chf/hypertension/pvd...and eclampsia are true hypertensive emergencies c. both of these conditions...

CHF/Hypertension/PVD

John W. Hafner, Jr., MD, MPH, FACEP

Clinical Assistant Professor of Surgery, University of Illinois College of Medicine at Peoria; Attending Physician, Department of

Emergency Medicine, OSF Saint Francis Medical Center, Peoria

Notes

CHF/Hypertension/PVD Page 1

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CHF/HYPERTENSION/PVD

I. HYPERTENSIVE EMERGENCIES

Definition: Those situations that require immediate blood pressure (BP) reduction to limit damage to target organs. (Note: The absolute BP is not essential for diagnosis. The organs at risk are the brain, heart, kidneys and mother/fetus. The rate of rise is most important.)

Epidemiology 1. 25% of the U.S. population has hypertension 2. Only 10% develop severe hypertension 3. Only 1-2% develop true hypertensive emergency 4. 30% of patients presenting to an ED have a BP ≥ 140/90 mm Hg

History

1. Symptoms (usually progressive)

a. CNS: mental status/visual changes, headache, focal neuro deficits

b. CVS: angina, CHF, back pain c. Past medical history d. Medications, compliance

Physical Exam

1. Search for end-organ dysfunction: neuro, cardiac, pulmonary and renal 2. Funduscopic exam: papilledema, hemorrhages, cotton wool

exudates. 3. Pregnancy

Labs

1. CBC, electrolytes, BUN, and creatinine 2. CXR – evaluate for CHF, aortic dissection or coarctation 3. EKG – may reveal changes consistent with coronary ischemia,

electrolyte abnormalities, strain or LVH 4. UA – assess for protein 5. Pregnancy test – women of childbearing potential 6. CT if altered mental status or a focal neuro deficits

Treatment

Notes


1. General Considerations a. Hemodynamics BP= Cardiac Output (CO) [(Stroke Volume

(SV) X Heart Rate (HR)] X Systemic Vascular Resistance (SVR)

b. Usually if SVR is increased, CO somewhat decreased c. Therapeutic goal: decrease SVR without further decrease to

CO and resultant decrease blood flow to critical organs. The Mean Arterial Pressure (MAP) = (1/3[Systolic Blood Pressure (SBP) – Diastolic Blood Pressure (DBP)]) + DBP. This should be done in a controlled, graded manner, using improvement in the patient’s condition as a guide. In severe hypertensive conditions, such as hypertensive encephalopathy, the MAP should be reduced by 25% or a diastolic pressure of 100 to 110 mm Hg over a period of 1 hour. Excessive and rapid reduction of BP should be avoided to prevent cerebral ischemia from dysfunctional cerebral autoregulation.

2. Cerebral Autoregulation a. Cerebral blood flow (CBF) is normally maintained at constant

flow despite systemic BP fluctuations. However, cerebral autoregulation is maintained at different levels for normal and chronic hypertensives.

b. Normal individuals: i. MAP = 60-120 mm Hg → constant CBF ii. MAP <60 mm Hg → unable to maintain CBF →

hypoperfusion and ischemia iii. MAP >120 mm Hg → increased CBF → hyperperfusion

and ischemia c. Chronic hypertensives

i. Curve is shifted to the right so that they still maintain CBF, but at a higher MAP range (100-160 mm Hg)

ii. This allows a tolerance to very high BP before having end-organ damage

iii. Unable to tolerate BP reduction to “normal” range, as hypoperfusion will result

d. Therapeutic goal i. To maintain CBF, reduce MAP slowly to level baseline

for individual or a 20-25% MAP reduction ii. Rate of reduction depends on clinical syndrome

e. “Ideal” antihypertensive agent i. Potent, titratable IV medication ii. Rapid onset/short duration of action iii. Reduces SVR without adverse hemodynamic effects (CO,

BF, coronary or renal BF) iv. Minimal alteration of mental status v. Minimal potential for side effects

f. Although fast acting nifedipine had been widely used in the

Notes


G.

past for symptomatic hypertension, numerous serious adverse effects related to uncontrolled hypotension have been reported. Its use in hypertensive emergencies is contraindicated

Specific Presentations of Hypertensive Emergencies

1. Hypertensive Encephalopathy

a. Uncommon syndrome resulting from an abrupt, sustained rise of BP that exceeds the limits of cerebral autoregulation of the small resistance arteries in the brain

b. Excessive reduction of blood pressure must be avoided to prevent the increased cerebral ischemia that results if the pressure falls below autoregulation.

c. Acute in onset and reversible d. Patients present with altered mental status, vomiting, seizures

and focal neurological deficits which may progress to coma and death

e. Focal deficits do not follow a singular anatomic pattern. They may occur on opposite sides of the body or may have a patchy distribution

f. Papilledema is usually present along with significant hypertensive retinopathy

g. Rapid measured reduction of BP is mandatory. Standard treatment regimen is IV nitroprusside with the careful reduction of MAP by 25% over an hour, with a minimum diastolic pressure of 110 mmHg. Starting dose is 0.3 µg/kg/min, titrating to a maximum dose of 10 µg/kg/min. Fenoldopam , nicardipine and labetalol are now also widely used, and are second-line agents for hypertensive encephalopathy

2. Stroke Syndromes a. Onset and progression are more rapid than hypertensive

encephalopathy b. 85% are ischemic in nature and 15% are hemorrhagic c. In most cases, elevated BP is the result of the physiologic

response to the stroke itself and is not the immediate cause. d. In most instances, antihypertensive therapy for ischemic

stoke is unnecessary and may be harmful. Some have recommended careful antihypertensive treatment for patients with persistent extreme BP elevations after a stroke with DBP >140 but this data is lacking. If fibrinolytic therapy is to be administered, patients should not have a BP of > 185/110 mm Hg

e. If BP reduction is pursued in these patients, vasodilating agents such as nitroprusside or nitroglycerin should be avoided. They increase ICP, impair cerebrovascular

Notes


reactivity, and CPP for a given level of BP reduction. f. Labetalol is the agent of choice in this setting. This agent

shifts cerebral autoregulation while preserving cerebral blood flow at lower pressures. Nicardipine is an alternative agent

3. Pulmonary Edema a. Hypertension is usually a result of increased SVR caused by

elevated catecholamines b. This increased SVR causes decreased LV function which

increases PCWP and leads to pulmonary edema c. BP must be reduced to reverse the process and nitroglycerin

