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NM706 > Module 7 Unit A > Flashcards

Module 7 Unit A Flashcards

1
Q

Describe mild intermittent asthma?

A 
Symptom frequency
    Two days per week or less
Nightime awakenings
    Two times per month or less
Interference with normal acitivity
    None
FEV1 or peak flow
     More than 80%
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2
Q

Describe mild persistent asthma.

A 
Symptom frequency
     More than 2 days per week but not daily 
Nightime awakenings
     More than twice per month
Interference with normal acitivity
     Minor limitation
FEV1 or peak flow
     More than 80%
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3
Q

Describe moderate persistent asthma.

A 
Symptom frequency
     Daily symptoms
Nightime awakenings
     More than once per week
Interference with normal acitivity
     Some interference
FEV1 or peak flow
     60% to 80%
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4
Q

Describe severe persistent asthma.

A 
Symptom frequency
     Throughout the day
Nightime awakenings
     4 times per week or more
Interference with normal acitivity
      Extremely limited
FEV1 or peak flow
     Less than 60%
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5
Q

What are the maternal implications of asthma?

A

Sig relationship b/w decreased FEV1 during pregnancy and ↑risk of LBW and prematurity

Even early asthma stages may be dangerous d/t smaller functional residual capacity and increased pulmonary shunting→ susceptibility to hypoxia and hypoxemia

Slight increase (studies not consistent) - stillbirth, preeclampsia, PTL, FGR, perinatal mortality, abruption, previa, PROM, GDM

Morbidity more linked to severe disease, poor control, or both

Status asthmaticus can → morbidity, muscle fatigue, resp arrest, pneumothorax, pneumomediastinum, acute cor pulmonale, cardiac arrhythmias

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6
Q

What are the fetal implications of asthma?

A

Fetal implications

Fairly uncommon, if any risk it is slight and studies are not consistent

SAB

PTL/PTB

FGR - with increased asthma severity

Abruption/previa

PROM

Fetal response to maternal hypoxemia → ↓umbilical blood flow, ↑systemic and pulmonary vascular resistance, ↓cardiac output

Possible teratogenic or adverse effects of meds

Slight risk for abnormalities - cleft lip and palate, autism spectrum disorders

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7
Q

How does pregnancy affect asthma severity?

A

Variable - 23% improved symptoms, 30% became worse

Pregnant who have asthma, even mild or well-controlled disease, need monitoring w/ PEFR and FEV1 testing as well as tracking symptoms throughout pregnancy

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8
Q

What are the differential diagnoses for a patient with asthma?

A

Dyspnea of pregnancy

GERD

Chronic cough from postnasal drip

Bronchitis

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9
Q

How should the nurse midwife assess for asthma in pregnancy?

A

Asthma symptom review - onset, duration, time of day, severity, recurrence

Chest tightness, SOB, difficulty w/respiration or wheezing, nonproductive cough

Relief measures used and their effects

Medical and surgical hx

Allergies, meds (quick and long-acting for asthma), asthma hx, chronic diseases

Exposure to triggers - allergens, irritants, pets, drugs, mold, air, exercise

Social hx - race/ethnicity, smoking or exposure, air quality, living conditions

Risk for development - atopy, rhinitis, hay fever, eczema, indoor air exposure

Physical ex - VS, general appearance, skin, color, pallor, cyanosis, pale nasal mucosa

Respiratory eval - breathing, auscultation, hyperinflated chest, prolonged expiratory phase, accessory muscle use, retractions, upright breathing easier, percussion

Evidence of resp distress - nasal flaring, retractions, peripheral cyanosis, ↑pulse or resp rate, grunting or wheezing

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10
Q

What non pharmacologic approaches can the nurse midwife use to manage asthma in pregnancy?

A

Control of triggers

Herbal remedies - NOT in place of asthma meds

Licorice, ginkgo Biloba, coltsfoot, hops

Fish oil, vitamin C

Yoga, acupuncture, biofeedback

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11
Q

What pharmacologic methods should the nurse midwife use to manage Intermittent asthma?

A

For mild - SABAs are usually enough

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12
Q

What pharmacologic method should the nurse midwife use to manage my who managed mild persistent asthma?

A

Low-dose ICS + SABA

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13
Q

What pharmacologic methods should the nurse midwife use to manage moderate persistent asthma?

A

High dose ICS + LABA + SABA

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14
Q

What pharmacologic methods should the nurse midwife use to manage severe persistent asthma?

A

High dose ICS + LABA + OCS + SABA

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15
Q

What is the clinical presentation of superficial thrombophlebitis?

