Cardiology




(1)
Interventional Cardiologist, Calgary, AB, Canada

 




Aortic Dissection



Differential Diagnosis



CARDIAC





  • myocardial—myocardial infarction, angina, myocarditis


  • valvular—aortic stenosis, aortic regurgitation


  • pericardial—pericarditis


  • vascular—aortic dissection


RESPIRATORY





  • parenchymal—pneumonia, cancer


  • pleural—pneumothorax, pneumomediastinum, pleural effusion, pleuritis


  • vascular—pulmonary embolism, pulmonary hypertension


GI

—esophagitis, esophageal cancer, GERD, peptic ulcer disease, Boerhaave’s, cholecystitis, pancreatitis


OTHERS

—musculoskeletal, shingles, anxiety


Pathophysiology



ANATOMY

—layers of aorta include intima, media, and adventitia. Majority of tears found in ascending aorta at right lateral wall where the greatest shear force is produced


AORTIC TEAR AND EXTENSION

—aortic tear may produce a tearing, ripping sudden chest pain radiating to the back. Aortic regurgitation can produce diastolic murmur. Pericardial tamponade may occur, leading to hypotension or syncope. Initial aortic tear and subsequent extension of a false lumen along the aorta may also occlude blood flow into any of the following vascular structures:



  • coronary—acute myocardial infarction (usually RCA)


  • brachiocephalic, left subclavian, distal aorta—absent or asymmetric peripheral pulse, limb ischemia


  • renal—anuria, renal failure


  • carotid—syncope/hemiplegia/death


  • anterior spinal—paraplegia/quadriplegia, anterior cord syndrome


CLASSIFICATION SYSTEMS





  • Stanford—A = any ascending aorta involvement, B = all others


  • D e B akey—I = ascending and at least aortic arch, II = ascending only, III = originates in descending and extends proximally or distally


RISK FACTORS





  • common—hypertension, age, male


  • vasculitis—Takayasu arteritis, giant cell arteritis, rheumatoid arthritis, syphilitic aortitis


  • collagen disorders—Marfan syndrome, Ehlers–Danlos syndrome, cystic medial necrosis


  • valvular—bicuspid aortic valve, aortic coarctation, Turner syndrome, aortic valve replacement


  • others—cocaine, trauma


Clinical Features



RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC AORTIC DISSECTION?



















































 
LR+
LR–

H istory

Hypertension
1.6
0.5

Sudden chest pain
1.6
0.3

Tearing or ripping pain
1.2–10.8
0.4–0.99

Physical

Pulse deficit
5.7
0.7

Focal neurological deficit
6.6–33
0.71–0.87

Diastolic murmur
1.4
0.9

CXR/ECG

Enlarged aorta or wide mediastinum
2.0
0.3

LVH on ECG
0.2–3.2
0.84–1.2




  • APPROAC H—“presence of tearing, ripping, or migrating pain may suggest dissection. Pulse deficit or focal neurological deficits greatly increase likelihood of dissection. Absence of pain of sudden onset decreases likelihood of dissection. Normal aorta and mediastinum on CXR help to exclude diagnosis”

JAMA 2002 287:17


Investigations



BASIC





  • labs—CBCD, lytes, urea, Cr, troponin/CK × 3, glucose, AST, ALT, ALP, bilirubin, albumin, lipase, INR/PTT


  • imaging—CXR, echocardiogram (TEE), CT chest or MRI chest


  • ECG


SPECIAL





  • aortography


Diagnostic and Prognostic Issues



CXR FINDINGS

—wide mediastinum (>6 cm [2.4 in.]), indistinct aortic knuckle, pleural cap, difference in diameter between ascending and descending aorta, blurring of aortic margin secondary to local extravasation of blood, pleural effusion or massive hemothorax, displaced calcification (separation of the intimal aortic calcification from the edge of the aortic shadow >1 cm [0.4. in.])


PROGNOSIS





  • type a—with surgery, 1-month survival 75–80%, 10-year survival 55%


  • type b—with aggressive hypertensive treatment, 1-month survival >90%, 10-year survival 56%


Management



ABC

—O 2 to keep sat >95%, IV, antihypertensive therapy (keep HR <60 and SBP <120 mmHg. Labetalol 2 mg/min IV loading drip, then 2–8 mg/min (target heart rate 55–60) or 20–80 mg IV q10 min, maximum 300 mg, then 200–400 mg PO BID. If SBP still >120 mmHg, sodium nitroprusside 0.25–0.5 μg/kg/min IV initially, then 0.25–3 μg/kg/min, maximum 10 μg/kg/min)


TREAT UNDERLYING CAUSE

—Type A (emergent surgical repair, endovascular stenting, long-term blood pressure control). Type B (medical blood pressure control). Monitor over time with serial CT/MR chest


Related Topics

Acute Coronary Syndrome (p. 28)

Stroke (p. 337)


Acute Coronary Syndrome


ACCF/AHA 2013 STEMI Guidelines

ACCF/AHA 2007 UA/NSTEMI Guidelines

ACCF/AHA UA/NSTEMI 2012 Focused Update


Differential Diagnosis of Chest Pain



CARDIAC





  • myocardial—myocardial infarction, angina (atherosclerosis, vasospasm), myocarditis


  • valvular—aortic stenosis


  • pericardial—pericarditis


  • vascular—aortic dissection


RESPIRATORY





  • parenchymal—pneumonia, cancer


  • pleural—pneumothorax, pneumomediastinum, pleural effusion, pleuritis


  • vascular—pulmonary embolism


GI

—esophagitis, esophageal cancer, GERD, peptic ulcer disease, Boerhaave’s, cholecystitis, pancreatitis


OTHERS

—musculoskeletal (costochondritis), shingles, anxiety


Pathophysiology


































 
Pathologic changes
Clinical presentation

Pre-clinical
Atherosclerosis
Asymptomatic

Angina
Luminal narrowing
Central chest discomfort; worsened by exertion,emotion, and eating; relieved by rest and nitroglycerine

Unstableangina
Plaque ruptureor thrombus
Worsening pattern or rest pain; no elevation in troponin,with or without ECG changes of ischemia

NSTEMI
Partial occlusion
Non-ST elevation MI; elevation in troponin, with or withoutECG changes of ischemia

STEMI
Complete occlusion
ST elevation MI; elevation in troponin, with distinct ST segment elevation in ≥2 contiguous leads, new LBBB, or posterior wall MI with reciprocal ST depression in precordial leads on ECG


THIRD UNIVERSAL DEFINITION OF MYOCARDIAL INFARCTION (MI)





  • type 1—spontaneous MI due to a primary coronary event (atherosclerotic plaque rupture or erosion with acute thromboembolism)


  • type 2—MI secondary to an ischemic imbalance (supply demand mismatch)


  • type 3—MI resulting in death when biomarker values are unavailable (sudden unexpected cardiac death before serum biomarkers collected for measurement)


  • type 4—MI related to PCI (4A) or stent thrombosis (4B)


  • type 5—MI related to CABG


RISK FACTORS





  • major—diabetes, hypertension, dyslipidemia, smoking, family history of premature CAD, advanced age, male gender


  • associated—obesity, metabolic syndrome, sedentary lifestyle, high-fat diet


  • emerging—lipoprotein abnormalities, inflammation (↑ CRP), chronic infections, chronic kidney disease


POST–MI COMPLICATIONS

—arrhythmia (VT/VF, bradycardia), sudden death, papillary muscle rupture/dysfunction, myocardial rupture (ventricular free wall, interventricular septum), ventricular aneurysm, valvular disease (especially acute mitral regurgitation), heart failure/cardiogenic shock, peri-infarction pericarditis, post-cardiac injury pericarditis (Dressler’s syndrome)


Clinical Features



CHEST PAIN EQUIVALENTS

—dyspnea, syncope, fatigue, particularly in patients with diabetic neuropathy who may not experience chest pain


