Chest Pain

In terms of typical pathogens associated with infective endocarditis, which organisms are considered part of the HACEK group?

- Haemophilus sp. - Aggregatibacter sp. - Cardiobacterium hominis - Eikenella corrodens - Kingella sp.

Considering each of the patient specific factors below in isolation (i.e. each of these choices stands alone), which of the following patients are more likely to experience atypical symptoms of angina or MI? - women - men - diabetics - elderly

- women - diabetics - elderly Women, diabetics, and the elderly are more likely than men to experience cardiac related chest pain differently than the "typical" or classic description. They may present primarily with SOA; they may describe the CP differently than the classic description of squeezing or chest pressure; they may have no chest pain at all. ANY patient, regardless of race, sex, or age with risk factors for CAD (smoking, HTN, hyperlipidemia, family history of CAD, and diabetes), should have their complaints of CP taken seriously. Do not assume that the absence of classical angina-like pain eliminates the potential for ACS or angina, especially in the setting of risk factors for CAD.

From question #1, in terms of a conglomeration of signs and symptoms that make up clinical presentation, the absence of SOA, DOE, orthopnea, PND, crackles on lung exam, JVD, and lower extremity edema in this patient effectively places which diagnosis at the bottom or completely off of the DDx? A) CHF B) CAD C) Unstable angina D) PE E) Pericarditis

A) CHF Together, the combination of SOA, DOE, orthopnea, PND, crackles upon lung exam, JVD, and lower extremity edema is heart failure until proven otherwise. These signs and symptoms together are very sensitive and specific for this condition. The other conditions may or may not have some of these features; but they are not known to cause them all together as you would see in CHF.

Chest pain can be caused by organ systems other than the heart. When patients present atypically for any cause, it can be very hard to formulate a differential diagnosis. However, regardless of how the quality of the pain is described, what is the one specific characteristic that distinguishes ischemic cardiac chest pain from all other causes of chest pain? A) Its reproducibility with exertion or emotional stress B) Its reproducibility upon palpation of the affected area C) Its reproducibility upon movement or change in position D) Its association with SOA E) Its association with deep breathing

A) Its reproducibility with exertion or emotional stress Reproducible chest pain upon exertion is the hallmark feature of ischemic cardiac pain (i.e. anginal pain), which is why stress EKG testing is considered a valuable diagnostic tool. Angina, which is the pain of CAD is ischemic in nature, which means pain will occur any time myocardial oxygen demand exceeds supply. Reproducible pain upon palpation of the affected area or pain upon certain movements/position changes is typical of musculoskeletal-related pain or pain due to inflammation. While chest pain associated with SOA can be a feature of ischemic cardiac pain, the presence or absence of SOA does not rule in or out ischemic-related CP, (i.e. one can have anginal chest pain without SOA), thus SOA is not a specific distinguishing characteristic. For example, PE can cause pleuritic CP along with SOA. Anginal pain is not associated with pain with deep breathing, which is pleuritic in nature. Anginal pain is not pleuritic; the hallmark feature of angina is exertional chest pain.

A patient well-known to you with HTN, hyperlipidemia, DM and inconsistent refill history, approaches the pharmacy counter to pick up his prescriptions. You notice he doesn't look to well and he's rubbing his chest. You ask him if he's OK. He says his chest just started hurting after walking in and he feels like he might pass out. You have him sit down and he says his pain is abrupt, 9/10, described as sharp and knife-like that is radiating to his back. Pain is unaffected by breathing and changing positions. He has not had any recent changes in usual daily activities, recent injuries or trauma, or changes in dietary habits. You take his BP in both arms and notice a significant systolic difference (> 20 mmHg) between the right and left arms. Based on this subjective and objective information, you call 911. What should be at the very top of your differential as you provide information to the dispatcher? A) acute aortic dissection B) pericarditis C) acute pulmonary embolism D) acute panic attack/hyperventilation syndrome E) infective endocarditis F) stable angina

A) acute aortic dissection Abrupt onset of severe, knife-like pain that radiates to the back, especially in someone with cardiac risk factors is highly suggestive of acute aortic dissection; this is the typical pain description. This patient also has HTN with a history of medication non-adherence. Uncontrolled HTN and dyslipidemia are risk factors for this condition. Additionally the objective finding of a significant (i.e. 20 mmHg or more) difference of systolic BP between the right and left arms is considered a hallmark finding. If you ever come across this presentation, call 911 immediately, as an acute dissection can be fatal if not addressed quickly.

