Category Archives: #Cardiology

MR with Moyukh + Dr. Chitale: Stress Tests and Coronary Fistulas

A middle aged female with a vague history of “extra coronaries” who presents with worsening dyspnea on exertion. Her initial stress echo was negative, but when here symptoms progressed 2 years later she had an MRI which confirmed 2 extra coronary fistulas. Although she did not meet strict criteria for repair, the repair was ultimately done due to her persistent symptoms, and she is now symptom-free!
*When should we order a stress echo instead of the usual treadmill EKG stress test? 
The bottom line – for the most part, we should start with treadmill EKG tests, not exercise echoes!
-Hard indications: an uninterpretable EKG (LBBB, TWI, paced), evaluation of exercise-related LVOT, AS, and pulmonary hypertension
-Soft indications: as in this case, we sometimes order it when our pre-test probability for ACS so high that we aren’t going to believe a negative EKG treadmill
-Contraindications: baseline wall motion abnormalities, severe CHF (hard to see wall motion abnormalities) or poor images with prior echoes (as in morbid obesity), other contraindications to exercise (will need a nuclear test)
*Coronary Fistulas
What? Extra coronary arteries that connect with a) the RA/RV chamber or b) the PA, creating a L-> R shunt
Inline image 2
Why are these a problem, and how can they present?
a) they can cause ischemia by coronary steal -> angina or angina equivalent (in this patient, SOB)
b) overtime lead to pulmonary hypertension
How do you decide when to repair these?
There are certain criteria, including angina, evidence of pulmonary hypertension, and a high shunt fraction. This patient did not meet any of these strict criteria, but was still repaired because of refractory symptoms. As Nishant aptly pointed out, it is possible that shunt fractions worsen with exercise, so people with exercise-related symptoms may not meet the criteria even though they could benefit from the repair.

MR with Liezel + Dr. Meadows: Acute Aortic Insufficiency and Shone’s Syndrome

A young man w/ Shone’s syndrome (, asthma, and alcohol use presents with subacute SOB, lower extremity edema, and back pain. He has good functional status and no history of heart failure in the past. On initial presentation, he was found to have a low grade fever, new afib, and a wide pulse pressure; these vitals alone pointed towards the ultimate diagnosis of aortic endocarditis cause acute aortic insufficiency. 
1. The physical exam can be KEY in helping you diagnose new AI
The findings are not subtle and no special maneuvers are required – you just need to know what to look for.
-Wide pulse pressure (this patient’s was 147/47)
-Bounding pulses and PMI
-Decrescendo diastolic murmur at LSB (for me, this is not always as easy as the first two findings – sometimes it’s very loud and other times hard to hear)
2. Why is acute AI so different from chronic AI?
a) Cardiac output drops rapidly in acute AI: In chronic AI, the heart dilates to maintain cardiac output (though ejection fraction drops as regurgitation develops, the dilation allows the stroke volume to remain the same). In acute AI, this doesn’t happen, so both ejection fraction AND stroke volume rapidly drop off. This can cause cardiogenic shock.
b) Pulmonary congestion is much worse in acute AI: The dilated hearts of chronic AI can better accommodate the regurgitation and pressure increases only slightly. In acute AI, new regurgitation against stiff hearts cause rapid pressure increases, backing up into the lungs and causing pulmonary edema.
Inline image 1
3. How do you manage acute AI?
Valve replacement! Medical management is limited but includes maintaining a good HR (if you drop it too low, regurgitant volume increases and CO decreases), diuresis if needed, and possibly dobutamine (reduces afterload and improves inotropy).

Thursday NF Interesting Case with Sonia and Dr. Robbins : Afib


An eldely man with a hx of hypothyroidism, recent L TKR and a hx of DVT 1 year prior who was called to come to the ED for a heart rate in the 130s found to be in new afib.


Key Learning Points

*Don’t treat subclinical hypothyroidism unless T4 is > 10 or thyroid antibody is +; the reason for treating subclinical hypothyroidism is risk of progressing to an overt hypothyroid state

*IV metop vs. PO Metop

-Per Kaiser Guidelines – oral beta blocker therapy is preferred over IV therapy in the setting of acute MI; oral administration should be initiated within the first 24 hours for MI patients who do not have any of the following (a) heart failure, (b) low output state, (c) increased risk for cardiogenic shock, or (d) other relative contraindications (PR > 240 msec, 2nd or 3rd degree heart block, active asthma or reactive airway disease).   Early aggressive IV beta blockade can pose a net hazard in hemodynamically unstable patients.

*Number to transfuse in setting of ACS?

