Prepared by md, PhD., Associate Professor Marta R. Gerasymchuk, pathophysiology department

1. Hypertension

2. ActualityActuality
 Arterial hypertension is a very commonArterial hypertension is a very common
condition. Cerebral, coronary and renal vesselscondition. Cerebral, coronary and renal vessels
are mainly affected byare mainly affected by the deleterious effect ofthe deleterious effect of
this condition, and both acute and chronic organthis condition, and both acute and chronic organ
failure may ensue.failure may ensue.
 Exacerbation of underlyingExacerbation of underlying pathophysiologicpathophysiologic
conditions or new precipitating factors can leadconditions or new precipitating factors can lead
to hypertensive crisis, either urgencies orto hypertensive crisis, either urgencies or
emergencies.emergencies.
 During hypertensive emergencies, a quick raiseDuring hypertensive emergencies, a quick raise
in arterial pressure may lead to acute andin arterial pressure may lead to acute and
significant organ dysfunction,significant organ dysfunction, such as aorticsuch as aortic
dissection, acute myocardial infarction,dissection, acute myocardial infarction,
intracranial bleeding or acute renal failure.intracranial bleeding or acute renal failure.
 PerioperativePerioperative hypertension often takes thehypertension often takes the
shape of a crisis and it can be related toshape of a crisis and it can be related to
hypothermia, pain, neuro-hormonal response tohypothermia, pain, neuro-hormonal response to
surgical trauma or antihypertensive drugssurgical trauma or antihypertensive drugs
withdrawal.withdrawal.

3. CONTENTCONTENT
• 1. Factors which predetermine the level of blood pressure for a1. Factors which predetermine the level of blood pressure for a
man, basal tone of vessels.man, basal tone of vessels.
• 2. Pressor and depressor systems of organism, their description.2. Pressor and depressor systems of organism, their description.
• 3. Arterial hypertensions: kinds, classification. Degrees of high3. Arterial hypertensions: kinds, classification. Degrees of high
arterial pressure.arterial pressure.
• 4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.
• 5. Etiology and pathogenesis of endocrinal hypertension.5. Etiology and pathogenesis of endocrinal hypertension.
• 6. A role of the sympathetic nervous system in pathogenesis of6. A role of the sympathetic nervous system in pathogenesis of
nerogenic hypertension.nerogenic hypertension.
• 7. Salt hypertension: etiology, mechanisms of development.7. Salt hypertension: etiology, mechanisms of development.
• 8. Etiology and pathogenesis of essential hypertension.8. Etiology and pathogenesis of essential hypertension.
• 9. Complication of essential hypertension.9. Complication of essential hypertension.
• 10. Reasons and mechanisms of arterial hypotension.10. Reasons and mechanisms of arterial hypotension.

4. Determinants of Blood Pressure
• Components of B/P
– Pressure of blood against the walls of
the arteries
– The elasticity of the artery walls
– The volume and thickness of the blood

5. • Systolic Blood Pressure (SBP) pressure measured in brachial
artery during systole (ventricular emptying and ventricular
contraction period)
• Diastolic Blood Pressure (DBP) pressure measured in brachial
artery during diastole (ventricular filling and ventricular
relaxation)
• Mean Arterial Pressure (MAP) "average" pressure throughout the
cardiac cycle against the walls of the proximal systemic
arteries (aorta)
• estimated as: .33(SBP - DBP) + DBP
• Total Peripheral Resistance (TPR) - the sum of all forces that
oppose blood flow
• length of vasculature (L)
• blood viscosity (V)
• vessel radius (r)
Definitions
TPR = ( 8 ) ( V ) ( L )
( p ) ( r 4
)

6. Physiological factors affecting Arterial Blood pressurePhysiological factors affecting Arterial Blood pressure
AgeAge::
 New born: 80/40 mmHgNew born: 80/40 mmHg
 4 years: 100/65 mmHg.4 years: 100/65 mmHg.
 Adults: 120/80 mmHgAdults: 120/80 mmHg
 After that: Gradually increase due to increase elasticity of arteries.After that: Gradually increase due to increase elasticity of arteries.
SexSex::
 Children: have equal Blood pressure.Children: have equal Blood pressure.
 Adults before 45 years: male more than female.Adults before 45 years: male more than female.
 Adults after 45 years: the diastolic B.P. is more in female than males.Adults after 45 years: the diastolic B.P. is more in female than males.
RaceRace:: ABP in oriental is less than in European and American.ABP in oriental is less than in European and American.
GravityGravity:: B.P. in upper parts of the body is more than the lower partsB.P. in upper parts of the body is more than the lower parts
especially during standing.especially during standing.
Meals:Meals: Digestion increases the arterial blood pressure.Digestion increases the arterial blood pressure.
Emotions and exerciseEmotions and exercise:: increase the arterial blood pressure.increase the arterial blood pressure.
SleepSleep:: Deep quiet sleep decrease A.B.P., while sleep with dreamsDeep quiet sleep decrease A.B.P., while sleep with dreams
increase A.B.P.increase A.B.P.

7. Measurements of Blood PressureMeasurements of Blood Pressure
1- Direct Method1- Direct Method
 The most accurate means for measuring bloodThe most accurate means for measuring blood
pressure is directly within an artery (intra-arterial)pressure is directly within an artery (intra-arterial)
using a catheter.using a catheter.
 But because this method is invasive, it is neitherBut because this method is invasive, it is neither
practical nor appropriate for repeated measurementspractical nor appropriate for repeated measurements
in non-hospital settings, or for large-scale publicin non-hospital settings, or for large-scale public
health screenings.health screenings.
2- The mercury-filled sphygmomanometer2- The mercury-filled sphygmomanometer
 The usual method of measurement, therefore, is aThe usual method of measurement, therefore, is a
noninvasive means that uses a sphygmomanometer,noninvasive means that uses a sphygmomanometer,
which includes either a column of mercury orwhich includes either a column of mercury or
pressure-registering gauge.pressure-registering gauge.

