EMERGENCIES/BIOCHEMICAL MARKERS
From the American Academy of Family Physicians’ 2006 Scientific Assembly, Washington, DC
| ROADSIDE AND IN-FLIGHT EMERGENCIES —Robert J. Dachs, MD, Clinical Assistant Professor, St. Clare’s
Family Medicine Residency, Albany Medical College, and Assistant Director, Department of Emergency Medicine,
St. Clare’s Hospital, Schenectady, NY
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| Ethics and emergency care: World Medical Association (1983)—physician shall give emergency care as humanitarian
duty, unless assured others willing and able to give such care; Canadian Medical Association (1990)—
ethical physician shall, except in case of emergency, have right to refuse to accept patient and will render all possible
assistance to patient; American Medical Association (AMA; 1992)—physician shall, in provision of appropriate
care, except in emergencies, be free to choose whom to serve; Hippocratic oath—“for the benefit of the sick, I
will keep them from harm and injustice” (implies ethical responsibility to respond to emergency situations)
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| Medicolegal issues: legal principles established by 1950—no legal obligation to treat emergencies outside of hospital;
if physician assists, expected standard of care modified by circumstances of situation; if aid given, it only
needs to be stabilization; implied consent exists to treat victim if he or she lacks capacity to consent (eg, patient unconscious);
criteria apply regardless of whether physician paid for services; 1958—physicians became averse to
giving Good Samaritan care; AMA suggested physicians should give emergency care; 1959—first Good Samaritan
act passed in California; 1970s—all 50 states had Good Samaritan laws
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| General principles of Good Samaritan laws: no legal obligation to provide aid, except in states with failure-to-
act laws (ie, Vermont, Louisiana, and Minnesota); physician has immunity from malpractice suit if aid provided,
except in cases of gross, willful, or wanton negligence or lack of good faith; legal immunity withdrawn if physician
accepts payment for aid; laws restricted to acts outside of hospital (laws undergoing change); recipient of aid must
not object to aid rendered; California in-hospital law—staff physician of hospital who treats another physician’s
patient in hospital in response to medical emergency protected by Good Samaritan laws; Good Samaritan provision
of Aviation Medical Assistance Act passed in 1998 (“so you’re covered in the air also”); as of end of 2004, no documented
cases of suit successfully brought against physician or suit allowed to go to jury for providing emergency
care outside of hospital setting in such scenario
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| At scene of emergency or accident: physicians may feel challenged or helpless; bystanders or victims may become
agitated, irrational, and uncooperative; physician may conflict with emergency medical services (EMS;
quickly decide who can handle situation best); be concerned about personal safety; cardiopulmonary resuscitation
(CPR)—1% to 2% chance of survival after cardiac arrest; if proper CPR performed at scene, chance of survival
doubles or triples
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| ABCs of CPR: open airway—use head-tilt, chin-lift method unless patient has trauma (use jaw thrust in case of
trauma); class IIB recommendation, ie, no good data; breathing—if patient not breathing, health care professionals
trained to listen for breath sounds and to give 2 rescue breaths; new guidelines state lay public does not
have to give rescue breaths and may proceed to compressions; compressions—chest compression to ventilation
ratio 30:2 for 1- or 2-person CPR; ≈100 compressions/min; push hard and fast; avoid interruptions (eg, pausing
for intubation or checking femoral pulse)
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 | Equipment: airway—options include bag-valve-mask, endotracheal tube, laryngeal mask airway (LMA), and
Combitube; optimal method of obtaining airway varies based on provider experience; choose more comfortable
method; with bag-valve-mask, use 30:2 ratio; with advanced airway, use 8:10 ratio (go lower and slower;
overinflation results in barotrauma or hypotension due to increased intrathoracic pressure); summary of new
Acute Cardiac Life Support (ACLS) guidelines—1) remember ABCs; 2) bagging as good as intubating, so “if
you can’t get the tube in, don’t be a hero”; 3) use lower and slower ventilations; 4) push compressions hard and
fast