NEW YORK HEART ASSOCIATION (NYHA) CLASSIFICATION





  • I = no symptoms with ordinary physical activity


  • II = mild symptoms with normal activity (walking >2 blocks or 1 flight of stairs)


  • III = symptoms with minimal exertion


  • IV = symptoms at rest


CANADIAN CARDIOVASCULAR SOCIETY (CCS) CLASSIFICATION





  • I = angina with strenuous activity


  • II = slight limitation, angina with meals/cold/stress


  • III = marked limitation, angina with walking <1–2 blocks or 1 flight of stairs


  • IV = unstable angina



    • IV a = unstable angina resolves with medical treatment


    • IV b = unstable angina on oral treatment, symptoms improved but angina with minimal provocation


    • IV c = unstable angina persists, not manageable on oral treatment or hemodynamically unstable


KILLIP CLASS CLASSIFICATION





  • I = no evidence of heart failure


  • II = mild to moderate heart failure (S3, lung rales less than half way up, or jugular venous distension)


  • III = overt pulmonary edema


  • IV = cardiogenic shock


RATIONAL CLINICAL EXAMINATION SERIES: IS THIS PATIENT HAVING A MYOCARDIAL INFARCTION?


































































































 
LR+

H istory

Pain radiation to the shoulderOR both arms

4.1

Pain radiation to right arm

3.8

Radiation to left arm
2.2

Radiation to both arms

9.7

Vomiting

3.5

Ex-smoker

2.5

Diaphoresis
2.0

Pleuritic chest pain
0.2

Sharp or stabbing chest pain
0.3

Positional chest pain
0.3

Chest pain reproducible by palpation
0.2–0.4

Physical

Hypotension
3.1

S3
3.2

Pulmonary crackles
2.1

EC G

New ST elevation ≥1 mm
5.7–53.9

New Q wave
5.3–24.8

Any ST elevation
11.2

New conduction defect
6.3

New ST depression
3.0–5.2

Any Q wave
3.9

Any ST depression
3.2

T wave peaking or inversion ≥1 mm
3.1

New T wave inversion
2.4–2.8

Any conduction defect
2.7

Multivariate Prediction Models
 

ACI-TIPI (Acute Cardiac Ischemia Time Insensitive Predictive Instrument)

3.9–12

Goldman Protocol

2.9–3.6




  • APPROAC H—“radiation of chest pain, diaphoresis, hypotension, and S3 suggest acute MI. Chest pain that is pleuritic, sharp or stabbing, positional or reproduced by palpation decreases likelihood of acute MI. On ECG, any ST ↑, new Q waves, or new conduction Δ make acute MI very likely. Normal ECG is very powerful to rule out MI”

JAMA 1998 280:14



  • UPDATE—“after clinical symptoms are used to identify patients with possible ischemia, the ECG and troponin results take precedence in making the diagnosis. The presence of diabetes, HTN, or dyslipidemia should not affect clinician’s probability estimate that an episode of chest pain represents an ACI”

The Rational Clinical Examination. McGraw-Hill, 2009


Investigations



BASIC





  • labs—CBCD, lytes, urea, Cr, troponin/CK × 3 q6-8 h, BNP or NT-pro-BNP, AST, ALT, ALP, bilirubin, INR/PTT, Mg, Ca, PO4, albumin, lipase, fasting lipid profile, random and fasting glucose, HbA1C


  • imaging—CXR, echocardiogram (first 72 h), MIBI/thallium (>5 days later)


  • EC G—q8h × 3 or with chest pain


  • stress tests—ECG, echocardiogram, MIBI once stable (>48 h post-MI)


  • coronary catheterization


Diagnostic and Prognostic Issues



RISK STRATIFICATION FOR STABLE CORONARY DISEASE





  • EC G exercise stress test



    • absolute contraindications—recent myocardial infarction (<4 days), unstable angina, severe symptomatic LV dysfunction, life-threatening arrhythmia, acute pericarditis, aortic dissection, PE, severe symptomatic aortic stenosis


    • goal—keep on treadmill until subject reaches 85–90% of age-predicted heart rate (220–age)


    • ischemia criteria— ≥ 1 mm horizontal or down-sloping ST ↓ over multiple leads, or ST ↑ → myocardial ischemia (sens 68%, spc 77%) → proceed to angiogram


    • inconclusive—premature termination due to chest pain/poor exercise tolerance → proceed to pharmacological stress test


    • duke treadmill score—(exercise time in minutes) – 5 × (maximum ST ↓ in mm) – 4 × (treadmill angina index [0 = none, 1 = non-limiting, 2 = exercise limiting]). Low risk ≥ +5 (4-year survival 98–99%), moderate risk −10 to +4, high risk ≤ −11 (4-year survival 71–79%)


  • dipyridamole/adenosine MIBI—dipyridamole (Persantine) causes vasodilation. In CAD, the coronary artery is already maximally dilated to compensate, so addition of dipyridamole will not change perfusion to diseased vessel(s) further. This results in a relative perfusion mismatch compared to areas with normal dilatory reaction. Contraindicated in asthma/COPD. Antidote is aminophylline or caffeine


  • dobutamine echocardiography—assesses wall motion abnormalities. Compared to MIBI, echocardiogram is more specific and less sensitive. Contraindicated in severe hypertension and arrhythmias


APPROACH TO DIAGNOSIS OF STABLE CAD

—start with history, physical, rest ECG, and CXR. If low probability, do not investigate further. If high probability, proceed with management. If intermediate probability → stress test → cardiac CT, MIBI or stress echo → angiography


DIFFERENTIAL DIAGNOSIS OF TROPONIN ELEVATION





  • cardiac—myocardial infarction, myocarditis, congestive heart failure, pericarditis, vasospasm, tachycardia with supply–demand mismatch, drug/cocaine ingestion, stress (takotsubo) cardiomyopathy


  • pulmonary—pulmonary embolism


  • hepatic—liver failure


  • renal—chronic kidney disease


  • neurologic—stroke, intracranial hemorrhage


  • systemic—sepsis, prolonged strenuous exercise


SERUM MARKERS





  • troponin i/t—rises within 4–6 h, peaks at 18–24 h, remains elevated 7–10 days (sens 40% at presentation, 40–70% after 6–9 h of symptoms)


  • ck / ckmb—rises within 4–6 h, peaks at 18–24 h, remains elevated 3–4 days (sens 35–50% at presentation, 90% after 3 h in ER)


  • myoglobin—rises within 1–2 h, peaks in few hours

Therefore, measure markers (e.g., troponin) at least twice separated by 6–8 h with serial ECG. Despite all appropriate investigations, missed MI rate is 2–5%


ECG CHANGES IN ACUTE MI

—see APPROACH TO ECG p. 73


TIMI SCORE FOR PATIENTS WITH UNSTABLE ANGINA/NSTEMI





  • scoring (out of 7)—age ≥65, ≥3 CAD risk factors, known CAD (stenosis >50%), ASA use within prior 7 days, ≥2 angina episodes within 24 h, ↑ cardiac markers, ST deviation ≥0.5 mm


  • risk groups—low = 0–2, intermediate = 3–4, high = 5–7. Consider GPIIb/IIIa and early angiography with revascularization in intermediate or high-risk groups


  • risk of death, MI or revascularization in 14 days—0/1 = 4.7%, 2 = 8.3%, 3 = 13.2%, 4 = 19.9%, 5 = 26.2%, 6/7 = 40.9%


GRACE RISK SCORE FOR PATIENTS WITH UNSTABLE ANGINA/NSTEMI





























Riskcategory
GRACErisk score
In-hospitaldeath (%)

Low
≤108
<1

Intermediate
109–140
1–3

High
>140
>3
























Riskcategory
GRACErisk score
6-monthdeath

Low
≤88
<3

Intermediate
89–118
3–8

High
>118
>8


TIMI SCORE FOR PATIENTS WITH STEMI





  • scoring (out of 14)—age (3 points = ≥75, 2 points = 65–74), any of diabetes, hypertension, or angina (1 point), systolic BP ≤100 mmHg (3 points), HR >100 (2 points), Killip class II–IV (2 points), weight <67 kg (1 point), anterior ST elevation or LBBB (1 point), time to reperfusion >4 h (1 point)


