Pregnancy Complications

Maternal death

When a birthing person dies during pregnancy or up to 42 days after giving birth from health problems r/t pregnancy

Pregnancy-related death

When a birthing person dies during pregnancy or within 42 days after birth from all deaths irrespective of cause

CVD in pregnancy

Maternal HTN

Peripartum cardiomyopathy

Myocardial infarction

Thromboembolic dz

Factors that increase the risk of CVD in pregnancy

Rising # of individuals w/ congenital heart dz of childbearing age, lifestyle trends that delay pregnancy and increase prevalence of risk factors such as obesity and substance use, and other chronic medical conditions like diabetes and HTN

How do risk factors contribute to CVD in pregnancy?

Chronic conditions and risk factors put added stress on the heart during pregnancy, labor, and childbirth, increasing the risk of complications

Classification of HTN disorders in pregnancy

Chronic HTN

Gestational HTN

Preeclampsia

Classified based on cause and timing of onset

Why is the incidence of HTN disorders in pregnancy increasing?

D/t rising rates of obesity and AMA

Racial disparities w/ HTN disorders in pregnancy

Significant rise in prevalence of chronic HTN among pregnant or PP African American individuals, also at higher risk of death from HTN d/o compared to other racial groups

Chronic HTN in pregnancy

Characterized by high BP levels of 140/90 or higher that occur before the 20th week of gestation or pesist beyond 12 weeks PP

Classification of chronic HTN

Can be classified into types --> primary/essential, secondary, severe, and superimposed

Primary/essential HTN

Elevated BP, no underlying cause

Secondary HTN

Elevated BP caused by underlying condition, such as atherosclerosis, endocrine d/o, renal dz, or certain meds

Severe HTN

BP 160 systolic and/or 110 diastolic or higher on 2 separate occasions 4 hours apart

Superimposed HTN

Sudden increase in baseline HTN, proteinuria, elevated liver enzymes, new onset thrombocytopenia

Maternal risks d/t chronic HTN

CVA, pulmonary edema, renal failure

Pregnancy complications --> PPH, C-section, placental abruption, superimposed preeclampsia

Fetal/newborn complications d/t chronic HTN

Fetal complications --> IUGR preterm birth, stillbirth and neonatal death

Gestational HTN

New onset high BP of 140/90 or higher AFTER 20 weeks gestation, without the presence of proteinuria or other multisystem features consistent w/ preeclampsia

Confirming gestational HTN dx

BP readings should be elevated on at least 2 separate occasions, at least 4 hours apart

Consideration w/ gestational HTN during PP period

If BP levels do not return to normal in the PP period, the condition may be considered chronic HTN

Most cases of gestational HTN arise at or after...

37 weeks gestation

Complications of gestational HTN

Thrombocytopenia, liver dysfunction, long-term CV risk, including development of chronic HTN

Differentiation of chronic and gestational HTN

Can be difficult if HTN emerges after 20 wks gestation or during PP period

Duration of gestational HTN to resolve is not definitively established, may take up to 2 years for BPs to normalize --> follow-up BP eval important

Preeclampsia

Onset of HTN after 20 weeks gestation, along with either proteinuria or multisystem disturbances indicative of dz severity

Note w/ proteinuria & preeclampsia

Used to be a diagnostic criterion but is no longer required because other severe s/sx of multi-organ involvement can accompany HTN

Underlying patho of preeclampsia

Not fully understood, theories suggest it occurs d/t changes in maternal CV, hematologic, and renal systems during pregnancy --> changes disrupt normal physiological adaptations during pregnancy and result in systemic vascular dysfunction

Factors that contribute to preeclampsia

Genetic predisposition, inflammatory responses, immunologic factors, maternal factors such as pre-existing CVD or metabolic syndrome, or a combination of these processes may result in abnormal placentation, contributing to placental ischemia and preeclampsia development

