Category Archives: Cardiovascular Medicine

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 – https://lifeinthefastlane.com/ecg-library/sa-exit-block/

 

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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.

KEY PEARLS:

  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

Normal:

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

Abnormal:

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 – http://www.onlinejacc.org/content/68/4/411

https://www.evernote.com/shard/s307/sh/6e60d9c4-b324-47bb-a162-03a79c64cb19/bde254d93bdd9f603bd4e3be123b31f2

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)

https://www.evernote.com/shard/s307/sh/c214c30c-a21c-46f6-a447-cd73bcbc2bc4/aafe54bf6c950077c1d6e738d608cced

Moffitt Pearls 10.24.17 – Cardiology Report – SLE and Tamponade

Thank you to Laura for presenting a fascinating case of a middle aged woman with a hx of SLE c/b APS presenting with progressive dyspnea and CP. Her Physical exam was notable for an elevated JVP and muffled heart sounds and negative pulses paradoxes (initially). Her INR was 10, she was thought to have a mild SLE flar and she was found to have a large, progressive hemorrhagic pericardial effusion resulting in tamponade requiring urgent pericardial drainage.

Key Pearls

  1. Think about tamponade in a patient who presents with hypotension, tachycardia and elevated neck veins.
  2. Tamponade is a CLINICAL diagnosis with the BECK’s triad: 1) elevated JVP 2) muffled heart sounds 3) hypotension with pulses paradox.
  3. Echocardiographic signs suggestive of tamponade include 1) presence of pericardial effusion 2) diastolic collapse of the RV or RA and 3) IVC dilation. See link for amazing videos. (https://web.stanford.edu/group/ccm_echocardio/cgi-bin/mediawiki/index.php/Tamponade)
  4. Remember that there are several drug-drug interactions with warfarin. As we saw in this case this patient’s INR rose to 10 after she was treated with levofloxacin!!

Cardiac Tamponade

Definition: Hypotension that immediately reverses with pericardial drainage

Physiology:

  • Pericardial effusion of significant volume OR rapidly accumulated leads to increased pressure in pericardial space throughout the cardiac cycle
  • During inspiration, as RV volume increases, the RV is unable to expand into the  left, decreasing LVEDV and thereby decreasing cardiac output, causing a decrease in SBP during inspiration maximally stretched pericardium. Therefore, the interventricular septum bulges to left, decreasing LVEDV and thereby decreasing cardiac output, causing adecrease in SBP during inspiration
  • Diastolic equalization of pressures
  • Acute vs. subacute tamponade: small volumes at fast rates vs. abilility for pericardial stretch if fluid gradually accumulates
  • In both acute and subacute, there is a point at which intrapericardial pressure decompensation reaches an almost vertical ascent with a small amount of fluid -> acute

 

Etiologies:

  • Acute tamponade:
    • Usually due to traumatic rupture of ventricle as a result of a procedure or blunt trauma; also in aortic dissection or myocardial infarction with ventricular rupture; hemorrhage as in our case
  • Subacute tamponade:
    • Infection: More commonly purulent than viral
    • Malignancy: Particularly lung, breast, Hodgkin’s, mesothelioma
    • Post-MI, post-CT surgery, post-procedure
    • Uremia
    • Post-XRT
    • Drugs
    • Collagen-vascular disease: in particular SLE
    • Idiopathic
    • HIV
    • External to pericardial sac (pleural effusions have caused tamponade physiology)

 

Treatment:

    • IV fluids to temporize (sometimes brings out tamponade physiology and physical
    • signs)
    • Pericardiocentesis: paraxiphoid (left), needle at 15 degree angle to skin, toward left
    • shoulder, with patient sitting forward
    • Pericardial drain or window

Moffitt Cardiology Pearls 10/10/17 – Congenital Heart Disease and SVC Syndrome

Thank you so much to Nick and Matt for presenting the case of a young man with a history of congenital pulmonary atresia and hypoplastic RV decades status post a bidirectional Glenn procedure coming in with shortness of breath and chest pain. The patient was found to have a severely dilated aortic root with resultant aortic insufficiency and severe pulmonary hypertension.

