Hospitalist housestaff handbook

The prior editors of the Handbook, as well as C. Alex Wiles, MD the 2 nd edition's editor-in-chief, whose guidance was instrumental in the transition between editions. Michael J. Nitropaste see Sliding Scales: Nitropaste. If patient is not already on aspirin and has no contraindications, have patient chew and swallow ASA mg.

Arrange for emergent CT scan or echo and call vascular surgery. If pneumothorax suspected, get CXR and call surgery for chest tube placement. Insert a 14 gauge angiocath into the 2nd intercostal space at the midclavicular line on the side of the pneumothorax.

Begin anticoagulation if there are no contraindications while you are waiting for the results. Be sure to obtain post-pain ECG and document the event. Lee TH, Goldman L.

Evaluation of the patient with acute chest pain. Normal urine output is typically at least 0. First, do you believe the numbers? Look for daily weights. Examine the patient and assess volume status.

The abrupt absence of urine output altogether anuria most often suggests obstructive uropathy. Rule out obstructive uropathyearly by checking a post—void residual by inserting Foley after patient voids. Some reasons for urinary retention include prostatic hypertrophy, anticholinergic side—effects of medications narcotics, Benadryl, anesthetics, etc.

Work-up: Renal failure is caused by prerenal, renal, and postrenal causes. Many laboratory indices exist to differentiate these see Renal: Acute Reversible Renal Dysfunction , but if patient is not volume overloaded or obstructed and has no history of CHF, then a fluid challenge is usually appropriate cc NS IV bolus. If they respond, however, your job is not quite done yet. Do the workup described under the Renal section.

If patient is in CHF or is volume overloaded, initiate diuresis. Remember, though, that unless the patient is truly volume overloaded, diuresis just for the sake of increasing urine output is pointless—treat the patient, not the numbers.

Sometimes patients in renal failure can still respond to high dose furosemide while waiting for the renal consult mg IV slowly. Complications: acute oliguria is associated with higher rates of infection, gastritis, GI bleeding, AMS, and arrhythmias. Klahr S, Miller SB. Acute oliguria. If there is any question of physical injury, call security. No matter how many years of commando training you have, it is not your responsibility to restrain patients in a safe manner.

Also, patients generally tend to calm down for the most part when they are confronted by overwhelming numbers of people who are responsive to their needs or anxieties. Try to do as much of an altered mental status workup as you can see Neurology: Altered Mental Status. If you suspect an underlying reason for the agitation pain, sundowning, hypoxia, medication , then obviously treat the underlying reason. If you feel physical restraints are needed, there are always forms that need to be completed specifying the type of restraint and the reasons for initiating.

They must be renewed every 24 hours. Generally, try to initiate the least restrictive type of restraint; after all, would you want to be tied down? Further, restraints have actually been shown to increase the rate of falls and injuries in delirious patients.

Four point cloth restraints limit the movement of arms and legs. They are more restrictive than a Posey but may be necessary if patient is pulling out lines, etc. ICU psychosis: poor terminology because altered mental status in the ICU is no different from delirium in any other hospitalized patient.

Be sure to fully evaluate any significant change in the mental status of your ICU patients. Common causes include: Metabolic disturbances: provide adequate nutrition and treat underlying metabolic derangement. Electrolyte imbalance: monitor and treat as indicated. Withdrawal syndromes: often missed; treat as indicated. Acute infection: search for source and treat.

Head trauma, intracranial lesions: evaluate with head CT. Medications: common medications given in the ICU setting that can cause delirium: propofol, lidocaine, fentanyl, morphine, atropine, anti-convulsants, H 2 blockers, omeparzole, and virtually any antibiotic including beta-lactams, cephalosporins, macrolides, quinolones, and aminoglycosides.

Intensive care unit syndrome: a dangerous misnomer. Arch Intern Med ; Practice guideline for the treatment of patients with delirium. American Psychiatric Association. Am J Psychiatry. FALLS 1. Assess patient for any injury.

Any focality on exam must be worked up in the appropriate manner e. Try to find out the circumstances of the fall. By whom? Broad differential diagnosis, with appropriate workup. Musculoskeletal: arthritis, pain, deconditioning, weakness.

Other: anemia, poor eyesight, dim lighting, room change, bed rails left down, wet floor. If the patient has a focal neurologic deficit that is new, you must get a head CT. Indications for computed tomography in patients with minor head injury. Obtain a brief history by asking the nurse or evaluating the patient yourself to see if there is any underlying, potentially treatable problem that is causing the insomnia e.

Differential diagnosis: psychological anxiety, grief , physical pain, decreased mobility, dyspnea , delirium, infection, metabolic, polyuria diuretics given at night , incontinence, underlying medical condition, sleep apnea. Generally start with antihistamine, e. Watch out for anticholinergic side-effects, especially in older patients e. Low dose trazodone is often effective. Sedative doses usually mg po qhs prn although some patients may need up to mg.

