Free CONO Clinical Sciences Clinical Cases

Rationale

Prolonged pressure-like substernal chest pain radiating to the arm and jaw, accompanied by diaphoresis, nausea, and dyspnea, is highly concerning for acute myocardial ischemia.

Why the other options are incorrect

• A. Costochondritis: Usually produces localized, reproducible chest-wall tenderness.
• B. GERD: May cause burning retrosternal discomfort but usually lacks diaphoresis and classic radiation.
• D. Pericarditis: Pain is generally sharp, pleuritic, worse when supine, and relieved by leaning forward.

Rationale

Suspected acute coronary syndrome is a medical emergency. Emergency medical services should be activated immediately because rapid ECG evaluation, monitoring, and reperfusion treatment may be required.

CONO safety point: Do not delay emergency referral while performing a complete naturopathic assessment.

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A 12-lead ECG should be performed urgently in suspected acute coronary syndrome to identify ST-segment elevation, ischemia, or other cardiac abnormalities.

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High-sensitivity cardiac troponin is the preferred biomarker for detecting myocardial injury. Serial measurements may be required because an early value can be normal.

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ST elevation in leads II, III, and aVF indicates an inferior myocardial infarction.

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The right coronary artery most commonly supplies the inferior wall and is frequently responsible for inferior STEMI.

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Right-sided ECG leads, particularly V4R, may identify right ventricular involvement in an inferior myocardial infarction.

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Right ventricular infarction can reduce right ventricular output and cause hypotension. These patients may depend on adequate venous return.

Exam trap: Nitrates can worsen hypotension in right ventricular infarction because they reduce preload.

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Aspirin inhibits platelet aggregation and reduces mortality in acute coronary syndromes. Emergency protocols commonly use a chewable loading dose when there is no serious allergy or active bleeding.

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Routine oxygen is not necessary when oxygen saturation is adequate and the patient has no evidence of respiratory failure.

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STEMI management requires rapid restoration of coronary blood flow, preferably through primary percutaneous coronary intervention when available.

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Dietary and naturopathic interventions may support long-term cardiovascular risk reduction but are not substitutes for emergency treatment.

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Progressive PR prolongation followed by a dropped QRS complex describes Mobitz type I, or Wenckebach AV block.

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Ventricular fibrillation produces ineffective ventricular activity and cardiac arrest. Immediate CPR and defibrillation are required.

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Left ventricular dysfunction may cause pulmonary congestion, dyspnea, orthopnea, crackles, and reduced ejection fraction.

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A Mediterranean-style eating pattern emphasizes vegetables, fruits, legumes, whole grains, nuts, olive oil, and fish and supports cardiovascular risk reduction.

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Smoking cessation substantially reduces future cardiovascular risk. Behavioural support and approved smoking-cessation therapies may improve success.

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High-dose omega-3 supplementation may have antiplatelet effects. Medication review and individualized risk assessment are required.

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Naturopathic care may support nutrition, physical activity, smoking cessation, stress management, sleep, weight management, and medication adherence. It should complement—not replace—appropriate cardiovascular care.

Rationale

Atrial fibrillation is characterized by an irregularly irregular rhythm, absent organized P waves, and variable R–R intervals. A rapid ventricular response is present because the ventricular rate is approximately 145 beats/min.

Why the other options are incorrect

• A. Sinus tachycardia: Usually has identifiable P waves before every QRS complex and a regular rhythm.
• C. Complete heart block: Usually causes atrioventricular dissociation and often produces bradycardia.
• D. Ventricular tachycardia: Usually produces a regular wide-complex tachycardia.

Rationale

Atrial fibrillation produces disorganized atrial electrical activity. Organized P waves are absent, and variable conduction through the AV node causes irregular ventricular intervals.

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Initial assessment must identify hypotension, shock, ongoing ischemic chest pain, altered mental status, acute heart failure, severe respiratory distress, or other evidence of instability. Hemodynamic status determines whether urgent synchronized cardioversion may be required.

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Hypotension, shock, acute pulmonary edema, severe ischemic symptoms, or altered consciousness suggests unstable tachyarrhythmia requiring emergency management.

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In a hemodynamically stable patient with atrial fibrillation and rapid ventricular response, initial management commonly includes controlling the ventricular rate while evaluating the cause, duration, symptoms, and thromboembolic risk.

