Chest pain

Chest pain - CTSP

...clutch your chest and think.

When called for a patient with CP, angina or MI may be of course your first thoughts. However, the most important tool in identifying the cause of CP is a good history. The patient should be assessed immediately. Never manage CP over the phone. Before you hang the phone, ask the nurse for vital signs.

Initial verbal orders should include:

  • Stat ECG

  • O2 by NC at 2 L/min

  • NTG, 0.4 mg SL q5 min x 3 (Hold if SBP <90 mm Hg)

  • ASA, 325 mg PO stat

  • Confirm IV access.

Major causes: Think about acute, potentially life-threatening conditions:

  • Heart: Angina, MI, acute pericarditis, AS, aortic dissection

    • MI and injury: CAD. Ischemia can also result from psychological stress, fever, large meals, compromised O2 delivery due to anemia, hypoxia, HOCM, HTN.

  • Lungs: Pulmonary embolus, spontaneous pneumothorax, pneumonia, pleuritis, pulmonary HTN.

  • GI: Esophageal spasm, Boerhaave syndrome, PUD, GERD, pancreatitis, gall bladder disease,

  • Others: Herpes zoster, costochondritis, cervical disc disease, arthritis of should and spine, panic attack, anxiety state.

In order of frequency:

  • Gastroesophageal disease: 42%; includes: GERD, PUD, esophageal motility d/o, gallstones.

  • Ischemic heart disease: 31%

  • Chest wall syndromes: 28%

  • Pericarditis: 4%

  • Pleuritis/pneumonia: 2%

  • Pulmonary embolism: 2%

  • Lung cancer: 1.5%

  • Aortic aneurysm: 1%

  • Aortic stenosis: 1%

  • Herpes zoster: 1%

HISTORY:

  • Check hemodynamic stability before anything else.

  • Description of pain: ChLoRIDE PP. Know the time of onset

  • Retrosternal chest discomfort, pressure, fullness, squeezing, pain lasting >15 min. Myocardial ischemia is usually associated with gradual intensification of the pain over a periods of minutes.

    • Chest pain that does not change with body position or respiration. Chest pain not associated with chest wall tenderness. When any of these three features is present, it is less likely to be from CAD.

  • Pain that fleeting or has lasted for hours without any ECG changes is not likely to be ischemic in origin.

  • Radiation to jaw, shoulders, neck, back or inbetween shoulder blades.

  • Light headedness, fainting, sweating, N/V, SOB (shortness of breath), anxiety, distress, leg pain or swelling, fever, dysphagia/odynophagia, impending doom.

  • Sometime epigastric distress may be the only symptom of ischemia.

  • Older females or diabetic patients may present as SOB or nausea as their main symptom.

  • Risk factors for CAD: HTN, DM, obesity, BMI: 30 or above, dyslipidemia, HDL <40 (HDL >60 is protective), elevated LDL, physical inactivity, cigarette smoking, microalbuminuria (urine albumin/cr ratio of 30 - 300 mg/g), GFR: 60 ml/min or less, renal insufficiency (Sr. Cr 1.5 or more), age: >45 in males, and >55 in females. If FH/o of CVD is positive in males relatives: <55 yrs and female relatives: <65 years, including SCD (sudden cardiac death), carotid artery disease, PAD, AAA, hyperhomocystinemia, high CRP and circulating fibrinogen.

Focused Exam:

  • General Survey: How distressed does the Pt appears? Check ABCs

  • Vitals: Hypotension is an ominous sign. Tachycardia may be from PE or from pain. Bradycardia may be from AV block with inferior MI. Take BP in both arms and legs, to check for possible Aortic dissection. Check pulse oximetry.

  • Skin: pallor, cool, clammy extremities, capillary refill, (shock states)

  • Neck: Assess JVD. Check carotids (one at a time), and listen for any bruit.

  • Thorax/Lungs: Check for ACW tenderness and any skin lesions. Anterior posterior compression of patient's thorax. Is the pain completely reproducible. Assess for crackles, absent breath sounds on one side, friction rub. Crepitus of subcutaneous emphysema - PTx or esophageal rupture. Tenderness on the ribs and sternum without crepitance suggests a fracture.

  • Heart: Inspect the apical impulse - if localized or presence of heaves (Rt and Lt). Feel for thrills over the respective valvular areas. Listen for murmur, rubs, or gallops. Assess JVD. Muffled heart sounds. S3 (dilated LV), S4 (LVH) in chest pain may reflect changes in the compliance of the ventricles resulting from myocardial dysfunction. Holosystolic murmur of mitral regurgitation (papillary muscle dysfunction).

  • Abdomen: Tenderness, bowel sounds.

  • Extremities: Edema or evidence of DVT. If dissection is suspected, examine pulses bilaterally in both UE and LE. Check the radial and femoral pulses simultaneously, as these pulses may be an important sign to diagnose aortic or subclavian stenotic disease.

  • Labs:

    • ECG for all patients with chest pain.