  • risk of death in 30 days—0 = 0.8%, 1 = 1.6%, 2 = 2.2%, 3 = 4.4%, 4 = 7.3%, 5 = 12.4%, 6 = 16.1%, 7 = 23.4%, 8 = 26.8%, >8 = 35.9%


IN-HOSPITAL OUTCOMES

































 
NSTEMI (%)
STEMI (%)

Death
4
6

Reinfarction
0.9
1.1

Cardiogenic shock
2.8
6.4

Stroke
0.7
0.8

Major bleeding
10
12

ACTION registry 2008/2009 data


Acute Management



ABC

—O2 to keep sat >95%, IVs, inotropes, consider balloon pump if hemodynamically unstable


PAIN CONTROL

—nitroglycerin (nitro drip 25 mg in 250 mL D5W, start at 5 μg/min IV, then ↑ by 5–10 μg/min every 3–5 min to 20 μg/min, then ↑ by 10 μg/min every 3–5 min up to 200 μg/min, or until relief of pain, stop titration if SBP is <100 mmHg. Nitro patch 0.4 mg/h daily. Nitro spray 0.4 mg SL q5min × 3. Beware if suspect right ventricular infarction or if patients on sildenafil). Morphine 2–4 mg IV every 5–15 min PRN


CLOT CONTROL





  • antiplatelet—ASA 162–325 mg PO chew × 1 dose, then 75–100 mg PO daily indefinitely. P2Y12 receptor blockade with clopidogrel 300–600 mg × 1 dose then 75 mg PO daily for 1 year; or ticagrelor 180 mg × 1 dose, then 90 mg PO BID for 1 year; or prasugrel (with PCI only; do not give if history of CVA or TIA, or age ≥75 years) 60 mg × 1 dose then 10 mg daily for 1 year. Combination ASA plus clopidogrel for minimum of 1 month (ideally 1 year)-post PCI with bare-metal stent, or minimum 12 months (possibly indefinitely) for drug-eluting stents. Consider G PIIb/IIIa inhibitor if intermediate/high-risk NSTEMI, treated with PCI, and pain unresponsive to nitroglycerin (tirofiban 0.4 μg/kg/min × 30 min IV, then continue 0.1 μg/kg/min × 18–24 h; eptifibatide 180 μg/kg IV bolus, then 2 μg/kg/min × 18–24 h; or, abciximab 0.25 mg/kg IV bolus, then 0.125 μg/kg/min × 12 h)


  • anticoagulation—options include LMW H (enoxaparin 30 mg IV bolus, then 1 mg/kg SC BID for STEMI [no IV bolus for NSTEMI], caution if renal failure or age >75) or unfractionated heparin (unfractionated heparin 70 U/kg [up to 4,000 U] IV bolus, then 18 U/kg/h [up to 1,000 U/h] and adjust to 1.5–2.5× normal PTT for 72 h). Factor Xa inhibitors (fondaparinux 2.5 mg SC daily until discharge or 8 days, caution if renal failure). Direct thrombin inhibitors (bivalirudin 0.1 mg/kg IV bolus then 0.25 mg/kg/h initially, followed by second 0.5 mg/kg bolus before PCI and 1.75 mg/kg/h during PCI, then continue infusion for up to 4 h post-PCI, if needed)


  • reperfusion therapy—see PCI for details. Fibrinolytics for STEMI (alteplase 15 mg IV over 2 min, then 0.75 mg/kg over 30 min [maximum 50 mg], then 0.5 mg/kg over 60 min [overall maximum 100 mg]; or tenecteplase IV bolus over 5 s, weight-based dosing: 30 mg for weight <60 kg, 35 mg for 60–69 kg, 40 mg for 70–79 kg, 45 mg for 80–89 kg, 50 mg for ≥90 kg])


RATE CONTROL

—start with metoprolol tartrate [immediate release] 25 mg PO q6-12 h. Titrate as tolerated up to maximum dose of metoprolol tartrate [immediate release] 100 mg PO q12h or metoprolol succinate [extended release] 200 mg PO daily. Alternatively, carvedilol 6.25 mg PO BID and titrate as tolerated up to 25 mg PO BID. The goal heart rate is 50–55 with normal activity. If ongoing ischemia or refractory hypertension at the time of presentation, may also consider metoprolol tartrate 5 mg IV q5min, up to 3 doses. Avoid if HF, low-output state, presence of prolonged first-degree or high-grade AV block, history of reactive airways disease, or MI precipitated by cocaine use. If β-blocker contraindicated, consider non-dihydropyridine calcium channel blockers (diltiazem 30–120 mg PO QID or verapamil 80–120 mg PO TID [contraindicated if LV dysfunction])


LIPID CONTROL

—high-intensity statin such as atorvastatin 80 mg PO daily or rosuvastatin 40 mg PO daily


BLOOD PRESSURE SUPPORT

—for patients with cardiogenic shock, consider IV fluids, inotropes (dobutamine/dopamine), balloon pump, and early revascularization


OVERALL APPROACH






































































 
Stable angina
Unstable angina or NSTEMI
STEMI

ASA
✓
✓
✓

Nitrates
✓
✓
✓

Morphine
±
✓
✓

β-blockers
✓
✓
✓

ACE inhibitors or ARBs
✓
✓
✓

HMG-CoA inhibitors
✓
✓
✓

Heparin or antithrombin
NO
✓
✓

P2Y12 inhibitors
NO
✓
✓

GPIIb/IIIa inhibitors
NO
✓ (consider)
NO

Fibrinolytics or PCIa

NO
NO
✓

Cardiology consult
Outpatientb

CCUc

CCUc


aIf initial presentation is to a PCI-capable hospital, then primary PCI should be performed within 90 min from time of first medical contact (FMC). If initial presentation is to a non-PCI-capable hospital, then arrange urgent transfer to PCI-capable hospital if primary PCI can be performed within 120 min from time of FMC. If timely PCI cannot be provided, administer fibrinolytic within 30 min of FMC. Urgent CABG is also an option post-catheterization

bOutpatient cardiology for stress test

cCCU consult for risk stratification, monitoring, PCI, and/or CABG


CAUTIONS IN TREATMENT OF ACUTE MYOCARDIAL INFARCTION

—avoid negative inotropic agents such as β-blockers and non-dihydropyridine calcium channel blockers if clinical heart failure. Avoid administration of nitroglycerin, morphine, and diuretics to patients with right ventricular infarction as these medications can cause venodilation and decrease preload, leading to hypotension


Long-Term Management of Coronary Artery Disease



ANTIANGINAL

—nitroglycerin (nitro patch 0.4–0.8 mg/h daily; nitro spray 0.4 mg SL q5 min × 3; isosorbide mononitrate 30 mg PO daily, maximum 240 mg), β-blocker (metoprolol tartrate [immediate release] 25–100 mg PO BID, metoprolol succinate [extended release] 50–200 mg PO daily, carvedilol 6.25–25 mg PO BID, bisoprolol 5–10 mg PO daily), calcium channel blocker (amlodipine 5–10 mg PO daily)


ACE INHIBITOR

—ramipril 2.5–10 mg PO BID, lisinopril 2.5–10 mg PO daily, trandolapril 0.5–4 mg PO daily, perindopril 2–8 mg PO daily. If ACE inhibitor not tolerated, use ARB


ANTIPLATELET

—ECASA 81 mg PO daily indefinitely. P2Y12 receptor blockade (clopidogrel 75 mg PO daily; ticagrelor 90 mg PO BID, or prasugrel 10 mg PO daily) generally for 1 year after ACS. Combination ASA plus clopidogrel for minimum of 1 month (ideally 1 year)-post PCI with bare-metal stent, or minimum 12 months (possibly indefinitely) for drug-eluting stents. Consider ticagrelor or prasugrel if received PCI