8. Cardiovascular Hemodynamic Basics
Flow (Q)
Pressure (MAP) P aorta – P vena cava
= =
Resistance (TPR) (8) (V) (L)
(p) (r 4
)
Flow (Q) = () (Pa – Pv) (r 4
)
(8) (V) (L)
V = viscosity of fluid (blood) flowing through the pipe
L = length of pipe (blood vessel)
r = radius of the pipe (blood vessel)
Pa = aortic pressure
Pv = venous pressure
Normally Resting Q is
about 5 - 6 liters / minute
BP = CO x PRBP = CO x PR

9. RA
RV
LUNGS LA
LV
AORTA
ARTERIOLES
SYSTEMIC
ARTERIES
VEINS
(CAPACITANCE VESSELS)
(100)
(92)
(40)
low compliance
13% of blood volume
high compliance
64% of blood volume
PO2 = 40 PCO2 = 46
(0)
(2)
PO2 = 100
PCO2 = 40
PO2 = 160
PCO2 = .3
CAPILLARY
BEDS
7% of blood volume
9% of blood volume
(7)
(13) (3)
Ohms Law: Flow (Q) = upstream pressure – downstream pressure
resistance
Systemic Circulation = 100 mmHg – 0 mmHg = 100 ml / sec = 6 liters / min
Flow (Q) 1 mmHg sec / ml
The “Closed” Cardiovascular
Hemodynamic System
Mean arterial pressures in red
(20)

10. Blood Pressure RegulationBlood Pressure Regulation
 Systemic arterial pressure is a function ofSystemic arterial pressure is a function of
stroke volume, heart rate, and totalstroke volume, heart rate, and total
peripheral resistanceperipheral resistance
 The major organs involved in regulation ofThe major organs involved in regulation of
blood pressure are the heart (HR & SV),blood pressure are the heart (HR & SV),
the SNS (TPR-total peripheral resistance),the SNS (TPR-total peripheral resistance),
and the kidneys (ECF – extracellular fluidand the kidneys (ECF – extracellular fluid
volume & secretion of renin).volume & secretion of renin).
 (Wynne, Woo, & Olyaei, 2007, p. 1093)(Wynne, Woo, & Olyaei, 2007, p. 1093)

11. Factors Influencing BPFactors Influencing BP
CardiacCardiac
•Heart rate
•Inotropic state
•Neural (pons and medulla)
•Humoral (hormones)
CardiacCardiac
•Heart rate
•Inotropic state
•Neural (pons and medulla)
•Humoral (hormones)
Cardiac OutputCardiac Output
Renal Fluid Volume ControlRenal Fluid Volume Control
•Renin–angiotensin
•Aldosterone
•Atrial natriuretic factor
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

12. Regulative systemsRegulative systems
Sympathetic Nervous SystemSympathetic Nervous System
BaroreceptorsBaroreceptors
– Nerve cells in carotid artery & aortic archNerve cells in carotid artery & aortic arch
– Maintain BP during normal activitiesMaintain BP during normal activities
– React to increases & decreases in BPReact to increases & decreases in BP
BP – impulse to brain to inhibit SNS; HR &BP – impulse to brain to inhibit SNS; HR &
force of contraction; vasodilation of arteriolesforce of contraction; vasodilation of arterioles
BP – activates SNS; vasoconstriction ofBP – activates SNS; vasoconstriction of
arterioles; HR & heart contractilityarterioles; HR & heart contractility
1. Barroreceptors of aorta arch and sinus caroticus

13. Sites of
Cardiorespiratory
Control

14.  Increased BP send inhibitory
impulse to sympathetic
vasomotor center in
brainstem;
 In long-standing
hypertension, baroreceptors
adjust to elevated BP and
reads it as normal; doesn’t
make adjustments; also
becomes less responsive in
some older adults

15. On standing up venous return fallsOn standing up venous return falls
Cardiac output diminishesCardiac output diminishes
Arterial blood pressure is reducedArterial blood pressure is reduced
Baroreceptor afferent firing reducedBaroreceptor afferent firing reduced
Medullary centres inhibition reducedMedullary centres inhibition reduced
THE BARORECEPTOR REFLEX - AN EXAMPLETHE BARORECEPTOR REFLEX - AN EXAMPLE
CORRECTION OF POSTURAL HYPOTENSIONCORRECTION OF POSTURAL HYPOTENSION
Effect of gravity onEffect of gravity on
venous returnvenous return
Preload diminishedPreload diminished
- Starling’s Law- Starling’s Law
Subject possibly feels faintSubject possibly feels faint
as cerebral flow is reducedas cerebral flow is reduced
Due to reduced arterial B.P.Due to reduced arterial B.P.
VasoconstrictionVasoconstriction
TachycardiaTachycardia
Raised stroke workRaised stroke work
Tend to
restore
arterial
blood
pressure
Increased sympathetic tone toIncreased sympathetic tone to
arteriolesarterioles
Reduced vagal tone to s.a.Reduced vagal tone to s.a.
nodenode
Increased myocardial sympathetic toneIncreased myocardial sympathetic tone

16. Sympatetic activitySympatetic activity
Increase BP
Increases
heart rate
and
contractility
Increase
cardiac
output
Vasoconstriction
increasing
peripheral
vascular
resistances
Increases
sodium and
water
reabsorption
Increases
vascular tone at
precapillary
level
Induces
vascular
remodelling
Increase
diastolic
pressure
Chronic
Ischemia
and AMI
Increased left
ventricular
hypertrofy and
oxygen
consumption

18. Blood pressure regulation by the renin-angiotensin systemBlood pressure regulation by the renin-angiotensin system
and the central roles of sodium metabolism in specificand the central roles of sodium metabolism in specific
causes of inherited and acquired forms of hypertension.causes of inherited and acquired forms of hypertension.
Components of theComponents of the
systemic renin-angiotensinsystemic renin-angiotensin
system are shown in black.system are shown in black.
Genetic disorders thatGenetic disorders that
affect blood pressure byaffect blood pressure by
altering activity of thisaltering activity of this
pathway are indicated inpathway are indicated in
red;red; arrowsarrows indicate sitesindicate sites
in the pathway altered byin the pathway altered by
mutation. Genes that aremutation. Genes that are
mutated in these disordersmutated in these disorders
are indicated inare indicated in
parentheses. Acquiredparentheses. Acquired
disorders that alter blooddisorders that alter blood
pressure through effectspressure through effects
on thison this pathway arepathway are
indicated in blue.indicated in blue.
(From Lifton RP, et al:
Molecular genetics of
human blood pressure
variation. Science 272:676,
1996.)

