Heart Failure with Preserved Ejection Fraction

 Today's morning report was about a man who developed flash pulmonary edema in the context of an NSTEMI.

Follow this link for a great CMAJ review of the management of acute decompensated heart failure. 

One thing that was touched on was the concept of congestive heart failure with preserved ejection fraction, aka "Diastolic Dysfunction" which occurs in 1/3 of patients with heart failure.

This type of dysfunction occurs as a result of concentric LV hypertrophy, and impaired ventricular relaxation as a result. As the ventricle does not sufficiently relax in diastole, filling (and thus forward flow) are impaired.

Risk factors include age, female gender, hypertension, coronary artery disease, diabetes mellitus, restrictive cardiomyopathy from infiltrative causes.

Diagnosis: Clinical evidence of heart failure with an ejection fraction greater than 50%. Echocardiogram can be helpful as it may show alterations in the E:A ventricular filling ratio (E is early, A is for atrial kick), as well as left atrial enlargement (more than 4cm), or evidence of hypertrophy (IV septum greater than 1cm, LV mass greater than 100gm/m2 body surface area).

Treatment: There is a lack of evidence when it comes to treating CHF with preserved EF. Guidelines (ACC/AHA) recommend controlling blood pressure, treating edema and controlling heart rate to allow greater LV filling time.


Follow this link for a NEJM review on the subject. 

Cellulitis and mimickers

Yesterday's Morning Report was on cellulitis and mimickers.

One key point made was the distinction between cellulitis and erysipelas, which is an infection of the superficial skin layers caused by beta-hemolytic streptococci. Unlike cellulitis, the borders of erysipeloid areas are very well demarcated. 

From a previous morning report on cellulitis:

Predisposing factors: saphenous vein harvesting, venous insufficiency, mastectomy with lymph node dissection, liposuction, "skin popping" in IVDU

Source: portal of entry in skin (e.g. tinea pedis, ulcer)- by far most common; other possibilities include osteomyelitis, bacteremia. 
Unusual sources: seawater (vibrio vulnificus), fresh water (aeromonas hydrophilia), fish (strep iniae)

Micro: 
80% gram +ve (staph, strep), 20% gram -ve. Aspirates/swabs are not indicated (unless ulcer) 
Broader coverage may be indicated in pts with DM2. 
Blood cultures are indicated in lymphedema, buccal, periorbital, water exposure, chills or fever. Otherwise, bacteremia is rare (less than 4%).

Empiric treatment: Cefazolin or cephalexin. Other possibilities: cloxacillin, clindamycin, penicillin, amoxicillin-clavulin. May want broader coverage (e.g. gram -ve coverage) in diabetics

Ancillary measures: Elevation, immobilization. Interdigital dermatophytic infections should be treated (e.g. clotrimazole and miconazole), terbinafine, etc
Click here for a review of cellulitis from NEJM

Important Conditions that Masquerade as Cellulitis:

Infectious:
- Necrotising fasciitis/ Clostridial myonecrosis

Non-infectious:
- Just plain edema with or without changes of chronic venous stasis- highly probable if bilateral
- Lymphedema
- Lipodermatosclerosis (in patients with chronic venous stasis)  fibrosing panniculitis characterized by advanced hyperpigmentation and induration involving most of the leg circumferentially.
- Superficial thrombophlebitis/DVT
- Contact dermatitis
- Systemic drug reaction
- Gout: in addition to arthritis, often have overlying skin induration and involvement of tendons
- Sweet's syndrome: acute febrile neutrophilic dermatosis associated with AML
- Well's syndrome aka eosinophilic cellulitis: urticarial lesions, transient systemic eosinphilia.


Click here for a great Annals review of diseases that masquerade as cellulitis. 

Staphylococcus Aureus and other goodies

Today we talked about a woman with a paraspinal abscess and Staphylococcus Aureus in the blood.

Some pearls of the discussion were:

- Causes of paraspinal/epidural abscess include: IVDU, endocarditis, contiguous spread from GI/GU infections

- Psoriasis is a risk factor for SA bacteremia. These patients should also have their psoriasis treated (note psoriatic skin lesions do not count as a removable source of infection)

- Psoas abscess is often a clue that there is a vertebral infection (as the infection spreads into the psoas from the vertebral/paravertebral space). Thus, if patient has a psoas abscess, consider getting a spine MRI as well.

