Hypotensive Syndromes in Geriatric Patients

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Editors
Kannayiram Alagiakrishnan Maciej Banach
Division of Geriatric Medicine Polish Mother’s Memorial Hospital
University of Alberta Research Institute (PMMHRI)
Edmonton, AB Lodz, Poland
Canada

ISBN 978-3-030-30331-0    ISBN 978-3-030-30332-7 (eBook)

https://doi.org/10.1007/978-3-030-30332-7

© Springer Nature Switzerland AG 2020

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v
Contents

1 Orthostatic Hypotension ��������������������������������������������������������������������������   1

Wilbert S. Aronow
2 Postprandial Hypotension ������������������������������������������������������������������������   9
Kannayiram Alagiakrishnan and Darren Mah
3 Carotid Sinus Syndrome �������������������������������������������������������������������������� 23
Anna Kasperowicz, Maciej Banach, Marek Maciejewski,
and Agata Bielecka-Dabrowa
4 Vasovagal Syncope ������������������������������������������������������������������������������������ 35
Kannayiram Alagiakrishnan
5 Post-exercise Hypotension in the Elderly������������������������������������������������ 45
Agata Bielecka-Dabrowa, Marcin Adam Bartłomiejczyk,
Marek Maciejewski, and Maciej Banach
6 Nocturnal Hypotension������������������������������������������������������������������������������ 57
Kannayiram Alagiakrishnan
7 Non-pharmacological Management of Hypotensive Syndromes���������� 65
Kannayiram Alagiakrishnan
8 Update on Pharmacological Management of Hypotensive
Syndromes in the Elderly�������������������������������������������������������������������������� 75
Kannayiram Alagiakrishnan and Darren Mah
9 Challenges with the Diagnosis and Management of Hypotensive
Syndromes in the Elderly�������������������������������������������������������������������������� 83
Kannayiram Alagiakrishnan
10 Hypertension and Hypotensive Syndromes�������������������������������������������� 97
Kannayiram Alagiakrishnan
11 Diabetes Mellitus���������������������������������������������������������������������������������������� 105
Paulina Gorzelak-Pabiś and Marlena Broncel
12 Hypotensive Syndromes and Heart Failure�������������������������������������������� 117
Kannayiram Alagiakrishnan, Darren Mah, and Ali Ahmed

vii
viii Contents

13 Hypotensive Syndromes and Chronic Kidney Disease �������������������������� 129

Jolanta Malyszko and Adrian Covic
14 Stroke and Hypotensive Syndromes�������������������������������������������������������� 139
Mariusz Stasiolek
15 Parkinson’s Disease and Hypotensive Syndromes���������������������������������� 157
Kannayiram Alagiakrishnan
16 Falls and Hypotensive Syndromes in the Elderly������������������������������������ 167
Kannayiram Alagiakrishnan
17 Hypotensive Syndromes and Cognitive Impairment/Dementia������������ 179
Kannayiram Alagiakrishnan and Kamal Masaki

Index�������������������������������������������������������������������������������������������������������������������� 193
Contributors

Ali Ahmed Washington DC VA Medical Center and George Washington University

and Georgetown University, Washington, DC, USA
Kannayiram Alagiakrishnan Division of Geriatric Medicine, University of
Alberta, Edmonton, AB, Canada
Wilbert S. Aronow, MD, FACC, FAHA Cardiology Division, Department of
Medicine, Westchester Medical Center and New York Medical College, Valhalla,
NY, USA
Maciej Banach Department of Hypertension, Chair of Nephrology and
Hypertension, Medical University of Lodz, Lodz, Poland
Department of Cardiology and Congenital Diseases of Adults, Polish Mother’s
Memorial Hospital Research Institute (PMMHRI), Lodz, Poland
Marcin Adam Bartłomiejczyk Department of Hypertension, Medical University
of Lodz, Lodz, Poland
Agata Bielecka-Dabrowa Department of Hypertension, Chair of Nephrology and
Hypertension, Medical University of Lodz, Lodz, Poland
Department of Cardiology and Congenital Diseases of Adults, Polish Mother’s
Memorial Hospital Research Institute (PMMHRI), Lodz, Poland
Marlena Broncel Department of Internal Diseases and Clinical Pharmacology,
Medical University of Lodz, Lodz, Poland
Adrian Covic Grigore T. Popa University of Medicine, Strada Universității, Iasi,
Romania
Paulina Gorzelak-Pabiś Department of Internal Diseases and Clinical
Pharmacology, Medical University of Lodz, Lodz, Poland
Anna Kasperowicz University Hospital, Clinical Department of Cardiology,
Zielona Gora, Poland
Marek Maciejewski Department of Cardiology and Congenital Diseases of
Adults, Polish Mother’s Memorial Hospital Research Institute (PMMHRI), Lodz,
Poland