20. Increase BPIncrease BP
Renin
Angiotensin II
AldosteroneAldosterone
VasoconstrictionVasoconstriction
on systemic andon systemic and
renal vasselsrenal vassels
Left ventricularLeft ventricular
hypertrophyhypertrophy
andand
myocardialmyocardial
ischemiaischemia
Increase leftIncrease left
ventricularventricular
wallwall
tensiontension
Alteration of renalAlteration of renal
arterial andarterial and
capillarycapillary
vessels’ wallvessels’ wall
Glomeruar ischemia,Glomeruar ischemia,
parenchymal damage,parenchymal damage,
proteinuria, end-stageproteinuria, end-stage
renal failurerenal failure
ADHADH
Sodium andSodium and
water renalwater renal
retentionretention
HHypervolemiaypervolemia
Effect of renin-angiotensin systemEffect of renin-angiotensin system
on cardiovascular homeostasison cardiovascular homeostasis
2.2. ReninRenin––angiotensinangiotensin systemsystem

21. Mutations altering blood pressure in humans.Mutations altering blood pressure in humans.
A diagram of a nephron, the filtering unit of the kidney, is shown. The molecular pathways mediating NaCl reabsorption in
individual renal cells in the thick ascending limb of the loop of Henle (TAL), distal convoluted tubule (DCT), and the cortical
collecting tubule (CCT) are indicated, along with the pathway of the renin-angiotensin system, the major regulator of renal
salt reabsorption. Single gene defects that manifest as inherited diseases affecting these pathways are indicated, with
hypertensive disorders in red and hypotensive disorders in blue. Abbreviations: Al, angiotensin I; ACE, angiotensin
converting enzyme; All, angiotensin II; MR, mineralocorticoid receptor; GRA, glucocorticoid-remediable aldosteronism;
PHA1, pseudohypoaldosteronism, type 1; AME, apparent mineralocorticoid excess; 11b-HSD2, 11b-hydroxysteroid
dehydrogenase-2; and DOC, deoxycorticosterone. (From Lifton RP, et al: Molecular mechanisms of human hypertension.
Cell 104:545, 2001.)

22. Regulative systems
3. Renin–angiotensin-aldosteron system
Renin Actination of
suprarenal glangs
(cortical layer)
Na reabsorbtion
in kidney increase
Angiotensin 2
Aldosteron
excretion
Na concentration in
blood increase,
blood osmotic
pressure increase
Move of extravascular
fluid inside the
vessels
Increase of circulative
blood volume
(CBV)
CО increase

23. Mechanism of Action of AldosteroneMechanism of Action of Aldosterone
Increases CO by increasing blood volume
.

24. BP Regulation: EndotheliumBP Regulation: Endothelium
Nitric oxideNitric oxide is secreted by endothelial cellsis secreted by endothelial cells
which results in relaxation of blood vesselswhich results in relaxation of blood vessels
It also produces local vasodilators, suchIt also produces local vasodilators, such
asas prostacylcinprostacylcin andand endothelium-derivedendothelium-derived
hyperpolarizing factorhyperpolarizing factor
EndothelinEndothelin is an extremely potentis an extremely potent
vasoconstrictor and also stimulatesvasoconstrictor and also stimulates
vascular smooth muscle growthvascular smooth muscle growth
(Wynne, Woo, & Olyaei, 2007, p. 1094)(Wynne, Woo, & Olyaei, 2007, p. 1094)

25. Healthy LifestyleHealthy Lifestyle
Maintain a Healthy Blood Pressure:
Blood PressureBlood Pressure
ClassificationClassification
Systolic BPSystolic BP
(mm Hg)(mm Hg)
Diastolic BPDiastolic BP
(mm Hg)(mm Hg)
NormalNormal < 120< 120 < 80< 80
PrehypertensionPrehypertension 120 – 139120 – 139 80 – 8980 – 89
Stage 1 HypertensionStage 1 Hypertension 140 – 159140 – 159 90 – 9990 – 99
Stage 2 HypertensionStage 2 Hypertension 160 – 179160 – 179 100 – 109100 – 109
Stage 3 HypertensionStage 3 Hypertension
(Hypertensive crisis)(Hypertensive crisis)
≥≥ 180180 ≥≥ 110110
Source: Clinical Practice Guidelines Management of Hypertension, 3rd
Ed. 2008
February;MOH/P/PAK/156.08(GU)

26. Hypertension:Hypertension: DefinitionDefinition
Persistent elevation ofPersistent elevation of
 Systolic bloodSystolic blood pressurepressure ≥140 mm Hg≥140 mm Hg
oror
 Diastolic blood pressureDiastolic blood pressure ≥90 mm Hg≥90 mm Hg
 Worldwide an estimatedWorldwide an estimated 1 billion1 billion peoplepeople
have hypertension; about 1 in 3have hypertension; about 1 in 3
Americans affectedAmericans affected
 Direct relationship between hypertensionDirect relationship between hypertension
and cardiovascular disease (CVD)and cardiovascular disease (CVD)

28. ClassificationClassification
Arterial hypotensionArterial hypotension
Arterial hypertensionArterial hypertension
AcuteAcute
ChronicChronic
SecondarySecondary
AP above 139/89 mm HgAP above 139/89 mm Hg
PrimaryPrimary
AP less than 100/60 mm HgAP less than 100/60 mm Hg

29. Primary HypertensionPrimary Hypertension
►Etiological TheoriesEtiological Theories
►Inability of kidneys to excrete sodiumInability of kidneys to excrete sodium
►Overactive renin/angiotensin systemOveractive renin/angiotensin system
►Overactive sympathetic nervous systemOveractive sympathetic nervous system
►Decreased vasodilatory reactionDecreased vasodilatory reaction
►Resistance to insulin actionResistance to insulin action
►Genetic Inheritance (polygenic)Genetic Inheritance (polygenic)