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Beta blockers are commonly used to slow AV-nodal conduction and reduce the ventricular response. A nondihydropyridine calcium-channel blocker may also be considered in selected patients without significant reduced-ejection-fraction heart failure.

CONO clinical point: Medication selection depends on blood pressure, ventricular function, comorbid disease, and clinical stability.

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Atrial fibrillation causing acute hemodynamic deterioration requires urgent synchronized electrical cardioversion.

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Potentially life-threatening cardiovascular instability must be treated immediately. Naturopathic assessment or counselling must not delay emergency intervention.

Score calculation

Risk factor Point s

Congestive heart failure 0

Hypertension 1

Age 75 years or older 0

Diabetes mellitus 1

Previous stroke, TIA, or embolism 0

Vascular disease 0

Age 65–74 years 1

Sex category: female 1

Total 4

Rationale

Validated thromboembolic-risk assessment helps guide anticoagulation decisions. Current recommendations emphasize estimating annual thromboembolic risk rather than relying only on the score number.

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Ineffective atrial contraction promotes blood stasis and thrombus formation. Embolization of a cardiac thrombus may obstruct cerebral circulation and cause ischemic stroke. Stroke prevention is a major component of atrial fibrillation management.

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Reduced atrial contraction promotes blood stasis, particularly in the left atrial appendage. A thrombus may subsequently embolize into the systemic circulation.

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Anticoagulation decisions are individualized according to estimated thromboembolic risk, bleeding considerations, comorbidities, contraindications, and shared decision-making. Aspirin is not recommended as a substitute for anticoagulation in patients who are appropriate anticoagulation candidates.

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Direct oral anticoagulants are generally preferred over warfarin in eligible patients with atrial fibrillation, except in important situations such as mechanical heart valves or significant mitral stenosis.

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Echocardiography evaluates:

• Left ventricular systolic function
• Chamber size
• Left atrial enlargement
• Valvular abnormalities
• Structural heart disease
• Evidence of heart failure

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Hyperthyroidism may increase sympathetic activity and predispose to atrial fibrillation. Thyroid function testing is therefore commonly included in the evaluation.

Rationale

Potential contributors may include:

• Electrolyte abnormalities
• Thyroid disease
• Infection
• Anemia
• Renal impairment
• Myocardial ischemia
• Medication effects
• Alcohol exposure
• Structural heart disease

Investigations should be selected according to clinical presentation.

Rationale

Persistent rapid ventricular rates may impair ventricular function and contribute to cardiomyopathy or heart failure.

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Sleep-disordered breathing is an important potentially modifiable associated condition. Weight management, appropriate sleep evaluation, blood-pressure control, physical activity, and alcohol reduction may form part of comprehensive risk-factor management.

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Risk-factor modification is an important component of atrial fibrillation care. Cardiovascular risk management includes healthy physical activity, weight management, avoidance of tobacco, moderation or avoidance of excessive alcohol, treatment of hypertension, and attention to sleep health.

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Appropriate naturopathic care may support:

• Heart-healthy nutrition
• Gradual weight management
• Blood-pressure control
• Appropriate physical activity
• Smoking cessation
• Reduction of excessive alcohol intake
• Sleep-apnea evaluation and treatment adherence
• Stress-management strategies
• Medication adherence
• Screening for supplement–drug and botanical–drug interactions

Naturopathic interventions should complement—not replace—indicated cardiology care, rate or rhythm management, or stroke-prevention therapy.

Rationale

The combination of sudden unexplained dyspnea, pleuritic chest pain, tachycardia, hypoxemia, hemoptysis, recent major orthopedic surgery, immobility, and unilateral calf swelling is highly suspicious for acute pulmonary embolism originating from a lower-extremity deep-vein thrombosis.

Why the other options are incorrect

• B. Costochondritis: Usually causes reproducible chest-wall tenderness and does not explain hypoxemia or unilateral calf swelling.
• C. GERD: More commonly causes burning retrosternal discomfort and does not explain acute hypoxemia and signs of DVT.
• D. Stable angina: Usually occurs with exertion and improves with rest. Pleuritic pain and unilateral leg swelling suggest an alternative diagnosis.

