Lecture Outline
Caring for the Critically Ill Review normal cardiopulmonary physiology of pregnancy Pregnant Patient Address management of critical illness duringgp pre gnanc y 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 ventilator y 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 disease Supportive care, restoration of uterine tone Treatment 50% of patients die within one hour of onset Discontinue tocolytic (if not already done) Risk of recurrence is unknown O2, diuretics, nitrates
5 Asthma in Pregnancy Asthma in Pregnancy
Most common medical condition occurring during Most common medical condition during pregnancy pregnancy (8%) Pre-pregnancy control is most important factor Women with asthma have higher rates of: Rule of 1/3’s Preeclampsia Important factors: Uterine hemorrhage, Placenta Previa, Hyperemesis Changes in physiology Preterm birth Hyperpnea IUGR or low-birth weight Effects of weight gain Perinatal death Changes in hormones, cortisol Strong association between asthma control during Coexistence of GERD, sinusitis/rhinitis, pulmonary edema, PE pregnancy and fetal outcome Medication adherence* Education is paramount Early recognition and treatment paramount Early intubation; higher complications; delivery options
Thromboembolic Disease When asthma gets bad… in Pregnancy Pulmonary embolism is leading cause of death among pregnant or peripartum women in the US Most acute exacerbations due to medication non- Affects 1 in 1000 pregnancies in US compliance (not using inhaled steroids:18% vs. 4%) Increased risk of VTE during/after pregnancy: 5-6X Initiation of inhaled steroids/β-agonists during hospitalization led to 12% readmission rate vs. 33% in Risk is higher in post-partum period gpgroup dischar ged on β-ag(p)gonists alone (p<0.047) Risk factors: Combination of close maternal and fetal monitoring Obesity Older age May need to follow PCO2 and intubate early for impending respiratory failure Personal/family history Inherited thrombophilia If RA O2 saturation is <95%, if PEF<70%, or if fetal compromise, consider ICU Anti-phospholipid antibody syndrome Consider early delivery if fetal maturity permits Trauma Cesarean delivery (2X risk of DVT) Pereira, A. and B. Krieger. Clin Chest Med 25 (2004) Immobility Increased parity
Clotting and Pregnancy Management of VTE in Pregnancy
Virchow’s Triad Treatment 1. Stasis: Increased venous capacitance, compression Can’t use warfarin in pregnancy on veins by gravid uterus Heparins, including LMWH, are safe 2. Endothelial Injury: Particularly during delivery Prompt initiation of IV heparin with aPTT monitoring 3. Hypercoagulability: Increases in “pro” clotting factors, decrease in protein S Manyyg advocate following anti-Xa level for LMWH Diagnosis: Should continue for minimum of three to six months Clinical signs/sx non-specific Timing of delivery and cessation of anticoagulation D-dimer not helpful Resume anticoagulation as soon as possible post- LE doppler Usd, spiral CT>VQ, potential use for partum (6-12 hrs) MRI (safety not established) Role of IVC filters DVT’s more likely to arise in the pelvic veins Thrombolysis if life-threatening
6 Aspiration in Pregnancy Pneumonia in Pregnancy
“Mendelsson’s rd Syndrome” 3 leading cause of maternal death Factors leading to No difference in either incidence or mortality aspiration during Decreased cell-mediated immunity may increase pregnancy: susceptibility to viral or fungal pathogens ↑ abdominal pressure Influenza Delayed gastric emptying Varicella Relaxed GE sphincter Coccidiomyces tone Safe antibiotics in pregnancy: Penicillins, Peri-labor factors macrolides, cephalosporins, neuraminidase Usually chemical inhibitors, acyclovir pneumonitis, but can lead to infection or Avoid fluoroquinolones, tetracyclines, sulfa, ARDS chloramphenicol
When the lungs go bad: ARDS The Particularly-Plagued Pregnancy
ARDS = Acute onset, severe impairment of gas 28 yo woman, 33 6/7 wks pregnant, presents exchange characterized by non-cardiogenic to the ED with dyspnea, cough, and chest pulmonary edema tightness. Not common in pregnancy, but high mortality PMH notable for asthma, typicall y mana ged Amni o tic Flu id Em bo lism, asp ira tion, pneumonia/sepsis, preeclampsia, DIC with albuterol inhaler Ventilator strategy adapted, if possible For last 3 months, describes using MDI 4-5 Maintain higher PaO2 times a day May be less tolerant of “permissive hypercapnia” For last week has been using it “too much” If critical, maternal over fetal health (roughly every 2-3 hrs while awake)
Taking a history: Classifying Asthma Severity What do you want to know next?
