reason for a bolus.

HCM, commotio cordis and syncope risk

In obstructive hypertrophic cardiomyopathy the thick septum and mitral leaflet narrow the outflow tract when the ventricle is small and squeezing hard. Merck: the murmur grows louder with maneuvers that lower preload (Valsalva, squat-to-stand) and softer with those that raise preload or afterload (hand grip, passive leg raise), and drugs that reduce preload or afterload, nitrates and diuretics among them, should generally be avoided. The ECG often shows LVH with deep T-wave inversions. So a hypotensive HCM patient is laid flat with legs raised and given fluid; drugs that make the heart beat harder or faster narrow the outflow further. HCM is a recognized cause of sudden death in young athletes and of unexplained exertional syncope.

Commotio cordis is ventricular fibrillation from a blow over the heart in a structurally normal heart. Peng and colleagues (2023) describe a 15 ms vulnerable window on the upstroke of the T wave in animal work, with impacts around 40 mph most likely to trigger VF; registry patients averaged 15 years of age, 95% were male, and baseball accounted for about half. Survival was about 40% when resuscitation began within 3 minutes and about 5% when it was later. It is a shockable arrest: CPR and the AED or defibrillator immediately, not decompression or pericardiocentesis.

NASEMSO lists high-risk causes of syncope as cardiac (MI, aortic stenosis, HCM, PE, dissection, dysrhythmia), neurovascular and hemorrhagic (ectopic pregnancy, GI bleed, aortic rupture), and high-risk ECG features as QT over about 500 ms, delta waves, the Brugada pattern and HCM. Merck adds syncope while lying down, without warning, with a murmur, in older age, with a family history of sudden death, or with injury. Vasovagal syncope comes upright after a trigger with nausea, sweating or blurred vision, and recovery is prompt. NASEMSO leaves any non-transport decision for a suspected low-risk cause to medical direction. Bystander reports of brief jerking fit syncope; see emt-by-complaint.

Chest pain mimics and lead reversal

Merck warns that pain worsened by palpation, breathing or movement is not specific for the chest wall, and that some patients with myocardial ischemia describe only indigestion or a very tender chest wall. NASEMSO notes atypical presentations are more common in women, older and diabetic patients. A recent strain explains soreness; it does not explain new horizontal ST depression in contiguous leads. Treat as non-ST-elevation ACS, repeat the 12-lead and go to a hospital that manages ACS.

The reverse error is giving aspirin and nitro to a patient with a low chance of ACS. NASEMSO tells crews to defer both for likely non-cardiac chest pain, giving blunt chest trauma in a child as the example, and to treat pain under the pain guideline. Aspirin impairs clotting after trauma, and nitro response does not separate cardiac from non-cardiac pain. Monitor for dysrhythmia and repeat the ECG if symptoms change.

Ramadurai and colleagues (2025) found lead reversal in 1.5% of 1,000 ECGs, mostly limb leads. Right and left arm reversal makes the P, QRS and T negative in lead I and aVL, and aVR turns upright because it is now recording aVL. Left arm and left leg reversal inverts lead III. A flat limb lead is another warning sign. The machine read flagged none of the misplacements and can report infarction falsely; the tracing must be retaken after correct placement. Dextrocardia also inverts lead I but is congenital and changes the chest leads, so a pattern new since a recent normal ECG points to the electrodes.

Endocarditis, limb ischemia and SVC syndrome

Merck: prosthetic valves and intracardiac devices carry the highest risk of infective endocarditis, with IV drug use and indwelling catheters also named; 5-10% of cases are right-sided, much more often in people who inject drugs, and these send septic emboli to the lungs. Osler nodes are painful nodules near the fingertips; Janeway lesions are painless macules on the palms or soles; splinter hemorrhages and Roth spots also occur. About 35% have CNS effects such as TIA or stroke, and abscess near the conduction system can cause conduction abnormalities. Blood cultures (ideally 3 sets) are drawn before antibiotics, so report the suspicion.

