Chapter 22: Cardiovascular and Respiratory Distress Disorders Flashcards
(42 cards)
How often do HTN isues happen in pregnancy?
12-22% of the time in pregnancy
Accountable for 20% of maternal deaths in the U.S
HTN during pregnancy
Most common cause of HTN in pregnancy?
Causes remain unknown
What defines chronic HTN?
Chronic HTN: Prior to 20 weeks pregnancy or persisting after 12 weeks post-partum.
How do we classify chronic HTN?
Classification: Mild = Systolic 140-159 or Diastolic 90 - 109. Severe = Systolic 160+ or Dia 110+
30% of people with HTN in pregnancy develop this:
Pre-ecclampsia
What is gestational HTN? How often does it occur?
Gestational HTN: HTN that develops for the first time after 20 weeks gestation in the absence of proteinuria. Happens in 5 - 10% of pregnancies, with a 30% incidence in multigestational preg.
Does Gestationam HTN lead to pre-ecclampsia?
50% of these patients go on to develop pre-ecclampsia with 10% of ecclamptic seizures happening before overt proteinuria
How do we define pre-ecclampsia? Is edema an indicative physical exam finding?
Pre-ecclampsia: HTN with proteinuria after 20 weeks gestation. Edema is common, but its common anyway so this isn’t reliable.
Risk factors for pre-ecclampsia?
Risk factors: Nulliparity, Multifetal, Age 35+, Previous preecclampsia, chronic HTN, pregestational DM, Vascular disorders, Kidney issues, Antiphospholipid syndrome, obesity, being African American
Specific criteria for pre-ecclampsia
Criteria: 140+/90+ after 20 weeks in a woman who previously did not have HTN. Proteinuria with urinary excretion of 0.3g or higher in a 24 hour urine sample.
When do we classify pre-ecclampsia as “severe”?
Severe: Any of the following: 160+/110+ on 2 occasions at least 6 hours apart while patient is on bed rest. Marked proteinuria defined as urine dipstick with 3+ protein on two samples taken 4 hours apart or urine protein at 5g.
Oliguria less than 500mL in 24 hours. Cerebral or visual disturbances. Pulmonary edema or cyanosis. Epigastric/RUQ pain (probably due to subscapular hepatic hemorrhage or stretching of Glisson capsule with hepatocellular edema), evidence of hepatic dysfunction, thrombocytopenia, IUGR.
Why do we care about classifying severe vs regular pre-ecclampsia?
Why we care: Severe = deliver no matter gestational age or maturity. You would only wait in certain circumstances for steroids to kick in, but this is a rare step
What is ecclampsia?
Ecclampsia: Pre-ecclampsia with seizures, happens only 0.5 - 4% of pre-ecclamptic patients. Occur within 24 hours of delivery, but 10% of cases have it 2-10 days post-partum
What is HELLP? What are the criteria?
HELLP: Hemolysis elevated liver enzymes and low platelets. Indication for delivery to avoid jeopardizing health of the woman. Happens in 4 - 12% of patiens with pre or regular ecclampsia.
Criteria: Microangiopathic hemolysis, thrombocytopenia, hepatocellular dysfunction
What is the leading finding of HTN in pregnancy that we see in mom?
Pathophys of HTN in pregnancy - Maternal vasospasm is the leading finding
5 potential causes of vasospasm leading to HTN in pregnancy
- Vascular changes
- Hemostatic changes
- Changes to prostaglandins
- Changes to prostanoids
- Changes in endothelial derived factors
Why vascular changes in pregnancy could lead to vasospasm?
Vascular changes: Endothelial damage in vessels and inadequate maternal vascular remodeling (normally we see trophoblast-mediated vascular changes in the uterine vessels with decreased musculature in the spiral arterioles that leads to development of low resistance, low pressure, high flow system)
What hemostatic changes in pregnancy could lead to HTN?
Hemostatic changes - Particularly in pre-ecc. Increased platelet activation with increased consumption in microvasculature. Endothelial fibronectin levels are increased and anti-thrombin III and a2-antiplasmin levels decrease which reflect endothelial damage. Low AT3 are permissive for microthrombi development. Endothelial damage leads to further vasospasm.
What prostanoid changes in pregnancy can lead to vasospasm and thus HTN?
Changes to prostanoids - Prostacyclin and Thromboxane increase with pregnancy, favoring Prostacyclin. Pre-ecclamptics get a favor for thromboxane. Prostacyclin favors vasodilation and decreased platelet aggregation with the opposite for thromboxane. Thromboxane thus leads to vessel constriction.
What changes in endothelial derived factors during pregnancy can lead to vasospasm and HTN?
Changes in endothelium derived factors - Nitric Oxide, a potent vasodilator, is decreased in patients with pre-ecclampsia and may explain the evolution of vasoconstriction in these patients
What free radical/antioxidant changes during pregnancy can lead to vasospasm and thus HTN?
Lipid peroxide, free radicals, and antioxidant release: Lipid peroxids and free radicals have been implicated in vascular injury and are increased in pregnancies complicated by pre-ecclampsia. Lower antioxidant levels noted.
Discuss in general the hematologic effects seen in HTN pregnancy and what bad things can happen
Plasma volume contraction or hemoconcentration may develop with risk of rapid-onset hypovolemic shock when hemorrhage occurs.
We see this contraction of plasma with an elevated hematocrit.
Thrombocytopenia or DIC may also develop from the microangiopathic hemolytic anemia. Involvement of the liver may lead to hepatocellular dysfunction. Third spacing could occur due to increased blood pressure and decreased plasma oncotic pressure.
Why do we see renal effects in some pregnancies with HTN?
Renal effects: Decreased GFR (increasing serum creatinine) and elevated protein cause decreased uric acid filtration that can be picked up on maternal serum as elevated uric acid on the blood.