Category Archives: Cardiovascular Medicine

VA Ambulatory Report 4.4.18 – New Atrial flutter

Thanks Anne for presenting your patient from clinic last week.  The patient is a 60 yo F with a pmhx of HTN and DCIS who presented to clinic with dyspnea on exertion found to have atrial flutter with rates in the 130-150s.

Sam Brondfield joined us and dropped some knowledge bombs about DOACs

DOAC MOA Reversal agent? Things to consider
Dabigitran Thrombin inhibitor idraucizumab -Common SE: dyspepsia
Rivaroxaban Xa inhibitor -Once daily dosing
-Least amount of data in elderly patients
Apixaban Xa inhibitor -Lowest bleeding risk
-Least dependent on creatinine clearance, safest in renal disease
Other considerations: insurance coverage, drug interactions


How is Aflutter different from Afib?

  • Background
    • Afib – associated with some underlying heart disease causing large atrium, increased atrial pressures or inflammation
    • Typical Aflutter – reentrant circuit involves the cavo-tricuspid isthmus
      • sawtooth negative flutter waves in the leads II, III, and aVF
    • Atypical flutter – not involving the cavo-triscupid isthmus
  • Work-up of new onset of atrial flutter is the same as afib
    • Any disorder that causes Afib can also cause Aflutter
      • Also commonly occurs after treating Afib with an antiarrythmic or ablation
      • It is an uncommon complication of acute MI in the absence of other symptoms
    • Assess for hyperthyroidism, heart failure, pulmonary disease
    • Tests to order
      • Echo: Looking at size of artia and ventricles, ventricular function, and valves and TEE if plan for cardioversion without optimal anticoagulation
  •  Management
    • Rate Control: Same general approach as Afib, but harder to achieve
      • Use non-dihydropyridine CCB or BB
      • Consider dig or amio if decompensated HF
    • Rhythm control
      • Cardioversion should be urgently in patients with rates >150 or in those who have hemodynamic compromise or who have WPW
      • Ablation is the treatment of choice given the high rate of recurrence of aflutter and the high success rate of the procedure
    • Stroke prevention
      • Limited data to suggest the optimal approach to anticoagulation in atrial flutter given rarity of persistent A flutter and the frequency of co-existence with Afib
      • Thromboembolic risk may be lower than in Afib, but most recommend approaching anticoagulation the same as they would in a patient with Afib as these patients may also be having episodes of Afib

Moffitt Pearls 2/9/18 – DKA and NSTEMI

Thank you to Katie Sullivan for presenting the case of an elderly woman with history of type 1 diabetes and CAD s/p CABG presenting after colonoscopy with severe nausea/vomiting and diarrhea. The patient was found to be in DKA likely 2/2 to an NSTEMI with EKG changes suggestive of ischemia and a troponin of 25!

Key Pearls

  • Complications after colonoscopy are rare (approximately 3 per 1000 screening colonoscopies) and include complications of sedation, complications related to the preparation, bleeding, and perforation.
  • Never forget that Ischemia – acute MI – can precipitate DKA!! See the rest of the “I’s” below brought to you by our wonderful interns Noa and Hayley.
  • Any patient with ACS regardless of intervention (stent or no stent) should be treated with DAPT for 12 months b/c of improved cardiovascular outcome. Bleeding risk needs to be balanced against benefits and shorter durations are sometimes used. (See graph from the study)
  • Troponin elevation in the setting on non-ACS related demand is associated with worse f/u cardiac mortality in both low and high risk patients. In one study incidence of cardiovascular death or heart failure after adjusting for conventional risk factors (hazard ratio 1.84, 95% CI 1.30-2.61) [1].
  • Patient with the flu are at a much higher risk of ACS during and in the week after illness. A recent Canadian study in the NEJM showed that MI admissions were 6x more likely to occur in the week after a positive flu test!!

Remember the I’s for causes of DKA reviewed!!