- Staph Aureus bacteremia should be treated with 4-6 weeks of IV antibiotics unless all of the following conditions are met in which case can treat for 2 weeks (based on this 2003 Archives paper):

1. removable source
2. no evidence of metastatic infection
3. Resolution of fever by 72 hours of therapy
4. Negative blood cultures by 48-96 hours

For more on Staph Aureus bacteremia see this previous blogpost

For more on epidural abscess, see this previous blogpost as well as this NEJM paper 

Vasculitis

Dr Simon Carette took us through the approach to vasculitis as we discussed a patient with a case of Microscopic Polyangiitis (MPA).

This patient presented with mononeuritis multiplex as well as purpura of the legs.

Some pearls that he shared:

1) Mononeuritis multiplex: dysfunction of multiple named peripheral nerves. Pathognomonic for vasculitis. The most common causes are:
- Polyarteritis Nodosa
- Churg-Strauss Syndrome
- Cryoglobulinemia
- Connective Tissue Disease-Associated (note that not all CTDs cause vasculitis- the ones that do most commonly are lupus, rheumatoid arthritis and Sjogren's).

Mononeuritis mulitplex could, for example, present as an isolated foot drop. One important question when examining these patients is: how to distinguish a common peroneal nerve palsy  from an L5 radiculopathy (both cause foot drop).
Key distinction: Ankle inversion and thigh abduction are weak in L5 radiculopathy, but not in common peroneal nerve palsy. Weak dorsiflexion and eversion are seen in both conditions.

2) Skin lesions in vasculitis: presentation depends on which vessels are involved.
- Small vessel vasculitis- superficial vessels involved= petechiae, purpura (see lower image above), hemorrhagic bullae.
- Medium-sized vessel vasculitis- depper vessels involved= livedo reticularis (classic in PAN, see top image above), nodules, ulcers. Note that a standard punch biopsy will not reach the deeper layers and miss the diagnosis. In the presence of these skin lesions, a deeper punch or wedge biopsy is needed.

3) ANCA Antibody Testing:
- c-ANCA highly specific for anti-PR3 antibody and Granulomatosis and Polyangiitis (previously known as Wegener's)
- p-ANCA much less specific for anti-MPO- thus positivity on p-ANCA testing should prompt a follow-up ELISA test for anti-MPO (many other things including IBD can give you a positive p-ANCA that are not associated with vasculitis). If anti-MPO positive, 80% specific for a vasculitis (MPA, Churg-Strauss)


Finally, check out this NEJM CPC case on PAN for a good review of the approach to a patient with vasculitis.

Tamponade or PE?

Today we discussed a tricky case of a patient with both a pericardial effusion and a pulmonary emobolism. When they developed shock, the question became is this tamponade or a massive PE?

On physical exam, both groups of patients will have:

- sinus tachycardia

- hypotension

- high JVP

In tamponade: muffled heart sounds, pericardial friction rub, pulsus paradoxus

In massive PE: signs of DVT

Note that an increased pulsus (ie>10 mmHg) can also be seen in other conditions: profound hemorrhagic shock, obstructive lung disease... and massive pulmonary embolism!

In an unstable patient, bedside investigations would include an ECG...

ECG findings of tamponade: 

- sinus tachycardia

- low voltages (ie less than 5 in limb leads, less than 10 in precordial leads)

- pericarditis findings: ST elevation, PR depression

- electrical alternans (beat-to-beat variation in QRS amplitude, caused by swinging of the heart in the pericardial fluid) - rare but very specific.

ECG findings of pulmonary embolism:

- sinus tachycardia

- atrial arrhythmias

- S1Q3T3-rare but specific ECG pattern

- iRBBB/RBBB

- RAD

- non-specific ST/T wave changes

- precordial T-wave inversion (Rt heart strain pattern)

To definitively sort these two out, an echocardiogram is needed. 