30. Risk Factors R/T PrimaryRisk Factors R/T Primary
HypertensionHypertension
Age/HeredityAge/Heredity
SexSex
RaceRace
ObesityObesity
StimulantsStimulants
SodiumSodium
AlcoholAlcohol
StressStress
HyperlipidemiaHyperlipidemia
DiabetesDiabetes
SocioeconomicSocioeconomic
StatusStatus

31. Risk Factors forRisk Factors for -- Primary HypertensionPrimary Hypertension
Age (>55)
Alcohol
Cigarette smoking
Diabetes mellitus
Elevated serum lipids
Excess dietary sodium
Gender
– SBP rises with age Alcohol – excessive use strongly correlated
to hypertension
– Smoking – increases risk for CV disease ; vasoconstriction
– Diabetes – along with hypertension greater risk for target organ
disease and usually more severe
– Hyperlipidemia elevated in people with hypertension; increases
risk of atherosclerosis
– Some pts Na sensitive Males have higher rates of hypertension
<55 and increased in women>55

32. Risk Factors forRisk Factors for
Primary HypertensionPrimary Hypertension
Family historyFamily history
ObesityObesity
EthnicityEthnicity
Sedentary lifestyleSedentary lifestyle
StressStress

33. Primary HypertensionPrimary Hypertension
 Water and sodium retentionWater and sodium retention
• AA high sodium intake may resulthigh sodium intake may result
in water retentionin water retention
• Some people are Na sensitiveSome people are Na sensitive
(about 20%) ; not everyone(about 20%) ; not everyone
with high salt diet developswith high salt diet develops
hypertensionhypertension

34. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
 Water and sodium retentionWater and sodium retention
 Certain demographics areCertain demographics are
associated with “saltassociated with “salt
sensitivity”sensitivity”
 ObesityObesity
 Increasing ageIncreasing age
 African American ethnicityAfrican American ethnicity
 People with diabetes, renalPeople with diabetes, renal
diseasedisease

35. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
• Stress and increased SNS activityStress and increased SNS activity
– Produces increased vasoconstrictionProduces increased vasoconstriction
– ↑↑ HRHR
– ↑↑ Renin releaseRenin release
– Angiotensin II causes direct arteriolarAngiotensin II causes direct arteriolar
constriction, promotes vascularconstriction, promotes vascular
hypertrophy and induces aldosteronehypertrophy and induces aldosterone
secretionsecretion

36. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
Insulin resistance & hyperinsulinemia
High insulin concentration
stimulates SNS activity and impairs
nitric oxide–mediated vasodilation
Not present in secondary
hypertension and don’t improve
when hypertension is treated

37. Risk factors and aetiological influences in hypertensionRisk factors and aetiological influences in hypertension
Risk factor or aetiologicalRisk factor or aetiological
influenceinfluence
Possible rationale and commentPossible rationale and comment
MajorMajor
Family historyFamily history Inherited tendency – probably polygenicInherited tendency – probably polygenic
Dietary Na highDietary Na high Fluid retention; vascular wall oedema; ion pump defectFluid retention; vascular wall oedema; ion pump defect
ObesityObesity Possible artefact of measurement (problem with arm cuff)?Possible artefact of measurement (problem with arm cuff)?
Greater perfusion demands of increased body massGreater perfusion demands of increased body mass
Reducing weight can reverse borderline HPTReducing weight can reverse borderline HPT
AlcoholAlcohol Unknown mechanism; possibly 30% of HPT related to alcohol abuseUnknown mechanism; possibly 30% of HPT related to alcohol abuse
Sedentary lifeSedentary life Unknown mechanism; regular exercise lowers BPUnknown mechanism; regular exercise lowers BP
Renal diseaseRenal disease Overt or occult renal disease often implicated: cause or effect?Overt or occult renal disease often implicated: cause or effect?
MinorMinor
AgeAge
Stress or type A personalityStress or type A personality Overactive sympathetic nervous system → vasoconstriction and/or raised COOveractive sympathetic nervous system → vasoconstriction and/or raised CO
Difficult to quantify; effect may have been exaggeratedDifficult to quantify; effect may have been exaggerated
DietaryDietary
 Ca, K, Mg ↓Ca, K, Mg ↓
 Saturated fatSaturated fat
 Animal productsAnimal products
Some evidence,Some evidence,
May induce vasoconstriction via endothelial interactionsespecially for KMay induce vasoconstriction via endothelial interactionsespecially for K
Vegetarians may have lower BPVegetarians may have lower BP
Glucose intoleranceGlucose intolerance Complex interaction between insulin resistance, hyperlipidaemia and HPTComplex interaction between insulin resistance, hyperlipidaemia and HPT
RaceRace Increased average BP in urban Blacks: response to stress or dietary salt?Increased average BP in urban Blacks: response to stress or dietary salt?
SmokingSmoking NoNo sustained effect on BP itself but greatly exacerbates atheroscleroticsustained effect on BP itself but greatly exacerbates atherosclerotic
complicationscomplications
BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.

38. HypertensionHypertension
Clinical ManifestationsClinical Manifestations
 Referred to as the “silent killer”Referred to as the “silent killer”
 Frequently asymptomatic until targetFrequently asymptomatic until target
organ disease occursorgan disease occurs
 Or recognized on routine screeningOr recognized on routine screening

39. HypertensionHypertension
Clinical ManifestationsClinical Manifestations
often secondary to
target organ disease
Can include:
– Fatigue, reduced
activity tolerance
– Dizziness
– Palpitations, angina
– Dyspnea

40. Target Organ DamageTarget Organ Damage
 Caused by damage to the body’s blood vesselsCaused by damage to the body’s blood vessels
which particularly affect the following organs:which particularly affect the following organs:
 Blood VesselsBlood Vessels
 HeartHeart
 KidneysKidneys
 BrainBrain
 EyesEyes