ix
x Contributors

Darren Mah University of Alberta, Edmonton, AB, Canada

Jolanta Malyszko Department of Nephrology, Dialysis and Internal Medicine,
Warsaw Medical University, Warszawa, Poland
Kamal Masaki Division of Geriatric Medicine, University of Hawaii at Manoa,
Honolulu, HI, USA
Mariusz Stasiolek, MD, PhD Department of Neurology, Medical University of
Lodz, Lodz, Poland
Orthostatic Hypotension
1
Wilbert S. Aronow

Introduction

Orthostatic hypotension is diagnosed if there is a reduction of ≥20 mm in systolic

blood pressure or of ≥10 mm in diastolic blood pressure within 3 minutes of stand-
ing [1–5]. Patients being treated with antihypertensive drugs should have their blood
pressure measured in the sitting position and within 3 minutes of standing [2]. Their
blood pressure should not be measured immediately after eating as postprandial
hypotension may occur then [6, 7]. Orthostatic changes in blood pressure should be
measured at 1 minute and at 3 minutes after standing [8, 9].
Disorders associated with orthostatic hypotension include advanced age and dis-
orders associated with hypovolemia including anemia, overdiuresis, diarrhea, vom-
iting, poor food and fluid intake, hemorrhage, and reduced plasma volume [10].
Hypertension, diabetes mellitus, neurological disorders, cardiovascular disorders,
endocrine disorders, alcoholism, vascular insufficiency, connective tissue disorders,
vitamin B12 deficiency, uremia, amyloidosis, and porphyria are also associated with
orthostatic hypotension. Drugs associated with orthostatic hypotension include
alcohol, diuretics which may cause volume depletion, and vasodilators such as
angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium
channel blockers, hydralazine, nitrates, and prazosin which cause a decrease in sys-
temic vascular resistance and venodilation. Centrally acting antihypertensive drugs
such as alpha methyldopa, clonidine, guanethidine, hexamethonium, labetalol, mec-
amylamine, and phenoxybenzamine and drugs associated with torsades de pointes
are associated with orthostatic hypotension. Antidepressants, antipsychotic drugs,
anti-Parkinsonian medications are also associated with orthostatic hypotension
[10]. One study showed that enalapril and nifedipine were equipotent in reducing
blood pressure with enalapril reducing the number of orthostatic hypotensive

W. S. Aronow (*)
Cardiology Division, Department of Medicine, Westchester Medical Center and New York
Medical College, Valhalla, NY, USA

© Springer Nature Switzerland AG 2020 1

K. Alagiakrishnan, M. Banach (eds.), Hypotensive Syndromes in Geriatric
Patients, https://doi.org/10.1007/978-3-030-30332-7_1
2 W. S. Aronow

episodes and nifedipine increasing the number of orthostatic hypotensive episodes

[11]. The functional adenine insertion polymorphism in the endothelin gene is not
associated with hypertension or orthostatic hypotension in Chinese persons [12].

