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65 Cards in this Set

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Describe changes in of the
Heart during Pregnancy to:

-Position
-Size of cardiac silhouette
-End-diastolic dimension
-Structural changes
1. Displaced left and upward due to upward displacement of diaphragm and change in shape of rib cage

2. Increase in size of cardiac silhouette

3. Increase in left ventricular end-diastolic dimension (Due to expanded blood volume)

4. Structural changes in heart similar to those found in physical training (just like training for marathon)
How does Cardiac Output change in Pregnancy

By 5 weeks?
By 12 weeks?
Between 25-30 weeks?
By 34 weeks?
Remember CO = SV x HR

NET INCREASE: to an avg.of 30-50% greater than nonpregnant levels

Markers:

*By 5 weeks: CO starts to increase (1 wk past missed peiod and CO already inc!)

*By 12 wks: CO increased by 34-39% above non-pregnant levels

*B/w 25-30 weeks: CO peaks

*By 34 weeks: Inc 50% from 4.88 L/min to 7.34 L/min
How do you date pregnancies?
Date pregnancies:
From first day of last menstrual period!
(haven't even ovulated yet, not even pregnant yet)

Example: if period comes on April 15, ovulate 14 days later on April 29 --> then that's when fertilization would occur (when you ovulate) and one week later it will implant in your uterus

Important Dates:
*Pregnant 3 weeks after last period
*Beta? will be positive 4 weeks after, which is about 2 weeks after she ovulated
*First, second trimester - first, second 12 weeks
-Third trimester - after 24 weeks
*A full term pregnancy: 10 months, 40 weeks give due date
How does Heart Rate change in Pregnancy?
NET INCREASE!

Markers:
*By 5 weeks: Initial rise HR

* At 32 weeks: Peaks at 15-20 beats/min higher (equals a 17%increase!)
How does maternal position affect CO?
Supine vs. Sitting
On exam: CO depends on maternal position!

1. SUPINE position (laying flat) allows enlarged uterus to compress IVC -> reducing venous return, SV and CO

2. Prior to 24 weeks (6 months) no effect on CO observed b/c uterus isn't that large
How do women compensate for decrease in VR caused by compressing IVC to maintain CO?
Most women don't get symptomatic (dizzy, want to pass out) d/t hypotension
--> Compensate by inc. systemic vascular resistance (SVR)
--> Also have adequate paravertebral collateral circulation
--> so more VR from paravertebral veins to be able to keep HR up

5% don't have that paravertebral circ, so they become hypotensive and symptomatic
If fetal heart rate becomes non-reassuring after 6th months of pregnancy, how do you adjust position to maintain CO to get more O2 to baby?
If non-reassuring fetal heart rate pattern

1. It's imperative to maintain CO of mother
--> b/c uterus gets large amt. blood volume to perfuse, bring O2 to uteroplacental circulation!

2. Place in left lateral decubitus position!!
--> alleviate pressure on IVC to inc. CO
--> DO NOT put her on her back
How does IVC occlusion w/ supine position affect CO, SV, HR in most pregnant women? Exceptions?
Supine posit--> IVC occlusion

1. Reduced atrial filling -> reduced CO

2. Most women increase SVR and maintain arterial pressure

3. 5% of women become hypotensive due to poor paravertebral circulation and parasympathetic response
Describe changes in SVR in the first half of pregnancy affect?
1. SVR decreases to min @ MID-PREGNANCY w/ gradual rise until term (still 21% <er than non-preg values)

2. MECHANISM UNKNOWN, but most obvious cause for dec SVR is PROGESTERONE made by the placenta!
How does SVR change to maintain arterial pressure in pregnant moms, once IVC occlusion occurs?
SVR decreases to min @ MID-PREGNANCY with gradual rise until term (still 21% lower than non-pregnant values)
How does maternal position affect BP? Why is this important?
1. BP should always be measured in a SITTING position!!
--> to find out MAX bp
--> Remember this in relation to pre-eclampsia!
--> BP in sitting position indicates risk in pre-eclampsia pts who might seize if BP too high when sit up

2. Diastolic BP is Korotkoff 5

3. Ensure BP Cuff is large enough
How does venous pressure change in preganancy?
VENOUS PRESSURE
1. Upper extremities - unchanged

2. Lower extremities -
Progressive rise
--> Femoral venous pressure inc from 10cm H20 at 10 weeks to 25 cm H20 near term
Why is increased venous pressure in pregnancy a problem?
Pregnancy and increase in lower extremity venous pressure causes:
1. b/l lower extremity edema
2. Varicose veins
3. Increased risk of deep venous thrombosis
d/t INC. VENOUS STASIS, clots will form
Pregnancy causes a net
INCREASE in what central hemodynamic factors?

