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The epidemic of chest pain According to a study conducted by HHS, chest pain is the fourth most common for an emergency visit Accounted for more than 2 million ER visits last year Five percent of patients with normal or non diagnostic ekgs will go on to have an acute MI The missed diagnosis of acute MI is around 2%. Patients with acute MI (AMI) that are mistakenly discharged from the emergency room have a short term mortality rate 25%. This is twice the in hospital mortality rate for AMI

Chest pain is difficult to interpret

Case 1 A 64-year-old woman is evaluated in the emergency department 6 hours after the onset of severe crushing chest pain associated with diaphoresis, nausea, and vomiting. Her medical history is significant only for mild hyperlipidemia; her medications include atorvastatin and aspirin. Her blood pressure is 140/88 mm Hg, and her pulse rate is 88/min. The lungs are clear; she has no murmurs; examination of the abdomen and extremities is normal.

Key details in a chest pain history Quality In your own words, how would you describe the pain? What adjectives would you use? Location Point with your finger to where you are feeling the pain Radiation If the pain moves out of your chest, trace where it travels with your fingers Size of area or distribution What is the area on your chest where the pain occurs? Severity On a scale of 1 to 10, can you rate the severity of the pain? Time of onset Is the pain still present? Has it improved or worsened since it first started? When did it begin? How long is each episode of pain? Frequency How many times per hour or per day has it been occurring? First occurrence When was the first time you ever had this pain? Similar to previous episodes If you have had a heart attack or angina in the past are these symptoms similar to your previous symptoms?

Precipitating factors Pleuritic pain Is the pain worse if you take a deep breath or cough? Positional Is the pain made better or worse when you change body positions? What position makes the pain better or worse? Palpable If I press on your chest wall, does that reproduce the pain Exercise Does the pain come back or get worse when you exert yourself Relieving factors Are there any things that you can do to relieve the pain oce it has begun? Associated symptoms Do you typically get other symptoms when you get this chest pain?

Typical versus typical chest pain Substernal Pressure like sensation or heaviness in the chest Increased with exertion and relieved with stress or nitrglycerin Must meet all three requirements

Likelihood ratio The likelihood ratio for a positive result (LR+) tells you how much the odds of the disease increase when a test is positive .

The importance of a history Swap JAMA 2005 1.9 Worse than previous angina or similar to previous MI 1.8 Described as pressure 2.0 Associated with nausea or vomiting 2.3 Radiation to left arm 2.4 Associated with exertion 4.1 Radiation to both arms or shoulder 4.7 Radiation to R arm or shoulder Positive likelihood ratio Pain Descriptor

The importance of a history Swap JAMA 2005 0.8 Not associated with exertion 0.3 Reproducible with palpation 0.3 Described as sharp 0.3 Described as positional 0.2 Describes as pleuritic Positive likelihood ratio Pain Descriptor

Physical Exam General Appearance Vital Signs – temperature, tachycardia or bradycardia, hyper or hypotension, respiratory rate and oxygen saturation JVP Rate, rhythm, murmurs, S3, rubs Crackles or signs of pulm edema Peripheral edema, distal pulses, extremities are warm or cold

Treatment Reperfusion Indicated for STEMI within 12 hours of presentation Early invasive approach may be preferrred for high risk NSTEMI Patients in cardiogenic shock should have reperfusion therapy Medical Therapy Antiplatelet therapy – aspirin and clopodigrel Antithrombin – heparin Beta blocker – beneficial, PO is now preferred Contraindications include HR<60, SBP< 100, signs of pulmonary edema or cardiogenic shock, heart block. ACE inhibitors High dose statins shown to be beneficial Of note – calcium channel have not shown benefit in acute MI and there may be associated with an increased risk in the acute phase of an MI

PTCA, percutaneous transluminal coronary angioplasty. 5.0%- 6.5% 13%-15% 30% Pre-CCU Era CCU Era Reperfusion Era Improvement in Mortality

Case # 2 43 yo F with h/o of HTN presents with constant retrosternal chest pain for two days. The pain becomes worse when she sits up and leans forward. On physical exam the patient is afebrile with no other positive findings.