Pathophysiology

Orthostatic hypotension may be caused by an excessive decrease in blood volume

when the person assumes an upright position or from inadequate cardiovascular
compensation for a reduction in cardiac preload when the person assumes an upright
position [13]. When changing from a lying to standing position, about 500 ml of
blood pool in the lower extremities. Baroreceptors in the carotid sinus and aortic
arch are sensitive to the reduction in arterial pressure with postural change, resulting
in vagal inhibition and sympathetic stimulation [14]. Failure of these autonomic
mechanisms may cause postural hypotension. Increased left ventricular stiffness
with aging caused by increased interstitial fibrosis and cross linking of collagen in
the heart impairs left ventricular diastolic relaxation and filling [15]. Conditions that
further reduce left ventricular filling with a decrease in intravascular volume or
decreased venous return to the heart when the person assumes the upright position,
especially if they are receiving drugs which may contribute to orthostatic hypoten-
sion, may cause orthostatic hypotension [13–16].
Orthostatic hypotension in the elderly is associated with hypertension, impaired
left ventricular filling, altered sympathovagal balance, increased left ventricular
wall thickness, reduced left ventricular preload, and impaired diastolic filling of the
left ventricle [16]. Hypertension predisposes to orthostatic hypotension by impair-
ing baroreceptor reflex sensitivity and decreasing vascular and left ventricular com-
pliance [13–16]. Alcohol potentiates orthostatic hypotension by impairing the
vasoconstrictor response to orthostatic stress [17]. Impaired blood pressure stabili-
zation is more common as we become older and was reported in the Irish Longitudinal
Study on Ageing [18]. Middle-aged adults with orthostatic hypotension developed
after 23-year follow-up echocardiographic left ventricular hypertrophy (hazard
ratio = 1.97), reduced right chamber volume (hazard ratio = 1.74), and decreased
early diastolic tissue velocity in the left ventricular septal wall (hazard ratio = 1.47),
independent of traditional risk factors [19].

Prevalence

The prevalence of orthostatic hypotension in older persons was 8% in 476 persons

[1]. In this study, the prevalence of orthostatic hypotension was 13% in 257 persons
receiving cardiovascular or psychotropic drugs and 3% in 219 persons who did not
receive cardiovascular or psychotropic drugs [1]. The prevalence of orthostatic
hypotension was 15% in 168 patients [20], 18% of 5273 persons in the Cardiovascular
Health Study [4], 17% of 100 persons [21], 22% in 186 persons [22], 17.8% at
baseline, 10.4% at 1 year, 12.8% at 4 years, and 20.0% at 1 or more visits in 4733
1 Orthostatic Hypotension 3

diabetics in the Action to Control Cardiovascular Risk in Diabetes (ACCORD)

blood pressure trial [23]. The prevalence of orthostatic hypotension in 4736 persons
in the Systolic Hypertension in the Elderly Program cohort was 10.4% when mea-
sured at 1 minute after standing, 12.0% when measured at 3 minutes after standing,
and 17.3% when measured at both 1 and 3 minutes after standing [8].
The prevalence of orthostatic hypotension in 9361 persons mean age 67.9 years,
in the Systolic Blood Pressure Intervention Trial (SPRINT), was 16.6% in persons
randomized to a systolic blood pressure below 120 mm Hg versus 18.3% in persons
randomized to a systolic blood pressure below 140 mm Hg [24]. The prevalence of
orthostatic hypotension in 2636 persons aged 75 years and older, mean age
79.9 years, in SPRINT was 21.0% in persons randomized to a systolic blood pres-
sure below 120 mm Hg versus 21.8% in persons randomized to a systolic blood
pressure below 140 mm Hg [25]. In this study, the prevalence of orthostatic hypo-
tension with dizziness was 1.9% in persons randomized to a systolic blood pressure
less than 120 mm Hg versus 1.3% in persons randomized to a systolic blood pres-
sure less than 140 mm Hg [25].

Symptoms

Symptoms associated with orthostatic hypotension include dizziness, falls, fractures,

light-headedness, and syncope [2, 3, 15, 26–36]. In a study of 4127 Irish persons,
mean age 61.5 years, orthostatic hypotension was associated with an increased risk
of unexplained falls (relative risk = 1.52), all-cause falls (relative risk = 1.40), and
injurious falls (relative risk = 1.81) [34]. Of 352 patients, mean age 78 years, the
etiology of syncope was diagnosed in 243 patients (69%) [35]. Of the 352 patients,
vasovagal syncope was diagnosed in 12%, volume depletion in 14%, orthostatic
hypotension in 5%, cardiac syncope in 29%, carotid sinus hypersensitivity in 2%,
and drug overdose/others in 7% [35]. In a study of 11,429 participants followed for
a median of 27 years, orthostatic hypotension was associated with dizziness (odds
ratio = 1.49), falls (adjusted hazard ratio = 1.22), fractures (adjusted hazard
ratio = 1.16), syncope (adjusted hazard ratio = 1.40), motor vehicle crashes (adjusted
hazard ratio = 1.43), and all-cause mortality (adjusted hazard ratio = 1.36) [36].