When determining empiric antimicrobial therapy for infective endocardits (IE), the IE Guidelines recommend an evaluation of which of the following patient specific factors? [select all that apply] A. History of prior infections B. Epidemiologic clues C. Recent exposure to antimicrobials D. Clinical course of current infection E. Severity of current infection F. Other sites of infection associated with current IE infection

A. History of prior infections B. Epidemiologic clues C. Recent exposure to antimicrobials D. Clinical course of current infection E. Severity of current infection F. Other sites of infection associated with current IE infection In addition to an ID consult, the IE guidelines recommend evaluating all of these factors when determining appropriate empiric therapy.

What is an aortic dissection?

Aortic dissection is a serious and potentially life-threatening medical condition that occurs when the inner layer (intima) tears, causing it to separate from the middle layer (media). Blood then flows between the layers, creating a channel called a dissection. This channel may be referred to as the "false lumen." Reduced blood flow in the dissected aorta can lead to major organ damage, or the channel may rupture or burst open through the outer layer (adventitia), which can be fatal.

Using Table 2 in the "Pleuritic Chest Pain" article by Reamy et al., which of the following is NOT one of the components that, if present, raise the likelihood of CAD as a cause of chest pain? A) Males 55 and over or females 65 and over B) Known h/o vascular disease (CAD, occlusive vascular disease, cerebrovascular disease) C) Pain is NOT reproducible upon palpation D) Pain is worse with exercise or exertion E) Patient assumes pain is of cardiac origin F) None of the above (ALL of the above are components of CAD-related chest pain)

F) None of the above (ALL of the above are components of CAD-related chest pain)

T/F: In terms of therapeutic principles of antibiotic use in infective endocarditis, prolonged parenteral bacteriostatic therapy is required for attempted infection cure.

False - Prolonged, parenteral, BACTERICIDAL therapy is required for attempted infection cure for infective endocarditis.

In terms of therapeutic principles of antibiotic use in IE, [prolonged or abbreviated], [oral or parenteral], [bacteriostatic or bactericidal] therapy is required for attempted infection cure.

In terms of therapeutic principles of antibiotic use in IE, prolonged, parenteral, bactericidal therapy is required for attempted infection cure.

How can you distinguish between presentations of pleuritic chest pain that are chronically concerning vs possibly life-threatening vs potentially acutely lethal if not addressed?

Most potentially lethal causes of pleuritic chest pain (e.g., pulmonary embolism, myocardial infarction, aortic dissection, and pneumothorax) typically have an acute onset over minutes. In contrast, less immediately lethal causes of pleuritic chest pain (e.g., infection, malignancy, inflammatory processes) progress over hours to days or weeks.

Pain that worsens when the patient is supine and lessens when the patient is upright and leaning forward should prompt consideration for ________.

Pain that worsens when the patient is supine and lessens when the patient is upright and leaning forward should prompt consideration for pericarditis.

Symptoms such as weight loss, malaise, night sweats, or arthralgias indicate chronic inflammatory causes of pleuritic chest pain, such as ________, ________, or ________.

Symptoms such as weight loss, malaise, night sweats, or arthralgias indicate chronic inflammatory causes of pleuritic chest pain, such as tuberculosis infection, rheumatoid arthritis, or malignancy.

Tachycardia or tachypnea may be present with any of the serious causes of pleuritic chest pain but should raise suspicion for ________, ________, or ________.

Tachycardia or tachypnea may be present with any of the serious causes of pleuritic chest pain but should raise suspicion for pulmonary embolism, pneumothorax, or myocardial infarction.

Describe atypical symptoms of chest pain associated with acute MI and identify which patient populations are more likely to experience atypical symptoms.

Women, the elderly, and patients with diabetes more commonly present with atypical symptoms, including: • lightheadedness or dizziness • unusual fatigue • indigestion • neck or jaw pain • burning or stinging sensations • shortness of breath • palpitations when patients present with these atypical symptoms, they may or may not have any chest pain at all