(monitor central hemodynamic factors via catheters all over body)
Pregnancy - NET INCREASE
1. Cardiac Output
2. Heart Rate
(on exam)
Pregnancy causes a net
decrease in what central hemodynamic factors?
Pregnancy - NET DECREASE
1. SVR
2. Pulmonary vascular resistance
3. Colloid Oncotic Pressure
--> decreases in COP (d/t increased BV)
--> causes pregnant women to get pulmonary edema much faster and at much lower PCWP
What central hemodynamic factors do NOT change during pregnancy?
Pregnancy - NO CHANGE
1. Pulmonary capillary wedge pressure (PCWP)
2. Central venous pressure
3. Left ventricular stroke work index
Normal Pregnancy Changes

Dyspnea (can't catch breath)
- Most women have complaint by 20 weeks

- 75% of women experience by 3rd trimester

- MILD

- Does not prevent daily activities! Can still do laundry, walk up steps at work

- Does not occur at rest

*dyspnea d/t dec. COP in pulmonary vascular system
How does the decrease in SVR during pregnancy affect maternal BP?
Remember: BP = CO x SVR

Dec in maternal BP, which occurs by 8 weeks gestation, parallels dec. in SVR
--> nl BP in preg ladies very low, should be lower at all times than non-preg levels
What is the overall decrease in DBP and MAP?
Overall decrease in DBP and MAP is 5-10 mm Hg
BP is lowest in what maternal position?
BP lowest in lateral recumbent position
--> ex: if nl bp 120/70 will drop to 110/60
Where is most CO directed during pregnancy?
Most CO directed to:
uterus, placenta, breasts
Non-pregnant uterus receives 2-3% of CO and breasts 1%
vs.
By term 40 wks, uterus receives 17% (450-650 ml/min) and breasts 2%

*When give c-section, VERY bloody when cut into uterus!
Having twins adds what percent increase in CO to the pregnancy above singletons?
Twins increase CO by an additional 15% above singletons
What are three other normal changes in pregnancy?
1) Decreased exercise tolerance (can't run marathons like you used to)

2) Fatigue (even one week after fertilization)

3) Orthopnea, occasional syncope, occasional chest discomfort
What are yet three other normal changes in pregnancy?
1) Peripheral edema (80% of women) d/t decreased COP - increased BV dilutes plasma proteins

2) Mild tachycardia

3) Jugular venous distention after 20 weeks (pulsations of neck veins)
What are the normal changes in heart sounds that occur during pregnancy?
1) Lateral displacement of left ventricular apex
*Normal heart sounds and murmurs displace in that direction as well

2) Louder

3) Exaggerated splitting of S1, S2

4) S3 (80-90%)

5) Systolic ejection murmur (96%)

6) Diastolic murmurs (18%) - still want to do echo to double-check
What is the CV Effect of Labor on CO?
By end of 1st Stage (complete dilation to 10 cm, time to push!):

1) CO is 51% above baseline term pregnancy (50% above non-preg)
*Remember it was already increased 50% above non-pregnant levels

2) Contraction occurs->
Blood expressed from uterus into maternal circulation
*Increased venous return
*Increased SV, BP, CO
What changes in CO occur during the immediate Postpartum Period****?
*By 10-30 min after delivery:
CO reaches its max w/ further rise of 10-20%

*W/in 1 hr of delivery: CO returns to pre-labor baseline
*W/in 2-4 weeks: cardiac parameters return to pre-pregnant levels
What physical changes occur in the kidneys during pregnancy?
Kidneys enlarge in pregnancy by 1 cm dt:
Increased:
1) Renal vasculature
2) Interstitial volume
3) Urinary dead space
*Dilation of renal pelvis
*Dilation of calyces
*Dilation of ureters
What changes do the ureters undergo during pregnancy? What causes them?
Dilation of ureter
*By 8 weeks: Begins
*At 22 weeks: maximizes

1) Right dilated greater than left
*Diameter of ureter = 2 cm

2) Mechanical compression by enlarging uterus and ovarian venous plexus

3) Smooth muscle relaxation by progesterone
* By 6 weeks postpartum: resolves
What is the clinical significance of dilated ureters during pregnancy?
Predisposition to pyelonephritis!
What factors predispose pregnant women to pyelonephritis?

