Critical Care Obstetrics part 5 ppsx

When evaluating patients for cardiovascular compromise, it is important to be aware of the pregnancy - associated changes and how these changes infl uence the various maternal hemodynami

Critical Care Obstetric Nursing

10 Witcher PM Promoting fetal stabilization during maternal

hemody-namic instability or respiratory insuffi ciency Crit Care Nurs Q 2006 ;

29 ( 1 ): 70 – 76

11 Drummond SB , Troiano NH Cardiac disorders during pregnancy

In: Mandeville LK , Troiano NH , eds AWHONN ’ S High - Risk and Critical Care Intrapartum Nursing , 2nd edn Philadelphia : Lippincott ,

1999 : 173 – 184

12 Sala DJ Myocardial infarction In: NAACOG ’ s Clinical Issues in Perinatal and Women ’ s Health Nursing: Critical Care Obstetrics

Philadelphia : Lippincott , 1992 : 443 – 453

13 Centers for Disease Control and Prevention Guidelines for the

pre-vention of intravascular catheter - related infections MMWR Morbidity Mortality Weekly 2002 ; 51 ( RR - 10 ): 3 – 36

14 American Association of Critical Care Nurses Practice Alert: Preventing Catheter Related Bloodstream Infections Washington, DC ,

2005

15 Preuss T , Wiegand DLM Pulmonary artery catheter insertion (assist)

and pressure monitoring In: Wiegand DLM , Carlson KK , eds AACN Procedure Manual for Critical Care, 5th edn St Louis : Elsevier

Saunders, Inc , 2005 : 549 – 569

16 Chaiyakunapruk N , Veenstra DL , Lipsky BA , Saint S Chlorhexidine compared with providone - iodine solution for vascular catheter - site

care: A meta - analysis Ann Intern Med 2002 ; 136 : 792 – 801

17 Posa PJ , Harrison , D , Vollman KM Elimination of central line -

asso-ciated bloodstream infections: Application of the evidence AACN Advanced Critical Care 2006 ; 17 ( 4 ): 446 – 454

18 American Association of Critical Care Nurses Evaluation of the effects of heparinized and nonheparinized fl ush solutions on the patency of arterial pressure monitoring lines: the AACN “ Thunder

Project ” Am J Crit Care 1993 ; 2 : 3 – 13

19 Wallace DC , Winslow EH Effects of iced and room temperature injectate on cardiac output measurements in critically ill patients

with decreased and increased cardiac outputs Heart Lung 1993 ; 22 :

55 – 63

20 Troiano NH , Dorman K Mechanical ventilation during pregnancy

In: Mandeville LK , Troiano NH , eds AWHONN ’ S High - Risk and Critical Care Intrapartum Nursing , 2nd edn Philadelphia : Lippincott ,

1999 : 84 – 99

21 Troiano NH , Baird SM Critical care of the obstetrical patient In: Kinney MR , Dunbar SB , Brooks - Brunn JA , Molter N , Vitello - Cicciu

JM , eds AACN ’ s Clinical Reference for Critical Care Nursing , 4th edn

St Louis : Mosby , 1998 : 1219 – 1239

22 Martin - Arafeh J , Watson CL , Baird SM Promoting family centered

care in high risk pregnancy J Perinat Neonat Nurs 1999 ; 13 ( 1 )

23 Harvey MG Humanizing the intensive care unit experience

NAACOG ’ s Clinical Issues in Perinatal and Women ’ s Health Nursing: Critical Care Obstetrics 1992 ; 3 ( 3 ): 369 – 376

24 Jenkins TM , Troiano NH , Graves CR , Baird SM , Boehm FH Mechanical ventilation in an obstetric population: characteristics and delivery rates Am J Obstet Gynecol 2003 ; 188 ( 2 ): 549 –

552

25 North American Nursing Diagnosis Association NANDA Nursing Diagnoses: Defi nitions and Classifi cation Philadelphia : Lippincott ,