Rationale

Major surgery, hospitalization, trauma, and prolonged immobility increase venous thromboembolism risk. Orthopedic surgery involving the hip or knee is particularly important because immobility and tissue injury promote venous thrombosis.

Rationale

Virchow’s triad describes three major contributors to thrombosis:

1. Venous stasis
2. Endothelial injury
3. Hypercoagulability

Reduced lower-extremity muscle activity decreases venous return and promotes blood stasis.

Rationale

Suspected pulmonary embolism is a medical emergency because deterioration may lead to right-heart failure, obstructive shock, cardiac arrest, or death. Emergency evaluation should not be delayed for complementary treatment or extensive outpatient testing.

CONO Safety Point

Do not massage a leg when acute DVT is suspected. Do not delay emergency referral.

Rationale

Structured assessment tools such as the Wells or Geneva score help estimate the clinical probability of pulmonary embolism and guide the selection of D-dimer testing or diagnostic imaging.

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Traditional Wells criteria include findings such as:

Clinical feature Traditional points

Clinical signs of DVT 3

PE considered more likely than an alternative 3 diagnosis

Heart rate greater than 100 beats/min 1.5

Recent surgery or prolonged immobilization 1.5

Previous DVT or PE 1.5

Hemoptysis 1

Active malignancy 1

This patient has multiple high-probability features.

Rationale

D-dimer testing is highly sensitive but nonspecific. A negative result may help exclude acute PE when pretest probability is sufficiently low or intermediate. An elevated value does not independently confirm PE because surgery, inflammation, pregnancy, cancer, age, and other conditions may increase D-dimer levels.

CONO Examination Trap

A high-probability presentation should not be falsely reassured by waiting for a nonspecific screening test when definitive imaging is indicated.

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CT pulmonary angiography, or CTPA, directly evaluates the pulmonary arteries and is commonly preferred for confirming acute pulmonary embolism when imaging is indicated.

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A ventilation-perfusion, or V/Q, lung scan may be used when CTPA is unavailable or unsuitable. Clinical circumstances, chest imaging, local expertise, pregnancy status, renal function, and contrast safety affect imaging selection.

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Compression ultrasonography is used to identify lower-extremity deep-vein thrombosis. Detection of proximal DVT may provide important evidence of venous thromboembolism in a patient with symptoms suggesting PE.

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A significant pulmonary arterial obstruction can suddenly increase right ventricular afterload. Right ventricular dilation or dysfunction indicates increased physiologic stress and is important for severity assessment and prognosis.

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Acute pressure overload may cause right ventricular ischemia and myocardial injury. Biomarkers such as cardiac troponin are used with clinical findings and right-heart imaging to assist risk stratification.

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Persistent hypotension, refractory shock, severe right-heart failure, or cardiac arrest indicates the highest-risk presentation and requires immediate advanced management. The 2026 AHA/ACC framework places cardiopulmonary failure with persistent hypotension, refractory shock, or arrest in the most severe category.

Rationale

A large embolic obstruction increases pulmonary vascular resistance and right ventricular workload. Severe right ventricular dysfunction may decrease left ventricular filling and cardiac output, resulting in hypotension, obstructive shock, or cardiac arrest.

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Anticoagulants prevent clot extension and reduce the risk of recurrent venous thromboembolism while the body gradually breaks down the existing thrombus. Anticoagulation is the principal treatment for most patients with PE.

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The 2026 multisociety guideline recommends low-molecular-weight heparin over unfractionated heparin for many patients with acute PE who require initial parenteral anticoagulation. Treatment selection must still account for kidney function, bleeding risk, anticipated procedures, clinical instability, and other individual factors.

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Direct oral anticoagulants are generally recommended over vitamin K antagonists in eligible patients because they reduce recurrent venous thromboembolism while offering a favorable major-bleeding profile. Contraindications and special clinical circumstances must be considered.

Rationale

Thrombolytic therapy and advanced interventions such as catheter-directed treatment, mechanical thrombectomy, or surgical embolectomy are generally reserved for selected patients at the highest risk of deterioration. Potential benefits must be balanced against major bleeding risk.

CONO Examination Trap

Do not administer thrombolytic therapy routinely to every hemodynamically stable patient with pulmonary embolism.