What do you need to know in order to She tells you that she has been having daily categorize her asthma? symptoms, and wakes at night 3-4 times a Frequency/timing of symptoms for previous 4 wks week to use her inhaler. Lung function (FEV1, FEV1/FVC, PFM) Freqqyuency of “rescue” inhaler use She is unable to work. Number of exacerbations requiring oral steroids/yr FEV1 was 1.67 L (61%), and FEV1/FVC was Other risk factors: 66% two weeks ago History of intubations/respiratory failure She does not check her peak flows. ED visits, hospitalizations She was prescribed steroids but was afraid to Symptom “awareness” take them Psychosocial factors
7 Categorizing asthma control Asthma Severity
How would you categorize her asthma control? A. Intermittent B. Mild persistent C. Moderate persistent D. Severe persistent
Schatz, et. al. NEJM, 360:1862-1869, 2009
Before embarking on therapy…. Additional information
What else might you want to know? + chills, +myalgias, green phlegm What medication she’s used in the past No smoking, GERD, or allergy Whether there are any co-existing risk No recent aspiration but intake has been poor factors VS: 38. 3 134 140/55 24 94% on RA GERD Appears pale, fatigued Infectious symptoms, history, contacts Mild “accessory” muscle use Tobacco abuse Allergies Bilateral wheezing at end expiration Aspiration risk factors Regular tachycardia What might you want to order? Extremities cool, trace edema
Case, continued: Hospital course, con.
WBC 13.9, nl diff She spikes a fever to 38.7 ABG on 35% VM: 7.40/29/80/18 Cultures are performed. Which of the following organisms is she at What would you do greatest risk for? now? A. Intubate A. Influenza B. Order a CT scan B. Mycoplasma C. BIPAP C. Varicella D. Albuterol nebs, IV steroids, f/u ABG in 1 D. Streptococcus Pneumoniae hour
8 Gotta bug?
However, she really has Influenza! Later that day, you note she has decreased wheezing but looks “tired.” What i s th e nex t b es t st ep? A. Let her get some sleep B. Ask for an ABG C. Request a CT scan of the chest D. Ask respiratory to give her an extra nebulizer treatment
ABG shows 7.33/42/70/20 with 94% on 50% Preoxygenate VM Avoid too much Patient is sleeping and looks “comfortable.” bagging (or place Blood pressure is 95/60. NG) Nhtdd?Now what do you do? Smaller ETT A. Increase the O2 back up to 100% NRB mask B. Give an extra dose of albuterol Cricoid pressure C. Call resident to order an additional antibiotic Positioning D. Chest X-ray stat Fluids, drugs E. Mobilize to intubate
Over the next week….
Your patient’s follow-up blood gas is Happily, your patient’s infection improves 7.45/32/110/24 with 99% on FiO2 50% and she is weaned from the ventilator The intern says, “We should give her after 5 days. more sedation;;g she’s breathing too She is sent to the OB floor, but ICU is fast.” called 5 days later with the report that What do you say? the patient is short of breath. A. Yes What would your differential diagnosis B. No be? C. Can I call a friend?
9 The “Bounce Back” Differential Dx: 35 2/7 wks
Your patient appears to be in acute respiratory distress, breathing 30 times per min Oxygen saturation is 93% on 6L NC Exam is notable for accessory muscle use, occasional wheeze, rales at the lung bases, and 1+ peripheral edema She is on continuous nebulizer treatment
You convince the patient to have a chest x-ray A. B.
Differential Diagnosis Management, CXR A
CXR A: CXR B: BP is 140/70, HR 133 Peripartum Asthma Patient is not on tocolytics and has not cardiomyopathy Venous had any sign of aspiration Preeclampsia thromboembolism What would you do now ? Volume overload Other A. Intubate and start antibiotics ARDS B. Immediate delivery C. Trial of BIPAP, nitrates, diuretics D. Order TTE
Particularly-Plagued Pregnancy, Management, CXR B continued
BP is 140/70, HR 133 The patient’s CXR looked like “B” Patient says “this doesn’t feel like She received empiric heparin prior to asthma” scan What would you do now? A. Intubate B. Immediate delivery C. Heparin gtt and CT of the chest with PE protocol D. Stat albuterol nebs, trial of BIPAP
10 The Happy Ending…. Summary & Conclusions
Our particularly-plagued pregnant patient Complex physiologic alterations occur during pregnancy that serve to protect the mother and delivered a healthy baby boy at term fetus from hemodynamic or respiratory She continues on anticoagulation, derangements asthma management (inhaled steroid- The spectrum of pulmonary disease in LABA combination) pregnancy is best understood in the context of alterations in cardiopulmonary physiology Although thankfully uncommon, pulmonary disease is an important cause of morbidity and mortality in pregnancy
Questions? Resources
Bates, et. al. Chest 2008; 133: 844S-886S. Campbell, L and R. Klocke. Am J Respir Crit Care Med 2001; 163: 1051-1054. Cruickshank DP, et al. In Gabbe SG, Niebyl JR, Simpson JL [eds] Obstetrics: Normal And Problem Pregnancies, 3rd ed. 1996. Elkayam U et. al. Circulation 2005;111(16):2050-5 Mason: Murray & Nadel ' s Textbook of Respiratory Medicine , 4th ed. 2005. Martin, S. and M. Foley. Am Jnl Obs and Gyn 2006; 195: 673-689. Pereira, A. et. al. Clin Chest Med 2004; 25: 299-310. Schatz, M. and M. Dombrowski. NEJM 2009; 360(18): 1862-1869. UptoDate and Google online for figures Wise, R. et. al. Immunol Allergy Clin N Am 2000; 20(4): 663-672.
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