-The optimal transfusion threshold in the setting of ACS remains unresolved.  In general transfuse when the Hgb is < 8 g/dL and consider transfusion when the Hgb is between 8 and 10 g/dL.  Pilot trial of 110 patients with ACS demonstrated that a liberal transfusion strategy to raise the Hgb >/= 10 was associated with greater survival at 30 days

MR with Nishant + Dr. Kim: Leukocytoclastic Vasculitis and Endocarditis

A middle aged man presents with 6 days of severe myalgias, low grade fevers, and rash. He initially underwent a broad work-up for his rash including infectious and autoimmune etiologies; his blood cultures ultimately grew staph aureus and TEE showed new severe AI and an aortic vegetation.
1. Endocarditis can present in very atypical ways – in an unknown inflammatory condition, it is on the differential!
2. Staph Aureus is BAD
– This patient subsequently found to have septic cerebral emboli
IE due to Staphylococcus aureus is associated with complications more frequently than other pathogens (stroke 21 versus 14 percent, systemic emboli 27 versus 18 percent, persistent bacteremia 17 versus 5 percent, and in-hospital mortality 22 versus 14 percent) [1].
-Staph aureus infection is itself a criteria for surgical repair of left-sided endocarditis. See this excellent algorithm to decide who gets surgery:
3. Leukocytoclastic vasculitis (i.e. the histologic correlate to ‘palpable purpura’) is classically associated with HSP but actually can result from many etiologies (in this case, the patient’s lesions may have been a combination of septic emboli and true immunologic complex lesions)
– think big categories of vasculitis, chronic infections, and medications
– one rheum attending uses complement levels for the initial branch point:
Inline image 1

Thursday case presentation with Nishant and Dr. Meadows: VTach storm

An elderly woman with a pmh of Ebstein’s anomaly with an ICD, rheumatoid arthritis, Sjogren’s syndrome and ILD who presented with nonexertional chest pain found to be in VT storm on admission.
Know the workup of VT -> Thyroid function tests, electrolytes including K, Mg, and Calcium; if appropriate measure levels of digoxin and TCAs, Tox screens also may be helpful; and of course troponin
-Remember that you cannot rule out ischemia if a patient is in a paced rhythm
-Ebstein’s is commonly associated with an ASD and presents with hypoxia from a L->R shunt.  
-Shunt flow is driven by COMPLIANCE – the right side of the heart is more compliant, so therefore flow is left to right
-470 is a good cutoff to remember when thinking about prolonged QT
-VT Storm as Nishant pointed out is defined as 3 or more episodes of sustained VT or shocks from an ICD for VT in a 24 hour period

9/19 Monday case presentation with Alice: Cardiac tamponade

A man in his 60s with hx of OSA, HLD, HTN presents with 1 day hx of dyspnea, coughing and low grade fever found to have large pericardial effusion of likely viral etiology, positive tamponade physiology, s/p pericardiocentesis of 920cc serosanguineous effusion. 
Key Learning Points
-While the size of the pericardial effusion is important, it is the rate of fluid accumulation that has the greatest effect on hemodynamics
-Ddx for pericardial effusion
       Infectious:  Viral/Bacterial/Fungal/Parasitic
       Neoplastic – primary OR metastatic disease
       Cardiac – pericarditis/myocarditis/Dressler’s/dissecting aortic aneurysm
       Metabolic – hypothyroidism, uremia
-Important procedural complications of pericardiocentesis: myocardial puncture or laceration; vascular injury, pneumothorax, air embolism, arrhythmia, intraabdominal organ damage, acute hemopericardium
Sweet video link from the Stanford 25 demonstrating how to measure pulsus paradoxus:

9/14 Wednesday AM with Shawn: Endocarditis

An elderly woman with a pmh of moderate AS and a R TKA 5 years prior who initially presented to her PCP with R knee pain.  She was initially treated with a steroid injection as well as a course of PO prednisone.   Several weeks later she continued to have knee pain and was seen by ortho – arthrocentesis at that time revealed a WBC of 25K and culture grew out Step Milleri – she was started on antibiotics.  Plans were made for a 2 step knee replacement.  During pre-op workup, she was noted to be in atrial fibrillation. She was subsequently sent home with an event monitor and was called back to the ED after it detected 3rd degree heart block.  Subsequent ECHO demonstrated perivalvular abscess involving the aortic valve.  Unfortunately, she was deemed too high risk for surgery, and was sent home on hospice with plans for comfort care.

Learning Points

-Pay attention to surgical history – the presence of hardware in this patient’s knee increased her risk of septic arthritis

-TTE sensitivity for vegetation is 75% compared with sensitivity of TEE which is > 90%

-Heart block should raise suspicions for perivalvular abscess, specifically involving the aortic valve

Duke’s criteria for endocarditis:

Criteria for Diagnosis: 2 Major; 1 Major and 3 Minor; 0 Major and 5 Minor


1)       + Blood Cx for typical infective endocarditis organisms (S. Viridans or Bovis; HACEK, S. Aureus) from 2 separate blood cultures or 2 positive cultures from samples drawn > 12 hrs apart

2)       Echo with oscillating intracardiac mass or valve or supporting structures in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or abscess, or new partial dehiscence of prosthetic valve or new valvular regurgitation


1)       Predisposing heart condition or IV drug use

2)       Temp > 38

3)       Vascular phenomena: arterial emboli, pulmonary infarcts, mycotic aneurysms, intracranial bleed, conjunctival hemorrhages, Janeway lesions

4)       Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots; RF

5)       Microbiological evidence: positive blood Cx but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with endocarditis (excluding coag neg staph, and other common contaminants)

6)       Echo findings: consistent with endocarditis but do not meet a major criterion as noted above