Lecture Outline Caring for the Critically Ill Review normal cardiopulmonary physiology of pregnancy Pregnant Patient Address management of critical illness duringgp preg nancy Mary Anne Morgan, MD General supportive care Pulmonary & Critical Care Critical illness & pregnancy September 17, 2012 The Case of the Particularly-Plagued Pregnancy Physiologic Changes in Pregnancy: Hyperpnea of Pregnancy Cardiopulmonary System Alterations in: Early: VT increases, Ventilation & respiratory drive RR little change Oxygen consumption increased Ve Structural changes in chest (hyperventilation) wall and in airway mucosa Offsets ↑ metabolic Total body fluid and cardiac rate output Net result: ↓PaCO2 Systemic vascular resistance 40 28-32 respiratory alkalosis Hyperpnea of Pregnancy: Oxygen Exchange in Pregnancy Roles of Progesterone Change in minute Decreased maternal Progesterone ventilation affinity for O2 Direct stimulation Increased O2 Pregnancy of respiratory drive consumption (20%) Hypoxic ventilatory drive is twice normal Progesterone (estrogen) L shift, increased Even so, pregnant slope of CO2 women particularly response curve = susceptible to hypoxemia (low FRC, ↑ “responsiveness” Red: pregnant patient Blue: Non-pregnant control ↑ cardiac output) 1 Changes in Chest Wall Mechanics ABG in pregnancy Diaphragm ascends 4 cm Respiratory alkalosis with mild metabolic Subcostal angle increases acidosis 50% (relaxin) pH 7.40-7.47 Lower rib cage widens 5-7 cm pCO2 28-32 mm Hg HCO3 18-21 ↑ abdominal/end-expiratory st pressure PaO2 105-107 mm Hg (1 tm), ↓ by 5 mm by 3rd tm Decreased chest wall compliance (↓40%) Will see drop in PaO2 moving from sitting to supine of ± 13 mm ↓ total pulmonary resistance Increased A-a gradient by 3rd trimester Hemodynamics of Pregnancy Hemodynamic change in pregnancy 50% increase total body volume Results in decreased oncotic pressure, anemia Increase in cardiac output by 30-50% ↑ preload, ↓afterload, ↑ HR (15-20 bpm) Central venous pressure and contractility unchanged Decreased systemic vascular resistance High flow, low-resistance circuit (uteroplacental circulation is 30% of CO) Increased venous capacitance Increased arterial compliance Factors driving this are incompletely understood Positional Changes in Cardiac Cardiovascular changes of Output pregnancy Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed. 2 A word on anemia…. Summary: Changes in Maternal Physiology Respiratory Hemodynamic Physiologic intravascular change Plasma volume increases 50-70 % (begins wk 6) RBC mass increases 20-35 % (begins wk 12) Disproportionate increase in plasma volume> RBC volume Hemodilution = “physiologic” anemia Typically Hgb shouldn’t fall below 10 Increased respiratory drive to protect against acidosis, Anemia may contribute to dyspnea, due to increased hypoxemia O2 requirements and decreased O2 carrying capacity Heightened sensitivity to disruptions in CO2, O2 exchange (somewhat compensated for by increased CO) Increased ability to unload oxygen to the placenta ↑ cardiac output & total body volume, ↓ SVR: to protect against hypovolemia (hemorrhage), inadeq nutrient to fetus Physiologic Dyspnea of Pregnancy Fetal physiology Causes: Increased respiratory drive, increased load (chest Placental O2 delivery wall proprioceptors) affected by: Other factors: increased 1. Uterine artery blood pulmonary blood volume, flow anemia, nasal congestion 2. O2 content of uterine Note: exercise efficiency is unchanged, but ventilation at a artilbldterial blood given level of O2 consumption 3. Hb conc/sat is increased increased Protective mech: perception of respiratory effort Higher fetal [Hb] Abnormal to have RR >20, Left shifted Hb From UptoDate PaCO2<28 or >35 mm Hg dissociation curve Fetal “reserve” Adapting supportive care to the Pregnancy and Critical Illness pregnant patient Mechanical ventilation Need for ICU admission rare When intubating, anticipate difficult airway, poor reserve <1% of pregnancies in US; <2% of all ICU Maintain PaCO2 30 - 32 mmHg; goal PaO2 >70 mmHg Sedation admissions involve pregnancy Opiates are safe; midazolam thought to be more safe than lorazepam. Avoid NSAIDs. 