You are verifying medication orders in the ED. An order for ketorolac 15 mg IV x 1 comes across for a 54 yo man who presented with "chest pain" as his CC. In terms of medication appropriateness, the ED clinical note contains the HPI, but is otherwise not yet complete. HPI reveals: 54 yo man with no significant PMH and no recent illness, presents with left-sided, dull, chest pain brought on by certain movements of his shoulder and when he takes deep breaths. He is able to point directly to the painful area on the left upper side of his sternum. Onset was about 2 days ago, and is a new problem. He reports heavy lifting while moving recently. "Being still" is a relieving factor. He denies, SOA, DOE, chest pressure, exertional CP, orthopnea, PND, syncope, palpitations, leg cramps, hemoptysis. BP - 116/78; HR - 76; RR - 12; Temp - 98.5; O2 sat - 100% on room air. Cardiac exam reveals reproducible CP on upper left side of sternum upon palpation. Heart is RRR, no MRG, no JVD, R and L carotid pulses 2+ with no thrills or bruits. Lung exam reveals symmetric chest expansion, lungs are clear to auscultation bilaterally without friction rubs, crackles, wheezing, or rhonchi. Lower extremities are without edema; distal pulses 2+ in all extremities. All labs are pending. Diagnostic tests have not been ordered. What do you do about the medication order? A) Approve it, because most likely DDx is costochondritis B) Recommend aspirin instead because most likely DDx is angina pectoris C) Approve it, because the most likely DDx is pleurisy D) Recommend a GI cocktail containing famotidine, because the most likely DDx is esophagitis E) Recommend to d/c order and check D-dimer, because most likely DDx is pulmonary embolism

You are verifying medication orders in the ED. An order for ketorolac 15 mg IV x 1 comes across for a 54 yo man who presented with "chest pain" as his CC. In terms of medication appropriateness, the ED clinical note contains the HPI, but is otherwise not yet complete. HPI reveals: 54 yo man with no significant PMH and no recent illness, presents with left-sided, dull, chest pain brought on by certain movements of his shoulder and when he takes deep breaths. He is able to point directly to the painful area on the left upper side of his sternum. Onset was about 2 days ago, and is a new problem. He reports heavy lifting while moving recently. "Being still" is a relieving factor. He denies, SOA, DOE, chest pressure, exertional CP, orthopnea, PND, syncope, palpitations, leg cramps, hemoptysis. BP - 116/78; HR - 76; RR - 12; Temp - 98.5; O2 sat - 100% on room air. Cardiac exam reveals reproducible CP on upper left side of sternum upon palpation. Heart is RRR, no MRG, no JVD, R and L carotid pulses 2+ with no thrills or bruits. Lung exam reveals symmetric chest expansion, lungs are clear to auscultation bilaterally without friction rubs, crackles, wheezing, or rhonchi. Lower extremities are without edema; distal pulses 2+ in all extremities. All labs are pending. Diagnostic tests have not been ordered. What do you do about the medication order? A) Approve it, because most likely DDx is costochondritis B) Recommend aspirin instead because most likely DDx is angina pectoris C) Approve it, because the most likely DDx is pleurisy D) Recommend a GI cocktail containing famotidine, because the most likely DDx is esophagitis E) Recommend to d/c order and check D-dimer, because most likely DDx is pulmonary embolism

What is an aortic aneurysm?

a bulge or ballooning in the aorta due to a weakened wall

Pulmonary embolism has often been called "The Great Masquerader," because it can masquerade or mimic several other conditions. Describe the clinical presentation of a pulmonary embolism and risk factors for this condition.

clinical presentation: • sudden onset of sharp pleuritic chest pain that may occur anywhere in the peripheral lung field • chest pain may be accompanied by SOB, dyspnea, and/or calf pain risk factors: • post-op • hx of DVT • bedridden • any other reason for long periods of immobility (e.g., long car rides or flights)

List some clinical features of an aortic dissection. How is the pain different from anginal-type pain? [ hint: "the clinical triad" ]

clinical triad: • abrupt onset of severe ripping/tearing chest pain that radiates to the back; pain is the worst at onset • pulse or BP deficit between both arms • mediastinal widening on CXR

Describe the inoculum effect and the concept of antibiotic synergy.

inoculum effect: the biofilm/fibrin matrix that surrounds vegetations provides an environment where the bacteria are able to replicate freely until the microbial density has reached very high concentrations, at which point most organisms will stop actively dividing and remain in a static growth phase these factors hinder host defenses, as well as the ability of antimicrobials to produce sufficient kill → this is often seen with β-lactams and glycopeptides as their effectiveness can be significantly diminished with increased bacterial inoculum and stationary growth phase of the bacteria antibiotic synergy: bactericidal effects can be achieved by a combination of antibacterial drugs that alone only inhibit bacterial growth (bacteriostatic); the rate of bactericidal activity against some other organisms can also be enhanced by using the combination of a β-lactam plus an aminoglycoside

How is a panic attack or hyperventilation syndrome similar in presentation to cardiac related chest pain? How are they different?

pain quality can be identical, but there are usually paresthesias and circumoral paresthesias present with panic attack or hyperventilation syndrome that are not usually present with cardiac related chest pain circumoral parasthesias = numbness/tingling around the mouth

