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Morning Report. Nikhil Jariwala Dr. Ward July 12, 2010. MKSAP.

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morning report

Morning Report

Nikhil Jariwala

Dr. Ward

July 12, 2010

mksap
MKSAP
  • A 52-year-old woman presents to the emergency department for ongoing substernal chest pressure associated with nausea, diaphoresis, and lightheadedness. Her symptoms began 3 hours ago. She has hypertension and hypercholesterolemia. Her daily medications are hydrochlorothiazide, pravastatin, and aspirin.
  • On physical examination, her blood pressure is 84/62 mm Hg, pulse is 88/min, and respiration rate is 20/min. Her BMI is 29. Cardiac auscultation reveals distant heart sounds with an S4. The lungs are clear bilaterally; estimated central venous pressure is 9 cm H2O. The extremities are cool.
  • Electrocardiogram with right-sided precordial leads is done. (Leads V1 through V6 are recorded from the right side of the chest.)
which of the following should be given next in the treatment of this patient
Which of the following should be given next in the treatment of this patient?
  • A. Dobutamine intravenously
  • B. Metoprolol intravenously
  • C. Nitroglycerin sublingually
  • D. 0.9% saline intravenous bolus
slide5

hypotension, clear lung fields, and elevated estimated central venous pressure represent the classic triad of RV myocardial infarction.

  • The most predictive finding is ST-elevation on right-sided lead V4R. Therefore, all patients with an inferior STEMI should have a right-sided ECG performed.
  • RV contractility is reduced, resulting in higher RV diastolic pressure, lower RV systolic pressure, and reduced preload or filling of the LV. Volume expansion improves the hemodynamic abnormalities of RV MI because the gradient of pressure maintains filling of the LV
  • In addition to reperfusion therapy for STEMI, the acute treatment of RV MI is supportive. Volume expansion is the primary supportive treatment.
  • Inotropic support, specifically using intravenous dobutamine, is appropriate treatment in patients with RV MI whose hypotension is not corrected after 1 L of saline infusion.
slide7

History of Present Illness

  • At work, patient felt flushed, light-headed, diaphoretic. He got up to walk outside and lost consciousnesses for a few seconds; co-workers caught him.
  • Upon waking up, continued to feel diaphoretic and flushed for 2-3 minutes before symptoms resolved.
  • No chest pain, SOB, palpitations, tonic-clonic movements, incontinence, post-ictal period, tongue biting, fevers, chills, recent illness.
  • EMS was called and he was brought to the Emergency Room
slide8

Patient History

Past Medical History:

HTN

Medications:

Lisinopril/HCTZ

Allergies:

NKDA

Family History:

Mother died age 63 from unknown cause

Father died age 82 from lung cancer

No cardiac disease or sudden cardiac death

Social History:

Smoked 1 ppd x 12 years, but quit 24 years ago

Social drinker

No illicits

slide10
Syncope = sudden, brief LOC with a loss of postural tone with spontaneous recovery

Can be precipitated by pain, exercise, micturition, defecation, or stressful events

Often associated with prodromal symptoms (sweating and nausea)

Not to be confused with:

“Drop attacks” = falls without LOC

Dizziness and vertigo typically do not result in LOC or loss of postural tone

Seizures have disorientation after the event, slowness in returning to consciousness, and unconsciousness lasting more than five minutes

Both syncope and seizures can have associated rhythmic movements

Definition of Syncope

slide11

Causes of Syncope

  • Cardiac
    • Organic heart disease (4%)
      • Aortic stenosis, Hypertrophic cardiomyopathy
      • Pulmonary embolism
      • Pulmonary hypertension
      • Myxoma
      • Myocardia infarction; Coronary spasm
      • Tamponade
      • Aortic dissection
    • Arrhythmias (14%)
      • Bradyarrhythmias
        • Sinus node disease
        • 2nd- or 3rd-degree heart block
        • Pacemaker malfunction
        • Drug-induced
      • Tachyarrhthmias
        • Ventricular tachcardia
        • Torsades de pointes
        • Supraventricular tachycardia
  • Reflex Mediated
    • Vasovagal (18%)
    • Situational (5%)
      • Cough
      • Micturition
      • Defecation
      • Swallow
    • Other (1%)
      • Carotid Sinus
      • Neuralgia
  • Orthostatic hypotension (1%)
  • Medications (3%)
  • Psychatric (2%)
  • Neurologic (10%)
    • Migraines
    • TIA
    • Seizures
    • Subclavian steal
  • Unknown (34%)

Source: From five population-based studies between 1984-1990. Ann Intern Med. 1997 Jun 15; 126(12): 991.

slide12

Physical Exam

VITALS: T 36.3, P74, R 21, BP 123/83, O2 99% RA

Sitting BP 117/71, P 71; Standing BP 128/82, P 88

GEN: Well appearing, NAD, A&Ox3

HEENT: EOMI, PERRLA, no lymphadenopathy

CV: RRR. Normal S1 and S2. No M/R/G. No JVD. No edema.

PULM: CTAB. No wheezes, rhonchi, or rales.

GI: S/NT/ND. Normal bowel sounds. No hepatosplenomegaly. Small umbilical hernia.