  • Infection
  • Ischemia
  • Infant/pregnancy
  • Ingestion/intoxication
  • In-adherence to medications
  • Iatrogenic
  • (I)Other: hypercortisol and sympathetic surge

CURE trial



  1. Prognostic value of cardiac troponin I measured with a highly sensitive assay in patients with stable coronary artery disease. Omland T, Pfeffer MA, Solomon SD, de Lemos JA, RøsjøH,ŠaltytėBenth J, Maggioni A, Domanski MJ, Rouleau JL, Sabatine MS, Braunwald E, PEACE Investigators. J Am Coll Cardiol. 2013 Mar;61(12):1240-9. Epub 2013 Feb 13.

Cardiology Report Pearls – 1.30.18 – Infective Endocarditis

Thank you to our cards team (Manoj, Noa and Nicole) for presenting the case of an elderly woman with hx of AVR presenting both native and prosthetic valve enterococcus endocarditis involving in the mitral valve and aortic valve. She is awaiting more urgent cardiac surgery given worsening MR and heart failure. A fun case where we learned a ton about endocarditis and HH nailed the organism prior to speciation!


  • In a patient with a positive UA with negative nitrites one should think of gram-positive organisms including enterococcus.
  • Ceftriaxone is not active alone against enterococcus, however ampicillin and ceftriaxone (CTX) are used in conjunction b/c CTX augments the activity of ampicillin.
  • If you have a high concern for endocarditis send 3 sets of blood cultures prior to abx!

Approach to prosthetic valve endocarditis:

  • Early (<30d): often are virulent organisms including S aureus, GNRs. Fungemia is BAD!
  • Late: Similar organisms to native valve endocarditis (staph, step and enteroccus), plus fungal organisms.

Indications for TEE

  1. Evaluation of endocarditis after a poor/unclear TTE study or possible complications (eg, fistula, abscess)
  2. Evaluate for valve disorders pre or post operatively
  3. Evaluation for left atrial/LAA thrombus in a patient with atrial fibrillation/atrial flutter to facilitate clinical decision making regarding anticoagulation, cardioversion, or ablation
  4. Suspected acute aortic pathology (ie, dissection, transsection, intramural hematoma).
  5. Evaluation of source of embolism in a young (<50 years) patient for whom a TEE would be performed if the TTE was normal

Global Indications for Surgery in Valve Endocarditis – (see table below)

  1. Heart Failure
  2. Uncontrolled infection
  3. Persistent Emboli

See more info in this fantastic 2013 NEJM Infective Endocarditis review article by Hoen and Duval. Table 2 is a great summary below.

IE Surgery Capture

Definitions of early surgery

  • There is no consensus as to the optimal timing of early surgery.
  • The ESC guideline classifies surgical indications in IE as emergent (within 24 hours), urgent (within a few days), and elective (after 1-2 weeks of antibiotic therapy).
  • The AHA/ACC guideline defines early surgery as occurring during the initial hospitalization and before completion of a full therapeutic course of antibiotics.

 Favorite PEARL from Anne this am!

  • Early intervention for endocarditis related valve dysfunction is associated with significantly reduced composite end point of death from any cause and embolic events by decreasing risk of systemic embolism. See the NEJM original article here:
  • When advocating for your patients send this to your friendly CT Surgery colleagues 🙂

Moffitt Pearls 1.12.18 – Pleural Effusions s/p CABG

Thank you Kapil for presenting the case of an elderly man born in China presenting w/ cough found to have a unilateral exudative pleural effusion. After inpatient work-up w/ ddx initially including TB and malignancy, it was felt that this effusion is likely a result of his recent CABG (the date was signed out to the team was years prior when in fact it was weeks prior).

Key Pearls

  1. Always verify history, labs, medications and imaging for holdover patients as this can dramatically influence your approach and work-up. Trust, but verify!
  2. Light’s criteria (below) is positive when ONLY 1 out of the 3 criteria (below) are met. This test is extremely sensitive (98%) so as not to miss exudative effusions (see below).
  3. Pleural effusions are common after CABG with a reported prevalence of 40-75% 1 week after surgery. Most of these are asymptomatic, exudative, small, left-sided and resolve over several weeks.
  4. The cause of 15-20% of all plural effusions will remain unknown. See this article from Chest looking at non-malignant effusions. They found that bilateral, transudative effusions were associated with a one year mortality of 50%!