Risk factors for preeclampsia

AMA (> 40 y/o), obesity, chronic HTN, family hx of preeclampsia

Preeclampsia w/ a previous pregnancy, GDM/DM1, nulliparity

Preexisting medical or genetic conditions

Multiple gestation & assisted reproductive technology

S/Sx of mild preeclampsia

>140/90 (high BP), edema, and proteinuria

S/Sx of severe preeclampsia

Severe HTN (> 160 SBP and/or 110 DBP), severe HA unrelieved by meds, vision changes, photophobia, fatigue, N/V, epigastric pain, decreased UO, pulmonary edema, impaired liver function, decreased platelet levels

Assessment for preeclampsia

Baseline VS, lung sounds, DTRs, neuro status, and UO essential before initiating anti-HTN therapy or seizure prophylactic tx w/ mag sulfate

Intake and output while on mag sulfate for preeclampsia

Stric I&Os required because preeclampsia can cause reduced excretion of mag sulfate, increasing the risk of mag toxicity

S/Sx of mag toxicity

Loss of reflexes, resp depression, resp arrest, cardiac arrest

Preferred reversal agent for mag toxicity

Calcium gluconate

Pregnant individuals dx w/ HTN d/o

Lab assessment critical in monitoring for preeclampsia, evaluating presence of severe features, and detecting potential end-organ disturbances --> renal and liver functions tests and CBC w/ plt for hematologic evaluation, compare to baseline (some w/ pre-existing chronic HTN may have experienced renal dysfunction before latter half of pregnancy)

Renal function tests for preeclampsia lab assessment

24-hour urine or random UA --> look for proteinuria to determine presence of superimposed preeclampsia, CMP, protein/creatinine ratio

LFTs for preeclampsia lab assessment

AST, ALT, LDH

Hematologic evaluation for preeclampsia

CBC w/ platelets

Prevention of preeclampsia

Supplements --> calcium, zinc, mag, fish oil

High protein, low salt diet

Antihypertensive agents & loop diuretics

Low-dose aspirin (81 mg)

Primary tx for preeclampsia

Deliver the fetus or manage the condition until the fetus can be safely born

Management priorities for preeclampsia

Controlling HTN, providing seizure prophylaxis, monitoring for dz progression and severity, determining the appropriate timing of birth, and optimizing organ function

Acute severe HTN

Sustained high BP

Tx of acute severe HTN in preeclampsia

Urgent tx w/ first-line antihypertensive meds, such as labetalol, nifedipine, or hydralazine based on standardized EBP recs

Seizure prophylaxis for preeclampsia

Mag sulfate indicated for seizure prophylaxis if pt has severe features associated w/ preeclampsia --> given during labor & 24 hours PP, 6 gm bolus then 2gm/hour, ensure order for calcium gluconate on chart

Modes of birth for preeclampsia

Expectant management, induction of labor, c/s

Fetal surveillance tests for HTN d/o

Fetal doppler studies, AFI, NST, fetal growth US, BPP

Fetal doppler studies

Doppler US uses sound waves to detect movement of blood in vessels, can detect changes in flow or decreased flow in the umbilical artery

Normal AFI

5-25 cm

AFI in oligohydramnios

< 5 cm

AFI in polyhydramnios

> 25 cm

NST

2 or more accelerations 15x15 over 20-30 min for fetus 32 weeks or older

2 or more accelerations 10x10 over 20-30 min for fetus 32 weeks or younger

Fetal growth US in HTN d/o

Can detect SGA or IUGR

BPP

NST allows for FHR exam

Breathing, movement, muscle tone, AFI, can be scheduled once or twice a week

Antepartum fetal assessment in HTN pregnancies

Helps prevent perinatal morbidity and mortality --> pathophys of chronic maternal HTN often leads to placental insufficiency, fetal growth restriction, and stillbirth

Eclampsia

Severe complication of preeclampsia and is associated w/ significant maternal and fetal mortality

Onset of eclampsia

Can occur at any stage of pregnancy after 20 weeks gestation or during the PP period

Etiology of eclampsia

Exact physiological mechanism unclear, theories suggest that cerebral overperfusion triggers vasoconstriction in the middle cerebral artery as a protective mechanism for sensitive brain regions

Also believed that increased permeability of the BBB during preeclampsia, along w/ impaired autoregulation, contributes to the development of eclampsia

Main clinical feature of eclampsia

New onset of generalized tonic-clonic seizures

Seizures can occur in the antepartum, intrapartum, or PP period

How long do the generalized tonic-clonic seizures last in eclampsia?

