Use of Medication for Cardiovascular Disease During Pregnancy

CV Medications in Pregnancy

Table for Quick Review, I posted this article earlier in the year but not the Central Illustration 

Cardiovascular disease complicating pregnancy is rising in prevalence secondary to advanced maternal age, cardiovascular risk factors, and the successful management of congenital heart disease conditions. The physiological changes of pregnancy may alter drug properties affecting both mother and fetus. Familiarity with both physiological and pharmacological attributes is key for the successful management of pregnant women with cardiac disease. This review summarizes the published data, available guidelines, and recommendations for use of cardiovascular medications during pregnancy. Care of the pregnant woman with cardiovascular disease requires a multidisciplinary team approach with members from cardiology, maternal fetal medicine, anesthesia, and nursing.

Summary:

1. Labetalol and methyldopa are the agents of choice in treating pregnant patients with hypertension.
2. Although all antihypertensive agents cross the placenta, methyldopa and labetalol appear to be the safest antihypertensive agents in pregnant women.
3. ACE inhibitors (such as lisinopril), angiotensin receptor blockers (such as losartan), spironolactone, and direct renin inhibitors (aliskiren) are teratogenic and are therefore contraindicated during pregnancy. During the first trimester, these agents can cause central nervous system and cardiovascular malformations in the fetus. Second-trimester exposure can cause developmental malformations of the kidneys and genitourinary system.
4. A 2013 guideline published by the American College of Obstetricians and Gynecologists made a strong recommendation for initiation of pharmacologic therapy for pregnant women with persistent chronic hypertension at a systolic blood pressure of 160 mm Hg or higher or a diastolic blood pressure of 105 mm Hg or higher. However, other guidelines, including one from the European Society of Cardiology, continue to recommend initiation of pharmacologic therapy at a systolic blood pressure of 150 mm Hg or higher or a diastolic blood pressure of 95 mm Hg or higher in women without symptoms or evidence of end-organ damage due to hypertension

ESC Guidelines on the management ofcardiovascular diseases during pregnancy

Emergency Echocardiography in the ICU

This is a good video for basic 2D-echo at the bedside for patients in shock. Patients in septic shock and ARDS need frequent limited focused exams , probably every other day as LV (dys)funtion is an extremely dynamic process. Every patient admitted with shock to the ICU should get a baseline echo, which unfortunately does not happen very often.




Attached are a basic outline and summary of elementary echocardiography, the second title is more advanced with quantification of valvular lesions.

Remember that the IVC size and collapse during breathing only represent CVP and is prone to the same limitations as measuring CVP through a CVC. IVC  measurement in intubated patients is not reliable to assess CVP. Distensibility index on the other hand can be used in intubated patients.

Measurement of CVP is not without some merit, as long as the limitations are understood and what exactly is being  measured. Refuting the measurement altogether is not appropriate 

Oral Fluoroquinolones and Risk of Mitral and Aortic Regurgitation

Fluoroquinolones (FQs) are one of the most prescribed classes of antibiotics and are favored over other agents for their broad spectrum of antibacterial activity and high oral absorption. In recent years, a number of adverse events have been linked to these drugs. Some of these adverse events include retinal detachment, which has produced mixed results , but others, including aortic aneurysm and dissection , peripheral neuropathy , and cardiac arrhythmias , are more consistent with a causal link with FQs and are now included in a warning from the U.S. Food and Drug Administration (FDA)

Mechanistically, FQs are known to damage connective tissue by inducing oxidative stress within the tendon cells , reducing collagen production , and stimulating the activity of metalloproteinases , all of which may lead to reduction in the integrity of the extracellular matrix . FQs can damage type I and III collagen  that is present in the Achilles tendons , aorta , and aortic valves . The putative chain of pathophysiological events would include FQs that, through their high bioavailability and chelating properties, bind to the collagen leading to eventual degradation of the collagen matrix of the aortic or possibly the mitral valve. This can lead to subsequent aortic or mitral valve regurgitation. This hypothesis has been observed in at least 1 case report where a patient who took ciprofloxacin (750 mg twice daily) for 2 days developed symptoms of decompensation as a result of aortic valve prolapse that, following a cardiac work-up, could only be linked to ciprofloxacin use . The acute onset of collagen damage with FQs has also been shown to lead to rupture of large tendons within hours  and aortic dissection within days .

