1 / 94

Healthy Hearts: Promoting Potency, Preventing Predicaments, Perplexing Presenting Problems

Healthy Hearts: Promoting Potency, Preventing Predicaments, Perplexing Presenting Problems. 32 nd Annual Nicholas J. Thompson Women ’ s Health Conference April 18, 2012. Richard Pretorius, MD, MPH Professor of Family Medicine Professor of Geriatrics Assistant Dean for Quality & Primary Care

kamal
Télécharger la présentation

Healthy Hearts: Promoting Potency, Preventing Predicaments, Perplexing Presenting Problems

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Healthy Hearts: Promoting Potency, Preventing Predicaments, Perplexing Presenting Problems 32nd Annual Nicholas J. Thompson Women’s Health ConferenceApril 18, 2012 Richard Pretorius, MD, MPH Professor of Family Medicine Professor of Geriatrics Assistant Dean for Quality & Primary Care Research

  2. The heart is a dynamic organ that is always in motion. There are four components of the heart that must work in synergy: a) the pump b) the plumbing c) the wiring d) the gates We will explore how healthy physiology in women can prevent undesired pathology.

  3. obstetrics cardiology

  4. obste-trics cardio-logy

  5. Background • Speaker’s involvement with CV health: • 20+ yrs of practice in a country where 50% of pop dies from CV ds • 9 yrs as medical director of a nursing home • 2 bk chapters on heart health: • Pretorius R and Franklin M. Chapter 22 Chronic cardiac disease. Essentials of Family Medicine, editors Sloane P et al., 3rd edition, 1998. • Pretorius R. Chapter 27 Congestive heart failure. Ambulatory Geriatrics: A Practical Approach, editors Rosenthal T, Naughton B, Williams M, 1st edition, 2006.

  6. Background • Speaker’s involvement with OB: • 20+ yrs of deliveries • Advanced Life Support in Obstetric (ALSO) • Course instructor (4) • Course director (2) • National teaching faculty (3), ALSO Instructor Course • 34 consecutive vaginal deliveries in a hospital with a 41% c/s rate

  7. Background • Speaker’s involvement with an integrated, multidisciplinary approach to medical education: • Improve med student scores from 89% pass rate to 100% in Intro to Clinical Medicine • Improve scores in cardiology course from 84% pass rate to 98% • Improve USMLE Step 1 scores for class mean by 5 to 6%

  8. Outline • Introduction • A case based approach • Principles of cardiovascular health • Summary

  9. Learning Objectives • To understand the relationship between the 4 components of the heart. • To distinguish accurately between normal physiology and acute and chronic dysfunction. • To understand the interaction of the CV system with other systems (renal, hepatic, etc). • To appreciate the heart as a dynamic organ that is always changing. • To use sound clinical reasoning to solve clinical dilemmas.

  10. Case-Based Learning • Real cases will be used to illustrate important learning principles. • While not all cases may occur in the daily practice of the participants, the learning principles will apply.

  11. BACK TO BASICS If I were giving a young man advice as to how he might succeed in life, I would say to him, pick out a good father and mother, and begin life in Ohio. Wilber Wright, 1910

  12. Dayton claimed more patents per capita than any other U.S. city in 1900. U.S. Patent Office Grand Eccentrics: Turning the Century: Dayton and the Inventing of America by Mark Bernstein

  13. CASE #1 • A 20 yo primip at 32 wks gestation with a BMI 55 has gained 15 lbs in the past 4 wks and 50 lbs for the pregnancy. You admit her with a P.O. 88% on RA that improves to 95% on 4 l/min NC. CxR shows pul edema with small b/l pleural effusions. Labs show uric acid 5.2, BUN/creat 20/0.8, 350 mg protein in 24 hr urine.

  14. CASE #1: question In this pt, a diuretic: • Would improve the pt’s clinical status. • Would worsen the patient’s clinical status. • Is not relevant to the optimum therapeutic choices.

  15. CASE #1: another question In this pt: A. The intravascular space is contracted. B. The intravascular space is expanded. C. The renal endothelium has been injured. D. Two of the above. E. None of the above.

  16. obesity • Obesity rate 38% in reproductive age women in past decade. Ehrenberg, 2004, Am J Ob Gyn

  17. HTN in pregnancy: definitions Preexisting hypertension • SBP ≥140 mmHg and/or DBP ≥90 mmHg that either: • antedates pregnancy. • begins before the 20th wk of pregnancy. • persists longer than 12 wks postpartum. Gestational hypertension • Inc’d BP after 20 wks of gestation in the absence of proteinuria. Preeclampsia superimposed upon preexisting hypertension • new onset of proteinuria after 20 wks gestation in a woman with preexisting HTN. Preeclampsia-eclampsia • new onset HTN & proteinuria after 20 wks gestation. • worsening HTN with new onset proteinuria in a woman with preexisting hypertension.