Differentiate between pleurisy, pericarditis, and costochondritis in terms of location of pain.

pleurisy: • laterally at periphery of lung fields • may be described as right upper quadrant abdominal pain with pneumonia pericarditis: • substernal with radiation to left trapezius costochondritis: • cartilage between ribs and sternum

Differentiate between pleurisy, pericarditis, and costochondritis in terms of symptom presentation.

pleurisy: • sudden onset of severe sharp pain that is worse when breathing pericarditis: • sudden onset of severe sharp pain that is continuous/unremitting • swallowing, lying down, and deep breathing make it worse • shallow breathing and leaning forward make it better costochondritis: • mild to moderate dull aching pain that comes on gradually and only occurs when breathing • made worse by breathing or by shoulder/arm movement • palpation over the area replicates the pain

How is the nature of GI-related "chest pain" different from cardiac-related chest pain?

quality of pain is typically described as gnawing or burning and located epigastrically rather than retrosternal

The pain of angina feels the same, so how do you distinguish between stable angina pectoris and unstable angina?

stable angina pectoris can be relieved with SL NTG or by resting if brought on by exercise unstable angina is unremitting and occurs even at rest; SL NTG is not effective in relieving the pain

Differentiate between stable angina pectoris, unstable angina, and acute myocardial infarction in terms of their clinical presentation.

stable angina pectoris: • episodic chest pain or tightness that is crushing/squeezing and may radiate down left arm • brought on by specific activities (e.g., exercise) or intense emotions • SL NTG and/or rest is usually effective in relieving pain • associated symptom(s) include SOB unstable angina: • prolonged chest pain or tightness that is crushing/squeezing and may radiate down left arm • pain is unremitting and not relieved by SL NTG • defined as angina at rest, new-onset angina, or angina that has become more severe or longer in duration • associated symptom(s) include SOB myocardial infarction: • prolonged chest pain or tightness that is crushing/squeezing and may radiate down left arm • pain is unremitting and not relieved by SL NTG • associated symptom(s) include SOB, diaphoresis, N/V, syncope

Differentiate between stable angina pectoris, unstable angina, and acute myocardial infarction in terms of lab results & diagnostic findings.

stable angina pectoris: • no changes in cardiac enzymes or ECG abnormalities unstable angina: • no changes in cardiac enzymes or ECG abnormalities myocardial infarction: • no ST segment elevation in NSTEMI; ST segment elevation in STEMI • elevated troponin levels in both NSTEMI and STEMI • elevated CKMB and/or AST in STEMI

How is pleuritic chest pain usually described?

sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling exacerbated by deep breathing, coughing, sneezing, or laughing

What is the pathophysiology of pleuritic chest pain?

the pain is caused by inflammation of the parietal pleura → inflammatory mediators released into the pleural space trigger local pain receptors

Chest pain can be caused by several different organ systems. When patients present atypically for any cause, it can be very hard to formulate a differential diagnosis. However, regardless of how the quality of the pain is described, what is ONE very specific characteristic that distinguishes ischemic cardiac chest pain from all other causes of chest pain?

the pain occurs when there is increased oxygen demand

What is unique about IE in terms of antibiotic penetration?

the penetration of antibiotics is a significant issue in the treatment of IE because cardiac vegetations, which are composed of layers of fibrin and platelets, pose a considerable mechanical barrier between the antibiotic and the embedded targeted microorganisms the efficacy of antimicrobial drugs varies, depending on the degree of penetration into the vegetation, pattern of distribution within the vegetation, and vegetation size

What is the most useful historical information for narrowing the differential diagnosis of pleuritic chest pain?

time course of symptom onset

T/F: The penetration of antibiotics is a significant issue in the treatment of IE, because cardiac vegetations, which are composed of layers of fibrin and platelets, pose a considerable mechanical barrier between the antibiotic and the embedded targeted microorganisms.

true

Imaging findings consistent with aortic dissection:

• CTA with obvious defect

Imaging findings consistent with pulmonary embolism:

• CXR with abrupt hilar cutoff, oligemia, or pulmonary infarction • filling defect often detectable with CTA

Imaging findings consistent with malignant pleural effusion:

• CXR with unilateral or bilateral effusions

You are an Emergency Department pharmacist, and a patient presents with s/sxs concerning for dissection. Emergent surgery is not indicated at this time and the team wants to initiate aggressive medical management. The medical resident asks you for medication recommendations. What is/are the primary goal(s) of medical management of aortic dissection? (i.e., what are the most important things we need to control?)