ANTICOAGULATION

—controversial especially in combination with ASA and/or P2Y12 inhibitor. May be considered for patients post-STEMI or NSTEMI with one of the following criteria: (1) atrial fibrillation, (2) left ventricular thrombus, (3) significant left ventricular dysfunction with extensive regional wall motion abnormalities. Start warfarin 5 mg daily within 72 h and continue heparin/LMWH until INR is between 2 and 3 (unless planning angioplasty). Beware bleeding risk. If possible, minimize duration of “triple therapy” (i.e., ASA, P2Y12 inhibitor, and warfarin), consider GI protection with proton-pump inhibitor, and target lower INR (e.g., 2.0-2.5)


RISK REDUCTION ★ABCDEFG★





  • ASA/ACE INHIBITOR / ARB


  • B lood pressure control (see HYPERTENSION p. 65)


  • C holesterol control (see DYSLIPIDEMIA p. 70)


  • D iabetic control (see DIABETES p. 381)


  • E xercise (30 min of moderate-intensity exercise 3–4×/week)


  • F at reduction (see OBESITY ISSUES p. 457)


  • Get going to quit smoking! (see SMOKING ISSUES p. 480)


DRIVING POST-MYOCARDIAL INFARCTION

—see p. 490 for details


Treatment Issues



RIGHT VENTRICULAR INFARCTION

—evidence of inferior MI should automatically trigger one to check right-sided leads (V4R) to assess for the possibility of RV infarction, which occurs in about 50% of patients with inferior MI. May see increased JVP, Kussmaul sign, and clear lungs clinically. ST elevation in V4R is diagnostic and prognostic. Hypotension should be treated with fluid bolus to ensure good preload


POSTERIOR INFARCTION

—ST depression in V1–V2 in a regular ECG should automatically trigger one to request for posterior (V7–V9) leads to check for posterior MI. Posterior infarct may be associated with inferior infarcts (90%) and lateral infarcts (10%) as the PDA may be supplied by the right or left circumflex coronary artery


POST-MI RISK STRATIFICATION





  • extent of infarct / residual function—assessment is based on clinical factors (↑ HR, ↓ BP, Killip class, diabetes, renal failure, ↑ WBC, GRACE risk score, TIMI risk score), ECG, biomarkers (CK, troponin), imaging (echocardiogram, MIBI, cardiac MRI), and angiography. Early measurement of LV function, although of prognostic importance, is misleading as myocardium function may improve in first 2 weeks. Medical management according to risk


  • extent of myocardium at risk—assessment is based on exercise stress test, stress echocardiogram, stress sestamibi (ischemic tissue), thallium scan (viable tissue), PET scan, cardiac MRI, angiography. Angioplasty or CABG should be considered


  • risk of arrhythmia—high risk of VF/VT within the first 48 h, therefore monitor with telemetry. If it occurs after 48 h, consider antiarrhythmics and early ICD


BALLOON PUMP

—a long balloon in the descending aorta that deflates during systole and inflates during diastole to augment coronary perfusion and cardiac output as well as decrease afterload. Reasonable for severe refractory ischemia and hemodynamic instability. May be used in conjunction with inotropes. Contraindicated in aortic regurgitation, AAA, aortic dissection, uncontrolled sepsis bleeding disorder, and severe PVD


FIBRINOLYTICS USE





  • indications—>120 min anticipated delay from first medical contact to primary PCI, ≥30 min of chest pain, patient presentation within 12 h (ideal door to needle time <30 min), ECG criteria (>1 mm ST ↑ in ≥2 contiguous leads, or new LBBB with suggestive history, age <75)


  • absolute contraindications—any intracranial hemorrhage; ischemic stroke within 3 months (except acute ischemic stroke within first 4.5 h); structural cerebral vascular lesion; malignant intracranial neoplasm; closed-head or facial trauma within 3 months; intracranial or intra spinal surgery within 2 months); severe uncontrolled hypertension (unresponsive to emergency therapy); suspected aortic dissection; bleeding diathesis or active bleeding (excluding menses)


  • relative contraindications—chronic, poorly-controlled, severe hypertension; severe hypertension on presentation (>180/110 mmHg); ischemic stroke >3 months; dementia; other intracranial pathology (not already specified above); internal bleeding within 2–4 weeks; active peptic ulcer; major surgery within 3 weeks; non-compressible vascular punctures; use of anticoagulation therapy; pregnancy; traumatic CPR >10 min; prior exposure to streptokinase (if planning to use this fibrinolytic again)


  • risk of bleeding—average risk of severe bleed is 1.8%. Increased risk with women, BP >165/95 mmHg, age >65, weight <70 kg [<154 lbs], and lysis with TPA (+0.5% absolute risk/factor)


  • persistent ST elevation—look for resolution of symptoms and ST elevation to decrease by >50% within 90 min of fibrinolytic therapy. Persistent ST elevation may suggest failed fibrinolytic therapy, and requires urgent rescue catheterization. Other causes of ST elevation include pericarditis, ventricular aneurysm, hyperkalemia, LBBB, and early repolarization abnormality


Related Topics

Aortic Dissection (p. 27)

Asystole (p. 495)

Diabetes Mellitus (p. 381)

ECG (p. 73)

Hyperlipidemia (p. 70)

Hypertension (p. 65)

Pericarditis (p. 35)

Shock (p. 108)

Smoking Cessation (p. 480)


PERCUTANEOUS CORONARY INTERVENTION (PCI, PTCA)





  • indications for acute STEMI—patient presents within 12 h of chest pain (at a PCI-capable hospital, ideal time from first medical contact to device or “FMC-to-device time” ≤90 min; if at a non-PCI-capable hospital requiring transfer for primary PCI, then ideal “FMC-to-device time” ≤120 min), ECG criteria (>1 mm ST ↑ in ≥2 contiguous leads, new or presumed new left bundle branch block), contraindications to fibrinolysis, or in patients in cardiogenic shock irrespective of time of MI onset


  • indications for chronic stable CAD—single/double vessel disease refractory to medical therapy. Decision for revascularization (PCI vs. CABG) should follow assessment by heart team (interventional cardiology and cardiac surgery)


  • adverse events—access site (bleeding, hematomas, arteriovenous fistulae, pseudoaneurysms), contrast nephropathy, arrhythmia (VT, VF), stroke, dissection, myocardial infarction, death


  • bare metal stents vs . drug – eluting stents—in-stent restenosis is due to fibrosis of coronary vasculature and usually happens 3 months post-procedure. Drug-eluting stents (sirolimus, paclitaxel, everolimus, or zotarolimus) are designed to inhibit cell proliferation and decrease the risk of in-stent restenosis. There has been some controversy regarding higher adverse events in patients with first generation drug-eluting stents (sirolimus or paclitaxel). The most recent outcomes research analysis suggests that newer-generation drug-eluting stents (everolimus or zotarolimus) are associated with a decreased rate of repeat revascularization, stent thrombosis, and no significant difference in mortality


  • benefits—primary PCI is generally preferred given the superior outcomes compared to fibrinolysis, particularly if (1) fibrinolysis contraindicated, (2) previous history of CABG, or (3) cardiogenic shock. However, patients who are able to seek medical attention within 1 h of chest pain onset, have allergy to contrast dye, or do not have access to PCI in a timely fashion should consider fibrinolytics


OUTCOMES FOR FIBRINOLYTICS VS. PRIMARY PCI





























 
Fibrinolytics (%)
PrimaryPCI (%)

Non-fatal reinfarction
7
3

Stroke
2
1

Death (4–6 weeks)
7–9
5–7

Combined endpoint of death–fatal reinfarctionand stroke
14
8

NEJM 2007 356:1; NEJM 2007 356:10; NEJM 2007 357:16


CORONARY ARTERY BYPASS GRAFT SURGERY





  • coronary anatomy



    • right coronary (RCA)—gives rise to right marginal (RMA), right posterior descending (RPDA), and right posterolateral branches (RPL 1, 2, 3)