Especially useful in elderly patients. If above ineffective, benzodiazepines are often used next. Most commonly, medium half-life benzos are used such as temazepam Restoril mg or lorazepam Ativan 0. Medication dosing: normal vs. Ativan: start at 0. Restoril: start at 15 mg, max 30 mg. If above measures do not work, you may want to evaluate patient first before giving more powerful sedatives.

In addition, in any patient in whom you think sedation is potentially dangerous e. Treatment of insomnia in hospitalized patients. Ann Pharmacother ; Cardiology Victor Cheng, M. Joshua Lehrer-Graiwer, M. Gordon Fung, M. Bed rest until ruled out yes, this means bedpan, although bedside commode OK for soft rule out. NPO except meds if possible catheterization or functional study in AM most patients. Have patient chew and swallow first dose for rapid absorption.

NTP q6h to chest wall according to sliding scale; after 24 hours, wipe off q night 12am-6am. See Sliding Scales: Nitropaste. Beta—blocker: use if there are no contraindications as numerous trials have shown a mortality benefit. Alternatively, a trial of metoprolol 5 mg IV q 5 min x 3 can be given initially.

If this IV dose is tolerated you can usually start 25 mg PO bid, but be sure to write hold parameters. Colace mg PO bid — hold for loose stools When seeing patient for persistent chest pain, can give morphine in 1—2 mg boluses. If ever in doubt, call for back-up.

Thrombolysis - Early treatment can limit infarct size, preserve LV function, and reduce mortality. Best performed within first 12 hours after onset of pain. If suspect bleed discontinue all anticoagulation, get a head CT, and call neurosurgery. Continue at 75 mg PO QD at least 30 days post-stent. Contraindications: high risk for GI bleed, known allergy, or low platelets.

Maximum weight for dosing is kg. Contraindications: see Cardiology: Contraindications to anticoagulation. Nitroglycerin: gtt infusion for persistent chest pain or pulmonary edema. Watch for hypotension! After 24 hours, give 6h holiday to prevent tolerance and consider switch to PO nitrates or nitropaste. Consider IV amiodarone for patients with resuscitated sudden cardiac death.

Further dosing dictated by clinical course. ACE-inhibitor: Start within first 24 hours with Captopril 6. Write hold parameters for BP. Obtain right-sided leads and look for ST elevation in V 4R. The RV is preload dependent, and extra IV fluids may be required to maintain cardiac output. Avoid nitrates in RV infarct. A clinical trial comparing primary coronary angioplasty with tissue plasminogen activator for acute myocardial infarction.

N Engl J Med. Categorize according to overall clinical risk: all patients are assumed to have a clinically evident acute coronary syndrome. Management — critically unstable patients: these patients should be referred urgently for cardiac catheterization.

If catheterization is unavailable and the patient does not meet criteria for thrombolysis, the patient should be transferred immediately to a facility with catheterization facilities. Placement performed by cardiology only. Patient must be on heparin. Complications include infection, hemolysis, rupture manifests as ischemic lower extremity. If unable to give enoxaparin, give unfractionated heparin infusion.

See Sliding scales: heparin. First dose must be given early in ED or at presentation for patient to derive a benefit. Continue infusion for 18 hours post-PCI. In general, these patients should be managed with an early conservative approach, which includes stress testing either as an inpatient or as an outpatient, depending on patient stability. The patient should be referred for cardiac catheterization if any of the following features are present: - Persistent or recurrent ischemia.

JAMA ; Outcomes in patients with acute NQWMI randomly assigned to an invasive as compared with a conservative management strategy. Braunwald E, Antman EM, et al. Cohen M, Demers C, et al. A comparison of low-molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation.

Smoking: all ACS patients who smoke should be counseled to quit smoking. Document this in the medical record. Diet: all ACS patients should be counseled on a diet low in saturated fat and cholesterol. Provide the patient with educational materials if available. If they are already on a statin, the dose should be increased. Always contact the primary care physician to ensure adequate follow-up care.

UCSF Guidelines for management of acute coronary syndromes. Revised June 23, The following criteria apply mainly to thrombolytics e. However, it is well worth looking over these contraindications for all forms of anticoagulation e. You must weigh the risks and benefits of anticoagulation in all patients individually. Cocaine can and does not infrequently cause real myocardial ischemia and infarction in young healthy people.

Pathophysiology: prevention of norepinephrine and dopamine reuptake leading to alpha-1 activation; increased myocardial demand increased HR and afterload ; coronary and peripheral vasoconstriction; promotes in situ thrombus formation; can lead to premature atherosclerosis and LVH. History: chest pain usually 30 minutes to 4 hours after use, but can occur up to 24 hours after use or even longer with withdrawal up to 2 weeks.