IV (at elevated doses so that SVR is affected) or nitroprusside are the drugs of choice

d. Additional therapy includes oxygen, diuretics, morphine and ACE inhibitors

4. Cardiac Ischemia a. If severe hypertension is found concurrently with angina,

immediate lowering of BP is indicated to prevent myocardial damage

b. Drug of choice is IV nitroglycerin c. Addition of beta blocker will reduce mortality in case of MI

(calcium channel blockers may be useful if bronchospasm an issue)

d. ACE inhibitors are also useful in setting of MI to reduce mortality

5. Aortic Dissection a. Longitudinal cleavage of the aortic media created by

dissecting column of blood. b. Abrupt onset of “tearing” pain in the chest or back (>90% of

presentations) c. Medical therapy consists of lowering both the blood pressure

and heart rate to decrease shearing forces d. The goal is to lower pressure to a systolic pressure of 100-120

mmHg. The drugs of choice are: i. Beta blocker to control tachycardia ii. Nitroprusside to lower BP by vasodilation iii. The ganglionic blocker trimethaphan and the combined

alpha and beta blocker labetalol have also been used successfully

6. Renal Failure a. Most important cardiovascular complication of chronic renal

failure is hypertension and these two are intrinsically related b. Severe elevation of BP may lead to acute renal failure or

exacerbation of CRF c. Worsening renal function in the setting of elevated BP,

elevation of BUN and creatinine levels, proteinuria, or the presence of red cells and red cell casts in the urine, is considered a hypertensive emergency that requires immediate

Notes


reduction of blood pressure d. Nitroprusside is the drug of choice with the calcium channel

blocker nicardipine a reasonable alternative 7. Pregnancy-Induced Hypertension

a. Hypertension complicates 5-10% of pregnancies b. Usually, these elevations do not lead to life threatening

immediate complications. However, severe preeclampsia and eclampsia are true hypertensive emergencies

c. Both of these conditions can occur without an extreme elevation of BP

d. Any acute elevation of DBP above 100 mmHg in the pregnant patient represents a true hypertensive emergency

e. Patients may present with: i. Mild: often asymptomatic edema (rapid weight gain),

HTN, and proteinuria ii. Severe: as above but also symptoms related to end organ

damage iii. CNS- headache, visual changes, altered mental status iv. GI- epigastric pain, N/V v. Renal- oliguria vi. CV- pulmonary edema vii. Hematologic- DIC viii. Eclampsia- seizures associated with preeclampsia

f. Treatment i. Mild: close OB follow up ii. Severe and Eclamptics: prevent seizures with IV

magnesium, treat seizures with IV benzodiazepines. iii. Treat the hypertension with hydralazine (10-20 mg IV

dose or 10-50 mg IM dose). This is the classic iv. teaching although the potential complications of

tachycardia and hypotension exist (alternatives include fenoldopam, nicardipine, and nitroprusside. Nitroprusside should only be used as a last effort if others have failed due to the potential accumulation of cyanide in the uterus)

v. Prompt delivery is the only cure vi. Drugs to avoid:

• Calcium channel blockers: inhibit labor • Diuretics: volume depletion • Trimethaphan: crosses placenta which

can lead to birth defects II. HYPERTENSIVE URGENCIES

A Definition: occurs when the blood pressure elevation presents a risk for imminent target-organ damage. Although acute organ injury has not occurred in hypertensive urgency, the risk of injury is high if the elevated BP is allowed to persist. (You have to be psychic)

Notes


B. In many cases, elevated blood pressure in the presence of preexisting

conditions (renal disease, CHF, CAD or CNS disorders) increases the likelihood of target-organ damage

C Main challenge is to determine if end-organ dysfunction exists. If target-organ dysfunction does exist then it must be determined if chronic and at risk for further impairment. This may be difficult if no prior knowledge of the patient exists. If dysfunction does not exist, it must be determined whether damage to the CNS, cardiovascular, or renal system is impending (Again, psychic)

D. The treatment of hypertensive urgency is the gradual reduction of BP

within 24 hours by using oral antihypertensive medications. Because a common cause of this process is noncompliance with medications, restarting their meds is a reasonable starting regimen

E. Any patient with a diagnosis of hypertensive urgency should be

started on an antihypertensive medication with follow-up in 24 hours

F. Admission decisions depend on comorbid condition, and impression of the patient’s response to therapy

G. A common cause of hypertensive urgency is noncompliance with

medication, restarting a previously established medication regimen is appropriate

H. TREAT THE PATIENT AND NOT JUST THE BP

III. HYPERADRENERGIC STATES A. Drug Ingestions

1. Illegal: cocaine, amphetamines, PCP 2. OTC: decongestants, appetite suppressants 3. Treatment

a. Benzodiazepines b. Avoid beta blockers due to unopposed alpha activity and

therefore a possible paradoxical increased BP c. Decontamination

i. Activated charcoal ii. Time

B. Head Trauma

1. Post-traumatic injury leads to increased levels of catecholamines

and increased sensitivity of central sympathetic receptors

Notes


2. Cushing’s triad a. Increased BP b. Bradycardia c. Decreased RR

3. Treatment a. Nitroprusside b. Labetalol

C. Food and Drug Interactions with MAO Inhibitors

1. MAO normally inactivates tyramine and other sympthomimetic

amines. Ingestion of food/drugs containing tyramine in patients on MAO inhibitors causes increased norepinephrine release at the synapses and hypertension

2. Patients present with severe HTN, headache, palpitations and diaphoresis

3. Treatment a. Phentolamine + propranolol b. Nitroprusside + propranolol c. Labetalol d. Avoid beta blocker alone as may cause a paradoxical rise in

BP due to beta 2 blockade e. Pheochromocytoma

i. Catecholamine secreting tumor ii. Presentation and treatment same as interactions with

MAO inhibitors

IV. MEDICATIONS

A. Vasodilators

1. Nitroprusside a. Action: balanced arteriolar and venous dilator b. Indications: virtually all of the hypertensive emergencies (not

the drug of choice for pregnancy or acute coronary syndromes)

c. Advantages: immediate onset, short duration of 1-2 minutes, no effect on cardiac output or renal blood flow

d. Disadvantages: “coronary steal syndrome”, inhibits hypoxia-induced pulmonary vasoconstriction, and cyanide toxicity (worse in renal insufficiency, prolonged infusions over 48 hours, higher doses and fetal toxicity)

2. Nitroglycerin a. Action: venodilator at low dose but arteriolar and venodilator

at high doses b. Indication: severe HTN with angina, MI or CHF c. Advantages: dilates large and small coronary arteries (no

Notes


coronary steal), no increased V/Q mismatch d. Disadvantages: headache, tachycardia, increases ICP