    • left main (LM)—gives rise to left anterior descending (LAD) → diagonal (D1, 2 3) and septals; ramus intermediate (Ram Int); and left circumflex (LCX) → obtuse marginal (OM 1, 2, 3)


    • dominant artery—defined as the artery that supplies PDA and at least one posterolateral (PL) artery


  • indications—studies suggest CABG provides mortality benefit for specific subgroups, including patients with (1) left main disease >50% occlusion, (2) two vessel disease with significant involvement of proximal left anterior descending, and (3) diffuse triple vessel disease. Diabetic patients and those with reduced left ventricular function derive more benefit from bypass surgery. Angiographic disease severity should be assessed using the SYNTAX score. Decision for revascularization (PCI vs. CABG) should follow assessment by heart team (interventional cardiology and cardiac surgery)


  • morbidity benefit—95% have improvement of symptoms immediately after surgery, 75% symptom free at 5 years. Recurrent disease more common in vein grafts than artery grafts


  • grafts—saphenous veins from calf or thigh (SVG), internal mammary arteries (LIMA/RIMA), radial arteries (RA), and gastroepiploic artery from stomach (GA). A total of 90% of arterial graft and 50% of vein graft remain patent by 10 years


  • complications



    • cardiac—MI 2–4%, arrhythmia (AF 40%, sustained VT/VF 2–3%), AV block requiring pacemaker 0.8–4%, pericarditis/tamponade, aortic dissection


    • neurological—stroke, postoperative delirium, cognitive impairment, depression, phrenic nerve damage, intercostal nerve damage


    • others—renal failure, bleeding, infection, pleural effusions, death


  • medications—hold clopidogrel or ticagrelor 5–7 days prior to CABG. Continue ASA before and after surgery


Pericardial Diseases: Pericarditis and Tamponade



Differential Diagnosis



★MINT★





  • Metabolic—uremia, dialysis, hypothyroidism


  • Medications—procainamide, hydralazine, INH, phenytoin, penicillin


  • Infarction—MI (early, late)


  • Infectious—HIV, Coxsackie, echovirus, adenovirus, TB


  • I nflammatory—psoriatic arthritis, enteric arthritis, rheumatoid arthritis, SLE, mixed connective tissue disease


Idiopathic





  • Neoplastic—primary (mesothelioma), metastasis (breast, lung, melanoma), leukemia, lymphoma


  • Trauma—stab, gunshot wound, blunt, CPR, postpericardiotomy


Clinical Features



RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT WITH A PERICARDIAL EFFUSION HAVE CARDIAC TAMPONADE?














































































 
Sens (%)

H istory
 

Dyspnea
87–89

Fever
25

Chest pain
20

Cough
7–10

Physical

Tachycardia
77

Pulsus paradoxus >10 mmHga

82

Elevated JVP
76

↓ heart sounds
28

Hypotension
26

Hypertension
33

Tachypnea
80

Peripheral edema
21–28

Pericardial rub
19–29

Hepatomegaly
28–55

Kussmaul sign
26

EC G

Low voltage
42

Atrial arrhythmia
6

Electrical alternans
16–21

ST elevation
18–30

PR depression
18


aPulsus paradoxus LR+ 3.3, LR– 0.03




  • APPROAC H—“among patients with cardiac tamponade, a minority will not have dyspnea, tachycardia, elevated JVP, or cardiomegaly on chest radiograph. A pulsus paradoxus >10 mmHg among patients with a pericardial effusion helps distinguish those with cardiac tamponade from those without. Diagnostic certainty of the presence of tamponade requires additional testing”

JAMA 2007 297:16


DISTINGUISHING FEATURES OF ACUTE TAMPONADE AND CHRONIC CONSTRICTIVE PERICARDITIS




































 
Acute tamponade
Constrictive pericarditis

Vitals
Tachycardia, hypotension+++, pulsus paradoxus

Hypotension, pulsus paradoxus (rare)

JVP
Elevated, Kussmaul (rare)
Elevated, Kussmaul

Prominent x′ descentbut blunted y descent
Prominent x′ and y descent (Friedrich’s sign)

Apex beat
Impalpable
Impalpable

Heart sounds
Distant
Distant, early S3/knock

Other features
Dullness and bronchial breath sounds over left base (Ewart sign)
Hepatosplenomegaly, edema


Investigations



BASIC





  • labs—CBCD, lytes, urea, Cr, troponin, CK


  • imaging—CXR (calcification if constrictive disease), echocardiogram


  • EC G—may have sinus tachycardia, low voltages, and electrical alternans in tamponade/effusion; diffuse ST elevation (concave up) and PR depression may be seen in pericarditis


SPECIAL





  • pericardiocentesis—diagnostic or therapeutic (for tamponade, TB/bacterial pericarditis, or large persistent effusion)


  • pericardioscopy


  • CT/MRI chest—if suspect constrictive pericarditis


Management



ACUTE PERICARDITIS

—NSAIDs (indomethacin 25–50 mg PO TID, ibuprofen 600–800 mg PO TID × 2–4 weeks, or until resolution of pain) for most cases of idiopathic or viral pericarditis, but avoid after acute MI. If post-MI, ASA 650 mg PO TID × 3–4 weeks. Adjuvant colchicine 0.6 mg PO BID × 3 months in addition to NSAID/ASA to reduce risk of recurrence. Prednisone 0.25–0.5 mg/kg PO daily × 2 weeks (followed by taper) may be considered for connective tissue-mediated disease, although symptoms may recur upon withdrawal


RECURRENT PERICARDITIS

—ASA 650 mg PO TID × 4–8 weeks or NSAIDs (indomethacin 25–50 mg PO TID, ibuprofen 600–800 mg PO TID × 4–8 weeks). Add colchicine (0.6 mg PO BID × 3–6 months) for longterm prophylaxis. Avoid anticoagulation as risk of hemopericardium. Prednisone 0.25–0.5 mg/kg PO daily may also be useful, although symptoms may recur upon withdrawal


TAMPONADE

—ABC, O 2 , IV’s, bolus IV fluids, pericardiocentesis (subxyphoid blind approach, echocardiogram-guided parasternal or apical approach), pericardiectomy, pericardial window if recurrent/malignant effusion. Avoid nitroglycerin and morphine if tamponade as they may decrease preload, leading to worsening of cardiac output


CONSTRICTIVE PERICARDITIS

—complete pericardiectomy


Specific Entities



ACUTE PERICARDITIS

—may be preceded by upper respiratory tract infection. Diagnosis is based on any two of the following inflammatory signs (LR+ 5.4): fever, pericardial friction rub (three components), characteristic chest pain (better with upright position and leaning forward, or pleuritic), PR depression, and diffuse ST elevation. Large effusion without inflammatory signs or tamponade suggests chronic idiopathic pericardial effusion (LR+ 20)


RECURRENT PERICARDITIS

—returns in days to weeks upon stopping medications. Likely causes include rheumatologic disorders, Dressler’s syndrome, and post-pericardiotomy syndrome


TAMPONADE

—a clinical diagnosis based on dyspnea, tachycardia, hypotension, pulsus paradoxus, and elevated JVP. Tamponade causes restriction in left or right ventricular diastolic filling. Tamponade with inflammatory signs suggests malignant effusion (LR+ 2.9)


CONSTRICTIVE PERICARDITIS

—contraction of pericardium due to chronic inflammation, leading to left and/or right heart failure. May follow pericarditis or radiation. May be difficult to distinguish from restrictive cardiomyopathy clinically


Heart Failure


NEJM 2003 348:20

Canadian Heart Failure Guidelines 2006

Canadian Heart Failure Guidelines Updates 2017–2013


Differential Diagnosis of HF Exacerbation/Dyspnea



CARDIAC





  • myocardial—HF exacerbation, myocardial infarction


  • valvular—aortic stenosis, acute aortic regurgitation, mitral regurgitation/stenosis, endocarditis