Management: no randomized controlled trials benzodiazepines, aspirin, oxygen, NTG for persistent pain, calcium channel blocker, thrombolysis vs angioplasty. The conventional wisdom is that beta-blockers should be avoided in cocaine chest pain, since they can lead to unopposed alpha-stimulation and thus, theoretically, worsening of the underlying pathophysiology. Labetalol may be of use in this situation since it is a combined alpha-1 and beta blocker.

Cardiovascular complications of cocaine use. Diagnosis with BNP: if available at your hospital, this test can be helpful in distinguishing CHF from other causes of dyspneic patients who present to the ER. The level of BNP correlates to the severity of heart failure.

If inadequate response, double the dose. Monitor for hypotension! Furosemide is effective for approximately six hours. If inadequate diuresis with furosemide alone, try adding thiazide such as HCTZ 25 mg PO qd or metolazone mg PO qd give 30 min before furosemide or consider furosemide drip.

When stable, can convert to PO nitrate eg. ACE inhibitor: proven mortality benefit - Captopril 6. Beta-blockers: - Also shown to have mortality benefit.

However, you should not start beta-blockers in the acute setting; you may even wish to hold beta-blockers in acute CHF exacerbations due to systolic dysfunction. Increase q 3 hour by 0. If hypotension occurs, the infusion should be discontinued and restarted when the blood pressure has stabilized, at a 30 percent lower dose without a repeat bolus.

Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. New therapeutic options in congestive heart failure: Part I.

Circulation ; New therapeutic options in congestive heart failure: Part II. Colucci WS, Elkayam U, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. Nesiritide Study Group. If relatively stable, control rate, anticoagulate, and then proceed to cardioversion. CVA risk appears to be much lower than other a-fib subgroups. ICU patient because half-life only 9 min.

Rebolus in 15 min PRN with 0. Load mg IV over 10 minutes. Controls ventricular rate at rest, but not during exercise. Slower onset of action than Ca-blockers and b-blockers. Load 0. Start maintenance dose at 0. Daily dose will need to be adjusted in presence of renal failure, amiodarone, etc. Usually used as adjunctive therapy — rate will not be controlled immediately if only digoxin is given! Alternatively, if no evidence of atrial thrombus on early transesophageal echocardiogram TEE , the patient can safely be cardioverted followed by anticoagulation for weeks.

In the hospital setting, anticoagulate with unfractionated heparin or enoxaparin and overlap with warfarin until therapeutic INR of is obtained. If anticoagulation is not feasible or contraindicated e. GI bleed , transesophageal echocardiogram may be used to rule out left atrial thrombus prior to cardioversion.

Predictors of success: short duration of A-fib, normal left atrial size. Pre-treatment with Ibutilide 1 mg IV may increase the likelihood of cardioversion. QTc should be monitored if using ibutilide. Patient who have been in A-fib for greater than one year, or with enlarged left atria, are less likely to convert. Most common effective agent used at is amiodarone see antiarrythmics section.

Rate control vs. Disabling stroke, hospitalizations, and new arrhythmias were less in the rate control group and at 2 years of follow up, the survival curve was slightly better for the rate control group. Falk RH. Atrial fibrillation. Am Heart J. Initial response to vasodilator challenge predicts response to long-term therapy. Works by vasodilation, inhibition of platelet aggregation, and vascular remodeling. Given by continuous IV infusion with portable pump due to short half-life minutes.

Monitor for headache, jaw pain, cutaneous erythema, diarrhea, arthralgias, catheter-related infections and thrombosis. Usually use higher doses than for systemic HTN. Used for short-term therapy at ppm. Currently limited to research. Use warfarin to achieve INR of approximately 2. Channick RN, Simonneau G, et al. Effects of the dual endothelin-receptor antagonist bosentan in patients with pulmonary hypertension: a randomised placebo-controlled study.

Rubin LJ. Primary pulmonary hypertension. Kapoor WN. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med ; Aortic stenosis: Crescendo-decrescendo systolic murmur heard best in the aortic area, radiating to the supraclavicular fossa and carotids.

Rarely heard at the apex. Pulsus parvus et tardus, S2 softens, murmur peaks later as aortic stenosis progresses. Aortic sclerosis can mimic AS murmurs very closely. Aortic insufficiency: High-pitched blowing diastolic murmur at left sternal border, 3rd or 4th interspace.

Heard best with patient sitting, leaning forward, and holding breath at end-expiration. Austin-Flint: diastolic murmur in mitral area due aortic regurgitant flow impinging anterior mitral leaflet.

Pulmonic stenosis: Systolic murmur heard in pulmonic area, transmitted to the neck or left shoulder. A2 is decreased, P2 is delayed. RVH with parasternal lift. Pulmonic insufficiency: High pitched decrescendo diastolic murmur heard in pulmonic area; often associated with pulmonary hypertension. Intensity may increase with inspiration. Mitral stenosis: low-pitched rumbling diastolic murmur heard best at apex. Opening snap sometimes present.