2003 – 2004

Interpretation of these data indicates a normal baseline FHR,

presence of accelerations and absence of FHR decelerations In

addition, decreased uterine contraction frequency was noted and

uterine resting tone by palpation was normal Collectively, these

subsequent maternal and fetal assessment fi ndings were

consid-ered reassuring

Strategies to p repare n urses to c are for

c ritically i ll o bstetric p atients

When creating a program to care for critically ill obstetric

women, careful attention should be paid to the identifi cation of

nursing competencies necessary to create a safe practice

environ-ment The theoretical basis for this enhanced level of practice

should be presented in a consistent and organized fashion

Thorough discussion of content to be included would cover

maternal physiology and common pathophysiology of

preg-nancy complications that are common in the critically ill

obstetric population However, didactic material should be

accompanied by the opportunity for nurses to gain clinical

prac-tice in a mentored, supervised setting to verify competency of

skills The subject of critical care obstetric staff is addressed in

Chapter 2 of this text Additional resources are available in the

literature to address this subject

References

1 Clark SL , Phelan JP , Cotton DB , eds Critical Care Obstetrics Medical

Economics Books, Oradell, New Jersey, 1987

2 Hankins GDV Foreword In: Harvey CJ , ed Critical Care Obstetrical

Nursing Gaithersburg, Maryland : Aspen Publishers, Inc , 1991

3 Fedorka P Defi ning the standard of care In AWHONN ’ s Liability

Issues in Perinatal Nursing Philadelphia : Lippincott , 1997

4 American Nurses Association Standards of Clinical Nursing Practice

Washington, DC, 1991

5 Association of Women ’ s Health, Obstetric and Neonatal Nurses

Standards for Professional Nursing Practice in the Care of Women

and Newborns , 6th edn Washington, DC, 2003

6 Joint Commission for Accreditation of Healthcare Organizations

Comprehensive Accreditation Manual for Hospitals: The Offi cial

Handbook (CAMH) , 2007

7 Page A Keeping Patients Safe: Transforming the Work Environment of

Nurses Washington, DC : The National Academy Press , 2003

8 Baggs JG , Schmitt MH , Mushlin AI , Mitchell PH , Eldredge DH ,

Hutson AD Association between nurse - physician collaboration and

patient outcomes in three intensive care units Crit Care Med 200 ; 31 ,

956 – 959

9 Baird SM , Kennedy B Myocardial infarction in pregnancy J Perinat

Neonat Nurs 2006 ; 220 ( 4 ): 311 – 321

Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,

M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd.

Physiologic adaptations occur in the mother in response to the

demands of pregnancy These demands include support of the

fetus (volume support, nutritional and oxygen supply, and

clear-ance of fetal waste), protection of the fetus (from starvation,

drugs, toxins), preparation of the uterus for labor, and protection

of the mother from potential cardiovascular injury at delivery

Variables such as maternal age, multiple gestation, ethnicity, and

genetic factors affect the ability of the mother to adapt to the

demands of pregnancy All maternal systems are required to

adapt; however, the quality, degree, and timing of the adaptation

vary from one individual to another and from one organ system

to another This chapter reviews in detail the normal physiologic

adaptations that occur within each of the major maternal organ

systems A detailed discussion of fetal physiology is beyond the

scope of this review A better understanding of the normal

physiologic adaptations of pregnancy will improve the ability of

clinicians to anticipate the effects of pregnancy on underlying

medical conditions and to manage pregnancy - associated

complications

Cardiovascular s ystem

Critical illnesses that compromise the cardiovascular system are

among the most challenging problems affecting pregnant women

When evaluating patients for cardiovascular compromise, it is

important to be aware of the pregnancy - associated changes and

how these changes infl uence the various maternal hemodynamic

variables, including blood volume, blood pressure (BP), heart

rate, stroke volume, cardiac output, and systemic vascular

resis-tance (SVR) Factors such as maternal age, multiple pregnancy,

gestational age, body habitus, positioning, labor, regional

anes-thesia, and blood loss may further complicate the management

of such patients This section reviews in detail the effects of

preg-nancy on the maternal cardiovascular system, and the relevance

of this information in the management of the critically ill obstet-ric patient

Blood v olume

Maternal plasma volume increases by 10% as early as the 7th week of pregnancy As summarized in Figure 4.1 , this increase reaches a plateau of around 45 – 50% at 32 weeks, remaining stable thereafter until delivery [1 – 6] Although the magnitude of the hypervolemia varies considerably between women, there is a ten-dency for the same plasma volume expansion pattern to be repeated during successive pregnancies in the same woman [4,7] Moreover, the magnitude of the hypervolemia varies with the number of fetuses [7,8] In a longitudinal study comparing blood volume estimations during term pregnancy with that in the same patient after pregnancy, Pritchard [7] demonstrated that blood volume in a singleton pregnancy increased by an average of

1570 mL (+48%) as compared with 1960 mL in a twin pregnancy (Table 4.1 ) There is a similar but less pronounced increase in red cell mass during pregnancy (see Figure 4.1 ), likely due to the stimulatory effect of placental hormones (chorionic somato-mammotropin, progesterone, and possibly prolactin) on mater-nal erythropoiesis [9,10] These changes account for the matermater-nal dilutional anemia that develops in pregnancy despite seemingly adequate iron stores [11] Hemodilution is maximal at around