Prognosis

The Honolulu Heart Program included 3522 elderly men [37]. The prevalence of
orthostatic hypotension in this study was 6.9% and increased with age. At 4-year
follow-up, orthostatic hypotension was significantly associated with increased all-­
cause mortality by 1.64 times [37]. The Cardiovascular Health Study included 5273
community-dwelling adults, mean age 73 years [4]. The prevalence of orthostatic
hypotension was 18% in this study. We reported that propensity analysis of 883
persons with orthostatic hypotension and 2627 persons without orthostatic hypoten-
sion (mean age 74 years; 58% women) demonstrated at 13-year follow-up that
4 W. S. Aronow

orthostatic hypotension was significantly associated with incident heart failure by

1.24 times. Symptomatic orthostatic hypotension was significantly associated with
incident heart failure by 1.57 times. Asymptomatic orthostatic hypotension was
associated with incident heart failure by 1.17 times [4].
The Progetto Veneto Anziani (Pro.V.A.) study included 2786 community-­
dwelling Italians, mean age 76 years (59% women) [38]. The prevalence of ortho-
static hypotension was 9.3% in this study. At 4.4-year follow-up, orthostatic
hypotension was associated with increased all-cause mortality by 1.13 times [38].
The Swedish Malmo Preventive Project included 33, 346 persons, mean age
45.7 years (67% men) [39]. The prevalence of orthostatic hypotension was 6.2% in
this study. At 22.7-year follow-up, orthostatic hypotension was significantly associ-
ated with all-cause mortality by 1.21 times, with coronary events by 1.17 times,
with stroke by 1.17 times, and by the composite endpoint of death, coronary event,
or stroke by 1.18 times [39].
The Orthostatic Hypotension in Diabetics in the Action to Control Cardiovascular
Risk in Diabetes Blood Pressure (ACCORD BP) trial investigated the prevalence,
incidence, and prognostic significance of orthostatic hypotension in the ACCORD BP
trial [5, 23]. The 4266 participants, mean age 62.1 years (50% men), in this study were
at high risk for orthostatic hypotension because they all had type 2 diabetes mellitus,
hypertension, and were being treated with antihypertensive drugs. Orthostatic blood
pressure measurements were made in 1321 persons at baseline, in 2625 persons at
12 months, in 3702 persons at 48 months, and in 926 persons at all 3 visits.
The prevalence of orthostatic hypotension was 17.8% at baseline, 10.4% at
12 months, 12.8% at 48 months, and 20% at one or more visits [23]. At baseline, the
prevalence of orthostatic hypotension was 19.3% in hypertensive diabetics treated
to a systolic blood pressure less than 120 mm Hg versus 16.1% in hypertensive
diabetics treated to a systolic blood pressure less than 140 mm Hg (p not signifi-
cant). At 12 months, the prevalence of orthostatic hypotension was 9.5% in hyper-
tensive diabetics treated to a systolic blood pressure less than 120 mm Hg versus
11.4% in hypertensive diabetics treated to a systolic blood pressure less than
140 mm Hg (p not significant). At 48 months, the prevalence of orthostatic hypoten-
sion was 12.2% in hypertensive diabetics treated to a systolic blood pressure less
than 120 mm Hg versus 13.5% in hypertensive diabetics treated to a systolic blood
pressure less than 140 mm Hg (p not significant).
At 12 months, the incidence of orthostatic hypotension was 8.0% in hypertensive
diabetics treated to a systolic blood pressure less than 120 mm Hg versus 9.9% in
hypertensive diabetics treated to a systolic blood pressure less than 140 mm Hg (p
not significant). At 48 months, the incidence of orthostatic hypotension was 9.9% in
hypertensive diabetics treated to a systolic blood pressure less than 120 mm Hg
versus 11.0% in hypertensive diabetics treated to a systolic blood pressure less than
140 mm Hg (p not significant). Dizziness upon standing for the blood pressure mea-
surements was similar for both treatment groups at baseline and at 6 months but was
1 Orthostatic Hypotension 5