75% of ICU admissions happen post-partum Minimal data re. paralytics (cisatracurium is B) Maternal morbidity & mortality in the ICU Vasopressors Best to avoid, if possible (fluids, positioning) is high (up to 20%) Paucity of evidence regarding specific vasopressors (ephedrine preferred, neosynephrine is second) Management of pregnant patient often Monitoring requires multidisciplinary approach Generally recommended; both maternal and fetal Prophylaxis Little in the way of formal research… VTE HOB elevation 3 CPR in the pregnant patient Critical Illness in Pregnancy: Causes Specific to Pregnancy Peripartum cardiomyopathy Etiologies: PE (30%), hemorrhage (17%), sepsis (13%), cardiomyopathy or preeclampsia (10%); other Preeclampsia/Eclampsia (HELLP) Practicalities Postpartum hemorrhage Suspect magnesium toxicity: d/c infusions and give calcium Amniotic fluid embolism,tocolytic Left lateral decubitus with wedge under R hip or manual displacement of the uterus to the left pulmonary edema Continuous cricoid pressure, smaller ETT Nonspecific Asthma Higher chest compressions (but common) Remove fetal monitor before administering shocks Pulmonary Embolism Early delivery (if >24 wks gestation or 4 finger breadths above umbilicus): “5 minute rule” for cardiac arrest Gastric Aspiration Infection/sepsis Other: pneumothorax, sleep apnea Circulation/AHA guidelines for resuscitation, 2005. Postpartum hemorrhage Preeclampsia In US, occurs in 5% of births Definition: Hypertension and proteinuria after 20 wks Accounts for 11-49% of gestation admissions to ICU Eclampsia: above, plus seizure Causes: uterine atony (80%), US: 5-8% (14% worldwide) trauma, coagulation problems Pathogenesis not understood: “endothelial dysfunction” Definition: any bleed that causes symptoms & results in Reasons for ICU admission: signs of hypovolemia refractory hypertension neurological dysfunction (seizures, ICH, elevated ICP, AMS) Management is typically multidisciplinary and related renal failure to cause of bleeding liver rupture or liver failure Uterotonic agents pulmonary edema the HELLP syndrome Balloon tamponade Disseminated intravascular coagulation (DIC) IR embolization vs. surgery Mortality 10% Management of Preeclampsia HELLP Syndrome Treat complications: Hemolysis, Elevated Liver enzymes, Low Platelets HTN (≥160 systolic or ≥ 110 diastolic) Thought be a subset of Severe Preeclampsia (10- Labetalol, hydralazine, nifedipine, nicardipine 20%) Seizures (or risk of) Clinical manifestations IV magnesium Usually 3rd TM Elevated ICP/ICH Abdominal pain, nausea/vomiting Neurosurgical consult, mannitol, hyperventilation etc 15% won’t have proteinuria or htn Pulmonary edema Management Usually blood pressure control, O2; rarely diuretics (patients usually intravascularly dry because of capillary leak) Cornerstone is delivery of fetus DIC ICU level of care often indicated Anti-hypertensives, platelet transfusions Delivery! 4 Peripartum Cardiomyopathy Peripartum Cardiomyopathy Incidence: 1 in 3000 to 1 in 15,000 Diagnostic criteria: Cause & pathogenesis remain obscure Onset within last month of pregnancy or 5 months after delivery Absence of determinable cause Viral, autoimmune, familial, idiopathic Absence of preexisting heart disease Posited “over-reaction” to normal alterations in LV systolic dysfunction cardiac physiology during pregnancy Indications: Usual signs/sx of heart failure Treatment Cardiomegaly on CXR Dilated cardiomyopathy on TTE ACE-inhibitors not safe; caution with beta blockers Hydralazine, Digoxin, Furosemide, nitrates safe Inotropes in severe cases Consider anticoagulation, particularly if EF <30% Outcome of Peripartum Amniotic Fluid Embolism (AFE) Cardiomyopathy Prognosis Poorly-understood Largest study of 123 women: 10% mortality, 4% transplanted. High maternal/fetal mortality (60-90%) 50% had recovery of EF>50% by Incidence in US: 1 in 20,000-30,000 deliveries two years. Pathophysiology: “Anaphylaxis of Pregnancy” Predictors of persistent LV dysfunction: Intense inflammatory response to presence of amniotic fluid in maternal circulation LVEF ≤ 30% Lipid-rich material in AF activates complement LVED volume ≥ 6% or acute lung injury syndrome fractional shortening <20% Severe vasospasm pulm htn R then L heart Elevated troponin T collapse Risk of recurrence/worsening Also has procoagulant factors coagulation cascade with subsequent pregnancy high Elkayam U et. al. Circulation 2005;111(16):2050-5 DIC Amniotic Fluid Embolism Tocolytic Pulmonary Edema Generally occurs during or soon after delivery, but can Acute pulmonary edema during/within 24 hrs of receiving β-agonists occur up to 48 hours later Terbutaline, Albuterol, Ritodrine Estimated to occur in 6-15% Clinical Presentation Pathogenesis: Likely multifactorial Respiratory distress Pulmonary vasoconstriction, Capillary “leak,” volume overload, Cyanosis reduced oncotic pressure Cardiovascular collapse Risk factors SiSeizures (10-1%)15%) or coma MltilMultiple pregnanc ies Coagulopathy/hemorrhage Infection No specific diagnostic tool Preeclampsia Simultaneous Mg Sulfate Aspiration of amniotic fluid no longer felt to be diagnostic Use of corticosteroids for >48 hrs No specific Rx available Presence of preexisting cardiac