30 – 32 weeks of gestation

The physiologic advantage of maternal hemodilution of preg-nancy remains unclear It may have a benefi cial effect on the uteroplacental circulation by decreasing blood viscosity, thereby improving uteroplacental perfusion and possibly preventing stasis and resultant placental thrombosis [12] Blood volume changes are closely related to maternal morbidity, and hypervol-emia likely serves as a protective mechanism against excessive blood loss at delivery Pre - eclamptic women, for example, are less tolerant of peripartum blood loss because, although total body

fl uid overloaded, they have a markedly reduced intravascular volume as compared with normotensive parturients, due primar-ily to an increase in capillary permeability (Table 4.2 ) [13] The precise etiology for this increased capillary permeability in the

Pregnancy-Induced Physiologic Alterations

plasma volume as measured by Evans blue dye dilution in term pregnancies with normal and growth - restricted fetuses Pregnancies complicated by fetal intrauterine growth restriction (IUGR) had signifi cantly lower mean maternal plasma volumes

as compared with pregnancies with well - grown fetuses (2976 ± 76 mL vs 3594 ± 103 mL, respectively) Moreover, recent studies have found that low pre - pregnancy plasma volumes in formerly pre eclamptic women predispose to a recurrence of pre eclampsia and adverse pregnancy outcome in a subsequent preg-nancy [18] The physiologic mechanisms responsible for these pregnancy - associated changes in blood volume are not fully understood Pregnancy may best be regarded as a state of volume overload resulting primarily from renal sodium and water reten-tion, with a shift of fl uid from the intravascular to the extravas-cular space Indeed, in addition to fetal growth, a substantial part

of maternal weight gain during pregnancy results from fl uid accumulation Unlike other arterial vasodilatory states, preg-nancy is associated with an increase in renal glomerular fi ltration and fi ltered sodium load [19] , leading to an increase in urinary sodium and water excretion [20] To prevent excessive fl uid loss and resultant compromise to uteroplacental perfusion, mineralo-corticoid activity increases to promote sodium and water reten-tion by the distal renal tubules The increased mineralocorticoid activity results primarily from extra - adrenal conversion of pro-gesterone to deoxycorticosterone [21] It is also possible that another as yet unidentifi ed vasodilator(s) may be responsible for the volume expansion, since studies in pregnant baboons have demonstrated that systemic vasodilation precedes the measured increase in maternal blood volume [22] The net result of these two opposing mechanisms is an accumulation during pregnancy

of approximately 500 – 900 mEq of sodium and 6 – 8 L of total body water [23,24]

There is also evidence to suggest that the fetus may contribute

to the increase in maternal plasma volume Placental estrogens are known to promote aldosterone production by directly activat-ing the renin – angiotensin system, and the capacity of the placenta

to synthesize estrogens is dependent in large part on the avail-ability of estrogen precursor (dehydroepiandrosterone) from the fetal adrenal As such, the fetus may regulate maternal plasma

setting of pre - eclampsia is not clear, but it appears to involve

excessive levels of circulating antiangiogenic factors [14 – 16]

Normal maternal blood volume expansion also appears to be

important for fetal growth Salas et al [17] compared maternal

Figure 4.1 Blood volume changes during pregnancy (Reproduced with

permission McLennon and Thouin [1] )

Table 4.1 Blood and red cell volumes in normal women late in pregnancy and

again when not pregnant

Late

pregnancy

Non - pregnant Increase

(mL)

Increase (%) Single fetus (n = 50)

Blood volume 4820 3250 1570 48

Twins (n = 30)

Blood volume 5820 3865 1960 51

Reproduced by permission from Pritchard JA Changes in the blood volume

during pregnancy and delivery Anesthesiology 1965; 26: 393

Table 4.2 Blood volume changes in fi ve women

Non - pregnant Normal pregnancy Eclampsia

Blood volume estimation (chromium 51) during antepartum eclampsia, again

when non - pregnant, and fi nally at a comparable time in a second pregnancy

uncomplicated by hypertension

* Change in blood volume (%) as compared with non - pregnant women

Adapted by permission from Pritchard JA, Cunningham FG, Pritchard SA The

Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of

245 cases Am J Obstet Gynecol 1984; 148: 951

thereby providing a reasonable explanation for a lower mean arterial BP during the fi rst trimester

Systolic and diastolic BP continue to decrease until midpreg-nancy and then gradually recover to non - pregnant values by term A longitudinal study of 69 women during normal preg-nancy demonstrated that the lowest arterial BP occurs at around