  18. Interconnections • Preexisting HTN • Gestational HTN • Up to 25% develop proteinuria and thus progress to preeclampsia • 15% develop HTN • Preeclampsia superimposed upon preexisting hypertension • Up to 30% of women with chronic HTN develop preeclampsia • Preeclampsia-eclampsia • Up to 20% develop HELLP, however up to 20% pts with HELLP have no HTN nor proteinuria

  19. LV dysfunction common intrapartum & PP Melchiorrea 2011

  20. Diastolic dysfunction more common Melchiorrea, 2011

  21. Obese pregnant woman (2003): 14% all 7% white 21% black Aly, 2010

  22. obesity • For 1st trimester BMI > 30: • 20.8% developed preeclampsia • For normal wt: • 5.8% developed preeclampsia • Controlled for age and parity. • N=250 Aghamohammadi, 2011

  23. BMI sig increases risk of preeclampsia Vasudevan, 2010

  24. Inc’d BMI not associated with prematurity Aly, 2010

  25. Preeclampsia predicts future HTN Bilhartz, 2011

  26. CV changes with preg Simpson, 2012

  27. CV changes with preg

  28. Where is the excessive fluid? • Intravascular • Arterial? • Venous? • Lungs/pleural cavity • Peritoneal cavity • Extremities Where is Waldo?

  29. Where is the fluid? • A pt has a rise in baseline creatinine, say from 1.0 to 2.0. • Is the prerenal pt WET or DRY?

  30. Creatinine reaches nadir at dry wt.

  31. Or, more correctly, BUN/creatinine ratio reaches nadir at dry weight.

  32. Keeping score: multifactorial analysis

  33. Urine indices of prerenal causes of oliguriavs renal ATN Al-Khafaji A, 2002

  34. Preventing Maternal Death10 Clinical Diamonds • A preg pt reporting acute CP always should undergo an immediate CTA. • A pt with preeclampsia reporting SOB should undergo a CxR immediately. • Any hospitalized pt with preeclampsia with either a SBP 160 or a DBP 110 should receive an IV antihypertensive agent within 15 min. • Angiographic embolization is not meant to be used for acute, massive PP hemorrhage. • Any pt with identified structural or functional cardiac ds gets a maternal–fetal med consultation. Clark, 2012

  35. Preventing Maternal Death10 Clinical Diamonds • If more than a single dose of med is necessary to treat uterine atony, go to the pt’s bedside until the atony has resolved. • Never treat “PP hemorrhage” without simultaneously pursuing an actual clinical dx. • In the PP pt who is bleeding or who recently has stopped bleeding & is oliguric, furosemide is not the answer. • Any woman with placental previa and one or more c/s should be evaluated and delivered in a tertiary care medical center. • If your L&D does not have a recently updated massive transfusion protocol based on established trauma protocols, get one today.

  36. CV mortality in preg is rising

  37. upward trend in PRMR, black > white maternal deaths per 100,000 live births Callaghan, 2011

  38. changes in preg mortality • Trends • Better case identification and reporting • More deaths attributable to chronic medical conditions (indirect deaths) • Better OB care decreases direct deaths • More women come with preexisting medical conditions Callaghan, 2011

  39. CASE #2 • A 64 yo female with h/o well controlled metabolic syndrome and a coronary stent placed a yr early had c/o fatigue & diaphoresis for 30 min after planting rose bushes for an hr. • There was no CP, SOB, nausea. • A routine exercise stress test 6 days earlier was neg.

  40. CASE #2: questions • What do you think is going on? • What is your plan?

  41. Prevalence of Silent Ischemia • In pts with stable CAD: • asymptomatic ischemic occurs more often than symptomatic • ½ have transient ST depression on ambulatory ECG, likely representing ischemia • In pts with unstable CAD: • Nearly ½ with silent ischemia on continuous ECG monitoring Conti, 2012

  42. Silent Ischemia is Very Common

  43. Sequence of Events After Coronary Artery Occlusion Conti, 2012

  44. One solution: walking Dose-response between walking MET-h week and risk of total CVD. Boone-Heinonen, 2008

  45. CASE # 3 • A 91 yo female who has not seen a physician in 30 yrs comes to your office with a 2 month h/o fatigue & dyspnea and now cannot walk 10 feet without SOB. • PE shows 2+ LE edema, 2+ presacral edema, abd dullness 1/3 up flanks & thoracic dullness 2/3 up. • EKG shows a fib, otherwise neg, no evidence ischemia, infarct, atrial or ventr enlargement.

  46. CASE #3: question According to the NYHA, this pt has: • Class I heart failure (cardiac ds, no sxswith ordinary physical activity) • Class II heart failure (cardiac ds, no sxs at rest, sxs with ordinary physical activity) • Class III heart failure (cardiac ds, no sxs at rest, sxs with minimal activity) • Class IV heart failure (cardiac ds, sxs at rest)

More Related