41. HypertensionHypertension
ComplicationsComplications
• Target organ diseases occur mostTarget organ diseases occur most
frequently in:frequently in:
– HeartHeart
– BrainBrain
– Peripheral vasculaturePeripheral vasculature
– KidneyKidney
– EyesEyes

42. Hypertension-Hypertension-ComplicationsComplications
• Cerebrovascular diseaseCerebrovascular disease
– Stroke
• Peripheral vascular diseasePeripheral vascular disease
• Nephrosclerosis
• Retinal damageRetinal damage
• AtherosclerosisAtherosclerosis most common cause of cerebrovascular disease;
hypertension major risk factor for cerebral atherosclerosis and stroke
• AtherosclerosisAtherosclerosis in peripheral blood vessels too; can lead to PVD, aortic
aneurysm, aortic dissection
• Hypertension one of leading causes of end-stage renal disease, esp. in
African-Americans; some degree of renal dysfunction usual in person with
even mild BP elevations
• RetinaRetina is only place blood vessels can be directly visualized; if see damage
there then indicates damage in brain, heart, & kidney too; Can cause
blurring, retinal hemorrhage and blindness

43. Accelerated-malignant HTAccelerated-malignant HT
• Fundoscopic changesFundoscopic changes
– Retinal hemorrhagesRetinal hemorrhages
– ExudatesExudates
– PapilledemaPapilledema

44. Wong, T. Y. et al. N Engl J Med 2004;351:2310-2317
Examples of Mild Hypertensive Retinopathy
AV nicking
Focal
narrowing
AV nicking
Copper
wiring

45. Secondary HypertensionSecondary Hypertension
►It is caused by another diseaseIt is caused by another disease
process such as:process such as:
►Renal FailureRenal Failure
►Diabetes MellitusDiabetes Mellitus
►Cushing’s SyndromeCushing’s Syndrome
►Primary AldosteronismPrimary Aldosteronism
►Coarctation of the AortaCoarctation of the Aorta
►PheochromocytomaPheochromocytoma
►Sleep ApneaSleep Apnea

47. Secondary hypertension representSecondary hypertension represent
symptoms of such diseasessymptoms of such diseases
• 1. Diseases of kidneys: glomerulonephritis (14 %),
pielonephritis, interstitial nephritis due to abusing
analgetics, hereditary nephritis (syndrome Alport’s),
polycytosis kidney.
• 2. Stenosis of renal artery (1 %). Hypertension arises not in
each stenosis. The most often reason of stenosis, caused
atherosclerotic platelits(at 70-80 of %), which damage
usually proximal third of renal artery on the one hand.
Other reason of stenosis with hypertension its
fibromuscular hyperplasia of an average third of renal
artery. It, as a rule, double-side and more often happens at
the women. The mechanism of hypertension in stenosis of
renal artery – hyperproduction of renin.

48. Secondary hypertension representSecondary hypertension represent
symptoms of such diseasessymptoms of such diseases
• 3. Primary aldosteronism (Cоnn syndrome)3. Primary aldosteronism (Cоnn syndrome) – in 1 %– in 1 %
of cases. The reasons – unilateral adenomaof cases. The reasons – unilateral adenoma
glomerular zone adrenal glands or double-sideglomerular zone adrenal glands or double-side
diffuse hyperplasia of adrenal glands.diffuse hyperplasia of adrenal glands.
• 4. Paraganglioma (1 %)4. Paraganglioma (1 %) – tumour from chromaffin– tumour from chromaffin
cells of medullarcells of medullar layer adrenal glands or sympatheticlayer adrenal glands or sympathetic
nerves, as a rule –nerves, as a rule – benighnbenighn. In paraganglioma is. In paraganglioma is
increased both cardiac output, and peripheralincreased both cardiac output, and peripheral
resistance.resistance.
• 5. Coarctation of the aorta is an anatomic defect5. Coarctation of the aorta is an anatomic defect, in, in
which aorta in pectoral or abdominal department iswhich aorta in pectoral or abdominal department is
narrowed to such extend, that it represents seriousnarrowed to such extend, that it represents serious
barrier for blood circulation. In all vessels, whichbarrier for blood circulation. In all vessels, which
depart from the aorta proximal of narrowing, thedepart from the aorta proximal of narrowing, the
resistance increases and is increased arterialresistance increases and is increased arterial
pressure.pressure.

49. Pheochromocytoma
• A pheochromocytoma is a tumor of chromaffin tissue, which containsA pheochromocytoma is a tumor of chromaffin tissue, which contains
sympathetic nerve cells.sympathetic nerve cells.
• The tumor is most commonly located in the adrenal medulla but canThe tumor is most commonly located in the adrenal medulla but can
arise in other sites, such as sympathetic ganglia, where there isarise in other sites, such as sympathetic ganglia, where there is
chromaffin tissuechromaffin tissue. Although only 0.1% to 0.5% of persons with. Although only 0.1% to 0.5% of persons with
hypertension have an underlying pheochromocytoma, the disorder canhypertension have an underlying pheochromocytoma, the disorder can
cause serious hypertensive crises.cause serious hypertensive crises.
• Eight percent to 10% of the tumors are malignant.Eight percent to 10% of the tumors are malignant.
• Like adrenal medullary cells, the tumor cells of a pheochromocytomaLike adrenal medullary cells, the tumor cells of a pheochromocytoma
produce and secrete the catecholaminesproduce and secrete the catecholamines epinephrine andepinephrine and
norepinephrine.norepinephrine.
• TheThe hypertensionhypertension that develops is the result of a massive release ofthat develops is the result of a massive release of
these catecholamines. Their release may be paroxysmal, rather thanthese catecholamines. Their release may be paroxysmal, rather than
continuous, causing periodic episodes of headache, excessivecontinuous, causing periodic episodes of headache, excessive
sweating, and palpitations.sweating, and palpitations.
• HeadacheHeadache is the most common symptom and can be quite severe.is the most common symptom and can be quite severe.
Nervousness, tremor, facial pallor, weakness, fatigue, and weight lossNervousness, tremor, facial pallor, weakness, fatigue, and weight loss
occur less frequently. Marked variability in blood pressure betweenoccur less frequently. Marked variability in blood pressure between
episodes is typical.episodes is typical.
• Some persons with pheochromocytoma have paroxysmal episodes ofSome persons with pheochromocytoma have paroxysmal episodes of
hypertension, sometimes to dangerously high levels; others may havehypertension, sometimes to dangerously high levels; others may have
sustained hypertension; and some may even be normotensive.sustained hypertension; and some may even be normotensive.