28 weeks of gestation (Figure 4.2 ) [29] BP measurements can be affected by maternal positioning In this same series, BP was lowest when measured with the patient in the left lateral decubi-tus position, and increased by approximately 14 mmHg when patients were rotated into the supine position [29] (Figure 4.3 ) Despite the difference in absolute measurements, the pattern of

BP change throughout pregnancy was unaffected (see Figure 4.3 ) For the sake of consistency and standardization, all BP measure-ments in pregnancy should be taken with the patient in the sitting position

Blood pressure measurements are also subject to change depending on the technique used to attain the measurements In

a series of 70 pregnant women, Ginsberg and Duncan [30] dem-onstrated that mean systolic and diastolic BP were lower (by

− 6 mmHg and − 15 mmHg, respectively) when measurements were taken directly using a radial intra - arterial line as compared with indirect measurements using a standard sphygmomanome-ter Conversely, Kirshon and colleagues [31] found a signifi cantly lower systolic (but not diastolic) BP when using an automated sphygmomanometer as compared with direct radial intra - arterial measurements in a series of 12 postpartum patients

Heart r ate

Maternal heart rate increases as early as the 7th week of pregnancy and by late pregnancy is increased approximately 20% as com-pared with postpartum values [29] (Figure 4.4 ) It is likely that

volume through its effect on the placental renin – angiotensin

system [25] In support of this mechanism, pregnancies

compli-cated by IUGR have lower circulating levels of aldosterone and

other vasodilator substances (prostacyclin, kallikrein) as

com-pared with pregnancies with well - grown fetuses [17] However,

the fetus is not essential for the development of gestational

hyper-volemia, because it develops also in complete molar pregnancies

[26]

Blood p ressure

Blood pressure (BP) is the product of cardiac output and SVR,

and refl ects the ability of the cardiovascular system to maintain

perfusion to the various organ systems, including the

fetoplacen-tal unit Maternal BP is infl uenced by several factors, including

gestational age, measurement technique, and positioning

Gestational age is an important factor when evaluating BP in

pregnancy For example, a maternal sitting BP of 130/84 mmHg

would be considered normal at term but concerningly high at 20

weeks of gestation A sustained elevation in BP of ≥ 140/90 should

be regarded as abnormal at any stage of pregnancy Earlier reports

suggested that an increase in BP of ≥ 30 mmHg systolic or

≥ 15 mmHg diastolic over fi rst - or early second - trimester BP

should be used to defi ne hypertension; however, this concept is

no longer valid since many women exhibit such changes in

normal pregnancy [27,28]

Blood pressure normally decreases approximately 10% by the

7th week of pregnancy [6] This is likely due to systemic

vasodila-tion resulting from hormonal (progesterone) changes in early

pregnancy Indeed, studies in baboons have shown that the fall

in arterial BP that occurs very early in pregnancy is due entirely

to the decrease in SVR [22] The resultant increase in cardiac

output does not fully compensate for the diminished afterload,

mean ± SEM) Postpartum (PP) values drawn on the ordinate are used as a baseline, and dashed lines represent the presumed changes during the fi rst 8 weeks (Reprinted by permission of the publisher from Wilson M, Morganti AA, Zervodakis I, et al Blood pressure, the renin - aldosterone system, and sex steroids throughout normal pregnancy Am J Med 68: 97 Copyright 1980 by Excerpta Medica Inc.)

Pregnancy-Induced Physiologic Alterations

Figure 4.3 Sequential changes in BP throughout pregnancy with

subjects in the supine and left lateral decubitus positions (n = 69; values

are mean ± SEM) The calculated change in systolic (open triangles) and

diastolic (closed triangles) BP produced by repositioning from the left

lateral decubitus to the supine position is illustrated LLR, left lateral

recumbent; PP, postpartum (Reprinted by permission of the publisher

from Wilson M, Morganti AA, Zervodakis I, et al Blood pressure, the

renin - aldosterone system, and sex steroids throughout normal pregnancy

Am J Med 68: 97 Copyright 1980 by Excerpta Medica Inc.)