    • CXR for patients with sign and symptoms of CHF, VHD, pericardial disease, or aortic dissection or aneurysm

    • ABGs, CBC, CCP, CRP

    • Troponin-I q6h x 3, CK-MB

    • BNP, d-Dimer

    • V/Q scan, CT scan Thx with contrast for PE, Ao dissection

    • 2-D echo, TEE if dissection is suspected

    • Duplex dopper US LE

    • ECG: ST elev of >1 mm or more in 2 contiguous leads or new LBBB or sustained VT. Always try to compare with a prior ECG. ST depression of >1 mm or ischemic T waves (symmetrical)

    • Continuous cardiac monitoring

      • Patients who present with ST-segment depression can have either UA or NSTEMI, the distinction being based on the later detection of biomarkers of myocardial necrosis. Inverted T waves, especially if marked (greater than or equal to 2 mm [0.2 mV]), also can indicate UA/NSTEMI.

    • CXR.

    • Amylase, lipase, LFTs if indicated.

    • Provocative tests for CAD (stress test) are not appropriate for patients with ongoing chest pain. Rest myocardial perfusion scans can be considered. A normal scan reduces the likelihood of CAD and can help avoid admission of low-risk patients to the hospital.

    • CT thorax with contrast done promptly if Aortic dissection is considered. if time constrants, do U/S of aorta, or TEE.

      • Stable angina: exercise ECG, stress echocardiography, or stress perfusion imaging

Immediate Tx:

  • Cardiac:

    • ABCs

    • Bed rest

      • IV access, O2 by NC at 2 - 4 L/min, cardiac monitor.

      • ASA 325 mg (chew).

    • Sublingual NTG (0.4mg) q5minutes X 3 (hold if SBP <90), if pain persists, also add Morphine 2 - 4mg IV.

      • CXR

    • If evidence of acute MI on Hx, ECG, and +ve Troponin-I. Consider reperfusion Tx: Stat cardiology consult to transfer to Telemetry or Cath. Lab.

    • Fibrinolytic checklist

      • NTG IV 10 - 200 mcg/min

      • If STEMI:

        • Start adjunctive treatments:

          • Metoprolol 5 mg IV, repeat q5 minutes to max: 15 mg.

      • Heparin 60 U/kg (max: 4000 units) IVP, followed by infusion of 12U/Kg/Hr (max: 1000 units/hr) to 14U/Kg/Hr. OR LMWH

        • Clopidogrel (may be deferred until a revascularization decision is made - CABG candidate or not?)

        • Reperfusion strategy. Defined by patient and center criteria

          • PCI

          • Fibrinolysis

      • ACE-I/ARB, within 24 hours of symptom onset.

      • Statin.

      • If high risk UA/NSTEMI:

        • Start adjunctive treatments:

          • Metoprolol 5 mg IV, repeat q5 minutes to max: 15 mg.

        • Heparin 60 U/kg (4000 units) IVP, followed by infusion of 12U/Kg/Hr (1000 units/hr) to 14U/Kg/Hr. OR LMWH

        • Clopidogrel (may be deferred until a revascularization decision is made - CABG candidate or not?)

        • GP IIb/IIIa inhibitor lower mortality, particularly in those undergoing angioplasty.

        • No thrombolytic use

      • High-risk patient:

          • Refractory ischemic chest pain

          • Recurrent/persistent ST deviation

          • VT

          • Hemodynamic instability

          • Signs of pump failure

          • Early invasive strategy, including catheterization and revascularization for shock within 48 hours of an AMI

        • ACE-I/ARB, within 24 hours of symptom onset.

      • Statin.

Reperfusion goals:

    • Door-to-balloon inflation (PCI) goal of 90 minutes.

    • Door-to-needle (fibrinolysis) goal of 30 minutes.

Aortic dissection:

  • Arrange for immediate transfer to CCU/MICU.

  • Nitroprusside or labetalol for BP control.

  • Stat Vascular surgery/CT surgery consult.

Pulmonary:

  • If PE, ensure O2 and IV heparin, pain control.

  • PTx: Tension requires immediate needle thoracentesis (decompression) in the 2nd ICS in MCL, followed by chest tube. Other pneumothoraces involving >20% of the lung require chest tube.

GI:

  • Antacids such as aluminum hydroxide (Maalox), 30 mL PO PRN q4-6h

  • Famotidine (Pepcid), 20 mg PO bid, or omeprazole (Prilosec), 20 mg PO qd.

    • Elevate the head of the bed.

Dipyridamole or adenosine thallium stress test or dobutamine echo

Pt. who cannot exercise to a target HR >85% of MHR

COPD, amputees, deconditioned, weakness/paralysis, lower-extremity ulcer, dementia, obesity

Exercise thallium testing or stress echocardiography

ECG is unreadable for ischemia: LBBB, digoxin use, pacemaker in place, LVH

Indications for CABG

3-vessel with >70 stenosis

Left main disease, >70 stenosis

CAD equivalents: DM, PAD, carotid artery disease, aortic disease.

Therapies in ACS:

Always lower mortality: ASA, metoprolol, statin, clopidogrel, thrombolysis, PCI.