MSK: Normal bulk and tone. 5/5 strength all extremities

SKIN: No rashes or lesions

NEURO: CN II-XII intact. Sensation intact to light touch. Normal finger-to-nose, heel-to-shin. Normal gait

PSYCH: Normal mood and affect

slide13

Orthostatic Hypotension

  • Definition: within 2 to 5 minutes of quiet standing, one or more of the following is present
    • At least a 20 mmHg fall in systolic pressure
    • At least a 10 mmHg fall in diastolic pressure
    • Symptoms of cerebral hypoperfusion
slide15

It depends on what you find…

  • History and Physical guide your choice of tests!
    • History:
      • Postural symptoms, exertional symptoms, family history, palpitations, postictal symptoms, situational symptoms, use of medication, history of organic heart disease, and witness account
    • Physical:
      • Focus on cardiovascular, neurologic, and orthostatic vitals
  • Check an EKG in all patients
  • Routine use of basic labs is not recommended
  • If patient has neurologic symptoms (seizures, focal neurologic deficits), check EEG, CT/MRI, carotid dopplers
  • If you suspect exercise-associated syncope, check exercise stress test AFTER echocardiography (to rule out hypertrophic cardiomyopathy)
  • If you suspect arrhythmia, consider inpatient telemetry vs 24-hour holter monitoring
  • If the patient has unexplained recurrent syncope for which cardiac causes have been excluded, consider passive upright tilt-table testing
slide18

7.6 4.6

  • 137 101 21
  • 3.5 23 1.1

1.7 0.3/1.4

12.0

9.1

26 36

35.0

67

Labs

CK 79

MB 2.1

Trop <0.03

195

135

slide19

To Admit, or Not To Admit,

  • That is the Question…
slide20

Common Reasons to Admit

  • Admit for Diagnostic Evaluation
  • Structural heart disease
  • Symptoms suggestive of arrhythmias or ischemia
  • Electrocardiographic abnormalities
  • Neurologic disease
  • Admission for Treatment
  • Structural heart disease
  • Orthostatic hypotension
  • Older age
  • Discontinuation of offending drug or modification of dose
slide21

San Francisco Syncope Rules

(SFSR)

Clinical prediction tool to determine short-term (7day) outcome of patients presenting to ER with syncope

Serious outcomes included: death, MI, PE, arrhythmia, stroke, subarachnoid hemorrhage

Source: Ann Emerg Med. 2004 Feb; 43(2): 224-32.

slide22

San Francisco Syncope Rules

Congestive heart failure

Hematocrit <30%

EKG abnormalities

Shortness of breath

Systolic BP<90

Any patient with one positive item is at high risk for serious outcome

Sensitivity 96%

Specificity 62%

slide23

The plot thickens…

In the Emergency Room, the patient complains of abdominal pain and becomes diaphoretic and pre-syncopal.

Vitals are obtained: HR 43, BP 63/41

You obtain an EKG…

slide25

ACLS Bradycardia Algorithm

Source: “Management of Symptomatic Bradycardia and Tachycardia.” Circulation. 2005 Nov; 112; IV-68.

slide26

He receives 0.8mg IV atropine which improves his HR to 87 and his BP135/87.

Mental status improves and diaphoresis resolves.

The patient is admitted to Cardiology

slide27

More Labs/Studies

Lipase 120

Acute hepatitis panel: Non-reactive

RPI: 0.9

LDH 360

Haptoglobin 137

CT Angio Chest/Abdomen: No aortic dissection or aneurysm. Focal pancreatitis of tail without complication. Cholelithiasis without inflammation.

slide29

Studies

TTE: LV EF 61%, no wall motion abnormalities. LV and RV normal size and performance. No significant valvular disease

Exercise SPECT: SSS 8. Duke treadmill prognostic index 7 (low-risk). Mildly abnormal perfusion scintigraphy with evidence for mild exercise-induced completely reversible myocardial ischemia in multivessel distribution.

slide30

Vasovagal Syncope

  • Vasovagal syncope (aka neurally mediated syncope or neurocardiogenic syncope) occurs as a reflex response leading to vasodilatation and bradycardia which causes hypotension and cerebral hypoperfusion.
    • Occurs with the activation of receptors in ventricular wall or in other organs (bladder, carotid sinus, etc.)
    • Response to receptor activation is reflex increase in vagal efferent activity and subsequent sympathetic withdrawal.
  • Head-up Tilt-Table testing can be used to diagnose unexplained recurrent vasovagal syncope
    • Patients start with passive upright tilt-table testing at 60 degrees for 45 minutes
    • If test is negative, can repeat with isoproterenol
take home points
Take home points
  • History and physical are crucial for determining cause of syncope and further diagnostic workup
  • Always get an EKG!
  • Tilt table testing can help diagnose neurocardiogenic syncope when not clear based upon initial evaluation and ruling out neurocardiogenic syncope is important
  • Admit syncope patients who meet the CHESS Criteria/ San Francisco syncope rules
slide32

Hospital Course

  • We suspected the patient’s pancreatitis  vasovagal syncope  bradycardia episodes.
  • Patient was monitored on telemetry and had no more arrhythmias during his stay.
  • Electrophysiology was consulted regarding the bradycardia. They felt no pacemaker was indicated at this time.
  • For his pancreatitis, he was kept NPO initially and diet was advanced slowly. His abdominal pain improved.
  • The patient was discharged home with a 30-day event monitor.
  • He followed up in cardiology 3 weeks after discharge and had no further events
slide33

Works Cited

Kapoor, WN. “Syncope Review Article.” NEJM. 2000 Dec 21. 343(25):

1856-62.

Linzer, M; Yang, EH; et al. “Diagnosing Syncope. Part 1: Value

of History, Physical Examination, and Electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians.” Ann Intern Med. 1997 Jun 15; 126(12): 989-96.

Linzer, M; Yang, EH; et al. “Diagnosing syncope. Part 2: Unexplained

Syncope.” Ann Intern Med. 1997 Jun 15; 127(12): 76-86.

“Management of Symptomatic Bradycardia and Tachycardia.” Circulation.

2005 Nov; 112; IV-67-77.

Quinn, JV; Stiell, IG; et al. “Derivation of the San Francisco Syncope Rule to

predict patients with short-term serious outcomes.” Ann Emerg Med. 2004 Feb; 43(2): 224-32.