Figure 4.4 Sequential changes in mean heart rate

in three positions throughout pregnancy (n = 69;

values are mean ± SEM) PP, postpartum (Reprinted

by permission of the publisher from Wilson M,

Morganti AA, Zervodakis I, et al Blood pressure, the

renin - aldosterone system, and sex steroids

throughout normal pregnancy Am J Med 68: 97

Copyright 1980 by Excerpta Medica Inc.)

the increase in heart rate is a secondary (compensatory) effect

resulting from the decline in SVR during pregnancy [32]

However, a direct effect of hormonal factors cannot be entirely

excluded Although human chorionic gonadotropin (hCG) is an

unlikely candidate [33] , free thyroxine levels increase by 10 weeks

and remain elevated throughout pregnancy [33,34] The

possibil-ity that thyroid hormones may be responsible for the maternal

tachycardia warrants further investigation

In addition to pregnancy - associated changes, maternal

tachycardia can also result from other causes (such as fever,

pain, blood loss, hyperthyroidism, respiratory insuffi ciency, and cardiac disease) which may have important clinical implications for critically ill parturients For example, women with severe mitral stenosis must rely on diastolic ventricular

fi lling to achieve satisfactory cardiac output Because left ventricular diastolic fi lling is heart rate dependent, maternal tachycardia can severely limit the capacity of such women

to maintain an adequate BP, and can lead to cardiovascular shock and “ fetal distress ” As such, the management of patients with severe mitral stenosis should include, among other

women [39,40] Longitudinal studies using Doppler and M - mode echocardiog-raphy to interrogate maternal cardiac output throughout preg-nancy report confl icting results about the relative contributions

of heart rate and stroke volume Katz and colleagues [49] attrib-uted the elevation in cardiac output (+59% by the third trimester;

n = 19) to increases in both heart rate and stroke volume, whereas the study by Mashini et al [51] showed that the increase (+32%

in the third trimester; n = 16) was due almost exclusively to maternal tachycardia Laird - Meeter et al [50] have suggested that the initial increase in cardiac output prior to 20 weeks ’ gestation

is due to maternal tachycardia, whereas that observed after 20 weeks results from an increase in stroke volume due primarily to reversible myocardial hypertrophy Mabie and colleagues [54] ,

on the other hand, attributed the increase in cardiac output (from 6.7 ± 0.9 L/min at 8 – 11 weeks to 8.7 ± 1.4 L/min at 36 – 39 weeks;

n = 18) to augmentation of both heart rate (+29%) and stroke

between cardiac output and body surface area is lost in pregnancy

[35] This may be explained, in part, by the observation that the

du Bois and du Bois [36] body surface area nomogram widely

used to calculate cardiac index is based on nine non - gravid

sub-jects and, as such may not apply to pregnant women

Linhard [37] was the fi rst to report a 50% increase in cardiac

output during pregnancy using the indirect Fick method Others

have studied maternal cardiac output by invasive catheterization

[38 – 41] , dye dilution [42 – 46] , impedance cardiography [47,48] ,

and echocardiography or Doppler ultrasound [49 – 53] Despite

controversy about the relative contributions of stroke volume

and heart rate, maternal cardiac output increases as early as 10

weeks ’ gestation and peaks at 30 – 50% over non - pregnant values

by the latter part of the second trimester This rise, from 4.5 to

6.0 L/min, is sustained for the remainder of the pregnancy

Nulliparous women have a higher mean cardiac output than

multiparous women [53]

Table 4.3 Cardiovascular parameters

Systemic vascular resistance (SVR) dynes/sec/cm − 5

= HR (beats/min) × SV (mL/beat)

Pregnancy-Induced Physiologic Alterations

midpregnancy values) Stroke volume was increased by 8 weeks, with maximal values (+32% over midpregnancy levels) attained

at 16 – 20 weeks Overall, maternal cardiac output increased from 4.88 L/min at 5 weeks to 7.21 L/min (+48%) at 32 weeks The mechanisms responsible for the increase in maternal cardiac output during pregnancy remain unclear An increase in circulat-ing blood volume is unlikely to contribute signifi cantly to this effect, because hemodynamic studies in pregnant baboons have shown that the increase in cardiac output develops much earlier than does the gestational hypervolemia [22] Burwell et al [64] noted that the increase in plasma volume, cardiac output, and heart rate during pregnancy was similar to that seen in patients with arteriovenous shunting, and proposed that these hemody-namic changes are the result of the low - pressure, high - volume arteriovenous shunting that characterizes the uteroplacental cir-culation A third hypothesis is that hormonal factors (possibly steroid hormones) may act directly on the cardiac musculature

to increase stroke volume and hence cardiac output, analogous

to the mechanisms responsible for the decrease in venous tone seen in normal pregnancy [65] or after oral contraceptive admin-istration [66] In support of this hypothesis, high - dose estrogen administration has been shown to increase stroke volume and cardiac output in male transsexuals [67] To further investigate this hypothesis, Duvekot and colleagues [32] studied serial echo-cardiographic, hormonal, and renal electrolyte measurements in