A

Inflammation at the site
Leg pain
Localized heat
Palpation of a knot or cord, tenderness

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16
Q

What is the management of superficial thrombophlebitis?

A

Leg rest
elevation of the affected extremity
supportive stockings
nonsteroidal anti-inflammatory drug (NSAID) analgesia as needed.

17
Q

What is the clinical presentation of deep vein thrombosis?

A

Abrupt onset with leg pain worsening with motion or when standing
Generalized edema of ankle, leg, or calf
Mild tachycardia and possible slight elevation in temperature
Pain with calf pressure

18
Q

What is the management of deep vein thrombosis?

A

leg rest
elevation of the affected extremity
supportive stockings
(NSAID) analgesia as needed.

Anticoagulants for at least 6 months
Ambulation gradually as tolerated.
Supportive stockings .
Physician referral is indicated.

19
Q

What is the etiology of DVT in pregnancy?

A

Virchow’s triad:
(1) stasis, (2) hypercoagulable state, and (3) vascular trauma.

Venous-wall relaxation resulting from the effects of progesterone and pressure on the veins by the gravid uterus fosters venous stasis. Pregnancy is also a hypercoagulable state, and this state persists throughout the early postpartum period. Venous-wall inflammation and endothelial damage secondary to distension, in the setting of this hypercoagulable state, predisposes the woman to thrombus formation.

Prolonged venous compression during positioning for labor or birth may contribute to the problem. Cesarean section also is considered a risk factor for thrombosis; thus, mechanical thromboprophylaxis, such as alternating compression devices, is recommended before and after cesarean birth.

20
Q

What are the risk factors for developing a dvt in pregnancy?

A

Maternal hx ~ Obesity (BMI>30), smoking, age>35, thrombosis hx, inherited thrombophilias, antiphospholipid antibody syndrome, sickle cell disease, heart disease, diabetes, immobility (paraplegia)

Pregnancy ~ Hypercoagulable state, venous stasis, multiple pregnancy, preeclampsia

Labor and Birth ~ operative vaginal birth, c/s, infection, vascular trauma, immobilization, postpartum hemorrhage, preterm birth, stillbirth

21
Q

What is the clinical presentation of DVT in pregnancy?

A

Abrupt onset of pain and edema in leg and thigh, pain worsens w/ motion/standing, pain w/calf pressure

Tenderness - along course of involved vessel(s) w/possible palpable cord

Warmth

Mild tachycardia and possible slight elevation in temp

Occasionally reflex spasm → pale, cool extremity w/diminished pulsations

May be no symptoms at all

22
Q

What is the 1st line diagnostic testing used to assess for DVT in pregnancy?

A

Compression US w/ or w/o doppler imaging - remember normal findings for venous US doesn’t always exclude PE

23
Q

What diagnostic test is non specific for assessing for DVT in pregnancy and why?

A

D-dimer- positive isn’t really helpful but a negative D-dimer is reassuring.

24
Q

What complications can DVT in pregnancy lead to?

A

PE

Post-thrombotic syndrome - chronic leg paresthesias or pain, intractable edema, skin changes, leg ulcers

25
Q

What is the recommended management for DVT in pregnancy?

A

Warfarin

26
Q

What level of interprofessional collaboration is warranted when a DVT is diagnosed in pregnancy

A

Referral

27
Q

What is the etiology/cause of pulmonary embolism in pregnancy?

A

Virchow’s triad:
(1) stasis, (2) hypercoagulable state, and (3) vascular trauma.

Venous-wall relaxation resulting from the effects of progesterone and pressure on the veins by the gravid uterus fosters venous stasis. Pregnancy is also a hypercoagulable state, and this state persists throughout the early postpartum period. Venous-wall inflammation and endothelial damage secondary to distension, in the setting of this hypercoagulable state, predisposes the woman to thrombus formation.

Prolonged venous compression during positioning for labor or birth may contribute to the problem. Cesarean section also is considered a risk factor for thrombosis; thus, mechanical thromboprophylaxis, such as alternating compression devices, is recommended before and after cesarean birth.

28
Q

What are the risk factors for pulmonary embolism in pregnancy?

A

DVT - primary risk factor

29
Q

What is the clinical presentation of pulmonary embolism in pregnancy?

A

Signs and symptoms

Dyspnea, chest pain, cough, syncope, hemoptysis

Tachypnea, apprehension, tachycardia

Pulmonic closure sound, rales, and/or friction rub

Deceptively nonspecific - s/s and lab testing

30
Q

What diagnostic testing is used to assess for pulmonary embolism in pregnancy with with and without leg symptoms?

