This document discusses cardiac disease in pregnancy. It notes that cardiac disease affects 1-2% of pregnancies and is a leading cause of maternal mortality. Rheumatic heart disease is the most common in many countries. Physiological changes in pregnancy like increased cardiac output place extra burden on the heart. Close monitoring and management of cardiac patients is needed before, during and after pregnancy to optimize outcomes for both mother and baby. A multidisciplinary team approach is important for treating women with heart disease through pregnancy.
The increased cardiac output related to pregnancy can lead to heart failure, and the increased heart rate in the third trimester can lead to ischemic events. The potential obstetrical complications include preeclampsia or other hypertensive related disorders, premature birth, and small-for-gestational-age births.
Uterine Rupture
Deepa Mishra
Assistant Professor (OBG)
Introduction
Uterine rupture is when the muscular wall of the uterus tears during pregnancy or childbirth
Symptoms while classically including increased pain, vaginal bleeding, or a change in contractions are not always present.
Disability or death of the mother or baby may result.
Definition
Uterine rupture is giving way of gravid uterus or dissolution in the continuity of uterine wall anytime after 28 weeks of gestation with or without expulsion of the fetus.
Incidence
Rates of uterine rupture during vaginal birth following one previous C-section, done by the typical technique, are estimated at 0.9%
Rates are greater among those who have had multiple prior C-sections or an atypical type of C-section.
In those who do have uterine scarring, the risk during a vaginal birth is about 1 per 12,000
Risk of death of the baby is about 6%
Etiology
Risk Factors
Previous cesarean section
Myomectomy
Dysfunctional labor
Labor augmentation by oxytocin or prostaglandins
High parity
First pregnancy- very rare
Types of uterine rupture
Complete Rupture
All the layers including peritoneum are torn and the uterine contents escape into the peritoneal cavity.
Usually results in death
Incomplete Rupture
Visceral peritoneum is intact and usually the fetus remains in the uterine cavity
Sign & Symptoms
Uterine dehiscence and abdominal pain and vaginal bleeding
Deterioration of fetal heart rate
Loss of fetal station on manual vaginal exam
Hypovolemic shock due to intrabdominal bleeding
Chest pain between the scapulae, pain during inspiration due to irritation of blood below the perineum
Cessation of uterine contractions
Palpation of fetus outside the uterus
Signs of abdominal pregnancy
Post term pregnancy
Diagnosis
Signs of obstructed labor with dehydration, exhaustion, tachycardia raised temperature tonic contraction , pathological retraction ring
Absent fetal heart sound
On PV hot, dry vagina with a large caput over the presenting part
Prevention
Early diagnosis and management of CPD mal presentation and obstructed labor
Proper selection of cases for vaginal delivery
Carefull monitoring of oxytocin infusion specially in multipara
Avoid intra uterine manipulation no version in single fetus
Instrumental delivery after cervical dilatation
Immediate CS in obstructed labor
Hospital delivery for high risk cases
ECV should be avoided during general anaesthesia
Careful manual removal of placenta
Treatment
Resuscitation with adequate hydration and blood transfusion
Laprotomy
Hysterectomy
Repair
Complication
Rupture uterus with haemorrhage, shock and sepsis
Fetal loss is high in spontaneous and traumatic rupture
Mortality is low in LSCS scar rupture
ACOG
ACOG 2019 Guidelines
American College of Obstetrics and Gynecology
Practice Bulletin
CVD in pregnancy
Cardiovascular Diseases in pregnancy
Managing heart disease in pregnancy
Managing heart diseases after pregnanacy
post-partum management of heart diseases in pregnancy
New ESC guideline on cardiovascular disease in pregnancyArunSharma10
New ESC Guideline on Cardiovascular Disease in Pregnancy
Management of Cardiovascular Diseases During Pregnancy
Women with CVD
LMWH
Drugs during pregnancy and breastfeeding
Valvular heart disease
Coronary artery disease
Pregnancy is complicated by maternal disease in 1–4% of cases
The increased cardiac output related to pregnancy can lead to heart failure, and the increased heart rate in the third trimester can lead to ischemic events. The potential obstetrical complications include preeclampsia or other hypertensive related disorders, premature birth, and small-for-gestational-age births.
Uterine Rupture
Deepa Mishra
Assistant Professor (OBG)
Introduction
Uterine rupture is when the muscular wall of the uterus tears during pregnancy or childbirth
Symptoms while classically including increased pain, vaginal bleeding, or a change in contractions are not always present.
Disability or death of the mother or baby may result.
Definition
Uterine rupture is giving way of gravid uterus or dissolution in the continuity of uterine wall anytime after 28 weeks of gestation with or without expulsion of the fetus.
