(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
scoring (based on regression model)—age, SBP, HR, creatinine, Killip class, cardiac arrest at admission, presence of ST segment deviation, elevation in serum cardiac enzymes/markers. Risk score calculated using online software: www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html
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 |
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 |
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 |
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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