Acute pericarditis Most of the pericardium is insensitive to pain Noninfectious causes of pericarditis rarely cause pain In contrast, infectious causes usually involve the pulmonary pleura, so patients experience pleuritic pain Incidence – 5 percent of patients who present to the ER with chest pain, but no acute MI haver pericarditis

History Chest pain is usually retrosternal, sudden in onset, and pleuritic Increased pain when the patient lies down and improved when the patient is sitting forward As in MI, chest pain can radiate to the neck arms, or left shoulder

Physical Exam Eighty-five percent of patients with pericarditis have an audible friction rub at some point of their illness Corresponds to the movement of the heart within the pericardial sac Patients can develop pericardial effusion and subsequent tamponade so a pulsus paradoxus should be checked >10 mm Hg systolic arterial decrease suggests tamponade Body temperature > 38 degrees is uncommon and may indicate purulent pericarditis that could require drainage

Treatment NSAIDS are the mainstay of treatment for idiopathic pericarditis Symptoms should improve in two weeks Colchicine is generally reserved for patients who have recurrent or non resolving pericarditis Steroids are only given to patients who have connective-tissue disease or severely symptomatic recurrent pericarditis

Case #3 56 yo F with PMH of HTN, CAD s/p CABG 2004, hyperlipidemia presents with sudden onset of chest pain and dyspnea for the past three years. Patient was in her usual state of health before her symptoms began. She works as a corporate lawyer spending 10 – 12 hours per day. On physical exam the patient is uncomfortable with VS 100.6 120/70 120 27 92% RA

Pulmonary Embolism About 79% of patients who present with PE have evidence of DVT in their legs If DVT is not present then it is likely that the entire thrombus embolized PE occurs in 50% of patients with DVT Dual pulmonary circulation makes pulmonary infarction rare Obstruction of the pulmonary artery leads to increases in RV afterload Death ensues from RV failure

Incidence and risk factors Average incidence is 1 episode per 1000 patients Annually, 100,000 patients die from PE Risk factors include Hip and knee replacement Trauma and spinal cord injury Decreased mobility Prolonged air and ground transportation Sedentary occupations may also increase risk Cancer Prothrombotic states – protein c and s deficincy, Factor V Leiden, antiphosopholipid syndrome

Clinical manifestations Look for signs of a DVT – leg warmth, pain, swelling Dyspnea or chest pain Pleuritic chest pain Hemoptysis – usu occurs in pulmonary infarction Tachypnea and tachycardia are common, but non specific Elevated neck veins, loud P2 Possibility of massive PE should be considered in patients who have a sudden onset of near syncope or syncope, hypotension, extreme hypoxia, or cardiac arrest

Wells Prediction Score DVT symptoms or signs 3 points PE as likely as or more likely 3 than other diagnosis HR > 100 bpm 1.5 Immobilization or surgery 1.5 in previous 4 weeks Previous DVT or PE 1.5 Hemoptysis 1.0 Cancer 1.0 Total Score < 2 points – low pretest prob 2 to 6 points – moderate pretest prob > 6 points- high pretest prob

Making the diagnosis D – dimer has a high negative predictive value and a high negative likelihood ratio (ie if it is negative, then PE is unlikely) CTA chest has excellent sensitivity and specificity for detecting emboli in the main, lobar, or segmental pulmonary arteries V/Q scan is most likely to make the diagnosis in the absence of cardiopulmonary disease Normal perfusion scan effectively rules out PE TTE can be used in patients if there is hemodynamic compromise as it can diagnose elevated PA pressure and RV strain.

Treatment Anticoagulation with heparin and coumadin is the mainstay of treatment Although, they do not have thrombolytic properties themselves, they allow the thrombolytic mechanism to act unopposed thereby decreasing clot burden PTT goal 60 to 80 and INR goal 1-2 Indications for IVC filter Contraindication to anticoagulation Major bleeding complication Recurrent embolism with anticoagulation Thrombolytics should be considered in patients with massive PE and hemodynamic compromise

Case #4 77 yo M with h/o CAD s/p CABG 1998, HTN, hyperlipidemia, IDDM presents with severe chest pain four hours prior admission that came on suddenly. Patient describes a stabbing sensation that radiates to the jaw, but which has been improved over the past few hours. On physical exam, vital signs – 97.4 176/65 76 23 95% RA. Cardiac exam shows a diastolic murmur and reduced distal pulses.