  • pericardial—tamponade


  • dysrhythmia


RESPIRATORY





  • airway—COPD exacerbation, asthma exacerbation, acute bronchitis, bronchiectasis, foreign body obstruction


  • parenchyma—pneumonia, cryptogenic organizing pneumonia, ARDS, interstitial lung disease exacerbation


  • vascular—pulmonary embolism, pulmonary hypertension


  • pleural—pneumothorax, pleural effusion


SYSTEMIC

—sepsis, ARDS, metabolic acidosis, anemia, neuromuscular, psychogenic, anxiety


Pathophysiology



ANATOMIC/PHYSIOLOGIC CLASSIFICATION OF CARDIOMYOPATHY





  • dilated (dilatation and impaired contraction of one or both ventricles)—idiopathic, ischemic, valvular, viral, genetic, late manifestation of hypertrophic heart disease, tachycardia induced, alcohol induced, peripartum


  • hypertrophic (disorder with disproportionate hypertrophy of the left ventricle and occasionally right ventricle)—idiopathic (autosomal dominant inheritance with incomplete penetrance), storage disease (Fabry’s disease, Pompe disease, Hurler’s syndrome, Noonan’s syndrome), athlete’s heart, obesity, amyloid


  • restrictive (non-dilated ventricles with impaired ventricular filling)—idiopathic familial, infiltrative (amyloidosis, hemochromatosis, sarcoidosis), drugs, radiation, endomyocardial fibrosis


  • arrhythmogenic right ventricular (replacement of right ventricular free wall with fatty tissue)—arrhythmogenic right ventricular dysplasia


  • unclassifiable—endocardial fibroelastosis, left ventricular non-compaction


ETIOLOGIC CLASSIFICATION OF CARDIOMYOPATHY





  • ischemic cardiomyopathy (mostly dilated)—varying degrees of persistent ischemia, infarction, and left ventricular remodeling


  • valvular cardiomyopathy (mostly dilated)—abnormal loading conditions and secondary left ventricular remodeling and dysfunction


  • hypertensive cardiomyopathy (dilated, restrictive)—left ventricular hypertrophy and dysfunction


  • diabetic cardiomyopathy (dilated)—left ventricular dysfunction in the absence of atherosclerosis or hypertension


  • inflammatory cardiomyopathy (mostly dilated)—infectious (diphtheria, rheumatic fever, scarlet fever, typhoid fever, meningococcal, TB, Lyme disease, Leptospirosis, RMSF, poliomyelitis, influenza, mumps, rubella, rubeola, variola, varicella, EBV, Coxsackie virus, echovirus, CMV, hepatitis, rabies, mycoplasma, psittacosis, arboviruses, histoplasmosis, cryptococcosis, Chagas disease), autoimmune, idiopathic myocardial inflammatory diseases


  • metabolic cardiomyopathy (dilated, restrictive, and/or hypertrophic)—endocrine (thyrotoxicosis, hypothyroidism, acromegaly, pheochromocytoma), storage diseases (glycogen storage disease, Fabry’s disease, Gaucher’s disease, Niemann–Pick disease), nutritional deficiencies (Beriberi, Kwashiorkor, pellagra), deposition (amyloidosis, hemochromatosis, sarcoidosis)


  • muscular dystrophies (mostly dilated)—Duchenne, Becker’s, myotonic dystrophy


  • neuromuscular—Friedreich’s ataxia (hypertrophic), Noonan’s syndrome, lentiginosis


  • general systemic disease (mostly dilated)—connective tissue diseases (rheumatoid heart disease, ankylosing spondylitis, SLE, scleroderma, dermatomyositis), granulomatous (sarcoidosis, Wegener’s granulomatosis, granulomatous myocarditis), other inflammatory (giant cell myocarditis, hypersensitivity myocarditis), neoplasm (primary, secondary, restrictive pattern)


  • sensitivity and toxic reactions (mostly dilated)—alcohol, amphetamine, arsenic, catecholamines, cocaine, anthracyclines, zidovudine, radiation (restrictive as well)


  • peripartum (dilated)—see p. 471


FUNCTIONAL CLASSIFICATION OF HEART FAILURE





  • systolic dysfunction (↓ LVEF <45%)—S3 (dilated ventricle with volume overload). Mechanisms include decreased contractility and increased afterload. Causes include MI, cardiomyopathy (dilated, infiltrative), valvular (aortic regurgitation, mitral regurgitation, “burned out” aortic stenosis), “burned out” hypertension and myocarditis


  • diastolic dysfunction (normal LVEF)—S4 (stiff ventricle), LVH, ↓ ventricular relaxation, normal LVEF, ↑ chamber pressures. Mechanisms include decreased active relaxation and passive relaxation (stiff ventricle). Causes include ischemia, hypertension, valvular (aortic stenosis), cardiomyopathy (restrictive, hypertrophic), and pericardial disease


  • mixed dysfunction—in many cases, diastolic dysfunction is present with systolic heart failure


PRECIPITANTS OF HF ★FAILURE★





  • Forget to take medications (non-adherence)


  • Arrhythmia, anemia


  • Infection, ischemia, infarction


  • Lifestyle change


  • Upregulators (thyroid, pregnancy)


  • Rheumatic heart disease, acute valvular disease


  • Embolism


Clinical Features



DISTINGUISHING FEATURES BETWEEN COPD AND HEART FAILURE















































 
COPD
Heart Failure

History
Previous COPD
Previous HF
 
Medications
Medications

Inspect
Nicotine stain, barrel chest
  

Laryngeal height <4 cm

Cardiac exam
Subxyphoid cardiac pulse
Elevated JVP, S3, S4

Resp. exam
Hyperresonance
Bilateral crackles

Prolonged expiratory time

Investigations
CXR shows hypeinflation
CXR shows redistribution and cardiomegaly
 
ABG shows hypercapnia and hypoxemia
ABG shows hypoxemia

Elevated BNP


LEFT HEART FAILURE

—left-sided S3, rales, wheezes, tachypnea. Causes include previous MI, aortic stenosis, and left-sided endocarditis


RIGHT HEART FAILURE

—right-sided S3, ↑ JVP, ascites, hepatomegaly, peripheral edema. Causes include left heart failure, pulmonary hypertension, right ventricular MI, mitral stenosis, and right-sided endocarditis


GRADING OF PITTING EDEMA

—0 = no edema, 1 = trace edema, 2 = moderate edema disappears in 10–15 s, 3 = stretched skin, deep edema disappears in 1–2 min, 4 = stretched skin, fluid leaking, very deep edema present after 5 min


RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS DYSPNEIC PATIENT IN THE EMERGENCY DEPARTMENT HAVE CONGESTIVE HEART FAILURE?





























































































































































































































































