When are pregnant moms most at risk?

What % pregnancies involve pyelo?
Changes in urine, ureters due to progesterone and compression:

1) Asymptomatic bacteriuria
*2/3 have pre-existing bacteriuria d/t high levels of glucose and amnino acids in urine

2) Increased uretrocalyceal dilation (mild hydronephrosis)

3) Elevation in bladder trigone with increased vascularity (may see microhematuria)

4) Urinary stasis with decreased peristalsis of ureters

Timing/Frequency of Pyelonephritis in pregnancy:
*1-2% of all pregnancies
*2nd and 3rd trimester: highest risk
Why are pregnant moms often incontinent?
Compression of the trigone by baby's head eliminates angles that prevent involuntary evacuation of urine, esp. when cough

1) Decreased bladder capacity
2) Increased frequency of urinary incontinence
What are the Si/Sx of pyelonephritis?
Symptoms/Signs Pyelo:

1) High fevers
2) Chills
3) N/V
4) CVA tenderness - more common on right b/c right ureter more dilated than left
How do we manage pyelonephritis during pregnancy?
Management of Pyelo in pregnant mom:

1) Hospitalization (versus send home on AB if not preg)
2) IV antibiotics
3) Urine and blood cultures, CBC, Creatinine
4) Hydration
5) Monitor urine output
6) Follow-up
7) Suppression with antibiotics until end of pregnancy
*VERY DANGEROUS TO GET SICK WITH PYELO WHILE PREG!!
What changes in renal plasma flow occur during pregnancy?
1) RPF increases d/t increase in CO to kidney
*By 16 weeks: Rises 75% over nonpregnant levels

2) GFR increases
*By 5-7 weeks: increases
*By 12 weeks, 50% higher than prepregnant levels
*By 3 months postpartum: returns to normal
What changes in creatinine clearance (GFR) occur during pregnancy?
Creatinine clearance, GRF Increases:
*By 5-7 weeks: increases
to 150-200 ml/min from 120 ml/min
What is the clinical relevance of the increase in RPF, GFR?
1) Decrease in Plasma creatinine, BUN, Uric acid
2) In the standing position: RAAS kicks in to compensate for the decrease in SVR progesterone is causing-> retain more sodium and water when standing
3) Night time, lying in the lateral recumbent position (to minim IVC compression) will start peeing like racehorses b/c inced fluid in periphery must be peed off w/o venous stasis when standing up-->
Added water excreted, NOCTURIA
In response to decreased SVR during pregnancy, how does renal tubular function change during pregnancy?
Progesterone's effect to decrease SVR-> Increased RAAS:

1) High levels of aldo

2) Pregnant women to retain K+, but stored mostly in fetus and placenta
What changes can you see in the blood glucose of pregnant moms?
1) Glucose excretion increases: 3+ glucose on urine dip NOT nec. indicative of diabetes

2) Intermittent

3) Not related to normal or abnormal glucose levels

4) Unknown mechanism
In response to respiratory alkalosis of pregnancy,
how does renal tubular function change during pregnancy?
Pregnant women breath faster and breath off CO2 causing alkalosis:

1) Increased Excretion
-Amino acids
-Calcium
-Bicarbonate
Questions Likely on exam from first hour
1) Heart is displaced how?
2) CO increases when?
3) HR changes how?
4) List some normal findings in pregnancy
*So if someone comes in complaining of “I just can’t breath, I have the hardest time breathing – she would do what? vs.can’t get up lecture hall steps w/o becoming out of breath - nl or abnl?
5) When do all changes return to normal postpartem?
6) RPF, GFR - Inc. or Dec.?
7) Serum creatinine, BUN, uric acid - Inc. or Dec.?
Review- on exam:
1) Heart is displaced left and upwards
2) CO increases almost immediately
3) HR also increases
4) Normal findings in pregnancy: dyspnea (SOB), peripheral edema, fatigue, systolic ejection murmur
* So if someone comes in complaining of “I just can’t breath, I have the hardest time breathing – she works this up (vs.)
can’t get up lecture hall steps w/o becoming out of breath - (normal)
5) All changes do not return to normal postpartem until 2-4 weeks NOT hours to get back to normal pre-pregnancy
6) Inc. RPF, GFR
7) D/t inc. GFR-> lower serum creatinine, BUN, uric acid
Abnormal physical findings in pregnancy
1) Dyspnea that limits activity