More on Effusions after CABG

  • Bloody, exudative, effusions tend to occur to earlier ( < 4 weeks after surgery). These are usually easy to control with one to three therapeutic thoracenteses.
  • Non-bloody effusions tend to occur later (> 4 weeks after surgery) and have a relatively low LDH and high percentage of lymphocytes. These effusions tend to be more difficult to control.

See this article for a review of pleural effusions and these figures!

light's criteriapleural effusions


Moffitt Cardiology Pearls 12.5.17 – Sinus Exit Block and Endocarditis

Thank you Nadia (my co-fellow to be next year!!) for presenting an amazing cardiology case with Anne Thorson. She presented the case of a man w/ hx of crack cocaine use and recent strep pneumo meningitis p/w acute SOB found to have a diastolic murmur, PR prolongation, sinus exit block and an perivalvular abscess!! The patient was found to have severe chronic AI and was being evaluated by CT surgery for definitive management while on IV abx. Keep us updated!!

Key Pearls

  1. ECG conduction changes, from first degree AV block to complete heart block, are associated with increased mortality in patients with known endocarditis (Am Heart J 2001;142:280-5.)
  2. See this study in the American Heart Journal for more information about conduction abnormalities and endocarditis (remember that these will occur at the level of AV node).
  3. See Figure below for more information on sinus exit block.

For more information see –


Moffitt Pearls – 11.14.17 – Complete Heart Block and Cardiac Sarcoid

Thanks you, Arvind, for presenting a case of an older man with exercise-induced bradycardia found to have complete heart block 2/2 to cardiac sarcoidosis.


  1. In the consideration of bradycardia, one must first rule out MI. 15% of patients with an MI will present with complete heart block.
  2. Bradycardia in an inferior or posterior MI is driven by 1) ischemia AND 2) the Bezold-Jarisch Reflex. This is a cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle.
  3. Complete AV dissociation with Ps faster than SLOW QRSs suggests complete heart block.

Etiology of Bradycardia


  • Healthy children/adults during sleep (HRs in 30s, pauses up to 2 seconds may occur)
  • Well-conditioned athletes
  • Some elderly patients


An easy way to break down bradycardia is into extrinsic vs intrinsic causes.

  • Intrinsic
    1. Idiopathic degenerative d/o
    2. Ischemia (ACS or chronic)
    3. Lyme disease
    4. Viral myocarditis
  • Extrinsic
    1. Drugs – antiarrhythmics, b-blocker, calcium channel blocker
    2. Hypothyroid
    3. Hypothermia
    4. Hypoxia
    5. Vagal tone


Evaluation of Patient with Complete Heart Block

  1. Rule out Ischemia – ~15% of patient with an acute MI will have complete heart block (usually RCA)
  2. Check for systemic, reversible causes of heart block:
  • Meds: Digoxin, beta-blockers, calcium channel blockers, or anti-arrhythmics
  • Hypothermia
  • Electrolyte abnormalities – hypokalemia
  • Hypothyroid

3. Look for the primary cardiac causes in 3 broad categories:

  • Infiltrative: Amyloidosis, hemochromatosis, sarcoidosis
  • Inflammatory: SLE, scleroderma
  • Infectious: Rheumatic fever, Chagas, endocarditis, viral myocarditis,i syphilis, Lyme disease

Diagnostic Criteria for Cardiac Sarcoid

cardiac sarcoid

Here is a great JACC review on cardiac Sarcoidosis –

Moffitt Pearls 11/7/17 – Cards Report – Vasopressors and PA Catheters

Thank you Matt H for your help with these PEARLS!!!

Thanks to Chloe for presenting a fascinating case of a 65 year old man with history of HOCM (w/o obstruction) who presented with acute onset shortness of breath, ultimately thought secondary to flash pulmonary edema from paroxysmal hypertension. We had a great discussion on vasopressors to use in different types of shock. Below is a summary of some of the more common vasopressors, as well as brief information on key considerations in their use. Finally, there is a bit of info on the ESCAPE trial that led to reductions in use of PA catheters in management of cardiogenic shock.