Mitral insufficiency: loud, high-pitched holosystolic murmur heard best at apex, radiating to the left axilla when ant leaflet incompetent or to left sternal border when pos leaflet incompetent. Soft S1. Tricuspid insufficiency: high-pitched blowing systolic murmur best heard along the lower left sternal border, radiating to the right sternal border.

Intensity increases with inspiration. Pericardial friction rub: scratchy, leathery, scraping sound heard best along the left sternal border, 3rd interspace. Usually the first two components are present. Heard best with patient leaning forward at end exhalation. Does this patient have an abnormal systolic murmur? The rational clinical examination. Does this patient have aortic regurgitation? RVH 2. Lateral or anterolateral MI 3. WPW with left freewall pathway 4.

LAFB 2. Inferior MI 3. WPW with posteroseptal pathway 4. Numbers refer to widthof Q wave in milliseconds. SVT 1. Is there absence of an RS complex in allof the precordial leads V1-V6?

Note: antiarrhythmic drugs may give a false positive diagnosis of VT, under this criteria. Is there AV dissociation or V-A block? Are there morphologic criteria for VT present? A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.

Exercise increases myocardial O2 demand and unmasks hypoperfusion in patients with CAD. There is also a high false negative rate in patients with a history of coronary artery disease. Hypokinesis and akinesis of the LV wall is highly suggestive of ischemic heart disease, and can be used to determine distribution of culprit coronary artery stenoses. Try adding contrast to obtain higher-quality images in patients with emphysema, chest wall deformities, and obesity.

Difficult to perform due to movement and respiratory artifacts during exercise. Very useful for detecting regurgitant blood flow across the valves and any abnormal communications within the heart. Doppler velocities across a valve can be converted to pressure gradients; cardiac output and pressure gradient data can be used to calculate stenotic valve area. For instance, a PFO is unmasked by seeing bubbles flowing directly from the right to left atrium.

T32 Training Program. Lupus Education Sessions. Core Center Clinical Research. Internal Medicine Residency. Program Overview. Application Information. Our Team. Current Residents. Resident Life.

Medical Students. Research Symposium. For Faculty. Grants and Contracts. Employee Recognition. Follow us on Facebook. Educational Purpose: The Hospitalist Elective at MUH is structured to give Internal Medicine residents a broad-based experience in managing acutely ill general medicine patients, consulting on surgical co-management patients, triaging ED and outside hospital admissions, and conducting preoperative evaluations.

Residents are expected to: To enhance their history taking and physical diagnosis skills. To develop differential diagnoses and formulate a treatment plan on acutely ill patients. To manage the inpatient illnesses which are commonly cared for by the hospitalist. To learn how to medically optimize and risk assess surgical patients. To co-manage surgical patients with acute and chronic medical illnesses. To perform the role of admitting officer of the day, triage admissions, and provide safe handoff.

Medical Knowledge Goals and Objectives: Goal: Residents must demonstrate knowledge of established and evolving biomedical, clinical, epidemiological, and social-behavioral sciences and apply this knowledge to patient care. The cardiologists and hospitalists round on patients together and make medical decisions collaboratively. This highly successful co-management model allows for the best possible management of these complex patients--both their general medical problems and advanced cardiac disease.

In addition to daytime responsibilities, AHF Hospitalists take turns working night shifts, cross- covering and admitting new patients to the service. In addition, they assist the Division of Cardiology with cross-coverage of the low acuity Cardiology Procedures Service, the Advanced Lung Disease service, and occasionally assist with low acuity general cardiology admissions in partnership with the Cardiology Night Hospitalist.

The AHF Hospitalist Service is dedicated to providing excellent specialized medical care to patients with cardiac disease. Please contact Aline Zorian aline. This hospitalist is responsible for admitting patients to the General Cardiology service, both in and out of the Cardiac Intensive Care Unit in a collaborative open ICU model. In addition, the Cardiology Night Hospitalist cross-covers a subset of general cardiology patients, supervises medicine housestaff on the General Cardiology Service, and participates in nighttime education of housestaff.

The hospitalist provides clinical care for a 12 hour shift and signs out to the daytime General Cardiology housestaff teams in the morning. The Cardiology Night Hospitalist works collaboratively with the Cardiac ICU team attending, fellow, NP , the on-call cardiology team attending, resident , and as needed by the AHF Hospitalist overnight to ensure outstanding medical and cardiac care for patients overnight.

To best meet the needs of our diverse patient population, trainees, and the city of San Francisco, the Division of Hospital Medicine is specifically seeking applicants who demonstrate a unique contribution and commitment to diversity.