2) Orthopnea that is progressive or severe

3) Paroxysmal nocturnal dyspnea

4) Hemoptysis

5) Syncope during or immediately after exertion

6) Jugular venous distension

7) Cyanosis, clubbing

8) Pulmonary rales

9) Chest pain with activity
When during pregnancy are women more prone to heart failure?
1) 1st half of pregnancy:
most increase in CO occurs *Therefore, most failure occurs in 1st half of pregnancy
What might precipitate cardiac failure 2nd Half of Preg**?
Mostly associated with a precipitating factor
1) Anemia (baby steals iron)
-> causes high output failure
-Try to prevent with iron supplementation
-Treat with iron
2) Infection
-Aggressively treat with antibiotics
3) Excess metabolic activity
-> inc CO-> high output failure
-Check thyroid tests and treat

*MUST check in all unexplainable causes of CHF
*Must Treat precipitating factor
What is the primary cause of serious mitral valvular disease in women?
1) Rheumatic Fever
-although is uncommon in US
-Epidemics of Strep pharyngitis occur
-Can have 3% of untreated young adults develop RF
What cardiac diseases most commonly cause maternal mortality?
MORTALITY RATES
Eisenmenger syndrome: 30-70%
Marfan’s: 25-50%
Peripartum cardiomyop: 15-60%
Primary pulmonary HTN: 50%
Aortic valve disease: 10-20%
Mitral stenosis + A-fib: 14-17%
Tetralogy of Fallot: 12%
Coarctation of aorta: 5%
Mitral Stenosis ends up causing a murmor by what mech?
Contracted valve impedes blood flow from the left atrium to left ventricle

Left atrial pressure increases

Passive increase in pulmonary pressures

Fixed cardiac output--> Diastolic murmur at apex
How does pregnancy complicate management of mitral valve stenosis?

Symptoms?
Pathophysiology:
-Normal increase in CO in pregnancy can not be handled by stenotic valve
-Pulmonary edema occurs

Symptoms include:
1) Dyspnea - due to pulmonary venous congestion
2) Fatigue
3) Palpitations
4) Cough
5) Hemoptysis
How does mitral stenosis cause heart failure in pregnant patients?
1) Increase in HR not tolerated ->
2) Less time for diastolic filling ->
3) Increases left atrial pressures ->
4) Increases pulmonary pressure ->
5) Results in pulmonary edema
How do you treat sinus tachycardia? A-fib?
Due to inability to tolerate less time in diastole combined with increased CO ->
-Causes pulmonary edema
*Sinus tachycardia is treated with beta blockers
(slow heart rate to increase filling time and volume)
*Atrial fibrillation treated aggressively to improve atrial kick
How should you adjust labor management in mitral stenosis patients?
Labor management w/ mitral stenosis:
1) Epidural to decrease pain (which increases HR, which can't be tolerated)
2) Fluid restriction (do not want to increase preload)
3) Watch postpartum when CO reaches max - fluid from extremities returns to CO to be cleared
4) Endocarditis prophylaxis
Causes of pre-eclampsia
1) Uterine vascular modeling
*Defective second-phase trophoblastic invasion
*Poor perfusion