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| Defibrillators: determine whether monophasic or biphasic; automated external defibrillators (AEDs) biphasic;
monophasic—shock once at 360 J and continue with CPR; biphasic—shock once at 150 to 200 J if using
truncated exponential waveform; shock once at 120 J if using rectilinear biphasic waveform; if type of waveform
unknown, shocking once at 200 J acceptable
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| Emergencies in air: most major airline carriers have physician control on ground who can be contacted; emergencies
include syncope, trauma, burns, gastrointestinal (GI) emergencies, cardiac, respiratory, and neurologic emergencies;
physicians not obligated to treat in United States, Canada, and United Kingdom, but required to treat in
some European countries and Australia; minimum components of medical kit required by Federal Aviation Administration
(FAA)—blood pressure (BP) cuff and stethoscope; 3 oropharyngeal airways; 4 syringes; needles; intravenous
(IV) tubing and normal saline; 2 ampules of diphenhydramine; 1 ampule of dextrose (D-50-W); 1 ampule of
1:1000 epinephrine; 1 ampule of 1:10,000 epinephrine; nitroglycerin tablets; β-agonist metered dose inhaler
(MDI); AED required, except on small flights; first-aid kit—may be separate from medical kit; aspirin; acetaminophen;
ammonia inhalant; decongestant nasal spray; bandages; gloves; when in need of equipment or drugs not
included in kits, ask flight attendant to make announcement and ask passengers (eg, “does anybody have a finger-
stick glucometer?”); captain asks, “should we divert?”—safety issue; physician can make recommendation, but
pilot makes final decision; may take 35 to 40 min to reach ground; airport may not be able to handle plane; may not
be safe to divert; listen to pilot
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| BIOCHEMICAL MARKERS FOR CARDIOVASCULAR DISEASE —John R. Holman, MD, Program Director,
Naval Hospital, Camp Pendleton, Fallbrook, CA
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| Introduction: 50% of coronary artery disease (CAD) patients have below-average low-density lipoprotein (LDL)
levels; study of 15,000 middle-aged women found 77% had LDL <160 mg/dL and had coronary events, 46% had
LDL <130 mg/dL and had coronary events; low LDL does not prevent coronary events; high-sensitivity C-reactive
protein (hs-CRP) may help with management of intermediate-risk patients; apolipoprotein B (apoB) may be better
marker than LDL; homocysteine not causative factor for cardiovascular disease, but useful marker; fibrinogen risk
factor, but not useful because of assay problems
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| Case presentation: man 55 yr of age treated for hypertension with hydrochlorothiazide; no history of tobacco
smoking or diabetes, and no significant family history of CAD; BP 150/82 mm Hg; total cholesterol 185 mg/dL;
LDL 128 mg/dL (may not be candidate for lipid-lowering therapy); high-density lipoprotein (HDL) 33 mg/dL;
risk of having coronary event within next 10 yr 13% (intermediate risk); consider decreasing systolic BP to <140
mm Hg, but no strong evidence that this has significant impact on overall cardiovascular event rate
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| Hs-CRP: high-sensitivity test allows measurement of low values of CRP; hs-CRP binds to damaged lipoproteins
and helps to facilitate their removal by phagocytes in vascular system; directly affects vascular cells by inducing
cytokines and prothrombotic factors; synthesized in hepatocytes; influenced by cytokines; released from sites of
inflammation; found in smooth muscle cells, macrophages in atherosclerosis, neurons, renal tubular cells, lymphocytes,
and alveolar macrophages; atheromatous plaque formation—inflammation oxidizes LDL; CRP binds
to modified LDL, activating complement to allow uptake by macrophages; macrophages become foam cells,
leading to atheromatous plaque; CRP marker of inflammation; appears to be systemic (rather than local) effect
on cells; proatherothrombotic consequences of hs-CRP—increases cytokine release, which induces more CRP
and plaque formation; enhances expression of adhesive molecules (ie, encourages platelets to bind); increases
macrophage presence in vascular system; enhances endothelial cell dysfunction; activates coagulation cascade; benefits
of hs-CRP—facilitates immunity; limits tissue damage, acute inflammation, and autoimmune reactions; suggested
that hs-CRP not causative factor in cardiovascular disease, but reflects effects of coronary ischemia on
myocardium
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| Clinical evidence on hs-CRP: mostly epidemiologic; meta-analyses show increase in relative odds of 2.0 for major