 
Sens (%)
Spc (%)
LR+
LR–

History

Initial clinical judgment
61
80
4.4
0.45

Hx heart failure
60
90
5.8
0.45

Myocardial infarction disease
40
87
3.1
0.69

Coronary artery
52
70
1.8
0.68

Dyslipidemia
23
87
1.7
0.89

Diabetes
28
83
1.7
0.86

Hypertension
60
56
1.4
0.71

Smoker
62
27
0.84
1.4

COPD
34
57
0.81
1.1

PND
41
83
2.6
0.70

Orthopnea
50
77
2.2
0.65

Edema
51
76
2.1
0.64

Dyspnea on exertion
84
34
1.3
0.48

Fatigue and weight gain
31
70
1.0
0.99

Cough
36
61
0.93
1.0

Physical

S3
13
99
11
0.88

AJR
24
96
6.4
0.79

JVD
39
92
5.1
0.66

Rales
60
78
2.8
0.51

Any murmur
27
90
2.6
0.81

Lower extremity edema
50
78
2.3
0.64

Valsalva maneuver
73
65
2.1
0.41

SBP <100 mmHg
6
97
2.0
0.97

S4
5
97
1.6
0.98

SBP ≥150 mmHg
28
73
1.0
0.99

Wheezing
22
58
0.52
1.3

Ascites
1
97
0.33
1.0

CXR

Pulmonary venous congestion
54
96
12
0.48

Interstitial edema
34
97
12
0.68

Alveolar edema
6
99
6.0
0.95

Cardiomegaly
74
78
3.3
0.33

Pleural effusions
26
92
3.2
0.81

Any edema
70
77
3.1
0.38

Pneumonia
4
92
0.50
1.0

Hyperinflation
3
92
0.38
1.1

ECG

Atrial fibrillation
26
93
3.8
0.79

New T wave changes
24
92
3.0
0.83

Any abnormal finding
50
78
2.2
0.64

ST elevation
5
97
1.8
0.98

ST depression
11
94
1.7
0.95

BNP

BNP ≥ 250 pg/mL
   
4.6
 

BNP ≥ 100 pg/mL a
   
2.7
 

BNP ≥ 50 pg/mL
   
1.7

0.06


aFor patients with an estimated GFR of 15–60 mL/min/1.73 m2, a threshold of 201 pg/mL can be used




  • APPROAC H—“the features evaluated in more than one study with the highest LRs (>3.5) for diagnosing heart failure were the following: the overall clinical judgment, history of heart failure, S3, jugular venous distension, pulmonary venous congestion or interstitial edema on CXR, and atrial fibrillation on ECG. The features evaluated in more than one study with the lowest LRs (<0.60) for diagnosing of heart failure were the following: the overall clinical judgment, no prior history of heart failure, no dyspnea on exertion, the absence of rales, and the absence of radiographic pulmonary venous congestion, or cardiomegaly. The single finding that decreased the likelihood of heart failure the most was a BNP <100 pg/mL. While the findings of this study are useful when assessing dyspneic patients suspected of having heart failure, no individual feature is sufficiently powerful in isolation to rule heart failure in or out. Therefore, an overall clinical impression based on all available information is best. If the appropriate constellation of findings with high LRs for heart failure are present, that may be sufficient to warrant empirical treatment without further urgent investigations”

JAMA 2005 294:15

The Rational Clinical Examination. McGraw-Hill, 2009


RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE ABNORMAL CENTRAL VENOUS PRESSURE?





  • JVP VS. CAROTID—JVP has biphasic waveforms, is non-palpable, is occludable, decreases with inspiration, changes with position, and increases with abdominojugular reflux (AJR). To perform the AJR, the blood pressure cuff is pumped 6× and then pressed against the abdomen at 20–35 mmHg for 15–30 s. Normal = no change in JVP, or transient increase of >4 cm that returns to baseline before 10 s, or sustained increase <3 cm throughout. Positive AJR occurs when abdominal compression causes a sustained increase in JVP >4 cm (sens 24%, spc 96%, LR+ 4.4)

JAMA 1996 275:8



  • UPDATE—a JVP height ≥3 cm above the sternal angle in any position indicates an abnormal CVP. Clinical assessment of high JVP has a LR+ for high CVP of 3.1. An assessment of low JVP has a LR+ for low CVP of 3.4

The Rational Clinical Examination. McGraw-Hill, 2009


RATIONAL CLINICAL EXAMINATION SERIES: CAN THE CLINICAL EXAMINATION DIAGNOSE LEFT-SIDED HEART FAILURE IN ADULTS?















INCREASED FILLIN G PRESSURE—very helpful findings are radiographic redistribution and jugular venous distension. Somewhat helpful findings are dyspnea, orthopnea, tachycardia, decreased systolic or pulse pressure, S3, rales, and abdominojugular reflux. Edema is helpful only when present

SYSTOLIC DYSFUNCTION—very helpful findings are radiograph (cardiomegaly, redistribution), anterior Q waves, LBBB, and abnormal apical impulse (especially if sustained). Somewhat helpful findings are tachycardia, decreased blood pressure or pulse pressure, S3, rales, dyspnea, previous infarction other than anterior, and high peak CK (post-infarct). Edema and increased jugular venous pressure are helpful if present

DIASTOLIC DYSFUNCTION—very helpful finding is elevated blood pressure during the episode of increased filling pressure. Somewhat helpful findings are obesity, lack of tachycardia, older age, and absence of smoking or CAD. Normal radiographic heart size is helpful if present

APPROAC H—“in patients without known systolic dysfunction, ≤1 finding of increased filling pressure can exclude diagnosis, ≥3 findings suggests increased filling pressure. In patients with known systolic dysfunction, absence of finding of increased filling pressure can exclude diagnosis, ≥1 finding suggests increased filling pressure. For systolic dysfunction, can exclude diagnosis if no abnormal findings, including no sign of increased filling pressure are present (LR– 0.1). ≥3 findings are needed to confirm the diagnosis (LR+ 14)”

JAMA 1997 277:21


Investigations



BASIC





  • labs—CBCD, lytes, urea, Cr, troponin/CK × 3, BNP or NT-pro-BNP, D-dimer, TSH, albumin


  • imaging—CXR, echocardiogram (check E/A ratio if diastolic dysfunction)


  • EC G


SPECIAL





  • further imaging—MIBI, MUGA


  • stress test—to assess ischemic heart disease


  • cardiac catheterization


  • AB G—if severe dyspnea


Diagnostic and Prognostic Issues



B-TYPE NATRIURETIC PEPTIDE/N-TERMINAL PROHORMONE OF BRAIN NATRIURETIC PEPTIDE





  • diagnosis—BNP and NT-proBNP levels are elevated with HF, PE, pulmonary hypertension, LVH, ACS, AF, renal failure, overload, and sepsis. Generally, can rule-out HF if BNP <100 pg/mL or NT-proBNP <300 pg/mL; may rule-in if BNP >500 pg/mL, NT-proBNP >900 pg/mL (if age 50–75 years), or NT-proBNP >1,800 pg/mL (if age >75 years). Best used in combination with clinical scoring system when diagnosis is uncertain


  • Baggish clinical scoring system—elevated NT-proBNP [>450 pg/mL if age <50 years, or >900 pg/mL if age ≥50 years] (+4), interstitial edema on CXR (+2), orthopnea (+2), lack of fever (+2), age >75 years (+1), lack of cough (+1), use of loop diuretic prior to presentation (+1), rales (+1). If score 0–5, low likelihood of HF; if 6–8, intermediate likelihood of HF; if 9–14, high likelihood of HF


  • prognosis—BNP >80th percentile is associated with a >50% increase in long-term mortality


HF PROGNOSIS

—33% 1-year mortality, 75% 6-year mortality


Acute Management



ABC

—O2 to keep sat >95%, IV’s


SYMPTOM CONTROL

—★LMNOP★ L asix/furosemide 20–120 mg IV PRN, M orphine 2–5 mg IV PRN, N itroglycerin 0.4 mg SL PRN, O 2, Position (upright)


Long-Term Management



★DDDD★





  • DIET—low salt (<100 mmol/day, 1.5–2 g/day), fluid restriction (1.5–2 L/day)


  • DIURETICS—furosemide 20–120 IV/PO daily-BID with daily adjustments (try to use smallest dose possible to allow ACE inhibitor) ± metolazone 2.5–5 mg PO 30 min before furosemide, spironolactone 12.5–50 mg PO daily or eplerenone 25–50 mg PO daily VASODILATORS—ACE inhibitor (captopril 6.25–50 mg PO TID, enalapril 1.25–10 mg PO BID, ramipril 2.5–10 mg PO BID, lisinopril 2.5–20 mg PO daily, perindopril 2–8 mg PO daily). ARB (valsartan 40–160 mg PO BID, candesartan 8–32 mg PO daily). Hydralazine 10–50 mg PO QID and nitrates (nitropatch 0.4 mg topical daily or isosorbide mononitrate 30–90 mg PO daily). β-blockers (metoprolol tartrate 50–100 mg PO BID, carvedilol 3.125–25 mg PO BID, bisoprolol 2.5–10 mg PO daily)