50. Peripheral Arterial DiseasePeripheral Arterial Disease
(PAD)(PAD)
§ PAD is equivalent in risk to ischemic heart disease.PAD is equivalent in risk to ischemic heart disease.
§ Any class of drugs can be used in most PAD patients.Any class of drugs can be used in most PAD patients.
§ Other risk factors should be managed aggressively.Other risk factors should be managed aggressively.
§ Aspirin should be used.Aspirin should be used.

51. Hypertension in OlderHypertension in Older
PersonsPersons
§ More than two-thirds of people over 65 have HTN.More than two-thirds of people over 65 have HTN.
§ This population has the lowest rates of BP control.This population has the lowest rates of BP control.
§ Treatment, including those who with isolated systolic HTN,Treatment, including those who with isolated systolic HTN,
should follow same principles outlined for general care ofshould follow same principles outlined for general care of
HTN.HTN.
§ Lower initial drug doses may be indicated to avoid symptoms;Lower initial drug doses may be indicated to avoid symptoms;
standard doses and multiple drugs will be needed to reach BPstandard doses and multiple drugs will be needed to reach BP
targets.targets.

52. Postural HypotensionPostural Hypotension
§ Decrease in standing SBP >10 mmHg, when associatedDecrease in standing SBP >10 mmHg, when associated
with dizziness/fainting, more frequent in older SBPwith dizziness/fainting, more frequent in older SBP
patients with diabetes, taking diuretics, venodilators, andpatients with diabetes, taking diuretics, venodilators, and
some psychotropic drugs.some psychotropic drugs.
§ BP in these individuals should be monitored in the uprightBP in these individuals should be monitored in the upright
position.position.
§ Avoid volume depletion and excessively rapid doseAvoid volume depletion and excessively rapid dose
titration of drugs.titration of drugs.

53. Hypertension in WomenHypertension in Women
Hypertensive disorders complicate 6% to 8% ofHypertensive disorders complicate 6% to 8% of
pregnancies.pregnancies.
They are the second leading cause, after embolism, ofThey are the second leading cause, after embolism, of
maternal mortality in the United States, accounting formaternal mortality in the United States, accounting for
almost 15% of such deaths.almost 15% of such deaths.
Hypertensive disorders also contribute to stillbirths andHypertensive disorders also contribute to stillbirths and
neonatal morbidity and mortality.neonatal morbidity and mortality.
The incidence of hypertensive disorders of pregnancyThe incidence of hypertensive disorders of pregnancy
increases with maternal age and is more common inincreases with maternal age and is more common in
African-American women.African-American women.

54. Classification of High Blood Pressure inClassification of High Blood Pressure in
PregnancyPregnancy
Classification Description
GestationalGestational
hypertensionhypertension
Blood pressure elevation, without proteinuria, that isBlood pressure elevation, without proteinuria, that is
detected for the first time during midpregnancy anddetected for the first time during midpregnancy and
returns to normal by 12 weeks postpartum.returns to normal by 12 weeks postpartum.
ChronicChronic
hypertensionhypertension
Blood pressure ≥140 mm Hg systolic or ≥90 mm HgBlood pressure ≥140 mm Hg systolic or ≥90 mm Hg
diastolic that is present and observable before the 20thdiastolic that is present and observable before the 20th
week of pregnancy. Hypertension that is diagnosed forweek of pregnancy. Hypertension that is diagnosed for
the first time during pregnancy and does not resolvethe first time during pregnancy and does not resolve
after pregnancy also is classified as chronicafter pregnancy also is classified as chronic
hypertension.hypertension.
Preeclampsia-Preeclampsia-
eclampsiaeclampsia
Pregnancy-specific syndrome of blood pressure elevationPregnancy-specific syndrome of blood pressure elevation
(blood pressure >140 mm Hg systolic or >90 mm Hg(blood pressure >140 mm Hg systolic or >90 mm Hg
diastolic) that occurs after the first 20 weeks ofdiastolic) that occurs after the first 20 weeks of
pregnancy and is accompanied by proteinuria (urinarypregnancy and is accompanied by proteinuria (urinary
excretion of 0.3 g protein in a 24-hour specimen).excretion of 0.3 g protein in a 24-hour specimen).
PreeclampsiaPreeclampsia
superimposedsuperimposed
on chronicon chronic
hypertensionhypertension
Chronic hypertension (blood pressure ≥140 mm Hg systolicChronic hypertension (blood pressure ≥140 mm Hg systolic
or ≥90 mm Hg diastolic prior to 20th week ofor ≥90 mm Hg diastolic prior to 20th week of
pregnancy) with superimposed proteinuria and with orpregnancy) with superimposed proteinuria and with or
without signs of the preeclampsia syndromewithout signs of the preeclampsia syndrome

56. 1st period
functional violations
(heart hypertrophy)
2d period
Pathological changes in arteries and arterioles (dystrophy):
- Arterioles sclerosis
- Arteriole’s wall infiltration by plasma (leads to dystrophy)
- Arterioles necrosis (hypertonic crisis arises in clinic)
- Vein’s wall thickening
Arterial hypertension after-effects