Incidence
Rates of uterine rupture during vaginal birth following one previous C-section, done by the typical technique, are estimated at 0.9%
Rates are greater among those who have had multiple prior C-sections or an atypical type of C-section.
In those who do have uterine scarring, the risk during a vaginal birth is about 1 per 12,000
Risk of death of the baby is about 6%
Etiology
Risk Factors
Previous cesarean section
Myomectomy
Dysfunctional labor
Labor augmentation by oxytocin or prostaglandins
High parity
First pregnancy- very rare
Types of uterine rupture
Complete Rupture
All the layers including peritoneum are torn and the uterine contents escape into the peritoneal cavity.
Usually results in death
Incomplete Rupture
Visceral peritoneum is intact and usually the fetus remains in the uterine cavity
Sign & Symptoms
Uterine dehiscence and abdominal pain and vaginal bleeding
Deterioration of fetal heart rate
Loss of fetal station on manual vaginal exam
Hypovolemic shock due to intrabdominal bleeding
Chest pain between the scapulae, pain during inspiration due to irritation of blood below the perineum
Cessation of uterine contractions
Palpation of fetus outside the uterus
Signs of abdominal pregnancy
Post term pregnancy
Diagnosis
Signs of obstructed labor with dehydration, exhaustion, tachycardia raised temperature tonic contraction , pathological retraction ring
Absent fetal heart sound
On PV hot, dry vagina with a large caput over the presenting part
Prevention
Early diagnosis and management of CPD mal presentation and obstructed labor
Proper selection of cases for vaginal delivery
Carefull monitoring of oxytocin infusion specially in multipara
Avoid intra uterine manipulation no version in single fetus
Instrumental delivery after cervical dilatation
Immediate CS in obstructed labor
Hospital delivery for high risk cases
ECV should be avoided during general anaesthesia
Careful manual removal of placenta
Treatment
Resuscitation with adequate hydration and blood transfusion
Laprotomy
Hysterectomy
Repair
Complication
Rupture uterus with haemorrhage, shock and sepsis
Fetal loss is high in spontaneous and traumatic rupture
Mortality is low in LSCS scar rupture
ACOG
ACOG 2019 Guidelines
American College of Obstetrics and Gynecology
Practice Bulletin
CVD in pregnancy
Cardiovascular Diseases in pregnancy
Managing heart disease in pregnancy
Managing heart diseases after pregnanacy
post-partum management of heart diseases in pregnancy
New ESC guideline on cardiovascular disease in pregnancyArunSharma10
New ESC Guideline on Cardiovascular Disease in Pregnancy
Management of Cardiovascular Diseases During Pregnancy
Women with CVD
LMWH
Drugs during pregnancy and breastfeeding
Valvular heart disease
Coronary artery disease
Pregnancy is complicated by maternal disease in 1–4% of cases
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. PREGNANCY AND HEART DISEASE
Cardiac disease affects 1-2%
of all pregnancies.
One of the leading causes of
maternal mortality and
morbidity
Higher incidence of fetal and
neonatal adverse events
3. PREGNANCY AND HEART DISEASE
Rheumatic heart disease is the most common
heart disease complicating pregnancy in our
country
Congenital heart disease is encountered as
advances in medical and surgical treatment
have resulted in improved survival.
CAD is expected to grow because of advanced
maternal age and higher incidence of risk
factors
5. Abrupt hemodynamic changes occur secondary
to pain anxiety and uterine contractions
With each uterine contraction extrusion of
approximately 500ml of blood into central
venous system
CVS Physiology
Periods of greatest risk of cardiac events
24-28 wks
Early 3rd trimester
Delivery
Immediate postpartum
6. CVS Physiology in Labour
Rapid increase in HR and BP
Cardiac output is often 50% above
baseline during 2nd stage, may be even
higher at the time of delivery
After delivery, abrupt increase in venous
return (due to autotranfusion and release of
IVC compression)
7. CVS Physiology in Labour
Excessive blood loss in normal vaginal
delivery / C-section can alter cardiac status
Cardiovascular adaptations associated with
pregnancy regress by approx. 6wks after
delivery
8. Decreased exercise capacity
Tiredness
Dyspnoea
Palpitations
Lightheadedness
Presyncope
Symptoms during normal pregnancy
that may mimic cardiac disease
14. Pre-conceptional counselling
Obstetrician and cardiologist should
work together
Prevent an unwanted pregnancy and
asses the risks associated with
pregnancy
Continuation OR Termination
15. CHD in offspring of a parent with CHD
CHD in a Parent Risk of CHD in Offspring(%)
IC shunts- ASD 3 - 11
VSD 4 - 22
PDA 4 - 11
Obstruction to flow
Lt sided 3 - 26
Rt sided 4 - 15
HCM 50 (AD)
Marfan’s syndrome 50 (AD)
Risk is 4% Vs 0.4 - 0.6% in general population
16. Maternal mortality risk and cardiac disease
Group Cardiac disease Associated mortality risk
I Mitral /aortic stenosis, NYHA Class I, II
Atrial septal defect* <1%
Aortic/Mitral regurgitation
Pulmonary/tricuspid valve disease
Corrected tetralogy of Fallot
Bioprosthetic valve
Small –moderate VSD/PDA
II Uncorrected tetralogy of Fallot 5% - 15%
Marfan’s syndrome with normal aorta
Mechanical prosthetic valve
Severe Mitral stenosis with AF or NYHA Class III, IV
Severe Aortic stenosis
Previous myocardial infarction
III Pulmonary hypertension—primary or secondary 25% - 50%
Coarctation of aorta with valvular involvement
Marfan’s syndrome with aortic involvement
Peripartum cardiomyopathy
17. Maternal Risk
Stenotic lesions on the left side are not well
tolerated as cardiac output is markedly reduced.