higher with a systolic blood pressure less than 120 mm Hg at 48 months (5.7%) than
with a systolic blood pressure below 140 mm Hg at 48 months (4.1%). This study
reassures us that hypertensive diabetics treated to a systolic blood pressure goal of
below 120 mm Hg will not have a higher prevalence or incidence of orthostatic
hypotension than hypertensive diabetics treated to a systolic blood pressure goal
below 140 mm Hg [5, 23]. This study also showed that orthostatic hypotension was
significantly associated with increased all-cause mortality by 1.62 times and with
heart failure death or hospitalization by 1.85 times but not with nonfatal myocardial
infarction, stroke, cardiovascular death, or their composite [23].
The Atherosclerosis Risk in Communities study included 12,433 community-­
dwelling black and white middle-aged men and women, mean age 54 years (57%
women and 28% black) [40]. Orthostatic hypotension was present in 5% in this
study. At 6-year follow-up, orthostatic hypotension was significantly associated
with coronary heart disease by 1.85 times [40]. At 7.9-year follow-up of 11,707
participants free of stroke and clinical heart disease at baseline in the Atherosclerosis
Risk in Communities study, orthostatic hypotension was significantly associated
with ischemic stroke by 2.0 times [41]. At 17.5-year follow-up of 12,363 persons
free of heart failure at baseline in the Atherosclerosis Risk in Communities study,
orthostatic hypotension was significantly associated with heart failure by 1.54 times
[42]. This association was similar across race and sex groups but was increased 1.90
times in persons aged 55 years and younger and increased 1.37 times in persons
older than 55 years [42]. Orthostatic hypotension was present in 76 of 103 new
patients (74%) attending a clinic on falls and syncope [43]. A sustained reduction in
systolic blood pressure of 30 seconds or longer was associated with a significant
increased use of vasopressors by 36% and a significant increased risk of all-cause
mortality at 5 years by 45% [43].
A meta-analysis of cardiovascular events and mortality associated with ortho-
static hypotension included 13 prospective studies with 121,913 persons [44]. At
5-year follow-up of 65,174 persons, orthostatic hypotension significantly increased
all-cause mortality by 1.5 times. At 6.4-year follow-up of 49,512 persons, ortho-
static hypotension significantly increased coronary heart disease by 1.41 times. At
6.8 to 24-year follow-up of 50,096 persons, orthostatic hypotension significantly
increased heart failure by 2.25 times. At 6.8-year follow-up of 58,300 persons,
orthostatic hypotension significantly increased stroke by 1.64 times [44].
A meta-analysis of 8 published papers from 7 cohorts included 64, 782 partici-
pants [45]. At 15.2-year follow-up, orthostatic hypotension was associated with a
significant increased risk for coronary heart disease by 32% and for stroke by 19%
independent of conventional risk factors. This association was significant for both
middle-aged and older participants [45]. A meta-analysis of 4 prospective cohort
studies which included 51,270 participants and 3603 incident heart failure cases
showed that orthostatic hypotension was significantly associated with an increased
risk for heart failure by 30% [46].
6 W. S. Aronow

Treatment

Hypertension should be treated [2]. Persons who have orthostatic hypotension

should avoid immobilization, prolonged diurnal recumbence, and physical decon-
ditioning [3, 10, 47, 48]. They should also avoid large meals, isometric exercise, hot
weather, hot showers, rapid ascent to a high altitude, hyperventilation, standing
motionless, ingesting alcohol, straining at defecation or voiding, diet pills, vasodila-
tors, diuretics, beta agonists, and tricyclic antidepressants. They should gradually
rise from the supine and sitting positions, especially in the morning, after meals, and
after defecation and urination. Meals should be small. Sodium and water intake
should be increased for volume expansion unless heart failure is present. The head
of the patient’s bed should be raised to a 10°–30° angle during sleep to reduce noc-
turia, volume depletion, and supine hypertension. Elastic stockings and abdominal
compression bandages are recommended to reduce peripheral pooling in the lower
limbs and splanchnic region [3, 10, 47–49].
Pharmacological interventions include the direct alpha 1-adrenoreceptor agonist
midodrine 2.5 to 10 mg 2 or 3 times daily [47, 48, 50]. The norepinephrine precur-
sor droxidopa 100 to 600 mg 3 times a day may be used [48]. The acetylcholines-
terase inhibitor pyridostigmine 30 to 60 mg 2 or 3 times daily is generally
recommended only for neurogenic orthostatic hypotension [48]. The mineralocorti-
coid volume expander fludrocortisone 0.05 to 0.3 mg daily may be used [47, 48].
The efficacy of the direct and indirect alpha 1-adrenoreceptor agonist ephedrine/
pseudoephedrine 25/30 to 50/60 mg 3 times daily is controversial [47, 48]. The
efficacy of the vasopressin analogue volume expander desmopressin (nasal spray 5
to 40 micrograms daily; oral formulation 100 to 800 micrograms daily) which
increases water reabsorption and decreases nocturia is uncertain [48].