Acute arterial occlusion comes from an embolus from the heart or aorta (atrial fibrillation is the classic teaching source; Merck names the heart and aorta) or thrombosis on plaque. Merck lists pain, pallor, paresthesias, coldness and pulselessness, with paralysis as the sixth P; after 6-8 hours the muscles may be tender, and treatment is immediate angiography with embolectomy, thrombolysis or bypass. Hours count: record the onset time, give analgesia, avoid tight dressings and take the patient to a hospital with vascular surgery.

Superior vena cava syndrome (Shah 2023): malignancy causes about 60%, mostly lung cancer and lymphoma, and catheters or devices 30-40%. Face, neck and arm swelling with distended veins, dyspnea, cough, hoarseness and headache typically worsen lying flat; stridor means airway swelling. Head elevation helps; endovascular stenting is now standard care for many patients.

Oxygen targets, silent hypoxemia and non-cardiac edema

BTS 2017 limits the 88-92% target to patients at risk of hypercapnic failure: COPD, morbid obesity, cystic fibrosis, chest wall deformity, neuromuscular disease and bronchiectasis with fixed obstruction. Pulmonary fibrosis causes hypoxemic, not hypercapnic, failure, so the target is 94-98% or the highest achievable, with a reservoir mask at 15 L/min when SpO₂ is below 85%. A low EtCO₂ supports that the patient is not retaining CO₂. NASEMSO adds that permissive SpO₂ of 90% or more may suit COPD or other complex lung disease.

Silent hypoxemia is marked hypoxemia without dyspnea in an alert patient (Swenson 2021); these patients can deteriorate rapidly, and care follows standard hypoxemic-failure practice. In the awake prone positioning meta-trial (Ehrmann 2021), COVID-19 patients on high-flow oxygen who lay prone had less treatment failure (40% vs 46%) and fewer intubations.

Negative-pressure pulmonary edema (Ma 2023) follows a strong inspiration against a blocked upper airway: intrathoracic pressure can fall to about -50 to -100 cmH₂O, raising venous return and left ventricular afterload so fluid leaks into the alveoli. Laryngospasm after extubation is the commonest adult cause; choking, croup and epiglottitis also cause it. Signs are dyspnea, tachypnea, cyanosis and pink frothy sputum; onset is usually soon after the obstruction, rarely 1-6 hours later. Treatment is a patent airway, oxygen and positive pressure; diuretics are controversial because these patients are not overloaded, and most cases clear in 12-24 hours. Aspiration and cardiogenic edema are the main alternatives.

CDC describes EVALI as respiratory symptoms (cough, chest pain, dyspnea) with GI symptoms (nausea, vomiting, abdominal pain, diarrhea) and constitutional symptoms (fever, chills, weight loss). Most cases involved THC products from informal sources, and vitamin E acetate is strongly linked. Asking about vaping is the most critical step; admission is strongly considered for SpO₂ below 95% on room air or respiratory distress, and some mild cases worsen within 48 hours.

NASEMSO names dialysis noncompliance among causes of pulmonary edema. In an anuric patient CPAP and nitro buy time, only dialysis removes the fluid, and hyperkalemia is likely. Its airway guideline keeps CPAP on until hospital CPAP is ready or a physician asks for it to stop, because breaking the seal drops airway pressure and lets alveoli collapse; if the patient worsens on CPAP (falling mental status, rising EtCO₂, vomiting), remove it and escalate.

Neck bleeding, foreign bodies and mediastinal air

Post-tonsillectomy hemorrhage (Siu 2024) occurs in 2-5% and can happen up to 14 days after surgery; deaths are rare but higher in children with complex conditions. Any bleeding, even blood-tinged sputum, needs urgent assessment, and swallowed blood may show only as nausea or abdominal pain. Keep the child upright with suction at hand, or prone or on the side to keep blood out of the airway, place an IV, and avoid manipulating the throat, which can dislodge clot. The otolaryngologist decides on observation or operative control.