3. Fenoldopam a. Action: selective dopamine-1 agonist which dilates renal,

splanchnic, and skeletal muscle beds b. Indications: not clearly established but promising for

pregnancy-induced, and renal hypertensive emergencies c. Advantages: as effective as nitroprusside, rapid onset of 4

minutes, short duration of 10 minutes, enhances renal blood flow and cardiac output, no effect of CBF or ICP, no toxic metabolites and category B for pregnancy

d. Disadvantages: may increase intraocular pressure and may give rise to hypokalemia

4. Hydralazine a. Action: direct arteriolar vasodilator b. Indication: pregnancy induced hypertension c. Advantages: increases CO, increases cerebral/renal and

placental BF d. Disadvantages: reflex tachycardia, may invoke precipitous

fall of BP, flushing/nausea/headache 5. Trimethaphan

a. Actions: direct vasodilator and cholinergic/adrenergic ganglia blocker

b. Indications: aortic dissection c. Advantages: decreases CO, aortic pressure wave d. Disadvantages: tachycardia, tachyphylaxis with infusions >24

hours, parasympatholytic effect

B. Adrenergic Blockers

1. Labetalol a. Action: selective alpha-1 blocker and nonselective beta

blocker with ratio of alpha: beta of ~1:5 b. Indications: useful in most cases of hypertensive emergencies c. Advantages: no effect on CBF or mental status; no reflex

tachycardia d. Disadvantages: decreases CO, may aggravate heart block and

bronchoconstriction, prolonged duration of action (4 hours) 2. Esmolol

a. Action: selective beta-1 blockade b. Indication: cardiovascular or hyperadrenergic states c. Advantages: ultra-short acting d. Disadvantages: bronchoconstriction, complicated to bolus and

set up drip 3. Phentolamine

a. Action: direct adrenergic blocker (alpha 1 > alpha 2) b. Indications: catecholamine induced HTN

Notes


c. Advantages: relatively short duration of action at 15 minutes d. Disadvantages: reflex tachycardia

4. Trimethaphan a. Action: cholinergic blocking agent that acts at both the

sympathetic and the parasympathetic ganglion which interrupts the adrenergic control of arterioles, resulting in vasodilation

b. Indications: aortic dissection c. Advantages: decreases CO and aortic pressure wave d. Disadvantages: tachycardia, tachyphylaxis and

parasympatholytic effects

C. Central Alpha Agonists

1. Clonidine a. Action: stimulation of postsynaptic alpha 2 receptors in

vasomotor center of brainstem decreased sympathetic outflow → vasodilation

b. Indications: hypertensive urgencies c. Advantages: predictable reduction in BP d. Disadvantages: sedation, withdrawal syndrome

D. Calcium Channel Blockers

1. Nifedipine

a. Action: peripheral and coronary arterial vasodilator b. Indication: hypertensive urgencies (extended release only) c. Advantages: few to none for ED uses d. Disadvantages: may cause a precipitous drop in BP, reflex

tachycardia, cannot titrate, prolonged action, cerebral vasodilator (worsen cerebral edema and encephalopathy)

2. Nicardipine a. Action: peripheral arterial vasodilator b. Indications: hypertensive encephalopathy, pregnancy-induced

HTN and postoperative patients c. Advantages: titratable, less negatively inotropic, less

tachycardic than nifedipine, d. Disadvantages: still negative inotrope therefore caution in

patients with decreased LV, heavily metabolized by liver, headache and flushing

E. ACE Inhibitors

1. Captopril/Enalapril

a. Actions: inhibition of ACE prevents conversion of inactive angiotensin I to potent vasopressor angiotensin II

b. Indications: CHF, diabetic retinopathy

Notes


c. Advantages: hypotension has not been reported in literature, peak effects shown in 15 minutes

d. Disadvantages: no dose related response, angioedema, cough, renal failure in patients with bilateral renovascular disease

F. Diuretics

1. Furosemide

a. Actions: increases venous capacitance, decreases plasma volume

b. Indications: combination therapy with other antihypertensives which cause fluid retention

c. Disadvantages: worsens volume depletion, electrolyte imbalances

d. Dosage table for IV medications:

i. Summary

Condition Drugs of Choice Avoid Encephalopathy Nitroprusside/Esmolol

Labetalol Nifedipine Hydralazine Clonidine

Stroke Syndromes Rarely needed but: Labetalol

Nifedipine Hydralazine Clonidine

Coronary Syndromes Nitroglycerin Labetolol Esmolol

Hydralazine

Drug Onset Duration Dosage Nitroprusside Seconds-1 minute 3-5 minutes 0.2-6 mg/kg/min Nitroglycerin 1-2 minutes 3-5 minutes 10-150 ug/min Fenoldopam 4 minutes 8-10 minutes 0.1-0.9 ug/kg/min Hydralazine 10-20 minutes 3-8 hours 10-20 mg @ 0.5-

1.0 mg/min Labetalol 5 minutes 4-8 hours 20 mg q 10 min to

max 80 mg Q 10 min

Esmolol 5 minutes 30 minutes 0.5 mg/kg bolus then 0.05-0.3 mg/kg/min infusion

Phentolamine 1-2 minutes 3-10 minutes 5-10 mg q 5 min then 0.2-0.5 mg/min

Trimethaphan 1-5 minutes 10 minutes 0.5-5 mg/min

Notes


Aortic Dissection Nitroprusside/Esmolol Labetalol Trimethaphan

Nifedipine

Pregnancy-Induced Magnesium Hydralazine Labetalol Fenoldopam

Nifedipine Trimethaphan Diuretics Nitroprusside (last line agent)

Pulmonary Edema Nitroglycerin Nitroprusside

Labetalol Beta blockers Hydralazine

Hyperadrenergic States Phentolamine/Propranolol Nitroprusside/Propranolol Labetalol