10 pregnant women The authors propose that the inciting event may be the fall in SVR that leads, in turn, to a compensatory tachycardia with activation of volume - restoring mechanisms In this manner, the increased stroke volume may be a direct result

of “ normalized ” vascular fi lling in the setting of systemic after-load reduction These data support the conclusion of Morton and

co - workers [68] that early stroke volume increases are caused by

a “ shift to the right ” of the left ventricular pressure – volume curve (Frank – Starling mechanism)

The cardiovascular changes in women carrying multiple preg-nancies are greater than those described for singleton pregnan-cies Two - dimensional and M - mode echocardiography of 119 women with twins showed that cardiac output was 20% higher than in women carrying singletons, and peaked at 30 weeks of gestation [69] This increase was due to a 15% increase in stroke volume and 4.5% increase in heart rate

Systemic v ascular r esistance

Systemic vascular resistance (SVR) is a measure of the impedance

to the ejection of blood into the maternal circulation (i.e after-load) Bader et al [40] used cardiac catheterization to investigate the effect of pregnancy on SVR They demonstrated that SVR decreases in early pregnancy, reaching a nadir at around 980 dynes/sec/cm − 5 at 14 – 24 weeks Thereafter, SVR rises progres-sively for the remainder of pregnancy, approaching a pre - preg-nancy value of around 1240 dynes/sec/cm − 5 at term These

fi ndings are consistent with subsequent studies [41] which found

a mean SVR of 1210 ± 266 dynes/sec/cm − 5 during late pregnancy

volume (+18%) (Figure 4.5 ) The confl icting nature of these

studies can be attributed, in part, to the positioning of the patient

during examination (lateral recumbent versus supine position)

It must also be emphasized that although M - mode

echocardio-graphic estimation of stroke volume correlates well with

angio-graphic studies in non - gravid subjects, similar validation studies

have not been carried out during pregnancy [55,56] For this

reason, ultrasound measurements of maternal volume fl ow in

pregnancy have been validated only against similar

measure-ments attained by thermodilution techniques [57 – 61]

One criticism of the above studies is that the maternal

hemo-dynamic measurements in pregnancy are usually compared with

those from postpartum control subjects This comparison may

not be valid, however, because cardiac output remains elevated

for many weeks after delivery [60,62] To address this issue,

Robson et al [63] measured cardiac output by Doppler

echocar-diography in 13 women before conception and again at monthly

intervals throughout pregnancy Maternal heart rate was signifi

-cantly elevated by 5 weeks ’ gestation, and continued to increase

thereafter, reaching a plateau at around 32 weeks (+17% above

Figure 4.5 Hemodynamic changes during pregnancy and postpartum

(Reproduced by permission from Mabie W, DiSessa TG, Crocker LG, et al A

longitudinal study of cardiac output in normal human pregnancy Am J Obstet

Gynecol 1994; 170: 849.)

Whether atrial natriuretic peptide (ANP) has a role to play in the regulation of SVR in pregnancy is still unclear ANP is a peptide hormone produced by atrial cardiocytes, which promotes renal sodium excretion and diuresis in non - pregnant subjects

[73] In vitro , ANP has been shown to promote vasodilation in

vascular smooth muscle pretreated with angiotensin II Circulating ANP levels increase in pregnancy, suggesting that ANP may play

a role in decreasing maternal SVR [74,75] Earlier cross - sectional studies did not correlate ANP levels with blood volume and hemodynamic measurements In a prospective longitudinal study, Thomsen et al [76] demonstrated that plasma ANP levels were positively correlated with Doppler ultrasound estimates of peripheral vascular resistance Although their results substantiate the physiologic importance of ANP in the regulation of blood volume, the authors conclude that ANP does not function as a signifi cant vasodilator during pregnancy

Regional b lood fl ow

Signifi cant regional blood fl ow changes have been documented during pregnancy For example, renal blood fl ow increases by 30% over non - pregnant values by midpregnancy and remains elevated for the remainder of pregnancy [77,78] As a result, glomerular fi ltration rate increases 30 – 50% [70] Similarly, skin perfusion increases slowly to 18 – 20 weeks ’ gestation but rises rapidly thereafter, reaching a plateau at 20 – 30 weeks that persists until approximately 1 week postpartum [79] This is likely due