Regurgitant lesions are well tolerated
Congenital heart disease with L-R shunts are
well tolerated due to fall in SVR
R-L lesions and cyanotic lesions not tolerated
Pulmonary HT carries high risk
18. Risk Index
Preconception history of adverse cardiac events
Poor functional class before pregnancy(NYHA class >II)
Left heart obstruction -MVOA < 1 sqcm
AVA <1.5sqcm
Peak LVOT grd >30mmHg
LV EF <40%
Estimated risk of adverse cardiac event
0 ------- 5%
1 ------- 27%
>1 ------- 75%
Multicentric Canadian Study . Circulation104;155,2001
19. First Visit
Detailed history
The patient’s functional status as per
New York Heart Association(NYHA)
Cardiology consultation
ECG , ECHO
20. 6/9/2021 20
NEW YORK HEART ASSOCIATION
FUNCTIONAL CLASSIFICATION OF CARDIAC DISEASE
CLASS I No functional limitation of activity.
No symptoms of cardiac decompensation with activity.
CLASS II Patients are asymptomatic at rest. Ordinary physical
activity results in symptoms.
CLASS III Limitation of most physical activity.
Asymptomatic at rest
Minimal physical activity results in symptoms.
CLASS IV Severe limitation of physical activity results in
symptoms.
Patients may be symptomatic at rest/heart failure
at any point of pregnancy.
22. Termination of pregnancy
TERMINATION - <12wks OF PREGNANCY
Eisenmenger's syndrome
Marfan syndrome with aortic involvement
Severe Pulmonary hypertension
Coarctation of aorta
Symptomatic severe AS, MS
Severe left ventricular dysfunction EF<40%
Metallic prosthetic valve -complications
23. Antepartum Care
NYHA CLASS I or II
1. Limit strenuous exercise
2. Adequate rest
3. Iron and Vitamins to minimize anemia
4. Low salt diet if ventricular dysfunction
5. Regular cardiac and obstetric evaluation
Identify and treat early - infections, anemia,
hypertension, hyperthyroidism & arrthymias
24. NYHA CLASS III or IV
1. Hospitalisation for bed rest
2. Intensive Close monitoring
3. Cardiac intervention, surgery
4. Termination of pregnancy
Treat precipitating events – infections,
arrhythmia, anemia, hyperthyroidism
25. PREGNANCY AND DRUGS
STENOTIC LESIONS REGURGITATION LESIONS
• Bblocker: metoprolol ,propranolol
(class C ),atenolol (class D ).
• C channel antagonist: verapamil ,
diltiazem (class C)
• Digoxin : (class C).
• Diuretic: for patient with pulmonary
congestion.
• Vasodilators: only If BP is high :
• Hydralazine:(class C ).
• Nitrate :(class C ).
• Diuretic:
• Thiazide: ( class B).
• Loop diuretic: (class C ).
• Avoid hypotension & placental
hypoperfusion
ACE inhibitor ,ARBS (class X ).
26. Arrhythmia
Acute atrial flutter or atrial fibrillation, should be
treated promptly.
If possible, all antiarrhythmic drugs should
be avoided during the first trimester, and those
known to be teratogenic should be avoided
throughout pregnancy.
Because of their safety profiles, preferred drugs
include digoxin, beta-blockers and adenosine.