The results of this study found an association between oral fluoroquinolones and an increased risk of mitral and aortic regurgitation. As such, it might be prudent to consider antibiotics that are chemically distinct to FQs in patients with a previous history of valvular regurgitation who require antibacterial therapy. Future studies are urgently required to confirm or refute these findings

Podcast

Master Class: Utility of the EKG and CXR in Clinical Cases

This week, Mayo Clinic is hosting the Cardiovascular Board Review for Internal Certification and Recertification
Join Rick A. Nishimura, M.D, Samuel J. Asirvatham, M.D., and Carole A. Warnes, M.D. for a free LIVE stream

This is an example why the Mayo Clinic is THE premier institution in the country !

Left Atrial Pressure

Left atrial pressure, LAP, is becoming rapidly and important measurement to accurately treat patients in acute decompensated heart failure with congestion but also to rule out a component of pulmonary vascular congestion due to HfpEF.  Due to the dramatic decrease decline in use of pulmonary artery catheters, this is really the next best measurement we have for left ventricular filling/correlate to left ventricular end-diastolic pressure.

However in patients with moderate to severe ARDS that require proning due to severe hypoxemia, I still feel these patient's benefit from a pulmonary artery catheter.  Prior studies that  reviewed  the use of PA catheters was in all-comers in the MICU,  in a very inhomogeneous patient population, an Achilles heel in randomized control trials that limit any credibility regarding external validity.

Notable exception here is that a pulmonary artery catheter still remains a standard of care in post cardiac surgery patients, as well as stage IV class D for treatment decisions for in particular inotropic therapy with milrinone, heart failure patient and cardiogenic shock

I have posted earlier this year on diastolic function and a quick easy approach to assess intracardiac filling pressures.  This is a more complete article with the 2016 guidelines from ASE with attached PowerPoint presentation.

 Realize that most echocardiographic reports are quite inaccurate in determining the degree of diastolic dysfunction and are even more inaccurate in the determination of left atrial pressure. Tissue Doppler imaging from the lateral mitral annulus and medial mitral annulus has become a surrogate quick measure ( E/e' ratio)  for cardiologist and Intensivist ( by bedside US) to determine left atrial pressure. Nothing is farther from the truth : these numbers need to be correlated with additional markers and pressure measurements obtained by echocardiography to give an accurate value. This requires a comprehensive and somewhat time consuming procedure, particularly if done at the bedside.  In most patients on mechanical ventilation, it may not be possible to follow the guidelines to obtain all the measurements that go into the final determination of left atrial pressure/LAP

LBBB and Sgarbossa Criteria in acute MI

What is the diagnosis? What criteria are used to further analyze this EKG ?

Dr Rael Sundy from Tel-Aviv had the immediate answer: this tracing represent an acute anterior wall MI .

Ideally, diagnostic tests for life-threatening conditions (i.e. AMI) need to be highly sensitive.  The reason the original Sgarbossa criteria are limited in clinical practice is the low sensitivity (20%).  This is why a new LBBB alone is no longer a criteria for emergent cath lab activation. Recently, Steven Smith, MD from Dr. Smith’s ECG Blog published a new criterion to replace the third component of the original Sgarbossa Criteria using the ST/S ratio instead of discordant ST-elevation ≥ 5mm. 

 What are the new modified Sgarbossa Criteria?

Scandinavian Clinical practice guidelines for therapeutic hypothermia and post-resuscitation care after cardiac arrest

A little bit of an older article on TTM, but nevertheless a nice overview