Last 60-90 seconds in duration

Note w/ seizure warning signs in eclamptic patients

Significant proportion of individuals w/ eclampsia may not exhibit any warning signs before the onset of seizures

However, premonitory signs of cerebral irritation can precede onset of seizures

Premonitory or warning signs for impending seizures in eclamptic patients

Persistent HA, vision changes/disturbances, photophobia (sensitivity to light)

AMS, abdominal pain in epigastric region or RUQ, severe range BP/increase in BP to 160 SBP or greater and/or 110 DBP or greater

Preparing for seizure management in eclamptic patients

Immediate preparations include having O2 supplies, padded side rails, and an Ambu bag readily accessible for resuscitation

Management of eclamptic seizure during/after the seizure

Prevent aspiration by positioning pt on their side with the HOB slightly lowered

After the seizure, secure the airway (assess for apnea or hyperventilation), maintain O2 levels, monitor O2 sat and BP, and prepare to admin mag sulfate and anti-HTN meds

Document onset & duration of seizure, assess for s/sx of mag toxicity

Assessing fetal status after an eclamptic seizure

Important because decreased blood flow to the placenta (decreased uteroplacental perfusion) can lead to fetal bradycardia

Considering birth after eclamptic seizure

Initial interventions should focus on stabilizing pregnant pt before considering the expeditious initiation of a cesarean birth

HELLP syndrome

Hemolysis, Elevated Liver enzymes, Low Patelets

Onset of HELLP and relation to preeclampsia

Closely associated w/ preeclampsia, underlying endothelial dysfunction in preeclampsia contributes to the hematologic and hepatic effects seen in HELLP

Whether it is subset of preeclampsia or separate d/o is controversial because subset of HELLP pts may not have HTN or proteinuria

Typically manifests in 3rd trimester of pregnancy but can also occur in the PP period

S/Sx of HELLP

Nonspecific -- N/V, malaise, epigastric pain -- makes prompt and accurate dx difficult

Epigastric pain in HELLP

Can indicate hepatic involvement but may also be attributed to other conditions such as fatty liver dz or gallbladder dz

Complications of HELLP

Severe --> placental abruption, hepatic subcapsular hemorrhage/rupture, recurrent preeclampsia, renal failure, maternal/fetal death

Management of both HELLP syndrome and severe preeclampsia

Timely delivery and optimization of organ perfusion to minimize further complications for pregnant or PP person and fetus

Risk factors for HELLP syndrome

HTN d/o in pregnancy, chronic HTN, > 30 y/o

Multiparity, multiple gestation, European descent

Obesity, placental d/o, congenital anomalies

Chronic cardiac conditions, pre-pregnancy DM

Management of HELLP syndrome

Monitoring OB complications

Management of HTN

Seizure prophylaxis

Planning for delivery

Monitoring for OB complications in HELLP syndrome

Regular assessments of BP, liver function, PLT count, and other relevant parameters

Management of HTN in HELLP

Anti-HTN meds may be given to maintain BP w/i safe range

Seizure prophylaxis in HELLP

Mag sulfate commonly admin to prevent seizures

Planning for delivery in HELLP

Becomes essential, primary tx approach for HELLP --> immediate delivery of newborn and placenta regardless of gestational age

Incidence and onset of peripartum cardiomyopathy (PPCM)

Rare and complex conditions that primarily affects individuals during late pregnancy or early PP

Hemodynamic changes during pregnancy & PPCM

Increased preload and CO during pregnancy may be potential triggers but are not the sole cause, other factors are likely involved