• HR <60 BPM • SBP 100-120 mmHg • IV Beta-blockers (e.g., esmolol) first line; IV calcium channel blockers (e.g., nicardipine) second

ECG findings consistent with myocardial infarction:

• ST elevation in contiguous leads

Imaging findings consistent with pneumothorax:

• abnormal CXR indicating air in pleural space

Red flags for pneumothorax:

• acute onset dyspnea

Red flags for pulmonary embolism:

• acute onset dyspnea • hx of DVT • hx of malignancy • unilateral leg swelling/pain

What are some factors that can help determine the likelihood of coronary artery disease as a cause of chest pain?

• age/sex: men 55 years or older, women 65 years or older • known vascular disease (CAD, occlusive vascular disease, cerebrovascular disease) • pain worse with exercise • pain not elicited with palpation • patient assumes pain is of cardiac origin

Red flags for myocardial infarction:

• angina • headache • arm/neck pain • nausea/vomiting

What are some risk factors for aortic aneurysm?

• atherosclerosis • cerebrovascular disease • coronary artery disease • first-degree relative with abdominal aortic aneurysm • hx of other vascular aneurysms • hypercholesterolemia • hypertension • male sex • obesity • older age • tobacco use type B aortic dissection (does not require immediate surgical intervention) can lead to an aortic aneurysm because the leaking of blood through the torn inner layers can weaken/dilate the outter layers of the aorta

Physical exam findings consistent aortic dissection:

• blood pressure/radial pulse discrepancy • aortic murmur • possible cardiac tamponade

Imaging findings consistent with pneumonia:

• consolidated infiltrates on CXR (or CT)

Imaging findings consistent with tuberculosis:

• consolidation on CXR • lymphadenopathy • unilateral pleural effusion • cavitation

Physical exam findings consistent with pneumothorax:

• decreased breath sounds locally • hypotension • hypoxia • possible tracheal deviation • hyperresonance

Physical exam findings consistent with myocardial infarction:

• diaphoresis • hypotension • third heart sound

ECG findings consistent with pericarditis:

• diffuse concave upward ST segments • PR segment depression without T wave inversion

Physical exam findings consistent with tuberculosis:

• egophony • pleural rub • rhonchi

Physical exam findings consistent with pneumonia:

• egophony • ronchi • pleural rub

The determination of empiric antimicrobial therapy for endocarditis is relatively more difficult than many other types of infections. This is because there is a wide variety of potential pathogens that have been implicated, which is dependent upon several patient specific factors. Therefore ID consult is highly recommended when an IE diagnosis is strongly suspected. The IE Guidelines recommend an evaluation of six patient specific factors when determining empiric antimicrobial therapy. What are these?

• epidemiologic factors in table 6 from IE guidelines • hx of prior infections (including CV infections) • exposure to abx • clinical course • infection severity • extracardiac sites of infection associated with current infection

Red flags for tuberculosis:

• exposure to TB • hemoptysis (small amounts of blood mixed with sputum) • fever • night sweats • weight loss

Red flags for pneumonia:

• fever • productive sputum • dyspnea

Red flags for malignant pleural effusion:

• history of malignancy • night sweats • older age • tobacco use • weight loss

Physical exam findings consistent with pulmonary embolism:

• hypotension • hypoxia • sinus tachycardia • respiratory distress

Laboratory results (CBC) consistent with tuberculosis:

• leukocytosis

Laboratory results consistent with pneumonia:

• leukocytosis

Physical exam findings consistent with malignant pleural effusion:

• locally decreased breath sounds

Clinical factors that increase likelihood of MI in patients with acute chest pain:

• pain that radiates to both arms • third heart sound on auscultation • hypotension

Clinical factors that decrease likelihood of MI in patients with acute chest pain:

• pleuritic chest pain • sharp or stabbing chest pain • chest pain that is reproduced by palpation

Physical exam findings consistent with pericarditis:

• positional chest pain

Imaging findings consistent with pericarditis:

• possible cardiomegaly

What are the four potentially lethal causes of chest pain?

• pulmonary embolism • myocardial infarction • aortic dissection • pneumothorax

Red flags for pericarditis:

• recent or current viral infection • prior hx of pericarditis

Red flags for aortic dissection:

• tearing sensation • pain that radiates to back/abdomen • pain is most severe at onset

What are the causes of pleuritic chest pain?

• viruses (common) • aortic dissection • malignant pleural effusion • myocardial infarction • pericarditis • pneumonia • pneumothorax • pulmonary embolism (most common life-threatening cause) • tuberculosis