  • DI G ITALIS—digoxin 0.0625–0.25 mg PO daily


  • TREAT UNDERLYIN G CAUSE—CAD (PCI/CABG), aortic stenosis (AV replacement), sleep apnea (CPAP)


  • DEVICES—if ejection fraction <30–35%, consider cardiac resynchronization therapy (CRT/biventricular pacing) ± implantable cardioverter defibrillators (ICD). Ventricular assist devices may also be considered in selected cases of refractory HF


Treatment Issues



ACE INHIBITOR

(Garg, JAMA 1995)—hazard ratios for total mortality 0.77 and mortality/hospitalization 0.65 for any patients with LVEF <40%. Target dose = maximum tolerated. Contraindications include SBP <80 mmHg, bilateral renal artery stenosis, severe renal failure, and hyperkalemia


ARB

(CHARM)—consider substitution with ARB if ACE inhibitor not tolerated (e.g., cough). May also be used as adjunct to ACE inhibitor if β-blocker not tolerated. Contraindications similar to ACE inhibitor


HYDRALAZINE/NITRATES

(VHEFT I and II, A-HeFT)—less effective than ACE inhibitor. Particularly useful for pregnant patients, African Americans, or those who developed renal insufficiency while on ACE inhibitor, or as add-on therapy


ANGIOTENSIN RECEPTOR–NEPRILYSIN INHIBITOR

(McMurray, NEJM 2014, PARADIGM-HF)—combination sacubitril-valsartan demonstrated 16% reduction in all-cause mortality, 20% reduction in death from cardiovascular causes, and 21% reduction heart failure hospitalizations compared to enalapril


β-BLOCKERS

(Foody JAMA 2002)—hazard ratios for total mortality 0.65 and mortality/hospitalization 0.64. May worsen symptoms in first few weeks and may take up to 1 year to see full effect in LVEF. Useful for patients with NYHA II–III (and stable IV) and LVEF <40%, also NYHA I, LVEF <40%, and post-MI. Contraindications include fluid overload and severe asthma. Start only when patient euvolemic


SPIRONOLACTONE

(RALES 1999, EPHESUS 2003, EMPHASIS-HF 2011)—hazard ratios for all-cause mortality 0.7 and hospitalization for HF, 0.65 for patients with NYHA III–IV, LVEF <35%, and already on maximum medical therapy. Hazard ratios for cardiovascular death/HF hospitalization 0.63 and cardiovascular mortality 0.76 for patients with NYHA II and LVEF ≤30% (or LVEF 31–35% plus QRS duration >130 msec), and already on maximum medical therapy. Caution in elderly and renal failure patients as higher risk of hyperkalemia


DIGOXIN

(DIG 1997)—hazard ratios for total mortality 0.99 and mortality/hospitalization 0.92. Particularly useful for patients with both HF and atrial fibrillation, or symptomatic HF despite maximum medical therapy


OVERALL APPROACH

—treat underlying cause if possible. Non-pharmacological treatments (diet, exercise, smoking cessation) → add ACE inhibitor if LVEF ≤40% (or hydralazine/nitrates if renal failure, ARB if cough secondary to ACE inhibitor) → add β-blocker when euvolemic if LVEF ≤40% → add spironolactone/eplerenone if NYHA II-IV if LVEF ≤30% (or ≤35% and QRS duration >130 msec) → add digoxin ± ARB if still symptomatic. If ejection fraction is <30–35% despite optimal medical therapy, consider revascularization, implantable cardioverter defibrillator, cardiac resynchronization (if QRS is wide), and ventricular-assist device/heart transplant


Specific Entities



CAUSES OF FLASH PULMONARY EDEMA

—cardiac (ischemic heart disease, acute aortic regurgitation, acute mitral regurgitation, mitral stenosis/obstruction, arrhythmia), pulmonary (pulmonary embolism, pneumonia), renal (bilateral renal artery stenosis), systemic (hypertension crisis, fever, sepsis, anemia, thyrotoxicosis)


HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HOCM)





  • pathophysiology—autosomal dominant condition with mutated cardiac sarcomere, leading to massive ventricular hypertrophy (particularly septum). This results in left ventricular outflow tract obstruction, mitral regurgitation, diastolic dysfunction, and subsequently myocardial ischemia and overt heart failure. Cardiac arrhythmias may lead to sudden death (<1%/year). Other complications include atrial fibrillation and infective endocarditis


  • risk factors for sudden death—major risk factors include history of cardiac arrest (VF), sustained VT, unexplained syncope, non-sustained VT on Holter, abnormal BP response on exercise test, left ventricular wall thickness >30 mm, and family history of sudden death. Minor risk factors include left ventricular outflow obstruction (gradient ≥30 mmHg), diastolic dysfunction, microvascular obstruction, late gadolinium enhancement on cardiac MRI, and high-risk genetic defect


  • clinical features—most are asymptomatic although dyspnea, chest pain, syncope, and sudden death may develop. Family history should be obtained. Physical findings include brisk carotid upstroke, bifid carotid pulse, double apical impulse, systolic ejection murmur (LLSB, louder with standing and Valsalva) ± mitral regurgitation murmur


  • diagnosis—echocardiogram (septal thickening, systolic-anterior motion of mitral valve). Further workup includes 48 h Holter monitor and exercise testing annually


  • treatments—avoidance (dehydration and strenuous exercise), medical (β-blockers and non-dihydropyridine calcium channel blockers as first line, disopyramide as second line), interventional/surgical (septal myomectomy, alcohol septal ablation, dual-chamber pacing), prophylaxis (implantable cardioverter defibrillator for high-risk patients to prevent sudden cardiac death, anticoagulation if atrial fibrillation)

NEJM 2004 350:13


Digoxin Intoxication


Circulation 2004 109:24


Causes



OVERDOSE

—intentional, accidental (digoxin, foxglove, yellow oleander)


DRUG INTERACTIONS

—quinidine, amiodarone, verapamil, diltiazem, tetracycline, erythromycin, rifampin, cyclosporine, SSRIs


PHARMACOKINETICS (see precipitants below)





  • old age , renal failure


  • cardiac—ischemia, myocarditis, cardiomyopathy, amyloidosis, cor pulmonale


  • metabolic—hypokalemia, hypomagnesemia, hypernatremia, hypercalcemia, hypoxemia, acid–base imbalance


Pathophysiology



DIGOXIN LEVEL

—measurement of serum levels is not routinely necessary as dosing can usually be titrated according to clinical and hemodynamic effects. When measured, serum level should be collected at 12–24 h after the last dose (post-distribution phase). While the upper normal limit is 2.6 nmol/L [2.0 ng/mL], higher digoxin levels may be seen in asymptomatic patients. Low-dose digoxin, resulting in serum levels 0.5–0.9 nmol/L [0.4–0.7 ng/mL] is associated with possible survival benefit compared to ≥1 nmol/L [≥0.78 ng/mL] in HF patients


MECHANISM

—digitalis acts by inhibiting the membrane-bound Na/K ATPase transport system. This leads to intracellular loss of K and gain of Na. Increase in intracellular Ca leads to ↑ cardiac contractility. Digoxin also exerts a vagotonic action, which slows conduction through the SA and AV node and helps to control heart rate


PRECIPITANTS OF DIGOXIN TOXICITY

—toxicity is not merely related to serum levels, but also digoxin dosing (e.g., acute overdose), other medications (e.g., non-potassium sparing diuretics), and conditions (e.g., renal insufficiency, acute coronary syndromes, cardiac amyloidosis, hypothyroidism). For instance, hypokalemia, hypernatremia, hypomagnesemia and acidosis predispose to toxicity even at low-serum digoxin levels because of their depressive effects on the Na/K ATPase pump. In contrast, hyperkalemia occurs in acute toxicity and is directly related to prognosis

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Mar 26, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Cardiology

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