A

Compression ultrasound with leg symptoms
CXR without leg symptoms

ECG - right axis deviation and T-wave inversion in the anterior leads

Chest x-ray - results normal 40% of the time, otherwise may have atelectasis, infiltrate, cardiomegaly, or effusion

Most hypoxemic - normal arterial blood glass does not exclude PE

⅓ have PO2 value of >80mmHg

Alveolar-arterial oxygen tension difference more useful indicator - 86% have alveolar-arterial difference >20mmHg

31
Q

What is the recommended management for pulmonary embolism in pregnancy?

A

Immediate full coagulation

May consider vena caval filters - especially if c/s needed soon

Vena Caval Filters

Recent PE and must have c/s- particularly serious problem

Reversal of anticoagulation may be followed by another embolus, and surgery while fully anticoagulated frequently results in life-threatening hemorrhage or troublesome hematomas. In these cases, consider placement of a vena caval filter before surgery

Also indicated - If heparin therapy fails to prevent recurrent PE from pelvis or legs, or when embolism develops from these sites despite heparin treatment, a vena caval filter may be indicated.

Following massive emboli in patients who are not candidates for thrombolysis

Device inserted through either the jugular or femoral vein; can be inserted during labor

Routine filter placement has no added advantage to heparin given alone

Retrievable filters - short-term protection and then removed 1 to 2 weeks later

Thrombolysis

Compared w/heparin, thrombolytic agents provide more rapid lysis of pulmonary clots and improvement of pulmonary hypertension

Embolectomy

Given efficacy of thrombolysis and filters- surgical embolectomy uncommonly indicated

Although the operative risk to mother reasonable, the stillbirth rate is 20 to 40%

32
Q

What level of interprofessional collaboration liberation is warranted when a pulmonary embolism is diagnosed in pregnancy?

A

Refer

33
Q

What is the cause of amniotic fluid embolism?

A

Previously thought to be amniotic fluid and debris passing into maternal circulation - during normal birth, this is a normal occurrence

Now - Disrupted maternal-fetal interface allows material from fetal compartment to enter maternal circulation→ abnormal activation of proinflammatory mediator systems

This causes initial transient pulmonary vasoconstriction and HTN

Acute right ventricular failure is then followed by hemodynamic collapse from right ventricular infarction coupled w/ interventricular septum displacement to the left and ultimately decreased LT sided output

This is followed by cardiogenic pulmonary edema and systemic hypotension

Concurrently acute respiratory failure develops with severe hypoxemia from shunting.

Results in multiorgan failure.

If woman survives this, a consumptive coagulopathy comes next as the fetal material activates factor VII leading to the development of DIC

34
Q

What are risk factors for amniotic fluid embolism?

A

Risk factors

Predisposing conditions -

Rapid labor

Mec-stained fluid

Tears into uterine/other large pelvic veins - permits fluid exchange b/w mother & fetus

Other risks

Older maternal age

Post-term pregnancy

Labor induction or augmentation

Eclampsia

Cesarean, forceps, or vacuum delivery

Abruption or previa

Hydramnios

Fetal - male gender, fetal distress, premature ROM, intrauterine death

Maternal - AMA >35, multiparity, diabetes

Obstetric - c/s, induction, cervical laceration, instrument delivery, uterine rupture

Uterine hypertonus - likely effect rather than cause, hypertonus from oxytocin not implicated

35
Q

What is the clinical presentation of an amnionic fluid embolism?

A

Signs and symptoms

Classic triad - hemodynamic compromise, respiratory compromise, DIC

Classic example -dramatic, late stages of labor immediately postpartum start gasping for air

Seizures or cardiorespiratory arrest rapidly follows w/ massive hemorrhage from consumptive coagulopathy

Manifestations can be variable

Diagnostic Criteria for Amniotic Fluid Embolism

Abrupt onset of cardiorespiratory arrest, or both hypotension and respiratory compromise

Documentation of overt DIC - Coagulopathy must be detected prior to the loss of sufficient blood to cause dilutional or shock-related consumptive coagulopathy.

Clinical onset during labor or within 30 minutes of placental delivery.

No fever ≥38°C.

36
Q

What are potential complications of amniotic fluid embolism?

A

Death

Neurological impairments

37
Q

What is the emergency management for amniotic fluid embolism?

A

Immediate high quality CPR and ACLS

NM706 (10 decks)

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