Beta blocker alone

Peripheral Vascular Disease I. PATHOPHYSIOLOGY

A. Arteries are composed of:

1. Tunica intima: inner endothelial cells lining the lumen 2. Tunica media: made up primarily of smooth muscle cells

arranged in concentric layers. 3. Tunica adventitia: poorly defined outer layer of connective tissue

in which nerve fiber and small, thin walled nutrient vessels are dispersed

B. Atherosclerosis

1. Disease of large and medium sized muscular arteries 2. The atheroma is a raised focal plaque within the intima that has a

lipid core covered by a fibrous cap 3. As the atheroma enlarges it not only encroaches on the lumen but

also weakens the wall

C. Arterial Embolism

1. Thromboembolism a. Most arterial emboli originate from the heart (85%) b. LV thrombus is the majority of this (85%) c. Atrial fibrillation is present in 60-75% of peripheral arterial

embolic events d. Embolic occlusion most frequently occurs at major

bifurcation points 2. Atheroembolism

a. Refers to microemboli consisting of cholesterol, calcium and

Notes


platelet aggregates dislodged from atherosclerotic plaques b. Causes both central (TIA, strokes) and peripheral (blue toe

syndrome, cool painful toes) c. Infectious emboli from bacterial endocarditis can produce

septic infarcts

D. Arterial Thrombosis

1. In situ formation of a blood clot within the non-interrupted arterial vascular system

2. Usually from endothelial injury, abnormal flow, trauma and inflammation

E. Vasospasm

1. Abnormal vasomotor response in distal small arteries 2. Characterized by ischemic symptoms and the absence of tissue

loss 3. Examples are Raynaud’s syndrome, livedo reticularis

II. CLINICAL FEATURES

A. History

1. Pain, change in sensation, change in appearance (swelling, discoloration and temperature change), tissue loss (ulcers)

2. Associated conditions of atherosclerosis (MI, stroke, dysrhythmias)

3. Risk factors: smoking, diabetes, hypercholesterolemia, and hypertension

4. Acute Arterial Occlusion: a. 5 “Ps”: pain, pallor, pulselessness, paresthesia, and paralysis b. Acute in onset so that patients have sudden limb threatening

ischemia 5. Chronic Arterial Insufficiency:

a. Intermittent claudication: cramping pain, reliably reproduced by the same degree of exercise and completely relieved by rest

b. Rest pain: often begins in the feet. Pain is severe, unrelenting aggravated by elevation and unrelieved by analgesics

B. Physical Examination

1. Palpate pulses 2. Look for chronic ischemia: thickening of toenails, loss of hair

growth, muscle atrophy, and shiny skin

Notes


3. Blanch any area where there is concern of ischemia and compare to the other leg

4. Elevate the area and check if turns pale, also see if dependency causes hyperemia of reperfusion

5. Ankle Brachial Index (ABI): a. ABI is the best single evidence available concerning the

prevalence of arterial occlusive disease and its severity b. Measure the pressure of the dorsalis pedis or posterior tibial

by inflating cuff above the ankle and using a Doppler to measure pressure when signal returns. Compare this value to brachial blood pressure i. Normal >90% ii. Mild arterial insufficiency 70-90% iii. Moderate 50-70% iv. Severe <50%

6. Doppler and B-Mode Imaging: a. Can access all arteries in the body b. Best example is carotid duplex which is the sole diagnostic

test required for carotid endarterectomy and removes the risk of having a neurological event during an angiogram

c. Depends on the skill of the operator 7. Arterial Embolism

a. In general, patients with arterial embolus have few physical findings suggestive of longstanding peripheral vascular disease with normal, proximal, and contralateral limb pulses

b. Limb distal to occlusion is classically chalk white c. Demarcation between ischemic and nonischemic is tissue

may be sharp d. Cyanosis may occur e. Paralysis and paresthesia indicates limb-threatening ischemia f. Presence of light touch is best guide to viability

8. Arterial Thrombosis a. Physical findings associated with chronic atherosclerotic

disease b. Proximal and contralateral pulses are often diminished c. Due to collateral circulation, less well defined area of

ischemia d. May have bruits, thrills

9. Vasospasm a. Sharp border between ischemic and normal tissue b. Triphasic color change: pallor, cyanosis, and then erythema c. Attacks usually last 15-60 minutes

C. Diagnosis

1. Noninvasive

a. Doppler: by analyzing waveforms, significant arterial

Notes


occlusive disease can be detected but the location is difficult b. B-mode ultrasound: useful in detecting and evaluating

atherosclerotic plaques and thrombi c. Duplex scanning: allows both the image of a vascular

structure and the characteristic of blood flow velocity within it. This is the procedure of choice for most conditions

2. Invasive a. Angiography

i. The definitive test of abnormal peripheral artery anatomy ii. Inconclusive for the physiologic status of the tissues iii. Significant adverse effects

• Contrast media •• Directly toxic to the endothelium •• Renal failure •• Allergic reactions

• Catheter related complications •• Embolization •• Catheter breakage •• Vascular disruption

iv. Emergency angiography for: • Acute arterial embolus or thrombosis • Consideration of emergency vascular bypass • Grafting • Characterization of vascular abnormality before

emergency surgical correction 3. CT/MRI

a. CT is the most useful diagnostic modality for the evaluation of the abdominal aorta

b. MRI role unclear at this time but is the definitive test of anatomy

III. MANAGEMENT

A. Management depends on the degree and cause of ischemia

B. Limb threatening ischemia from embolism → Immediate Surgical/Vascular Consultation → Fogarty catheter embolectomy

C. Limb threatening ischemia from thrombosis → Immediate

Surgical/Vascular Consultation → direct or Fogarty embolectomy combined with vascular bypass grafting

D. Lesion that can’t be bypassed, irreversible ischemia or too ill→

primary amputation

Notes


E. Non-limb threatening ischemia from embolism → Surgical/Vascular Consultation → Fogarty embolectomy

F. Non-limb threatening ischemia from thrombosis→

Surgical/Vascular Consultation → systemic heparinization with consideration of intraarterial thrombolysis

G. Noninvasive Therapy

1. Heparin

a. Effective initial therapy for acute arterial thrombosis and arterial embolism

b. Minimizes clot propagation 2. Thrombolytic therapy

a. Low dose intraarterial thrombolytic therapy is being used for acute arterial occlusion

b. Not for limb-threatening ischemia as clot lysis takes 6-72 hours

c. Usually for thrombosis and non-limb threatening 3. Fibrinolytic Therapy

a. Low-dose intra-arterial fibrinolytic therapy is increasingly used for acute arterial occlusion.

b. Limb threatening ischemia patients are not candidates as clot lysis takes 6 to 72 hours

c. Reserved for in-situ thrombosis and non-limb-threatening ischemia

d. Streptokinase, urokinase and tissue plasminogen activator have all been used successfully

H. Invasive Therapy

1. Fogarty catheter thrombectomy

a. Most frequently used for iliac, femoral, and popliteal embolectomy, often with only local anesthesia

b. Can also be used for thrombosis if fresh and not had time to organize

c. Can’t use on venous side due to valves d. Results are disappointing distal to the inguinal ligament