27. Interventional or surgical Cardiac
management
Optimal time – second trimester
Balloon valvotomies preferred
Open heart surgery-- Higher risk of fetal
malformation and fetal loss in first trimester
(10-30%), Premature labour in third trimester
29. ANTICOAGULATION
Adjusted dose UFH bid subcutaneous throughout
pregnancy to achieve mid-interval aPTT at least twice
control
Adjusted dose LMWH bid subcutaneous 1mg/kg
throughout pregnancy to achieve a peak anti-Xa level
of 0.7-1.2 U/ml 4 hours after injection
UFH or LMWH (as above) until 12 weeks' gestation,
change to warfarin until the middle of the third
trimester, and then restart UFH or LMWH
30. ANTICOAGULATION
Current practical guidelines
Warfarin during entire pregnancy but
substitute heparin during peak teratogenic
period (6th to 12th week)
Warfarin upto 36 wks
Switch over to heparin 2 weeks before labour
32. Heparin & LMWH
Heparin does not cross placenta, no teratogenic
effect
Subcutaneous high dose (16,000 to 24,000
units/ day) to maintain APTT 1.5 to 2
Maternal thrombocytopenia, osteoporosis, sterile
abscesses, hematoma, maternal death 6-7%
33. Heparin & LMWH
LMWH – 1 mg/kg body wt (Enoxaparin)
Effective, easier to use & safe
Expensive, clinical trials needed
34. Warfarin therapy
Warfarin in the first trimester of pregnancy
is associated with increase -
foetal wastage
prematurity
low birth weight
Risk of valve thrombosis (3.9%)
Warfarin embryopathy in 6.4% of live
births.
35. Fetal intracranial bleeding: 4 - 10%
throughout pregnancy, during vaginal
delivery
Study of 55 pregnancies – Warfarin < 5 mg
No cases of embryopathy
36. ANTICOAGULANT THERAPY IN PREGNANCY
MATERNAL
DEATH
THROMBO
EMBOLISM
EMBRYOPATHY
THERAPY
1.8%
3.9%
6.4-10%
Vit k antagonist
throughout
pregnancy
40%
60%
0%
Low dose UFH
throughout
pregnancy
6.7%
25%
0%
Adjusted dose
UFH throughout
pregnancy
4.2%
9.2%
3.4%
UFH in 1st
trimester then Vit k
antagonist up to
36wk
37. Warfarin is the favored anticoagulant during
the 2nd, 3rd trimesters until the 36th wk
(Class IC ESC guidelines).
Warfarin is favored in the 1st trimester if the
dose <5mg /24hrs(Class IIaC ECS guidelines)
ESC Guidelines
38.
39. MODE OF DELIVERY
Normal vaginal delivery is advised in
patients who are hemodynamically stable
class IC (ESC guidelines)
Cesarean section is indicated in:
1. Aortic dissection.
2. Marfan syndrome with dilated aortic root.
3. Hemodynamically Unstabillity in particular
case of severe AS.
4. Obstetric causes .
40. MODE OF DELIVERY
Intensive Hemodynamic monitoring is
recommended in case of severe stenotic lesions
or low EF.
Admit few days before labour
Monitor pulse, BP, Oxygen saturation
Oxygen inhalation
41. Careful attention to volume status is
essential
NS < 75 ml/hr 30ml/hr
Inj. Frusemide , Digoxin
Asses pulmonary basal crepts, JVP
Treatment of arrhythmias
Epidural analgesia to provide analgesia
and thus avoid I in CO due to pain and
anxiety,
42. Obstetric procedures (ventouse / forceps) to
cut short the 2nd stage of labour will
decrease the hemodynamic consequences
Left Lateral decubitus position is preferred to
attenuate the hemodynamic effect of the
supine position .
Slight blood loss is beneficial, Inj Frusemide
43. ENDOCARDITIS PROPHYLAXIS
Required in patients of prosthetic valve / cardiac
device implants
Previous history of IE
Used routinely in all pts as an uncomplicated
delivery cannot always be anticipated (not
recommended by AHA)
44. POSTPARTUM CARE
Hemodynamics do not return to baseline for
many days after delivery
Patients at intermediate or high risk may
require monitoring for at least 72 hours
postpartum.
Lactation should be encouraged unless
patient is in failure.
45. POSTPARTUM CARE
Cardiac output is not compromised during
lactation.
Lactation is a pathway for fluid excretion
and diuretic requirement may actually fall.
46. CONCLUSION
PREPREGNANCY COUNSELLING AND RISK
STRATIFICATION SHOULD BE DONE TO ALL WOMEN
WITH HEART DISEASE
TREATMENT OPTIONS AT PROPER SHOULD BE GIVEN
SUCCESSFUL PREGNANCY IS POSSIBLE FOR GROUP I
& II PATIENTS WITH HEART DISEASE
OPTIMAL CARE REQUIRES A MULTIDISCIPLINARY
TEAM APPROACH