Aortic Dissection Acute aortic dissection occurs – only 7,000 cases per year in the US, but is potentially catastrophic Early mortality is as high as 1% per hour if left untreated Occurs when blood penetrated the medial layer of the aorta dissecting the wall causing a false lumen Type A dissections involve the ascending aorta and Type B involve are all other dissections.

Epidemiology and pathogensis Cystic medial degeneration Marfan’s Ehlers-Danlos Biscuspid aortic valves – risk factor for proximal dissection Woman in their third trimester are at increased risk Peak incidence is in the sixth and seventh decades of life and three-quarter of patients have hypertension.

Symptoms Chest pain is resent in up to 96% of cases Typically severe and of sudden onset with a decrescendo type pain Patients describe a tearing, ripping, sharp, stabbing pain Pain tends to radiate and follow the path of the dissection Less common presentations include heart failure and syncope

Signs and complications Hypertension – but only seen 36% patients with ascending dissection Hypotension can occur with acute aortic insufficiency Decreased pulses, AI murmur, and neurologic manifestations are more charactersitic of proximal rather than distal dissection AI murmur occurs in 1/3 of all cases and can be due to aortic root dilation or the dissection can travel proximally detaching an aortic flap CVA, renal failure, or mesenteric ischemia can occur branching arteries lose their blood supply due to the dissection.

Diagnosis Chest xray shows a widened mediastinum 81 to 90% of the time EKG may show an acute MI if the dissection flap involves the coronary artery CTA is the diagnostic modality of choice MRI/A can also be used if CT is contraindicated TEE is well suited to see the proximal ascending aorta, but may not be able to assess the proximal or distal ascending arch due to artifact from the trachea and bronchi

Management Blood Pressure Management Arterial bp monitering is perferred SBP should btw 100 -120 Beta blocking agents should be used to decrease the shear stress on intima Nitroprusside + beta blocker can be used Labetelol IV fenoldopam can be used in patients with renal failure Hydralazine should be avoided because the reflex tachycardia may exacerbate shear stress Definitive therapy is surgery to repair the dissection

Case # 5 A 52-year-old man telephones his physician to report a 4-week history of episodic left-sided chest pain lasting 3 to 5 minutes, often occurring at rest, and resolving spontaneously. He is unsure whether the episodes are related to meals. He has not had any shortness of breath, orthopnea, exertional dyspnea, nausea or vomiting. History is significant for hyperlipidemia. Patient has been sedentary for the past several years until 3 months ago when he began exercising. The patient is experiencing significant stress related to his job; he is also in the midst of a divorce. During the course of the phone interview, the patient is asked to determine whether he feels any pain while pressing on his chest over the lateral aspects of the sternum. The patient reports that this maneuver does vaguely reproduce his pain.

Costochronditis Most common cause of anterior chest musculoskeletal pain Local chest wall tenderness – reproducible pain by palpation. Occasionally, patients have swelling and inflammation over the costochondral joint The pain often occurs at rest and during chest movement Lasts up to several hours or days Ranges in severity from a dull ache to a throbbing intense discomfort May be increased with deep inspiration.

Case #6 48 yo M with PMH of CAD s/p PCI to LAD, hyperlipidemia, current smoker presents with mid strenal chest pain occasionally associated with cough. The patients symptoms can occur during exertion. The patient runs one mile every day with no symptoms. Chest pain is, however, increased when the patient is sleeping or in a recumbent position. Pain is not reproducible upon palpation. Of note, the patient does not report any new stressors in his life.

Gastroesophogeal reflux disease GERD is the common cause of non cardiac chest pain. The pathophysiology of GERD – related chest pain may be related to the fact the esophagus and heart share a common innervation. Prior acid reflux events may sensitive the nerves leading to chest pain. Patients often present with epigastric pain and dyspepsia often provoked by recumbency and swallowing. Usually, the patients are given a short trial of high dose PPi to make the diagnosis and treat the symptoms

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