coronary events for patients in lower third and upper third of hs-CRP levels; elevated hs-CRP associated with increase
in coronary events; in intermediate-risk patients, continue controlling traditional risk factors (eg, tobacco
smoking, BP); hs-CRP testing costs ≈$60; ≤1 mg/dL indicates low risk, 1 to 3 mg/dL indicates intermediate or
average risk, 3 to 10 mg/dL indicates high risk, >10 mg/dL considered to be from other sources (eg, rheumatoid
arthritis) rather than cardiovascular source (“you need to basically throw that out”)
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| Management of elevated hs-CRP: diet low in saturated fat can lower hs-CRP by 10%; diet high in plant sterols can
lower hs-CRP by up to 28%; aerobic exercise; statins shown to lower hs-CRP by 15% to 30%; β-blockers;
rosiglitazone; aspirin blocks overall inflammation, but does not specifically work on hs-CRP
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| Case management: man’s hs-CRP level 6.8 mg/dL; man placed on statin
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| Case presentation: Hispanic woman 57 yr of age with history of myocardial infarction at 55 yr of age; BP 122/82
mm Hg (currently on treatment); adult-onset diabetes (good control; hemoglobin A1c 6.5%); LDL 98 mg/dL (currently
on statin); positive family history for cardiovascular disease and diabetes; hs-CRP 0.8 mg/dL
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| Homocysteine: amino acid not used for protein synthesis; breakdown product of methionine; homocysteine converted
into cystathionine and cysteine using vitamin B6 as cofactor; elevated concentrations associated with male
sex, advanced age, poor diet, coffee drinking, tobacco smoking, excessive alcohol use, low physical activity, elevated
cholesterol, and hypertension; improves endothelial function; significant genetic component associated
with metabolism; lack of cystathionine- β-synthase (CBS) found to be associated with elevated homocysteine and
fairly early onset of arterial damage; 1976 retrospective study found patients with CAD and abnormal homocysteine
metabolism had more frequent coronary events than control group
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| Heart Outcomes Prevention Evaluation-2 (HOPE-2): study decreased homocysteine levels in high-risk patients using
vitamin B12 and folate; saw decrease in nonfatal stroke (no effect on coronary events or fatal stroke) and statistically
significant increase in hospital admissions for unstable angina; recommended against screening for or
treating elevated homocysteine
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| Case management: decrease LDL to 70 mg/dL; prescribe aspirin; look for other markers; consider metabolic syndrome
and apoB
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| Apolipoprotein B: may help stratify risk in patients with metabolic syndrome; synthesized in liver; required for assembly
of very low-density lipoprotein (VLDL) particles; found in intermediate-density lipoprotein and LDL after
removing apolipoprotein A (apoA), apolipoprotein E (apoE), and apolipoprotein C (apoC); measurement of
apoB reflects quantity of atherogenic particles (measurement of LDL reflects weight of particles, not necessarily
their number); small dense LDL particles may be more atherogenic than large fluffy LDL particles; patient with
normal LDL (eg, <100 mg/dL) and high apoB may be at higher risk than patient with higher LDL (eg, 130 mg/
dL) and low apoB; elevated apoB identifies high-risk individuals with small dense LDL particles and associated
with abdominal obesity, hyperinsulinemia, thrombosis, and inflammation (key factors in risk for coronary events
associated with metabolic syndrome); better marker than LDL for residual events in patients on statins; statins
treatment of choice for reducing apoB; automated and standardized assay available (measuring apoB accepted in
Canada as alternative to measuring LDL in certain groups)
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| Case management: woman’s apoB 145 mg/dL (>75th percentile); push harder with statin to lower apoB and to reduce
LDL to <70 mg/dL
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Educational Objectives
| The goal of this program is to educate the listener about legal principles of Good Samaritan laws, management of
roadside emergencies, and biochemical markers for cardiovascular disease. After hearing and assimilating this program,
the participant will be better able to:
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| 1. State general principles of Good Samaritan laws.