When describing the physiologic relationship between

pres-sure and fl ow, it is customary to report vascular impedance as a

ratio of pressure to fl ow (see Table 4.3 ) The observed decrease

in SVR during pregnancy results primarily from a decrease in

mean arterial pressure coupled with an increase in cardiac output

It is important to recognize the inverse relationship between

cardiac output and SVR

Peripheral arterial vasodilation with relative underfi lling of the

arterial circulation is likely the primary event responsible for the

decrease in SVR seen in early pregnancy [70,71] The factors

responsible for this vasodilation are not clear but likely include

hormonal factors (progesterone) and peripheral vasodilators

such as nitric oxide [72] The existence of a pregnancy - specifi c

vasodilatory substance has been postulated but it has yet to be

characterized Cardiac afterload is further reduced by the

pro-gressive development of the low - resistance uteroplacental

circu-lation The decrease in SVR in early pregnancy leads to activation

of compensatory homeostatic mechanisms designed to maintain

arterial blood volume by increasing cardiac output and

promot-ing sodium and water retention (summarized in Figure 4.6 ) This

is accomplished through activation of arterial baroreceptors,

upregulation of vasopressin, stimulation of the sympathetic

nervous system, and increased mineralocorticoid activity In

addition to vasodilation, creation of a high - fl ow, low - resistance

circuit in the uteroplacental circulation also contributes signifi

-cantly to the decline in peripheral vascular resistance [63]

Non-osmotic vasopressin stimulation

Stimulation of sympathetic nervous system

Activation of the renin–angiotensin–

aldosterone system

CARDIAC OUTPUT RETENTIONWATER PERIPHERAL ARTERIALVASCULAR AND RENAL

RESISTANCE

SODIUM RETENTION

MAINTENANCE OF EFFECTIVE ARTERIAL BLOOD VOLUME

Figure 4.6 Unifying hypothesis of renal sodium and water retention initiated by peripheral arterial vasodilation (Reprinted by permission from the American College of

Obstetricians and Gynecologists Obstet Gynecol 1991; 77: 632.)

Pregnancy-Induced Physiologic Alterations

throughout their pregnancies (Figure 4.7 ) Maternal heart rate was maximal (range, +13% to +20% compared with postpartum values) at 28 – 32 weeks of pregnancy, and was further elevated in the sitting position Stroke volume increased early in pregnancy, with maximal values by 20 – 24 weeks (range, +21% to +33%), followed by a progressive decline towards term that was most

to vasodilation of dermal capillaries [80,81] and may serve as a

mechanism by which the excess heat of fetal metabolism is

allowed to dissipate from the maternal circulation Pulmonary

blood fl ow increases during pregnancy from 4.88 L/min in early

pregnancy to 7.19 L/min at 38 weeks, an increase of around 32%

[82,83] A small decrease in pulmonary vascular resistance was

noted at 8 weeks without any subsequent signifi cant change

thereafter However, both non - invasive [82] and invasive studies

[40,41,84] have shown that mean pulmonary artery pressure

remains stable at around 14 mmHg, which is not signifi cantly

different from the non - gravid state

The most dramatic change in regional blood fl ow in pregnancy

occurs in the uterus Uterine blood fl ow increases from

approxi-mately 50 mL/min at 10 weeks to 500 mL/min at term [85,86] At

term, therefore, uterine blood fl ow accounts for over 10% of

maternal cardiac output This increase in blood fl ow is likely

related to hormonal factors, because animal studies have shown

a signifi cant decrease in uterine vascular resistance in response to

exogenous administration of estrogen and progesterone [87,88]

Effect of p osture on m aternal h emodynamics

Prior to the 1960s, clinical investigators did not fully appreciate

the effects of postural change on maternal hemodynamics and

patients were often studied in the supine position The unique

angiographic studies of Bieniarz et al [89,90] demonstrate that

the gravid uterus can signifi cantly impair vena caval blood fl ow

in > 90% of women studied in the supine position, thereby

pre-disposing pregnant women to dependent edema and varicosities

of the lower extremities Moreover, impairment of central venous

return in the supine position can result in decreased cardiac

output, a sudden drop in BP, bradycardia, and syncope [91]

These clinical features were initially described by Howard et al

[92] and are now commonly referred to as the “ supine

hypoten-sive syndrome ” Symptomatic supine hypotension occurs in 8%

[93] to 14% [94] of women during late pregnancy It is likely that

women with poor collateral circulation through the paravertebral

vessels may be predisposed to symptomatic supine hypotension,

because these vessels usually serve as an alternative route for

venous return from the pelvic organs and lower extremities [95]

In addition to impairing venous return, compression by the

gravid uterus in the supine position can also result in partial

obstruction of blood fl ow through the aorta and its ancillary

branches, leading, for example, to diminished renal blood fl ow

[77,96]