57. 33dd periodperiod
Secondary changes in organs and systemsSecondary changes in organs and systems
KidneyKidney
((nephrosclerosisnephrosclerosis andand chronicchronic
kidneykidney insufficiencyinsufficiency))
KidneyKidney
((nephrosclerosisnephrosclerosis andand chronicchronic
kidneykidney insufficiencyinsufficiency))
CNSCNS
–– brain hypoxiabrain hypoxia
–– neurons destructionneurons destruction
–– apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture
leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain
destructiondestruction))
CNSCNS
–– brain hypoxiabrain hypoxia
–– neurons destructionneurons destruction
–– apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture
leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain
destructiondestruction))
HeartHeart
Decompensate heart failureDecompensate heart failure
HeartHeart
Decompensate heart failureDecompensate heart failure
Organs of visionOrgans of vision
- retinopathyretinopathy ((retina’sretina’s vessels injuryvessels injury))
- hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of
retinaretina,, that leads to blindnessthat leads to blindness
Organs of visionOrgans of vision
- retinopathyretinopathy ((retina’sretina’s vessels injuryvessels injury))
- hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of
retinaretina,, that leads to blindnessthat leads to blindness
Endocrine systemEndocrine system
Glands atrophy and sclerosisGlands atrophy and sclerosis
Endocrine systemEndocrine system
Glands atrophy and sclerosisGlands atrophy and sclerosis
Arterial hypertension after-effectsArterial hypertension after-effects

59. Hypertensive crisisHypertensive crisis
 DefinitionDefinition

Severe elevation in BP ( >220/120 mmHg)Severe elevation in BP ( >220/120 mmHg)

Sub classified into emergency and urgencySub classified into emergency and urgency
 Hypertensive emergencyHypertensive emergency

Require an immediate reduction in BP ( 1 hr )Require an immediate reduction in BP ( 1 hr )

Rx IV therapy and in ICURx IV therapy and in ICU
 Hypertensive urgencyHypertensive urgency

No evidence of progressive end-organ injuryNo evidence of progressive end-organ injury

Require only gradual reduction in BP in 24-48 hrRequire only gradual reduction in BP in 24-48 hr

60. Laboratory TestsLaboratory Tests
§ Routine Tests
• Electrocardiogram
• Urinalysis
• Blood glucose, and hematocrit
• Serum potassium, creatinine, or the corresponding estimated
GFR, and calcium
• Lipid profile, after 9- to 12-hour fast, that includes high-
density and low-density lipoprotein cholesterol, and
triglycerides
§ Optional tests
• Measurement of urinary albumin excretion or
albumin/creatinine ratio
§ More extensive testing for identifiable causes is not generally
indicated unless BP control is not achieved

61. Collaborative CareCollaborative Care
Lifestyle ModificationsLifestyle Modifications
 Wt. reduction
 10 kg (22 lb) loss; SBP by 5-20 mm Hg
 DASH eating plan (dietary approaches to stop
hypertension)
 Na reduction
 <2.4 g of sodium/day
 Moderate alcohol intake
 Men: 2 drinks/day or less
 Women: 1 drink/day or less

62. Collaborative CareCollaborative Care
Lifestyle ModificationsLifestyle Modifications
Physical activity:Physical activity:
– Regular physical (aerobic) activity,Regular physical (aerobic) activity,
– At least 30 min, most days of weekAt least 30 min, most days of week
Avoidance of tobacco productsAvoidance of tobacco products
Stress managementStress management

63. ExperimentalExperimental models of arterialmodels of arterial
hypertensionhypertension..
 Models confirming a role of the nervous factor in increase ofModels confirming a role of the nervous factor in increase of
arterial pressure:arterial pressure:
 1.1. Arterial hypertension owing to an irritation ofArterial hypertension owing to an irritation of
hypothalamus nucleuseshypothalamus nucleuses. The irritation of a back nucleus. The irritation of a back nucleus
frequently resultsfrequently results toto hypertension, connected with increasehypertension, connected with increase
of cardiac output. The irritation of a central nucleus causesof cardiac output. The irritation of a central nucleus causes
hyperensionhyperension due todue to of peripheral resistance increase.of peripheral resistance increase.
Electricity stimulation ventro-medial nucleus givesElectricity stimulation ventro-medial nucleus gives
hypertension, which depends from simultaneoushypertension, which depends from simultaneouslyly increaseincrease
of cardiac output and peripheral resistance.of cardiac output and peripheral resistance.
 2.2. Arterial hypertension from double-side damage nucleusArterial hypertension from double-side damage nucleus
tractus solitarii totractus solitarii to medullamedulla oblongoblongataata of rats, where areof rats, where are
located primary synapsis of sinuaorticus baroreceptors.located primary synapsis of sinuaorticus baroreceptors.
Arterial pressure is increased immediately without changeArterial pressure is increased immediately without change
of frequency of cardiac rof frequency of cardiac rateate. The reason of hypertension is. The reason of hypertension is
the sharp increase of peripheral resistancethe sharp increase of peripheral resistance
 3.3. Reflexogenic hypertensionReflexogenic hypertension,, inin dogs and rabbits adogs and rabbits affterffter
section depressor nerve Ludvig-Cion or sinus nerves Heringsection depressor nerve Ludvig-Cion or sinus nerves Hering
..

64. ExperimentalExperimental models of arterial hypertensionmodels of arterial hypertension..
Models, which confirm participation renals factor in occurrence andModels, which confirm participation renals factor in occurrence and
stabilization of arterial hypertension:stabilization of arterial hypertension:
1.1. Vasorenal hypertensionVasorenal hypertension, which is caused by narrowing renals arteries., which is caused by narrowing renals arteries.
Conditions of reproduction: а) arteries should be narrowed only partially,Conditions of reproduction: а) arteries should be narrowed only partially,
instead of are blocked completely;instead of are blocked completely; bb) the narrowing should be double-) the narrowing should be double-
side; c) the variant is possible(probable): narrowing arteries of one kidneyside; c) the variant is possible(probable): narrowing arteries of one kidney
plusplus removalremoval of the other kidney.of the other kidney.
2.2. Renoprival hypertensionRenoprival hypertension it arises afterit arises after removelremovel both kidneys andboth kidneys and spendingspending
ofof animal on dialysisanimal on dialysis..
Models confirming a role of adrenal glands in fixing arterialModels confirming a role of adrenal glands in fixing arterial
hypertension:hypertension:
1.1. Mineral-corticoids hypertensionMineral-corticoids hypertension –– in the casein the case ofof longlong introduction ofintroduction of
aldosteron with simultaneousaldosteron with simultaneouslyly purpose of solution NaCl instead of water.purpose of solution NaCl instead of water.
2.2. Salty hypertensionSalty hypertension. Sodium chlorids in a fair quantity even without. Sodium chlorids in a fair quantity even without
additional hormonal effects is capable to cause hypertension.additional hormonal effects is capable to cause hypertension.
Model confirming role of the hereditary factor in etiology ofModel confirming role of the hereditary factor in etiology of
hypertonic disease.hypertonic disease.
Exists genetic (spontaneous) hypertension in rats.Exists genetic (spontaneous) hypertension in rats. InIn the animal withthe animal with
spontaneous hypertension is revealed higher, than in normal animals,spontaneous hypertension is revealed higher, than in normal animals,
permeability ions channels in membranes smoothmusclepermeability ions channels in membranes smoothmuscle cellscells of arteries.of arteries.
These membrane defects can have some significance in increase ofThese membrane defects can have some significance in increase of
arteries tonus and regulation of volume extracellular liquid. They can bearteries tonus and regulation of volume extracellular liquid. They can be
considered as one of the factors pathogenesis hypertonic disease.considered as one of the factors pathogenesis hypertonic disease.