For more information, refer to the UCSF Hospitalist Handbook and the MGH CCU handbook.

Key Pearls

  • Dobutamine is considered a first line pressor in cardiogenic shock b/c it improves contractility and drops SVR (watch out for dropping BPs).
  • HOWEVER, never write for a MAP goal and titration parameters when using dobutamine as patients MAPs will sometimes drop with up titration (this is why we sometimes start this with norepinephrine).
  • The ESCAPE (2005) showed no improved 6 month mortality in patient with decompensated heart failure randomized to management with PA catheter monitoring vs. usual care. See indications for when to us a PA catheter below.

Vasoactive/Inotrope medications

Class Drug Dose Mechanism
Vasopressor Phenylephrine 0-200 mcg/min α-1 agonist
Vasopressin 0.04 units/min V-receptor agonist
Mixed Norepinephrine 1-20 mcg/min α-1, β-1 agonist
Epinephrine 1-20 mcg/min α-1, β-1, β-2 agonist
Dopamine 1-3 mcg/kg/min

2-10 mcg/kg/min

10-20 mcg/kg/min

D agonist

β-1, β-2 agonist

α-1 agonist

Inodilator Dobutamine 2-5 mcg/kg/min β-1 > β-2 agonist
Milrinone 0.375-0.75 mcg/kg/min PDE III inhibitor


Receptor Action
α-1 Vasoconstriction
β-1 Inotropy
β-2 Vasodilation, bronchodilation
D Splancnic vasodilation – increases renal blood flow
V Vasoconstriction

Quick info on selected vasoactive agents:

Norepinephrine: 1st line pressor for sepsis, cardiogenic shock, undifferentiated shock.

Vasopressin: Often 2nd line pressor in sepsis. Use caution in patients with coronary or peripheral vascular ischemia. Not affected by acidosis (many other pressors are less effective in this situation)

Phenylephrine: Useful for pure vasodilatory hypotension (e.g. sedation-related hypotension). Generally avoid in cardiac patients as can cause reflex bradycardia with decreased cardiac output. HOWEVER, can be useful in unstable arrhythmias when beta agonism may be undesirable. Also useful in HOCM with dynamic outflow obstruction (‘stents’ open the obstruction) or fixed obstruction in AS as it increases SVR without changing afterload felt by the heart.

Epinephrine: Primary use is in ACLS, though can also be used as 3rd pressor in refractory hypotension. Adverse effects include tachycardia/tacchyarrythmias, peripheral vasoconstriction and end-organ damage

Dobutamine: Increases contractility while reducing SVR. Often decreases blood pressure, therefore should not be thought of as a vasopressor, should also not be titrated to MAP goals. Risk of arrhythmia with higher doses, also risk of myocardial ischemia from increased oxygen demand.

Milrinone: PDE-3 inhibitor, inhibits cAMP breakdown. Similar to dobutamine, results in both inotropy and decreased SVR (perhaps more reduction in afterload, but also more risk of hypotension, than dobutamine). Requires dose-reduction in renal impairment.

Indications for PA Catheters

ESCAPE trial (2005) – randomized patients with acute decompensated heart failure to therapy guided by PA catheter vs no PA catheter. No difference in 6 month mortality or days out of the hospital. Based on this trial and meta-analysis, PA catheters are no longer used routinely. They still have a role in shock of uncertain etiology or when initial management is unsuccessful.

AHA guidelines on PA catheters (2013):

  • Recommended in patients with respiratory distress or evidence of impaired perfusion when intracardiac filling pressures can’t be determined by clinical assessment (class I, level C)
  • Can be useful in heart failure with persistent symptoms despite standard therapy if any of the following are present: (class IIa, level C):
    • Uncertain volume status, perfusion, SVR, PVR
    • Persistent hypotension
    • Worsening renal function despite initial therapy
    • Need for vasoactive agents
    • Anticipated need for mechanical cardiac support
  • Routine use not recommended in normotensive patients with acute decompensated heart failure responding to diuresis and afterload reduction (class III, level B)