Etiology/causes/triggers of PPCM

Complex and multifactorial --> hemodynamic changes during pregnancy, viral infections (myocarditis-associated viruses like echovirus, Coxsackie, and parvovirus B19), hormonal changes, genetic factors, pro-inflammatory states, and autoimmune responses

Timing of PPCM

Typically manifests after 36 weeks of gestation or within the first month PP

Earlier presentation may occur in individuals w/ preexisting cardiac conditions, such as valvular or ischemic cardiomyopathy

S/Sx of PPCM

Can vary based on severity of dz at time of dz

R/t both HF and pregnancy --> paroxysmal nocturnal dyspnea, pedal edema, orthopnea, DOE, dry cough, palpitations, increased abdominal girth, lightheadedness, chest pain

Clinical examination findings for PPCM

S3 heart sound, JVD, displaced apical impulse, murmurs r/t mitral regurg -- reflect cardiac and hemodynamic changes characteristic of PPCM

Meds for PPCM

Caution w/ diuretics

ACE inhibitors and ARBs contraindicated d/t teratogenic effects

Good options include beta blockers (B1 selective in particular( and hydralazine

Inotropes like dobutamine and digoxin can be used in critical cases

Using diuretics in PPCM

Preload optimization through diuresis and fluid balance is essential, but caution is needed during pregnancy to avoids meds that can cause fetal harm

Can use HCTZ and furosemide cautiously w/ close monitoring

Anticoagulation for PPCM

Controversial, should be considered based on individual factors like Afib or presence of left ventricular thrombus

Advanced interventions for PPCM

ICDs and cardiac resynchronization therapy should be evaluated in context of dz's natural hx

Mechanical circulatory support w/ LVADs can be conisdered in severe cases

Maternal complications of PPCM

Thromboembolism, arrhythmias, progressive HF, and the potential for misdiagnosis as preeclampsia d/t overlapping symptoms -- significant risks to birthing person's health during pregnancy and PP period

Fetal complications of PPCM

Maternal heart dysfunction can cause fetal distress and hypoxia d/t reduced oxygen supply

Acute MI during pregnancy

Rare, more common during third trimester and PP

Risk factors for pregnancy-associated MI

Common causes --> HTN, obesity, DM, AMA

Pregnancy-specific factors --> PP infection and blood transfusion

Diagnostic challenges for pregnancy-associated MI

Typical pregnancy symptoms can resemble those of an MI, so any suspicion of cardiac involvement should trigger immediate evaluation through an ECG and labs

Dx of pregnancy-related MI

Elevated ST segments on ECG and cardiac troponin I suggest MI/acute coronary syndrome during pregnancy, requiring prompt tx

Most critical therapy for acute MI during pregnancy

Rapid reperfusion of the cardiac muscle, typically through PCI w/ placement of a bare metal stent to restore blood flow to the affected coronary artery

Primary goal of CVD management in pregnancy

Maximize CO while minimizing metabolic demand throughout pregnancy, labor, and birth

Common complications of pregnancy

HF and arrhythmias -- early detection and management critical, pregnant individuals w/ known CVD should receive thorough and regular evaluation

S/Sx of HF

Increased JVD, peripheral edema, adventitious lung sounds, or marked SOB

Arrhythmias in pregnancy

Should be promptly addressed if irregular HR or palpitations are reported

When necessary, cardioversion, pacing, or defibrillation may be used to address severe arrhythmias

Management of labor and birth in CVD

Interventions may be needed to optimize preload and afterload, thus maximizing CO based on underlying cardiac condition

Meds, intravascular volume adjustments, and pain management strategies should be carefully considered

Choice of delivery w/ CVD in pregnancy

Well-structured labor and vaginal birth approach is preferred unless there is a specific obstetric indication for an elective c/s

Anesthesia and pain management in birthing individuals w/ CVD

Early epidural anesthesia helps manage pain and mitigate sympathetic response to pain, which can trigger tachycardia and increase myocardial workload = early epidural helps decrease myocardial workload