 

KEY PEARLS:

  1. When assessing a patient with congenital heart disease, it is VITAL to obtain records outlining the pathophysiology and previous procedures in order to understand their current physiology and what might go wrong.
  2. As Anne Thorson shared with us, in a patient with congenital heart disease who was previously doing well and then decompensates, ALWAYS consider the possibility of infection (particularly endocarditis) as the cause.
  3. SVC syndrome is a clinical diagnosis – see some physical exam features below.

    Cyanotic Congenital Heart Lesions: There are 5 main lesions, often called the “5 Ts”, of congenital heart defects that can result in cyanosis at birth or in the neonatal period. Most of these conditions will require intervention within the first months of life.

     

    Here’s a review on cyanotic congenital heart disease in adults. Of note, it’s from 1975… my guess is many things have changed since then and we see significantly more adult survivors of congenital disease.

Pulmonary atresia and hypoplastic RV is NOT typically a cyanotic heart lesion. However, the small RV + atretic pulmonic valve can lead to a volume and pressure overloaded state on the right side the heart. The Bidirectional Glenn Procedure reduces blood flow to the hypoplastic RV (thus offloading the pressures) by diverting the SVC directly into the pulmonary arteries. Blood return from the IVC continues to enter into the RA.

 


While we most commonly see SVC Syndrome in the setting of extrinsic compression or internal invasion of the SVC in malignancy, remember that there are multiple other risk factors as well!

Risk factors for SVC syndrome:

  • Thoracic mass – lung cancer, lymphadenopathy, lymphoma, teratoma, thymoma
  • Vascular disease – aortic aneurysm, vasculitis, AV fistula
  • Scarring or Fibrosis – related to chronic infection (like histo as Harry mentioned or tuberculous mediastinitis as described by Schechter in 1954), radiation, or instrumentation
  • Cardiac causes – pericarditis, atrial myxoma OR, as in this case, severe pulmonary hypertension in patient whose SVC connects directly to the pulmonary veins!
  • Clot – with or without underlying malignancy or central venous catheter

Here’s another, more recent, review of SVC syndrome, describing the pathology, risk factors, diagnosis, and management.

Harry mentioned Pemberton’s sign, described in the linked NEJM images in Clinical Medicine article. Below are 2 YouTube videos showing the classic finding:  signs of SVC syndrome brought on by extending the arms over the head. The second is quite dramatic.

1) https://www.youtube.com/watch?v=r1dkasbE7v8

2) https://www.youtube.com/watch?v=m_ZecWGnb2A

 

Evernote: https://www.evernote.com/shard/s462/sh/d5befae6-e090-4f3e-ab15-7dfa8ed3e73a/6e88cb495f580e320334ed1c2932afb5

Moffitt Pearls 10.03.17 – Chest Pain in the Young , FFR & Myocardial Bridging

Thank you to Vaibhav for presenting the fascinating case of a young woman with a hx of myocardial bridging s/p unroofing p/w recurrent chest pain and elevated troponin to 1.8 of unknown cause. She has had an extensive prior work-up that has included abnormal MRI (initially thought to be Sarcoid, then reviewed normal), mild diastolic dysfunction and reduction in voltage c/f infiltrative disorder. She will get a repeated cardiac MRI (possibly PET), ANA, serum free light chains and ESR/CRP to help determine the cause.

Key Pearls

  1. Low voltage on the ECG is defined by < 5mm in limb leads and < 10mm in the precordial leads. Amyloid is the predominate infiltrative disease to consider with this finding as other diseases such as Sarcoid often does not present with low voltages.
  2. Myocardial bridging is present in up to 25% of people per autopsy/imaging reports AND it can be very difficult to determine if this is driving symptoms. 
  3. Medical management for myocardial bridging includes beta-blockers and calcium channel blockers to decrease inotropy. Nitrites are contraindicated as they increase contractility.