2. Peripheral percutaneous transluminal angioplasty a. Success depends on the location of the lesion and the extent

of atheromatous disease b. Proximal larger caliber arteries have the best success rate c. Discrete lesions have better long-term patency rates than

diffuse lesions d. Increasing number of “rebound” stenosis unless a stent used

3. Grafting a. Used to bypass arterial occlusion and reconstruct a diseased

Notes


arterial bifurcation. b. Either vein or prosthetic graft c. May develop thrombosis or false aneurysm at one or more

suture lines

IV. CHRONIC ARTERIAL INSUFFICIENCY

A. Arteriosclerosis

1. Responsible for 95% of chronic arterial disease 2. Men:Women → 5:1 3. 1/3 have existing CAD 4. Approximately 5% of lower extremity ulcerations are due to

arterial insufficiency. a. Distal to the ankle b. Painful c. Rim of ulcer is sharp and the base is gray, tallow or black

5. Approximately 90% of lower extremity ulcerations are due to venous insufficiency a. Proximal or at region of ankle b. Mildly painful c. Evidence of longstanding chronic venous insufficiency

(edema, superficial veins, stasis dermatitis) d. Ulcers are moderate in size with a weeping base and

extensive granulation tissue e. Management

i. Classify into either functional ischemia versus limb-threatening ischemia • Functional ischemia

•• Outpatient arrangements for noninvasive vascular testing or elective invasive arteriography to determine treatment options

• Limb threatening ischemia: •• Surgical emergency •• Angiography •• Immediate vascular consult

B. Buerger’s Disease

1. Idiopathic inflammatory occlusive disease primarily involving the medium and small arteries of the hands and feet.

2. Usually men between 20-40 years of age 3. Almost all use tobacco 4. Patients present with painful, tender, reddened, or dark nodule

over a peripheral artery with either a reduced or an absent pulse

Notes


5. Permanent complete abstinence from tobacco is the only known effective treatment for Buerger’s.

6. If patient continues to smoke, the disease progresses to severe pain at rest, tissue loss, and eventually amputation

V. ACUTE ARTERIAL OCCLUSION

A. Arterial Embolism

1. Management

a. Surgical emergency b. Successful salvage if ischemia less than 4-6 hours c. Full dose heparin immediately to prevent clot propagation d. Pretreatment angiogram is usually required and diagnostic e. Fogarty catheter embolectomy f. Intraarterial thrombolytic therapy an alternative for non-limb-

threatening ischemia

B. Atheroembolism

1. Microemboli break off from proximal atherosclerotic plaques or aneurysms and lodge in distal end arteries. This can cause TIAs and strokes in the central system and cool, painful cyanotic toes in the peripheral system

2. The classic presentation is sudden onset of a small painful area on the foot, typically the toe, which is cyanotic and tender

3. Management is aimed identifying and removing proximal source of atheroembolism. Angiography is the most accurate diagnostic method determine the source of emboli

C. Arterial Thrombosis

1. Approximately 50% of acute arterial occlusions are caused by

thrombosis 2. In patients with limb-threatening ischemia, angiography is

required to evaluate if emergency bypass is an option 3. Management

a. Systemic heparinization should be started b. Direct or Fogarty catheter embolectomy c. Primary amputation if too ill, irreversible ischemia d. Non-limb threatening should be managed nonoperatively with

heparin and consideration of intraarterial fibrinolytic therapy Vascular Abnormalities Caused by Drug Abuse

D. IV or intraarterial injuries may result in acute arterial ischemia, infected pseudoaneurysms, lymphatic obstruction or direct

Notes


neurologic injury

E. Distal ischemia after intraarterial injection most often occurs in the upper extremity after injection of the brachial or radial artery 1. Severe, burning pain at the time of injection is a characteristic

hallmark 2. Painful, edematous upper extremity with patchy blue-purple skin

discoloration 3. Distal pulses usually present but extremity is cool

F. Infected pseudoaneurysms have a painful mass develop several days to weeks after injection 1. Usually pulsatile 2. Associated bruit in ½

G. Management

1. Primarily conservative for acute ischemia as other interventions have shown not to be of use. Gradual resolution of symptoms without surgery is the most common outcome

2. Infected pseudoaneurysms require resection, debridement of infected tissue, and ligation of the proximal and distal unaffected arteries

Heart Failure I. EPIDEMIOLOGY

A. 5 million patients (2.2% of U.S. population) currently diagnosed

with heart failure (HF) and 550,000 new cases per year

B. Most common reason for hospital admission in patients >65 years old in whom the incidence is 10 per 1000

C. Direct cost costs of heart failure in 2004 was 28.8 billion dollars

D. 5 year mortality of 50%

II. PATHOPHYSIOLOGY

A. By definition cardiac output is decreased as a result of impaired myocardium

Notes


B. Contractility preload and afterload determine ventricular stroke volume

C. Heart rate (HR) and stroke volume (SV) determine cardiac output

(CO): [HR x SV = CO]

D. Usually, some myocardial injury or stressor typically induces HF

1. This activates endogenous biochemical pathways in an initial attempt to maintain adequate circulation a. Renin-angiotensin-aldosterone system (RAAS)

i. Decreased renal artery perfusion leads to rennin release by the kidneys

ii. Renin converts circulating angiotensinogen to angiotensin I

iii. Circulating angiotensin-converting enzymes (ACE) released by the vascular endothelium convert angiotensin I to angiotensin II

iv. Angiotensin II is a potent vasoconstrictor and stimulates the release of aldosterone by the adrenal cortex

v. Aldosterone promotes sodium and water reabsorption 2. Counterregulatory vasodilators are released by the failing heart

which includes B-natriuretic protein and atrial natriuretic peptide. They promote sodium excretion, decrease vascular resistance, and act to decrease levels of aldosterone

3. While CO may be maintained, it is at the cost of increased systemic vascular resistance and elevated intra-cardiac pressures

4. This cascade makes the heart more prone to subsequent dysfunction

5. Pulmonary edema: a. Results from elevated pulmonary hydrostatic pressure that

forces plasma ultrafiltrate across the capillary membrane into the interstitium

b. Normally, fluid in the interstitial space is cleared by the lymphatic system, however in heart failure the fluid in interstitial space overwhelms the lymphatic system causing pulmonary edema

c. Cardiac filling pressures are increased, the myocardium is unable to compensate, and hence pulmonary congestion and dyspnea result

d. Catecholamine levels and vascular resistance are increased e. Increased BP and afterload, further LV dysfunction, and

progressive increases in filling pressures with more pulmonary congestion

E. The body tries to compensate for decreased cardiac output by:

Notes


1. Increasing SV a. SV is directly affected by changes in preload, afterload and

contractility 2. Increasing HR 3. Increasing SVR 4. Cardiac hypertrophy: this is the primary mechanism of the heart

to compensate for pump failure 5. Neurohumoral responses

a. Renal: decreased GFR leads to activation of ACE and vasoconstriction

b. Central and autonomic: ADH release causes vasoconstriction and renal water retention. Increased catecholamine levels cause increased HR, BP and vascular tone

c. Cardiac neurohormonal response: increased atrial volume causes release of atrial natriuretic peptide (ANP), which causes inhibition of the renin-angiotensin-aldosterone system (RAAS). This causes some vasodilation and improves the ability to excrete salt. This system is overwhelmed when HF becomes severe