Rationale

Anticoagulation duration depends on whether the PE was associated with a major reversible factor, persistent risk factor, recurrent VTE, active cancer, thrombophilia, bleeding risk, and other clinical considerations. The 2026 guideline describes an initial three-to-six-month treatment phase and recommends considering longer treatment when no major reversible factor exists or a persistent risk factor remains.

Rationale

Appropriate adjunctive care may include:

• Supporting gradual return to appropriate physical activity
• Encouraging medication adherence
• Supporting healthy weight management
• Avoiding tobacco exposure
• Reviewing diet and cardiovascular risk factors
• Monitoring for recurrent symptoms
• Screening supplements and botanical products for possible bleeding interactions
• Reinforcing follow-up with the medical treatment team

Complementary care must not replace anticoagulation or specialist management. Patients receiving anticoagulants should not begin high-dose supplements or botanicals with potential antiplatelet or anticoagulant effects without a medication-interaction review.

Rationale

This patient has progressive dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rapid weight gain, elevated jugular venous pressure, pulmonary crackles, an S3 gallop, and extensive peripheral edema.

His severe hypoxemia and respiratory distress suggest acute cardiogenic pulmonary edema caused by worsening left-sided heart failure.

Why the other options are incorrect

• B. Stable COPD: Does not adequately explain the elevated JVP, S3 gallop, extensive edema, rapid weight gain, and pulmonary congestion.
• C. Costochondritis: Causes reproducible chest-wall pain and does not cause pulmonary edema.
• D. GERD: May cause retrosternal burning but does not explain hypoxemia, crackles, elevated JVP, or edema.

Rationale

Orthopnea is shortness of breath that develops or worsens while lying flat and improves when the patient sits or stands upright.

In heart failure, lying down increases venous return and redistributes fluid toward the chest, worsening pulmonary congestion.

Rationale

Paroxysmal nocturnal dyspnea involves sudden nighttime breathlessness that awakens the patient from sleep and may improve after sitting or standing.

It is an important indication of worsening pulmonary congestion.

Rationale

The patient has severe respiratory distress, an oxygen saturation of 84%, tachypnea, and probable acute pulmonary edema.

Immediate priorities include:

• Emergency medical activation
• Airway, breathing, and circulation assessment
• Upright positioning
• Oxygen support because significant hypoxemia is present
• Continuous monitoring when available
• Rapid hospital treatment

CONO Safety Point

Do not delay emergency transportation to provide supplements, botanical medicines, acupuncture, hydrotherapy, or prolonged counselling.

Rationale

Elevated jugular venous pressure reflects increased right atrial or central venous pressure and commonly indicates systemic venous congestion.

It may occur in:

• Right-sided heart failure
• Biventricular heart failure
• Severe volume overload
• Pulmonary hypertension
• Cardiac tamponade

Rationale

An S3 gallop occurs during rapid ventricular filling. In an older adult with dyspnea and congestion, it supports increased ventricular filling pressures and systolic heart failure.

Rationale

B-type natriuretic peptide and N-terminal pro-BNP are released in response to increased myocardial wall stress. They may support diagnosis and assist with severity assessment when interpreted with the clinical presentation.

Natriuretic peptide levels must not be interpreted in isolation. Renal function, age, body composition, rhythm disorders, and other clinical factors can affect results.

Rationale

Echocardiography evaluates:

• Left ventricular ejection fraction
• Ventricular size and function
• Wall-motion abnormalities
• Valve structure and function
• Myocardial thickness
• Selected filling-pressure findings

Echocardiography is a central investigation for classifying heart failure and identifying structural cardiac disease.

Rationale

Chest radiography may demonstrate:

• Cardiomegaly
• Pulmonary vascular congestion
• Interstitial edema
• Bilateral alveolar edema
• Pleural effusions

Chest radiography also helps assess alternative causes of respiratory symptoms, but it does not independently provide all information required to diagnose or classify heart failure.

Rationale

Stopping the prescribed diuretic reduced sodium and fluid elimination. High sodium intake likely promoted additional fluid retention.