The clinical signifi cance of supine hypotension is not clear

Vorys et al [97] demonstrated an immediate 16% reduction in

cardiac output when women in the latter half of pregnancy were

moved from the supine to the dorsal lithotomy position, likely

due to the compressive effect of the gravid uterus on the vena

cava (Table 4.4 ) To investigate the effect of gestational age on

the maternal cardiovascular response to posture, Ueland and

Hansen [44] measured changes in resting heart rate, stroke

volume, and cardiac output for 11 normal gravid women in

various positions (sitting, supine, and left lateral decubitus)

Figure 4.7 Effect of posture on maternal hemodynamics PP, postpartum

(Reproduced by permission from Ueland K, Metcalfe J Circulatory changes in pregnancy Clin Obstet Gynecol 1975; 18: 41; modifi ed from Ueland K, Novy MJ, Peterson EN, et al Maternal cardiovascular dynamics IV The infl uence of gestational age on the maternal cardiovascular response to posture and exercise

Am J Obstet Gynecol 1969; 104: 856.)

Table 4.4 Changes in cardiac output with maternal position

Late - trimester women ( n = 31) Change from supine (%)

Reproduced by permission from Vorys N, Ullery JC, Hanusek GE The cardiac output changes in various positions in pregnancy Am J Obstet Gynecol 1961; 82: 1312.)

Conventional wisdom teaches us that low blood pressure in pregnancy is reassuring, but recent studies suggest that sustained low blood pressure in the third trimester (defi ned as a maximum diastolic blood pressure < 65 mmHg) is a risk factor for stillbirth and growth restriction [105 – 108] The rise in blood pressure in the third trimester of pregnancy likely represents a healthy physi-ologic response of the maternal cardiovascular system to the rela-tive inability of the placenta to keep pace with fetal growth, and

nancy A change from the recumbent to standing position resulted

in a decrease in cardiac output of around 1.7 L/min at any stage

of gestation with a compensatory SVR augmentation (Table 4.5 )

Of note, the compensatory increase in SVR was signifi cantly

blunted in late pregnancy as compared with non - pregnant

subjects, which may be related to the altered response to

norepi-nephrine observed during pregnancy [99,100] In addition to

confi rming these fi ndings, Clark et al [101] were able to

Non - pregnant Early pregnancy Late pregnancy P *

MAP (mmHg) 78 ± 8.3 4.7 ± 7.7 5.0 ± 11.3 NS

Heart rate (bpm) 15.5 ± 9.2 25.7 ± 11.8 16.7 ± 11.2 NS

CO (L/min) − 1.8 ± 0.84 − 1.8 ± 0.79 − 1.7 ± 1.2 NS

Stroke volume (mL/beat) − 41.1 ± 15.8 − 38.7 ± 14.5 − 30.8 ± 17.5 NS

SVR (dynes/sec/cm − 5 ) 732 ± 363 588 ± 246 379 ± 214 0.005

Data are presented as mean ± SD

* Determined by analysis of variance

CO, cardiac output; MAP, mean arterial pressure; NS, not signifi cant; SVR, systemic vascular resistance

Reproduced with permission from the American College of Obstetricians and Gynecologists Obstet Gynecol

1988; 72: 550

Table 4.5 Net change in hemodynamic parameters

from recumbent to standing positions

Hemodynamic parameter Position

Left lateral Supine Sitting Standing

MAP (mmHg) 90 ± 6 90 ± 8 90 ± 8 91 ± 14

CO (L/min) 6.6 ± 1.4 6.0 ± 1.4 * 6.2 ± 2.0 5.4 ± 2.0 *

Heart rate (bpm) 82 ± 10 84 ± 10 91 ± 11 107 ± 17 *

SVR (dynes/sec/cm − 5 ) 1210 ± 266 1437 ± 338 1217 ± 254 1319 ± 394

PVR (dynes/sec/cm − 5 ) 76 ± 16 101 ± 45 102 ± 35 117 ± 35 *

PCWP (mmHg) 8 ± 2 6 ± 3 4 ± 4 4 ± 2

CVP (mmHg) 4 ± 3 3 ± 2 1 ± 1 1 ± 2

LVSWI (g/min/m − 2 ) 43 ± 9 40 ± 9 44 ± 5 34 ± 7 *

* p < 0.05, compared with left lateral position

CO, cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; MAP, mean arterial

pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; SVR, systemic vascular

resistance

Reproduced with permission from Clark SL, Cotton DB, Pivarnik JM, et al Position change and central

hemodynamic profi le during normal third - trimester pregnancy and postpartum Am J Obstet Gynecol 1991; 164:

884.)

Table 4.6 Hemodynamic alterations in response to

position change late in third trimester of pregnancy