Echocardiogram findings of massive PE:

- Increased RV size

- Decreased RV function

-Tricuspid regurgitation

Echocardiogram findings of tamponade:

- RA/RV diastolic collapse

- ventricular interdependence: reciprocal respiratory variation in volume in right and left heart, as well as flows across AV valves (as in figure above).

- IVC full, collapses by less than 50% on inspiration

Check out this NEJM review on Acute Cardiac Tamponade

Kidney injury and ACE inhibitors

Today in morning report we touched on the perils of volume depletion in patients who are taking ACE inhibitors. Have you ever wondered why this situation would precipitate acute kidney injury?



The issue is this: ACE inhibitors offload the glomerulus (and thus protect it from wear-and-tear) by causing efferent arteriolar dilatation. Normally in situations of volume depletion, the Renin-Angiotensin system is activated, and angiotensin II causes efferent arteriolar constriction, thus increasing the pressure in the glomerulus (think of it as a "squeeze") and thus preserving GFR. If you have a ACE inhibitor (or ARB) on board then you don't get the efferent constriction, thus no squeeze, thus drop in GFR. This causes AKI.

Patients on ACE inhibitors should be warned about this complex issue. While the ACE inhibitor protects their kidneys in the longterm, it can hurt them in the short term if your patients takes his ramipril while volume depleted. So please hold it if there is diarrhea, vomitting, decreased PO intake, bleeding etc.

Cheers! Have a great long weekend!

Secondary Causes of Hypertension & Hypertensive Emergencies

When to consider a secondary cause of hypertension:

1. sudden onset or worsening of hypertension at any age
2. onset of hypertension in those less than 30 years old (with no family history or obesity)
3. hypertension resistant to 3 drugs

Secondary causes of hypertension and their clues:
-Renovascular disease: abdominal bruit, rise in creat>30% upon ACE inhibitor or ARB initiation, atherosclerosis elsewhere, history of flash pulmonary edema with hypertensive episodes

-Pheochromocytoma: paroxysmal hypertension, typical spells (headache, palpitations, sweating, panic attacks, pallor), hypertension triggered by beta-blockers, MAO inhibitors or changes in abdominal pressure (ie. intraoperatively),adrenal mass

-Hyperaldosteronism (often missed!): hypokalemia  less than 3 .5 without diuretics or less than 3.0 on diuretics, adrenal incidentaloma on imaging

-Cushing's syndrome: typical appearance, history of exogenous steroids

-Sleep apnea: body habitus (including neck circumference more than 16 inches in women and more than 17 inches men), history of snoring/apneic spells/morning headache/daytime somnolence

-Medications: OCP, HRT, some NSAIDS, some antidepressants (eg Venlafaxine), sympathomimetics including decongestants

-Coarctation of the aorta: don't forget to check for brachiofemoral delay in this patients... has been detected for the first time in adulthood

-Hypothyroidism

-Hyperparathyroidism

Hypertensive Emergencies

"Urgency": SBP over ~180 or DBP over ~110 without end-organ damage- needs correction over days with oral agents
"Emergency": Above, but with acute end-organ damage, needing urgent lowering, usually with IV medications in a monitored setting.

End organ complications and specific treatments:

1) Aorta- dissection (B-blockade, nitroprusside after B-bl. No pure vasodilators)
2) Brain- encephalopathy (note that headache without neuro deficits does not count!)- sz, cerebral hemorrhage/infarction, raised ICP
3) Heart- MI, CHF (acute diastolic dysfunction leading to pulmonary edema)- careful with B-bl. May use nitro infusion
4) Kidney- renal failure- careful diuresis, calcium antagonists useful
5) Placenta (pre-eclampsia)- hydralazine, labetalol, delivery
6) Hemolysis (can look just like TTP with MAHA, fragments)

7) Eyes: papilledema, hemorrhages

Treatment Targets: 

-         emergency: lower BP by no more than 25% in minutes to 2 h using IV medications (exception: aortic dissection, where it must be lowered more rapidly)

-         urgency: lower BP over hours to days with PO

-         meds PO: amlodipine, captopril, hydralazine, clonidine

-         meds IV: labetalol, nitroprusside, nitroglycerin, hydralazine

Click here for the Canadian Hypertension Education Program (CHEP) guidelines from 2011