Common causes or contributors to heart-failure decompensation include:

• Medication nonadherence
• Excess sodium or fluid intake
• Acute myocardial ischemia
• Uncontrolled hypertension
• Atrial fibrillation or another arrhythmia
• Infection
• Worsening kidney function
• Anemia
• Thyroid disease
• Medication adverse effects

Rationale

Loop diuretics promote sodium and water excretion and are commonly used to treat substantial congestion in hospitalized patients with acute heart failure.

Response is monitored using findings such as:

• Urine output
• Body weight
• Dyspnea
• Edema
• Jugular venous pressure
• Blood pressure
• Electrolytes
• Renal function

Contemporary heart-failure hospitalization pathways emphasize repeated assessment of congestion and response throughout treatment.

Rationale

This patient has severe hypoxemia and respiratory distress. Oxygen therapy is appropriate while the cause is treated.

Oxygen supports oxygenation but does not independently remove pulmonary fluid or correct elevated cardiac filling pressures.

Rationale

Continuous positive airway pressure or bilevel positive airway pressure may improve oxygenation and reduce the work of breathing in selected cooperative patients with acute cardiogenic pulmonary edema.

The patient must be monitored closely. Invasive airway management may be necessary when respiratory failure progresses or noninvasive support is unsuitable.

Rationale

A vasodilator may reduce cardiac filling pressures and afterload in selected patients with acute pulmonary edema and adequate or elevated blood pressure.

Blood pressure and clinical response must be closely monitored.

CONO Examination Trap

Do not use vasodilators reflexively in patients with severe hypotension or shock.

Rationale

Cardiogenic shock involves inadequate cardiac output and impaired tissue perfusion.

Important findings may include:

• Persistent hypotension
• Altered mental status
• Cool or mottled extremities
• Weak peripheral pulses
• Reduced urine output
• Elevated lactate
• Progressive kidney or liver dysfunction

Patients require urgent advanced critical care. Selected patients may require inotropic support, vasopressor therapy, mechanical circulatory support, or other advanced interventions.

Rationale

Common ejection-fraction categories include:

Classificatio Left ventricular ejection fraction n

HFrEF 40% or lower

HFmrEF 41–49%

HFpEF 50% or higher

This patient has an ejection fraction of 28%, which is consistent with HFrEF.

Rationale

Core guideline-directed medical therapy for chronic HFrEF includes:

1. Angiotensin receptor–neprilysin inhibitor, when appropriate, or another indicated renin–angiotensin system treatment
2. Evidence-based beta blocker
3. Mineralocorticoid receptor antagonist
4. Sodium-glucose cotransporter-2 inhibitor

The treatment plan is individualized according to blood pressure, kidney function, potassium, tolerance, contraindications, and other clinical factors.

Rationale

Evidence-based beta blockers are important chronic HFrEF medications. However, initiation and dose escalation are generally deferred until the patient is sufficiently stabilized and compensated.

The 2024 ACC HFrEF pathway emphasizes that beta-blocker initiation or titration should be deferred until heart failure is compensated.

Rationale

Patients should understand their individualized action plan and monitor for worsening features such as:

• Rapid weight gain
• Increasing edema
• Increasing shortness of breath
• New or worsening orthopnea
• Sudden nighttime breathlessness
• Increasing fatigue
• Abdominal swelling
• Reduced activity tolerance
• New dizziness or confusion

Heart-failure self-management commonly includes symptom tracking, weight monitoring, blood-pressure management, medication adherence, and individualized sodium or fluid guidance.

Rationale

Appropriate adjunctive naturopathic care may include:

• Supporting medication adherence
• Identifying barriers to taking prescribed medication
• Helping implement the individualized sodium plan
• Supporting an appropriate heart-healthy dietary pattern
• Monitoring weight and symptoms
• Supporting gradual, medically appropriate physical activity or cardiac rehabilitation
• Supporting smoking cessation
• Limiting or avoiding alcohol according to the treatment plan
• Supporting sleep and stress management
• Reviewing supplements and botanical medicines for interactions
• Reinforcing cardiology and primary-care follow-up

Lifestyle recommendations should be individualized to disease severity, kidney function, blood pressure, medications, and the treating team’s guidance.

Rationale

Important findings include:

• Abrupt onset
• Maximum pain intensity immediately at onset
• Severe chest pain radiating to the back
• Marked hypertension
• Blood-pressure difference between the arms
• Pulse deficit
• New aortic-regurgitation murmur
• New focal neurologic symptoms
• Known thoracic aortic aneurysm

These findings strongly suggest an acute aortic syndrome.