III. CLASSIFICATION OF HEART FAILURE

A. Right Sided vs. Left Sided

1. Fluid accumulation “behind” the involved ventricle is responsible for many of the clinical manifestations

2. LV failure leads to primarily to pulmonary congestion with symptoms of orthopnea and dyspnea

3. RV failure leads to systemic venous congestion with such findings of elevated JVP, pedal edema and hepatic congestion

4. The two sides are however connected and eventually output from the two chambers equal

B. Systolic vs. Diastolic Failure

1. Systolic failure refers to impairment of contractility and usually

caused by myocyte destruction (MI, myocarditis) 2. Diastolic failure indicates a primary problem with the ventricles

to relax and fill normally (hypertrophic and restrictive cardiomyopathies)

3. Usually there is a component of both systolic and diastolic dysfunction

C. Forward vs. Backward Failure

1. Forward indicates inadequate systemic perfusion resulting from

low CO

Notes


2. Backward refers to symptoms of back pressure that “builds” behind the affected chamber

D. Output failure 1. Low output failure occurs when there is an inherent problem with

myocardial contraction 2. High output heart failure when functionally normal myocardium

cannot meet the excessive systemic demands (i.e. anemia, beriberi etc)

IV. CAUSES OF HEART FAILURE

A. Left

1. Ischemic heart disease 2. Hypertension 3. Valvular disease (aortic or mitral) 4. Idiopathic dilated cardiomyopathy 5. High output states (anemia, thyrotoxicosis, AV fistula, Paget’s) 6. Congenital heart disease

B. Right

1. LV failure (most common) 2. Pulmonary arterial hypertension 3. Valvular (tricuspid or pulmonic) 4. Myocarditis 5. RV infarction 6. PE 7. COPD

V. CLINICAL EVALUATION OF PATIENTS IN HEART FAILURE

A. Precipitating Causes of Acute Heart Failure

1. Myocardial ischemia or infarction 2. Noncompliance with medications 3. Dysrhythmias 4. Dietary indiscretion 5. Administration of drugs which impair cardiac function (beta-

blockers/CCB) or result in sodium retention (NSAIDs) 6. Increased baseline metabolic needs

a. Infection b. Trauma c. Pregnancy d. Environmental

Notes


e. Emotional 7. COPD 8. Cardiac disease progression 9. Acute valvular dysfunction

a. Aortic stenosis b. Aortic insufficiency c. Aortic dissection d. Mitral stenosis e. Mitral regurgitation f. Infectious endocarditis

10. PE

B. Symptoms

1. SOB, PND/orthopnea 2. Cough 3. Fatigue/weakness 4. Anxiety 5. Nocturia

C. Signs

1. Tachypnea 2. Tachycardia 3. Pale, clammy, skin 4. S3 (↓ ventricular compliance) or S4 5. JVD/Hepatojugular reflux 6. Pulsus alternans 7. Pleural effusion

D. ECG and Laboratory Evaluation

1. ECG and cardiac monitor

a. Pivotal for acute MI or rhythm disturbance b. Can assess electrolyte disorders and potential drug toxicity

(junctional rhythm with digoxin toxicity) 2. Laboratory

a. Cardiac markers to look for infarction b. Specific drug levels if required (digoxin, protime) c. CBC to look for anemia d. Electrolytes e. ABG: most patients have a component of lactic acidosis as

well as concomitant respiratory alkalosis. Once the respiratory reserve is compromised, a respiratory acidosis ensues

f. B-type natriuretic peptide i. B-type natriuretic peptide (BNP) is a polypeptide secreted

Notes


by the cardiac ventricles as a result of ventricular volume expansion and pressure overload

ii. N-terminal Pro-BNP (NT-pro-BNP) is a pre-pro-hormone BNP that is cleaved into active BNP; measurements correlate with BNP activity

iii. BNPs result in vasodilation, decreased aldosterone levels, inhibition of the renin-angiotensin-aldosterone system (RAAS), and decreased activity of the sympathetic nervous system

iv. Measuring the BNP or the NT-pro-BNP level improves diagnostic accuracy in dyspneic ED patients with suspected HF as it correlates well with cardiac function. In this manner, if a dyspneic patient has abnormal BNP, consider other causes of SOB

v. Actual BNP levels correlate with prognostic information (very high levels predict higher 6-month mortality and higher readmit rate)

vi. Serial BNPs can be used to monitor adequacy of HF therapy

vii. A rising BNP level post MI is strong indication of MI within the next year

3. Chest X-ray a. Poor sensitivity and specificity for all findings

i. Up to 53% of ED patients with mild to moderate elevated PCWP have no findings of pulmonary congestion on chest X-ray

b. Cardiomegaly is the first X-ray abnormality c. Vascular redistribution with a prominence of the pulmonary

vessels in the apices (cephalization). Usual PAWP 12-18 mm Hg

d. Enlargement of pulmonary vessels associated with Kerley B lines (horizontal markings at the periphery of lung fields) are also present. PAWP 18-25 mm Hg

e. Frank pulmonary edema occurs first in perihilar regions then progresses to “whiteout” the lungs. PAWP >25 mm Hg

4. Echocardiography a. The gold standard for confirming the presence of HF b. Provides information about contractility, chamber

size, valve status and ejection fraction VII. TREATMENT OF HEART FAILURE

A. Acute Pulmonary Edema

1. Place patient in sitting position with legs dependent 2. Oxygen (via high-flow mask) is the most important immediate

therapy

Notes


3. IV/monitor/pulse oximeter 4. Nitrates

a. Relaxes vascular smooth muscle b. At lower doses, primarily a venodilator but at higher doses

causes arterial dilation and thus decreases both preload and afterload

c. This improves pump function and decreases myocardial oxygen demands

d. IV nitroglycerin is a titratable agent with rapid onset and offset of action.

e. Hypotension is the most common adverse effect and may be transient; if persistent most likely due to volume depletion or right ventricular infarct