More on Myocardial Bridging

  • The major coronary arteries occasionally have a segmental intramyocardial course. During systole, this segment of the vessel is compressed, a condition referred to as milking or systolic “myocardial bridging.” On angiography, bridging is recognized as compression of a segment of a coronary artery during systole, resulting in narrowing that reverses during diastole. This occurs most often in the left anterior descending coronary artery or its septal perforator branches
  • Myocardial bridging, which causes coronary artery obstruction only during systole, would not be expected to reduce total myocardial perfusion significantly since almost two-thirds of blood flow in the left coronary system occurs in diastole.  

Differential Diagnosis of a young pt w/ Cardiac Chest Pain:

Always rule out MI first!

  • Atheromatous CAD
    1. Think of RF including hyperlipidemia, hyperhomocysteinaemia, lipoprotein a
  • Non-Atheromatous Coronary Artery anomalies
    1. Myocardial bridging – artery dives through myocardium instead to the epicardium (tx: with B-blockers and nondihydropurine calcium channel blockers)
    2. Coronary Dissection (surgical)
    3. Anomalous coronary (surgical)
    4. Embolism to the coronary arteries – septic or clot  (through PFO)
    5. Prizmental Angina – vasospam (tx amlodipine, nitrates)
  • Hypercoagulable States
    1. Antiphospholipid syndrome
    2. Nephrotic syndrome
    3. Factor V Leiden and Antithrombin III
  • HCOM w/ demand (tx maintain euvolumia, beta-blockers)
  • Microvascular d/o (treat as angina – risk factor reduction, beta-blockers, nitrates)
  • Pericarditis
Fraction Flow Reserve (FFR) is traditionally used to quantify the degree of coronary artery narrowing to evaluate for stenting during a catheterization. The FAME trial re-defined flow limiting lesions as < 0.8 which is used to decide which lesions to stent. Diastolic FFR has also been used in the evaluation of myocardial bridging with a flow rate < 0.76 do determine if a lesion should be stented or not. Interestingly enough, dobutamine is used in the cath lab and NOT adenosine (which is usually used) the determine whether myocardial bridging is causing flow limitation.
FFR

Moffitt Pearls 8.29.17 – Cardiology Report

  1. Management of atrial fibrillation (AF) is broken down into rate control and rhythm control – see details on AFFRIM trial below. Use the CHaDsVasC score to determine anticoagulation.
  2. In patient’s with a reduced ejection fraction do not use calcium channel blockers for rate control (class iii, level C evidence).
  3. Amiodarone and dofedilide are two options for anti- arrhythmia therapy in patient’s with HFrEF.
  4. See below for flow sheet on cardioversion of patient’s with hemodynamically stable AF.

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The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Trial (2002)

Bottom Line:  In patient’s with nonvalvular AF, there is no survival benefit between rate and rhythm control, but rhythm contol trends towards increased mortsality.

Major Points:

Multicenter, parallel group, RCT of > 4,000 patients w/ nonvalvular AF

Rate control (HR <80 at rest) was achieved with B-blockers, Ca++ channel blockers, and/or digoxin (n=2,027)

Rhythm control strategy varied considerably but included class 1a (procainamide), 1c (propafenone, flecanidie) and III (amiodarone, sotalol, dofetilide) (n=2,033)

Median follow-up: 3.5 years

Analysis: Intention to treat

Primary Outcome: All cause mortality at 5 years 25.9% vs 26.7% (HR 1.15, CI 0.99-1.34, P=0.08)

What if my patient cannot be anticoagulated??

Among patients with nonvalvular atrial fibrillation (AF), the majority of thrombi are located within or involve the left atrial appendage (LAA). The importance of the LAA in thromboembolic risk among patients with AF provides the rationale for ligation or occlusion of the LAA in patients who are candidates for but have either absolute or relative contraindications to long-term oral anticoagulation

Percutaneous approaches, referred to as LAA occlusion procedures, that mechanically prevent embolization of LAA thrombi have been developed and shown to be effective

The left artial appendage ligation or LARIAT procedure was developed here at UCSF and is used in such patients (video below)

Cardioversion of patient’s with hemodynamically stable AF.

**Remember unstable patients should be immediately cardioverted**

Cardioversion Flow.png

https://www.evernote.com/shard/s307/sh/b32ec2f6-aab5-4c75-a9ed-58727105f371/e40f23a849ddc915e16c00e9ca9e8986Key Pearls