Aortic dissection occurs when blood enters and separates layers of the aortic wall. The dissection may compromise blood flow to the brain, heart, kidneys, spinal cord, extremities, or other organs and may progress to aortic rupture.

Why the other options are incorrect

• B. Stable angina: Usually develops predictably with exertion and improves with rest. It does not explain pulse asymmetry or a new aortic-regurgitation murmur.
• C. Costochondritis: Typically causes localized, reproducible chest-wall tenderness.
• D. GERD: May cause burning retrosternal discomfort but does not explain sudden maximal tearing pain, pulse deficits, or neurologic findings.

Rationale

Acute aortic dissection classically produces sudden, severe pain that reaches maximum intensity immediately. Patients may describe the pain as tearing, ripping, stabbing, or sharp.

Myocardial ischemic discomfort is often described as pressure, heaviness, tightness, or squeezing and may build in intensity. However, symptom descriptions overlap, so urgent diagnostic evaluation is required.

Rationale

Suspected acute aortic dissection is a medical emergency. Rapid hospital assessment, advanced imaging, blood-pressure and heart-rate control, and urgent surgical evaluation may be lifesaving.

Immediate priorities include:

• Activate emergency medical services
• Assess airway, breathing, circulation, and neurologic status
• Keep the patient at rest
• Monitor vital signs when possible
• Avoid unnecessary exertion
• Communicate the suspected diagnosis to emergency personnel

Aortic dissection and rupture require immediate emergency treatment.

Rationale

Thrombolytic treatment may worsen bleeding into the aortic wall or contribute to catastrophic hemorrhage when acute aortic dissection is present.

Because acute aortic syndrome may mimic acute coronary syndrome, clinicians must consider dissection when high-risk findings are present, including:

• Abrupt severe pain
• Back radiation
• Pulse deficit
• Blood-pressure difference
• Neurologic deficit
• New aortic-regurgitation murmur
• Known aortic disease

CONO Safety Point

Do not assume that every patient with severe chest pain has myocardial infarction. Evaluate for life-threatening alternative causes.

Rationale

CT angiography can rapidly evaluate:

• The ascending aorta
• Aortic arch
• Descending thoracic aorta
• Abdominal aorta
• Intimal flap
• True and false lumens
• Branch-vessel involvement
• Malperfusion
• Pericardial or pleural complications
• Evidence of rupture

Acute aortic syndrome is evaluated with aortic CT angiography when clinically appropriate.

Rationale

Transesophageal echocardiography may be useful when a patient is unstable or cannot safely undergo immediate CT imaging.

It may identify:

• Proximal aortic dissection
• Intimal flap
• Aortic-regurgitation severity
• Pericardial effusion
• Cardiac tamponade
• Ventricular function

Imaging selection depends on hemodynamic stability, availability, expertise, anatomy, renal function, and the urgency of the clinical situation.

Rationale

A widened mediastinum may occur with thoracic aortic disease, but chest radiography does not definitively diagnose or exclude acute aortic dissection.

Additional possible radiographic findings include:

• Abnormal aortic contour
• Enlarged aortic shadow
• Pleural effusion
• Displacement of mediastinal structures

Definitive aortic imaging is still required.

CONO Examination Trap

A normal chest radiograph does not rule out aortic dissection.

Rationale

An ECG is important in acute chest-pain assessment, but no single ECG pattern excludes aortic dissection.

Troponin elevation may occur because of:

• Coronary-artery involvement
• Myocardial ischemia
• Severe hemodynamic stress
• Other concurrent myocardial injury

The complete clinical presentation must guide imaging and treatment. ECG and serial high-sensitivity troponin remain important components of acute chest-pain evaluation.

Rationale

The Stanford classification is based on involvement of the ascending aorta.

Stanford Aortic involvement classification

Type A Involves the ascending aorta, regardless of distal extension

Type B Does not involve the ascending aorta and begins distal to the left subclavian artery

This patient has ascending-aortic involvement and therefore has a Stanford type A dissection.