5. Morphine a. Reduces pulmonary congestion through a central

sympatholytic effect that causes peripheral vasodilation b. Potent sedative and analgesic that acts to calm the patient

down, relieve ischemic chest pain and reduce circulating catecholamines

c. No adequate studies demonstrating efficacy in acute decompensated heart failure; offers little benefit beyond oxygen, nitrates and diuretics

d. Avoid in patients with diminished respiratory effort or altered sensorium

e. Complications include hypotension, hypoventilation, sedation and nausea/vomiting

6. Loop Diuretics a. Work through inhibition of sodium resorption of the

ascending limb of the loop of Henle b. Also works in the first 30 minutes primarily by neuro humeral

mechanisms. This causes both a vasodilator (promotes both prostaglandin and NP secretion) and a vasoconstrictor (stimulating renin release)

c. For acute decompensated heart failure, diuretics should be administered intravenously

d. Diuretic response correlates with prognosis e. Aggressive diuresis can result in severe hypokalemia

7. Nitroprusside a. Potent titratable direct smooth muscle relaxing agent b. Balanced vasodilating effect so that both preload and

afterload are reduced c. Potential for “coronary steal” where less diseased vessels

dilate than diseased vessels and therefore more blood flow to these areas

d. Cumbersome setup that requires continuous invasive hemodynamic monitoring and potential for thiocyanate poisoning

Notes


8. Nesiritide a. First medication approved for HF by USFDA in over a

decade b. It is the recombinant DNA of endogenously produced B-

natriuretic peptide c. Represents an amplification of the natural compensatory

mechanism for neurohormonal and hemodynamic derangements i. Neurohormonal: serves as a counterpoint to renin-

angiotensin-aldosterone system (therefore diuresis) and antagonizes the sympathetic system

ii. Hemodynamic: causes vasodilation of both the systemic veins and arteries. Therefore a rapid and predictable decrease in right atrial pressure and PAWP. This causes an increase in the cardiac output

d. Overall Effects i. Decreases preload ii. Decreases afterload iii. Vasodilator (including coronary arteries) iv. Promotes free water loss v. Promotes sodium loss vi. Not arrhythmogenic vii. Not inotropic

e. Recent meta-analyses have questioned the safety of nesiritide, with greater mortality and renal failure noted. In 2005, an industry sponsored expert panel determined there was insufficient data to make recommendations regarding the adverse effects of nesiritide

9. Inotropic Therapy a. In the short term, these effects improve cardiac output and are

used most frequently as a bridge to definitive therapy. b. Hypotensive heart failure is probably the greatest clinical

management challenge in our specialty. All aspects of pathophysiology and pharmacology must be utilized for optimum patient management

c. Hypotension and heart failure may be attempted to be treated by a combination of both dopamine and dobutamine

d. Dopamine i. Dose dependent effects

• <20 mcg/kg/min, dilates renal, cardiac and splanchnic vessels

• 2.5-5 mcg/kg/min, beta-1 effects predominate • 5-10 mcg/kg/min, alpha and beta-1 • >10 mcg/kg/min, alpha predominates

e. Dobutamine i. Primarily a beta-1 agonist with some weak beta-2

stimulation

Notes


ii. Net effect increases cardiac output and lowers systemic vascular resistance, with little change in the BP. • Reduces wedge pressure • Increases cardiac index • Increases HR • Decreases SVR • Neutral if effect on BP

10. Noninvasive Respiratory Therapy a. Continuous positive airway pressure (CPAP) applied by tight

fitting face mask and biphasic positive airway pressure (BiPAP) applied via a plastic molded nasal mask increase functional residual capacity, reduce work of breathing, and result in decreased LV preload and afterload

b. Result in more rapid restoration of normal vital signs and oxygenation and fewer intubations

B. Treatment of Chronic Heart Failure

1. ACE-Inhibitors

a. Cornerstone of pharmacological therapy for HF b. All patients without contraindications to these agents should

be prescribed c. Decrease the overall mortality rate and combined end-point of

death d. Suppress levels of angiotensin II as well as decreasing

aldosterone production as well as augmenting levels of endothelium-protective bradykinins

2. Nitrates a. Improve exercise tolerance in chronic heart failure b. Improves mortality when combined with hydralazine

3. Diuretics a. Patients with chronic heart failure exhibit a reduced ability to

excrete a sodium and water load, with abnormal cardiac and hemodynamic adaptations to salt excess.

4. Loop diuretics remain the most commonly used a. For severe heart failure (Class II or IV), spironolactone in

combination with ACEI, beta-blockers, digoxin and diuretics showed a mortality reduction of 30%

5. Digoxin a. Improves clinical symptoms when therapy with ACEI’s and

beta-blockers is initiated b. Does not reduce mortality, but does decrease symptoms and

the incidence of hospitalization c. Multiple drug interactions

6. Beta-blockers a. Once contraindicated in HF, beta-blockers currently are

advocated for management of patients with HF due to

Notes


impressive mortality reduction data b. One study showed a 34% decreased mortality at one year

with metoprolol use added to HF regimen c. Probable reduction of sympathetic nervous system activity is

the major benefit

C. Therapeutic Approaches to be Avoided in Heart Failure

1. Calcium Channel Blockers a. Short term use may result in pulmonary edema and

cardiogenic shock b. Long-term use may lead to worsening CHF and death

2. NSAIDs a. Inhibit effects of diuretics and ACEIs, and can worsen cardiac

and renal function 3. Antiarrhythmics

a. Heart failure patients are extremely sensitive to pro-arrhythmic and cardio depressant effects of the antiarrhythmics

b. Suppression of asymptomatic ventricular arrhythmias are usually unnecessary

c. Class I antiarrhythmics (procainamide and quinidine) should not be used in HF, except for immediate treatment of life-threatening ventricular arrhythmias.

d. Amiodarone is not recommended for routine use to prevent sudden death inpatients already treated with mortality reducing drugs (ACEIs and beta-blockers)

Notes


CHF/HYPERTENSION/PVD

PEARLS

Hypertensive Disease 1. Hypertensive emergencies are not classified by absolute blood pressure but by damage to end organs (brain, heart and kidney). 2. Remember to understand the cerebral autoregulation of blood pressure. 3. Ischemic strokes rarely need acute blood pressure reduction. 4. For intracranial bleeds a cautious reduction of blood pressure to a diastolic blood pressure <120 mmHg is an option. 5. Acute coronary syndrome patients should have their blood pressures reduced with both nitrates and beta-blockers. 6. Heart failure patients should be treated with nitroglycerin (first and in high doses), diuretics, and oxygen in the immediate resuscitative phase. 7. Aortic dissection patients must have the slope of the change of pressure over time graph flattened by nitroprusside (blood pressure) and esmolol (heart rate) or by labetalol (both BP and HR). 8. Preeclamptic and eclamptic patients should be treated with magnesium and hydralazine. 9. Nifedipine has no role for BP management in either the emergent or urgent settings. 10. For all cases, avoid overshooting BP reductions. This can lead to other end organ damage and an entirely new group of morbidity and mortality. Use titratable meds with short half-lives. 11. Patients without acute end-organ damage rarely require urgent management of their blood pressure and may be safely referred for close follow-up.