The Difficult Airway Society guideline (Iliff 2022) puts haematoma needing emergency bedside intervention at up to about 1 in 400 thyroidectomies (haemorrhage overall 0.45-4.2%); most occur within 24 hours and about half within 6 hours, so patients sent home the next day are still at risk. Its DESATS triggers are difficulty swallowing, rising early warning score, swelling, anxiety, tachypnea and stridor, which may be late. Concern means immediate oxygen, head-up position and senior help. In hospital the wound is opened at the bedside (SCOOP: skin exposure, cut sutures, open skin, open muscles, pack), and intubation is done by experienced hands, ideally with videolaryngoscopy and front-of-neck access ready. Prehospital, sit the patient up, give oxygen, transport fast and call ahead.

In an adult series of airway foreign bodies (Sancho-Chust 2020), 69% lay in the right bronchial tree and 9% were dental prostheses or implants; flexible bronchoscopy removed 94%. A first one-sided wheeze after a lost crown is a foreign body until imaging says otherwise, and a partial response to albuterol does not exclude it. Abdominal thrusts are for complete obstruction, not an object in a bronchus.

Spontaneous pneumomediastinum follows alveolar rupture with air tracking into the mediastinum and neck. In Sahni 2013, 75% had chest pain, 58% subcutaneous emphysema, 49% dyspnea and 18% Hamman crunch; most were treated with rest, analgesia and oxygen. Merck: treatment is generally unnecessary, but the cause must be found to exclude esophageal perforation. Merck describes needle aspiration only for tension pneumomediastinum, so with equal breath sounds and stable vitals decompression is not indicated; a 12-lead is still reasonable for chest pain.

In CF, Merck lists hemoptysis among the pulmonary complications, discourages cough suppressants, and treats massive or recurrent bleeding with bronchial artery embolization. For massive hemoptysis Merck puts the bleeding lung dependent to protect the other lung from aspiration, which is the asphyxiation risk.

Prostacyclin pumps, Glenn circulation and home ventilators

Patients with pulmonary arterial hypertension on continuous IV epoprostenol or IV or SC treprostinil live close to right ventricular failure. The epoprostenol label gives a half-life of no more than 6 minutes and warns that even brief interruptions cause rebound pulmonary hypertension; patients keep a backup pump. Remodulin (treprostinil) has an SC terminal half-life of about 4 hours and its label warns against abrupt withdrawal. Ahern 2025: resume the home infusion promptly; hypoxia, hypercapnia and acidosis raise pulmonary vascular resistance; use small boluses of about 250 mL and avoid large ones; norepinephrine is the preferred vasopressor; intubation and positive pressure can cause collapse; consult the PH center early. NASEMSO bars nitrates in patients on IV epoprostenol or treprostinil.

In hypoplastic left heart syndrome the bidirectional Glenn (at 3-6 months) connects the superior vena cava to the pulmonary arteries, so about half of systemic venous return reaches the lungs passively; the Fontan (18-36 months) adds the inferior vena cava. Until then, desaturated lower-body blood still mixes, so SpO₂ stays low; in a 2026 survey of 35 cardiac intensive care providers most targeted 81-85% after a Glenn (range 70-90%, no consensus). Merck gives no normal range, so the family's emergency letter is the yardstick. Passive pulmonary flow is helped by spontaneous breathing, so avoid bagging a child who is moving air. Fontan circulations are preload-dependent, so diuresis should be cautious (Lindor 2024).

NASEMSO's airway guideline excludes chronically ventilated patients and sends crews to its tracheostomy guideline: in severe distress on a ventilator, take the patient off the vent and bag through the trach, then work through DOPE (displacement, obstruction, pneumothorax, equipment). The home go-bag (suction catheters, spare trach tubes, saline, lubricant) travels with the patient. A failing power supply is an equipment problem: manual ventilation bridges to a transport ventilator, and the caregiver knows the usual settings.

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Sources

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