Rationale

DeBakey Description type

Type I Begins in the ascending aorta and extends beyond the arch

Type II Begins in and remains limited to the ascending aorta

Type III Begins in the descending aorta, usually distal to the left subclavian artery

This patient’s dissection begins in the ascending aorta and extends into the descending aorta.

Rationale

Ascending aortic dissection may involve the aortic root and interfere with normal aortic-valve function.

Acute aortic regurgitation may cause:

• Early diastolic decrescendo murmur
• Rapid left ventricular volume overload
• Pulmonary edema
• Hypotension
• Cardiogenic shock

A murmur may be subtle or absent, particularly in an unstable patient.

Rationale

Extension of a dissection into an aortic branch vessel can reduce blood flow to organs or extremities.

Potential malperfusion complications include:

• Stroke or transient neurologic deficit
• Upper- or lower-extremity ischemia
• Myocardial ischemia
• Renal ischemia
• Mesenteric ischemia
• Spinal-cord ischemia

The guideline emphasizes assessment of branch-vessel involvement and malperfusion during imaging.

Rationale

Anti-impulse therapy reduces:

• Heart rate
• Blood pressure
• Left ventricular contractile force
• Rate of pressure change within the aorta

Reducing these forces may decrease continued stress on the injured aortic wall while definitive treatment is arranged.

Rationale

Intravenous beta-blocker therapy is generally recommended initially in acute aortic syndrome unless contraindicated.

Common hospital options may include:

• Esmolol
• Labetalol

The treatment goal is to reduce aortic-wall stress while maintaining adequate organ perfusion.

Rationale

Guideline targets for acute aortic syndrome include:

• Systolic blood pressure below 120 mmHg when tolerated
• The lowest blood pressure that preserves end-organ perfusion
• Heart rate approximately 60–80 beats/min

Treatment must be individualized according to perfusion, neurologic status, renal function, and hemodynamic stability.

Rationale

An intravenous vasodilator may be added when blood pressure remains above target after adequate beta blockade.

CONO Examination Trap

Do not begin a potent vasodilator before controlling reflex tachycardia when acute aortic dissection is suspected.

The beta blocker is generally administered first because vasodilation alone may provoke increased heart rate and contractility, potentially increasing aortic-wall stress.

Rationale

Acute Stanford type A dissection generally requires urgent surgical repair because of the risk of:

• Aortic rupture
• Cardiac tamponade
• Acute severe aortic regurgitation
• Coronary-artery involvement
• Myocardial infarction
• Stroke
• Organ malperfusion
• Death

Immediate operative repair is recommended for acute type A dissection, including presentations with renal, mesenteric, or extremity malperfusion.

Rationale

Extension or rupture of an ascending aortic dissection into the pericardial space may rapidly produce cardiac tamponade.

Possible findings include:

• Hypotension
• Elevated jugular venous pressure
• Muffled heart sounds
• Tachycardia
• Narrow pulse pressure
• Pulsus paradoxus
• Shock

This is an immediately life-threatening complication requiring urgent specialist management.

Rationale

Medical therapy is generally the initial treatment for uncomplicated acute type B dissection.

Intervention may become necessary when complications occur, including:

• Aortic rupture
• Branch-artery occlusion
• Organ malperfusion
• Progressive aortic enlargement
• Extension of the dissection
• Persistent or intractable pain
• Uncontrolled hypertension

When intervention is needed and anatomy is suitable, thoracic endovascular aortic repair may be preferred in selected patients.

Rationale

Appropriate adjunctive care may include:

• Supporting strict blood-pressure management
• Reinforcing prescribed beta-blocker and antihypertensive adherence
• Supporting smoking cessation
• Encouraging an individualized heart-healthy dietary pattern
• Supporting appropriate aerobic activity after specialist clearance
• Avoiding unapproved heavy lifting or intense isometric strain
• Reviewing supplements and botanicals for medication interactions
• Supporting stress management and recovery
• Reinforcing cardiology and surgical follow-up
• Reinforcing scheduled surveillance imaging
• Reviewing family history and recommended family screening

Long-term imaging surveillance is important because residual aortic disease may enlarge or develop additional complications. For patients with residual disease after dissection repair, or

those managed medically, CT or MRI surveillance is recommended after approximately 1 month, 6 months, 12 months, and annually thereafter when stable.