Peripheral Vascular Disease

1. Limb threatening ischemia from embolism→ immediate vascular surgery referral for Fogarty catheter embolectomy. 2. Limb threatening ischemia from thrombosis→immediate vascular

Notes


surgery referral for direct or Fogarty embolectomy combined with vascular bypass grafting. 3. Lesion that can’t be bypassed, irreversible ischemia or too ill→immediate vascular surgery consult for primary amputation. 4. Non-limb threatening ischemia from embolism→Fogarty embolectomy. 5. Non-limb threatening ischemia from thrombosis→systemic heparinization with consideration of intraarterial thrombolysis. Heart Failure

1. Don’t label a patient “congestive heart failure” without focusing on the reason why they are in this clinical situation. 2. For patients with known heart failure that present in acute decompensation, look for the reason for this decompensation and treat accordingly. 3. Always think of acute ischemic coronary disease as a primary reason for heart failure. 4. Cardiogenic shock and heart failure have a very high mortality rate despite appropriate medical management. 5. Management of acute pulmonary edema should include: A. Oxygen: High flow mask with early consideration BiPAP or CPAP B. Nitroglycerin (SL to start then titrate with IV at appropriately high doses to affect afterload) C. IV diuretics

Notes


REFERENCES

Hypertension . 1. Maisel JA, Hypertensive emergencies, Emergency Medicine Just the

Facts, Ma OJ-editor, second edition, pp 115-118, 2004. 2. Gray RO . Hypertension. Emergency Medicine: Concepts and Clinical

Practice, Rosen-editor, 7th Edition, pp 1075-1087, 2010. 3. Wu M, Chanmugam A. Hypertension, Emergency Medicine: A

Comprehensive Study Guide, Tintinalli-editor, 6th edition, pp 394-404, 2004.

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hypertension: what to treat, who to treat, and how to treat. Med Clin N Am. 2006; 90:439-451.

5. Vaidya CK, Ouellette JR. Hypertensive urgency and emergency.

Hospital Physician. 2007; 3:43-50. 6. Kamalakannan D, Rosman HS, Eagle KA. Acute aortic dissection. Crit

Care Clin. 2007; 23:779-800. 7. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the

Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC7 report. JAMA. 2003; 289:2560.

8. Chiang W. Asymptomatic hypertension in the ED. Am J Emerg Med.

1998; 16:1701. 9. Gilmore RM, Miller SJ, Stead LG. Severe hypertension in the

emergency department patient. Emerg Med Clin N Am. 2005; 23:1141-1158.

Peripheral Vascular Disease 1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Guidelines for

the management of patients with peripheral artery disease (lower extremity, renal, mesenteric, and abdominal aorta): executive summary. JACC. 2006; 47(6):1239-312.

Notes


2. Aufderheide TP. Peripheral Arteriovascular Disease. Emergency Medicine: Concepts and Clinical Practice, Rosen-editor, 7th Edition, pp 1103-1123, 2010.

3. Anand SS, Creager MA. Peripheral arterial disease. Am Fam Physician. 2002; 65(11):2321-2,.

4. Chopra A: Thrombophlebitis and occlusive arterial disease, Emergency

Medicine: A Comprehensive Study Guide, Tintinalli-editor, 6th edition, pp 415-418, 2004.

5. Kabrhel C, Peripheral vascular disorders, Emergency Medicine Just the

Facts, Ma OJ-editor, second edition, pp 121-124, 2004. 6. Hiatt WR. Medical treatment of peripheral arterial disease and

claudication. N Engl J Med. 2001; 344:1608-1621. 7. Dinh T, Scovell S, Veves A. Peripheral artery disease and diabetes: a

clinical update. Int J Low Extrem Wounds. 2009; 8:75-81. 8. Hankey GJ, Norman PE, Eikelboom JW. Medical treatment of peripheral

artery disease. JAMA. 2006; 295(5):547-553. 9. Khan NA, Rahim SA, Anand SS, et al. Does the clinical examination

predict lower extremity peripheral artery disease? JAMA. 2006; 295(5):536-546.

10. Sontheimer DL. Peripheral vascular disease: diagnosis and treatment. Am

Fam Physician. 2006; 73:1971-6. Heart Failure 1. Peacock WF: Congestive heart failure and acute pulmonary edema,

Emergency Medicine: A Comprehensive Study Guide, Tintinalli-editor, 6th edition, pp 364-372, 2004.

2. Silvers SM, Howell JM, Kosowsky JM, et al. Clinical Policy: critical

issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med. 2007;49:627-669.

3. Pfisterer M, Buser P, Rickli H, et al. BNP-guided vs. symptom-guided

heart failure therapy: the trial of intensified vs. standard medical therapy in elderly patients with congestive heart failure (TIME-CHF) randomized trial. JAMA. 2009; 301(4):383-392.

Notes


4. Wang CS, FitzGerald JM, Schulzer M, et al. Does this dyspneic patient

in the emergency department have congestive heart failure? JAMA. 2005;294:1944-1956.

5. Braunwald E. Biomarkers in heart failure. N Engl J Med.

2008;358:2148-59.

6. Onwuanyi A, Taylor M. Acute decompensated heart failure: pathophysiology and treatment. Am J Cardiol. 2007;99[suppl]:25D-30D.

7. Collins S, Storrow AB, Kirk JD, et al. Beyond pulmonary edema:

diagnostic risk stratification, and treatment challenges of acute heart failure management in the emergency department. Ann Emerg Med. 2008;51:45-57.

8. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic

peptide in the evaluation and man agent of acute dyspnea. N Engl J Med. 2004;350:647-54.

9. O’Brien JF, Falk JL: Heart Failure, Emergency Medicine: Concepts

and Clinical Practice, Rosen-editor, 7th Edition, pp 1036-1053, 2010. 10. Miller C. Congestive heart failure and acute pulmonary edema,

Emergency Medicine Just the Facts, Ma OJ-editor, second edition, pp 99-101, 2004.

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chf/hypertension/pvd...and eclampsia are true hypertensive emergencies c. both of these conditions...

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