65. ReferencesReferences
1.1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia:General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia:
Nova Knuha Publishers – 2011. – P.Nova Knuha Publishers – 2011. – P. 478478––489489..
2.2. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinicalRussell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical
pharmacy practice / Russell J. Greene, Norman D. Harris // Published by thepharmacy practice / Russell J. Greene, Norman D. Harris // Published by the
Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, LondonPharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London
SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rdSE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd
edition, USA. – 2008. – Chapter 4. – P. 208–234.edition, USA. – 2008. – Chapter 4. – P. 208–234.
3.3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.
– 2010. – P. 372–387.– 2010. – P. 372–387.
4.4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova //Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova //
Study guide for medical students and practitioners.Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. –Edited by prof. Zaporozan, OSMU. –
OdessaOdessa.. – 200– 20055. – P.. – P. 222222––229229..
5.5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &
Wilkins), Trade paperback (2003)Wilkins), Trade paperback (2003) // Carol Mattson Porth, Kathryn J. Gaspard. –ChapterCarol Mattson Porth, Kathryn J. Gaspard. –Chapter
16 – P. 274–290.16 – P. 274–290.
6.6. SilbernaglSilbernagl S.S. Color Atlas of PathophysiologyColor Atlas of Pathophysiology / S./ S. SilbernaglSilbernagl, F., F. LangLang //// ThiemeThieme..
StuttgartStuttgart.. New YorkNew York. –. – 20002000. – P. 206–215.. – P. 206–215.
7.7. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.
Copyright ВCopyright В.. – Lippincott Williams & Wilkins – 2008. –– Lippincott Williams & Wilkins – 2008. – Chapter 13. – P. 399–412, 426–Chapter 13. – P. 399–412, 426–
427, 431–435.427, 431–435.
8.8. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.
Banasic // Elsevier Inc. – 2010. – P. 374Banasic // Elsevier Inc. – 2010. – P. 374––395.395.
9.9. Robbins and Cotran Pathologic Basis of DiseaseRobbins and Cotran Pathologic Basis of Disease 88th edition./ Kumar, Abbas, Fautoth edition./ Kumar, Abbas, Fauto. –. –
20020077.. – Chapter 11. – P. 398–400.– Chapter 11. – P. 398–400.
10.10. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.
– New York, Milwaukee. – 2009. – P. 50–532.– New York, Milwaukee. – 2009. – P. 50–532.

66. ReferencesReferences
1.1. Donofrio, J., Haworth, K, Schaeffer, L. & Thompson, G., (Eds.). (2005).Donofrio, J., Haworth, K, Schaeffer, L. & Thompson, G., (Eds.). (2005). Cardiovascular careCardiovascular care
made incredibly easy.made incredibly easy. Ambler, PA: Lippincott Williams & Wilkins.Ambler, PA: Lippincott Williams & Wilkins.
2.2. Herman, A. (2010). Hypertension: The pressure’s on.Herman, A. (2010). Hypertension: The pressure’s on. Nursing Made Incredibly Easy, 8Nursing Made Incredibly Easy, 8(4), 40-(4), 40-
53.53.
3.3. McCance, K. L., & Huether, S. E. (2006).McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biologic basis for disease inPathophysiology: The biologic basis for disease in
adults and children,adults and children, (5(5thth
ed.). Philadelphia, PA: Elsevier Mosby.ed.). Philadelphia, PA: Elsevier Mosby.
4.4. Moser, D. K., & Riegel, B. (2008).Moser, D. K., & Riegel, B. (2008). Cardiac nursing: A companion to braunwald’s heartCardiac nursing: A companion to braunwald’s heart
disease.disease. Saunders Elsevier: St. Louis, MO.Saunders Elsevier: St. Louis, MO.
5.5. Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2008).Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2008). Brunner and suddarth’sBrunner and suddarth’s
textbook of medical-surgical nursing,textbook of medical-surgical nursing, (11(11thth
ed.). Philadelphia, PA: Lippincott Williams &ed.). Philadelphia, PA: Lippincott Williams &
Wilkins.Wilkins.
6.6. Smithburger, P. L. et al. (2010) Recent advances in the treatment of hypertensive emergency.Smithburger, P. L. et al. (2010) Recent advances in the treatment of hypertensive emergency.
Critical Care Nurse, 30Critical Care Nurse, 30(5),(5), 24-30.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., &24-30.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., &
Bridges, E. J. (2005).Bridges, E. J. (2005). Cardiac nursing,Cardiac nursing, (5(5thth
ed.). Philadelphia, PA: Lippincott Williams &ed.). Philadelphia, PA: Lippincott Williams &
Wilkins.Wilkins.
7.7. Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007).Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Pharmacotherapeutics for nurse practitionerPharmacotherapeutics for nurse practitioner
prescribers,prescribers, (2(2ndnd
ed.). Philadelphia, PA: F. A. Davis Company.ed.). Philadelphia, PA: F. A. Davis Company.
8.8. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation,The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure (JNC-VII)and Treatment of High Blood Pressure (JNC-VII)
9.9. American Heart Association WebsiteAmerican Heart Association Website