Lower mortality in certain conditions: ACE-I/ARBs if LVEF is low.

Do not lower mortality: O2, morphine, nitrates, CCB, lidocaine, amiodarone.

Complications of MI:

Cardiogenic shock

Valve rupture

Septal rupture

Myocardial wall rupture

Third-degree heart block

Right ventricular infarction

Myocardial markers:

Troponins, proteins of the thin filaments composing the myofibrils that regulate calcium-dependent ATP hydrolysis of actomyosin comes in 3 forms: Troponin I (inhibitory), T (tropomyosin binding), C (calcium binding)

ACC/AHA Guidelines for the Management of Pts with UA/NSTEMI

Guidelines and Critical Pathways For Acute Chest Discomfort

ACC/AHA.

    • Perform ECG on virtually all patients with CP who do not have an obvious noncardiac cause of their pain, and perform CXR for Pts with si and sx consistent with CHF, VHD, pericardial disease, or Ao dissection or aneurysm.

    • Exercise testing in low-risk patients, as well as in intermediate-risk patients. Stress testing is a way of increasing the intensity of detection of CAD beyond an ECG and enzymes. Testing done after Pts have been screened for high-risk features or other indications for hospital admission. Such Pt. can be safely observed in non-coronary care units, and undergo early exercise testing, or be discharged home.

    • LOS in a monitored bed for a patient who has no further sx is 12 hours of less if exercise testing or other risk stratification is done.

  • CK-MB and tropinin rise at 3-6 hours after chest pain. Same specificity, but CK-MB stays elevated for 1-2 days, while troponin stays elevated for 1-2 weeks.

  • Reinfarction a few days after initial infarction: Check CK-MB.

  • Myoglobin elevates earliest 1-4 hrs after onset of chest pain.

After PCI with stent.

ASA:

    • BMS: ASA, 325 mg qd x 1 mo

    • DES: ASA, 162-325 mg qd (based on risk of excess bleeding), x 3-6 months.

NSAIDs and ASA:

    • Due to interaction between ibuprofen and ASA, an alternative NSAID should be used, or ibuprofen should be taken at least 30 min after or at least 8 h before ASA

ADP receptor antagonists and other antiplatelet agents:

    • Thienopyridines—ticlopidine (can cause neutropenia, out of favor) and clopidogrel—are adenosine diphosphate receptor (P2Y12) antagonists approved for antiplatelet therapy.

    • Irreversible effect of thienopyridines. In the absence of loading dose, takes several days to have maximum effect.

Variant (Prinzmetal’s) Angina

Variant angina (Prinzmetal’s angina, periodic angina) is an unusual form of UA that usually occurs spontaneously, is classically characterized by transient ST-segment elevation, and spontaneously resolves or resolves with NTG use, usually without progression to MI.

Clinical Picture, Pathogenesis, and Diagnosis:

    • Anginal discomfort at rest, simulating UA/NSTEMI.

    • Attacks can be precipitated by emotional stress, hyperventilation, exercise, or exposure to cold and occur more frequently in the early morning.

    • Patients with variant angina are generally younger and, except for smoking, have fewer coronary risk factors.

    • Occasionally, prolonged vasospasm can result in MI, atrioventricular block, ventricular tachycardia, or sudden death.

    • The cause of variant angina is epicardial coronary artery spasm, most commonly focal but potentially at more than 1 site). ST-segment elevation implies transmural ischemia associated with complete or near-complete coronary occlusion.

    • The key to diagnosis is the documentation of transient ST-segment elevation during chest discomfort.

    • Both noninvasive tests (ambulatory ECG recording, morning treadmill exercise) and coronary angiography (which can include pharmacological

Treatment and Prognosis

    • NTG, long-acting nitrates, and calcium antagonists.

Cardiovascular “Syndrome X”

Cardiovascular “syndrome X” refers to with a syndrome of angina or angina-like discomfort with exercise, ST-segment depression on exercise testing or other objective signs of ischemia, and normal or nonobstructed coronary arteries on arteriography.

    • Syndrome X is more common in women than in men.

    • Chest discomfort can be typical or atypical, may occur with activity or at rest, and may or may not respond to NTG.

Cause of syndrome X is not well understood but has been postulated to involve microvascular dysfunction and/or abnormal pain perception. Other causes of chest discomfort, especially esophageal dysmotility, should be ruled out. C

Treatment

    • Beta blockers and calcium antagonists can reduce the number of episodes of chest discomfort.

    • Nitrates are effective in one-half of patients.

    • Imipramine 50 mg daily can benefit patients with chronic pain syndromes, including syndrome X.

    • Estrogen in postmenopausal women can reduce the frequency of chest pain episodes but can increase cardiovascular risk.

    • Statin therapy and exercise training can improve exercise capacity, endothelial function, and symptoms.

    • Cognitive behavioral therapy can be beneficial.

    • Transcutaneous electrical nerve stimulation and spinal cord stimulation have been used for pain control in highly symptomatic, refractory cases