2) Vessels contract in response to vasomotor agents
*VERY reactive to norepi, epi, angiotensin II
*All pregnant women have large amounts of AII in pregnancy
*Vasoconstriction in pregnancy systemically and regionally
What are the manifestations of pre-eclampsia***?
1) Hypertension (140/90 or >er)
2) Central Nervous System - everyting's spasming d/t vasoconstriction -> spots before their eyes, severe headache usually frontal
3) Eye
4) Liver - vasoconstriction pain in RUQ
5) Renal - less excretion of AA, glucose, uric acid
6) Uteroplacental Circulation - diminished d/t vascoconstriction - when oxygen doesn't get to baby you get late decelerations on fetal heart rate monitor
7) Coagulopathy, Intravascular Hemolysis
8) Edema - canckles
How does the SYSTEMIC VASCULATURE respond to pre-eclampsia?
Pre-eclampsia changes in systemic vasculature:
1) Increases PVR = HTN
How does the CNS respond to pre-eclampsia?
Pre-eclampsia changes in the CNS:
1) Sensitive to AII
2) Vasoconstriction causing hypoxemia and hypoperfusion
*Seizures (eclampsia) - very little oxygen gets into mom or baby
*Coma - check reflexes
*Cerebral edema - check reflexes
*Increased DTRs and clonus - may be first sign getting to be pre-eclamptic
*Intracranial bleeding can occur
How does the EYE respond to pre-eclampsia?
Pre-eclampsia changes in the eye:
1) Retinal artery vasoconstriction
2) Blindness

*Generally reversible
What are the manifestations of pre-eclampsia in the LIVER?
Liver in pre-eclampsia:
1) Sensitive to AII causing vasoconstriction
2) Hypoxic hepatic cellular damage
3) Pain in right upper quadrant (THIS AND HIGH BP ALONE = INDICATION FOR DELIVERY TO CURE PRE-ECLAMP)
4) Increased liver enzymes (AST, ALT)
*Above symp. generally reversible

5) Rarely get subcapsular hematoma/hepatic rupture
What are the manifestations of pre-eclampsia in the KIDNEY?
Kidney in pre-eclampsia:
1) Vasoconstriction decreases renal blood flow
2) Deterioration in renal function
3) Decreased urine output
4) Increased serum creatinine
5) Decreased creatinine clearance - d/t vasospasm (normally urination and CC should be way up)
*Above seen most with severe preeclampsia
What additional damage can pre-eclampsia do to the KIDNEY?
1) High vascular pressure & renal vasoconstriction
2) Ischemic & pressure damage to glomerulus
3) Alters selective filtration allowing large MW substances to filter
->PROTEINURIA

Vasoconstriction -> ischemic damage to glomerulus -> allows large molec weight protein to get through ->

**With Pre-eclampsia - Think: HIGH BP, VASOCONSTRICTION, PROTEINURIA, HIGHT URIC ACID
What additional changes can occur in the KIDNEY d/t pre-eclampsia?
1) Abnormality of proximal tubular function - damage to glomerulus

2) Increased lactic acid production b/c of hypoxemia in preeclampsia

3) Increased need to retain and exchange urate for lactic acid
What are the manifestations of pre-eclampsia in the UTEROPLACENTAL CIRCULATION?
Uteroplacental Circulation in pre-eclampsia:

1) Vasoconstriction of UP vascular bed
2) Decrease nutrient and oxygen supply to fetus
3) Fetal growth restriction
4) Acute, severe decrease in blood flow w/ vasospasms
5) Microhemorrhage in placenta
6) Placental separation -> placental abruption (abruptio can happen in a split second)
7) Abnormal tests of fetal well being (check on state of UP circulation, late decelerations after contractions)
How does pre-eclampsia cause COAGULOPATHY?
1) Decreased UP perfusion tilts normal balance of fibrin deposition & fibrinolysis
2) More fibrin deposition
3) Further aggravates UP circulation resulting in a consumption coagulopathy
4) Detected as thrombocytopenia early (will see drop platelet count 80k vs. 150k)
5) Can lead to generalized DIC
How do complications of pre-eclampsia lead to INTRAVASCULAR HEMOLYSIS?
1) Body detects decreased perfusion ->
2) Responds with increased CO ->
3) High CO aggravates HTN (BP 140/90 to 160/110)
4) Blood is flowing at high pressure against severe vasoconstriction
5) Mechanical injury to cellular components of blood
How does pre-eclampsia cause EXCESSIVE EDEMA?
1) High CO ->
2) High hydrostatic pressure ->
3) Low oncotic pressure, esp with proteinuria ->
4) Loss of fluid into interstitium ->
5) Decreased intravascular volume ->
6) Further compromise organ perfusion (people won't wear rings anymore)
How does pre-eclampsia cause PULMONARY EDEMA?
Same reason as for peripheral edema

1) High CO ->
2) High hydrostatic pressure ->
3) Low oncotic pressure ->
4) Loss of fluid into pulmonary interstitium ->
5) Pulmonary edema