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| 2. Perform cardiopulmonary resuscitation in accordance with newer guidelines.
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| 3. Provide care during an in-flight emergency.
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| 4. Use biochemical markers such as high-sensitivity C-reactive protein, homocysteine, and apolipoprotein B to
assess cardiovascular risk.
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| 5. Manage patients with cardiovascular risk factors, based on history and clinical findings.
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Discussed on This Program
Aspirin (acetylsalicylic acid; ASA) (several trade names)
Dextrose (D -glucose) [D-2.5-W, D-5-W, D-10-W, D-20-W, D-30-W, D-40-W, D-50-W, D-60-W, D-70-W]
Diphenhydramine HCl (several trade names)
Epinephrine (several trade names)
Folic acid (folacin; pteroylglutamic acid; folate) [Folvite]
Hydrochlorothiazide [Esidrix, Ezide, HydroDIURIL, Hydro-Par, Microzide Capsules, Oretic]
Hydroxocobalamin, crystalline (vitamin B12 ) [Hydro Cobex, Hydro-Crysti-12, LA-12]
Nitroglycerin (several trade names)
Rosiglitazone maleate [Avandia]
Suggested Reading
Abella BS et al: Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA 293:305, 2005;
Arai YC et al: The endoscopically measured effects of airway maneuvers and the lateral position on airway patency
in anesthetized children with adenotonsillar hypertrophy. Anesth Analg 100:949, 2005; Bruppacher H et al:
The effects of common airway maneuvers on airway pressure and flow in children undergoing adenoidectomies.
Anesth Analg 97:29, 2003; Dachs R: Emergency response. Am Fam Physician 67:2423, 2003; Danesh J et al: C-
reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J
Med 350:1387, 2004; Gausche M et al: Effect of out-of-hospital pediatric endotracheal intubation on survival and
neurological outcome: a controlled clinical trial. JAMA 283:783, 2000; Gross CP et al: The physician as ambivalent
Samaritan: will internists resuscitate victims of out-of-hospital emergencies? J Gen Intern Med 13:491, 1998;
Homocysteine Studies Collaboration: Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis.
JAMA 288:2015, 2002; Jagoda A et al: Medical emergencies in commercial air travel. Emerg Med Clin North
Am 15:251, 1997; Lonn E et al: Homocysteine lowering with folic acid and B vitamins in vascular disease. N Engl
J Med 354:1567, 2006; Reber A et al: Effect of common airway manoeuvres on upper airway dimensions and clinical
signs in anaesthetized, spontaneously breathing children. Br J Anaesth 86:217, 2001; Ridker PM et al: C-reactive
protein, inflammation, and coronary risk. Cardiol Clin 21:315, 2003; Sniderman AD: How, when, and why to
use apolipoprotein B in clinical practice. Am J Cardiol 90:48i, 2002; St-Pierre AC et al: Apolipoprotein-B, low-
density lipoprotein cholesterol, and the long-term risk of coronary heart disease in men. Am J Cardiol 97:997, 2006;
Wik L et al: Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA 293:299, 2005;
Williams K et al: Comparison of the associations of apolipoprotein B and low-density lipoprotein cholesterol with
other cardiovascular risk factors in the Insulin Resistance Atherosclerosis Study (IRAS). Circulation 108:2312, 2003;
Wilson PW et al: C-reactive protein and risk of cardiovascular disease in men and women from the Framingham
Heart Study. Arch Intern Med 165:2473, 2005.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue,
the faculty reported nothing to disclose.
Drs. Dachs and Holman spoke at the American Academy of Family Physicians’ (AAFP) 2006 Scientific Assembly,
presented September 27 to October 1, 2006, in Washington, DC. The Audio-Digest Foundation thanks the speakers
and the AAFP for their cooperation in the production of this program.
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