Conflict of Interest The author has no conflicts of interest.

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Postprandial Hypotension
2
Kannayiram Alagiakrishnan and Darren Mah

Introduction

Postprandial hypotension (PPH) is a significant drop in blood pressure after eating.

It is commonly defined as a supine systolic blood pressure (SBP) drop of 20 mmHg
or a SBP decrease to less than 90 mmHg when the preprandial SBP is greater than
100 mmHg, within 2 hours of eating [1–3]. In hypertensive subjects, one study
showed the cut-off for PPH may be better defined as a SBP drop of 30 mmHg within
2 hours of eating, instead of 20 mmHg [4]. However, there is no standardized defini-
tion of PPH. Although orthostatic hypotension (OH) is a common fall concern in
the elderly, PPH occurs more often than OH [5].

Epidemiology

PPH is seen in 13% of healthy older adults [6, 7]. Its prevalence increases with cer-
tain diseases like diabetes, Parkinson’s disease, and chronic renal failure [6, 8–10].
Its prevalence also appears to be increased in patients admitted to the ICU, even
after discharge. One small study reported that 29% of patients 65 years or older had
PPH 3 months after a stay in an ICU, with an average systolic drop of 10 mmHg
among all discharged patients [11]. A study of 85 frail hospitalized older adults
found that 67% had PPH compared to 52% with OH [12]. In nursing home subjects,
the prevalence of PPH ranges from 24% to 36% [13, 14].

K. Alagiakrishnan (*)
Division of Geriatric Medicine, University of Alberta, Edmonton, AB, Canada
D. Mah
University of Alberta, Edmonton, AB, Canada

© Springer Nature Switzerland AG 2020 9

K. Alagiakrishnan, M. Banach (eds.), Hypotensive Syndromes in Geriatric
Patients, https://doi.org/10.1007/978-3-030-30332-7_2
10 K. Alagiakrishnan and D. Mah

Causes

PPH is common in elderly patients with autonomic system dysfunction [15]. It occurs
in roughly 1/3 of patients with diabetes mellitus [16] and the majority of patients with
Parkinson’s disease (PD) [17–19]. It is also seen in patients with paraplegia [20, 21]
and Alzheimer’s disease [22]. Patients with heart failure [23] and hypertension have
also been noted to have postprandial blood pressure drops [24–26]. Diuretics like
furosemide can potentiate the postprandial blood pressure drop [27].

Pathophysiology

The pathophysiology of PPH is multifactorial (Fig. 2.1). Insulin-induced vasodila-

tion and/or increased postprandial splanchnic blood pooling is an important mecha-
nism [28, 29]. Other factors appear to be impairments in baroreflex function and
inadequate postprandial cardiac output increases, peripheral vasoconstriction, and
sympathetic nervous system compensation [2, 30]. Reduced baroreflex sensitivity is
seen with decreased heart rate variability in PPH [31, 32]. Attenuation of the gastro-
vascular reflex plays a role in the mechanism of PPH [33]. In healthy older subjects,
postprandial hypotension is associated with relatively more rapid gastric emptying
and attenuation of the rise in plasma noradrenaline levels in response to a meal [7,
34]. However, PPH is not fully explained by autonomic dysfunction alone [35]. A

Insulin-induced
Vasodilation
Impaired Macronutrient
Baroreflex Absorption
Function

Splanchnic Inadequate
Blood Postprandial Cardiac
Pooling Hypotension Output

Inadequate Vasodilatory
Sympathetic Gastrointestinal
Compensation Gastric Peptides
Dysmotility

Fig. 2.1 Pathophysiological mechanisms of PPH