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hypertension
Blood pressure (BP), sometimes it is called arterial blood
pressure, is the pressure exerted by circulating blood upon
the walls of blood vessel.
During each heartbeat, blood pressure varies between a
maximum (systolic) and a minimum (diastole) pressure.
Hypertension - Introduction




Silent Killer – painless complications
It is the leading risk factor –MI, HF, CRF
Stroke
25% of population
Complications bring to diagnosis but
late…
hypertension
Persistent SBP greater than 140mmhg , DBP
greater than 90mmhg or current use of
antihypertensive drugs
Which means heart is working harder than normal
,putting both heart and blood vessels under strain
Hypertension
Arterial BP = Cardiac Output (CO) x Systemic
vascular resistance (SVR)
Cardiac Output = stroke volume x beats per
min
Systemic vascular resistance = force opposing
the movement of blood within the blood
vessels
What is the effect on BP if SVR increased and
CO remains constant?
Mechanisms that Regulate BP

Sympathetic Nervous System

Vascular Endothelium

Renal System

Endocrine System
Regulation of BP:
BP = Cardiac Output x Peripheral
Resistance
 Endocrine Factors
 Renin, Angiotensin, ANP, ADH, Aldosterone.

Neural Factors
 Sympathetic & Parasympathetic

Blood Volume
 Sodium, Mineralocorticoids, ANP

Cardiac Factors
 Heart rate & Contractility.

Sympathetic Nervous System (SNS) –
Nor epinephrine released from sympathetic nerve
endings  Increases Heart Rate - chronoscopic
 Increased cardiac contractility - inotropic
 Produces widespread vasoconstriction in
peripheral arterioles
 Promotes release of rennin from the kidney

(SNS) –Sympathetic Vasomotor Center – located in the
medulla
 Baroreceptors: specialized nerve cells the carotid
arteries and the aortic arch
 Sensitive to BP changes:
 Increase: Inhibits SNS – peripheral vessel dilation.
Decreased heart rate, and decreased contractility of
the heart + increased parasympathetic activity (vagus
nerve) decreased heart rate
 Decrease: Activates SNS – peripheral vessel
constriction, increased heart rate, and increased
contractility of the heart
Hypertension
SNS Receptors Influencing B/P

Vascular Endothelium
 Single cell layer that lines the blood vessels
 Produce vasoactive substances:
 EDRF Endothelium-derive relaxing factor –
Helps maintain low arterial tone at rest
Inhibits growth of the smooth muscle layer
Inhibits platelet aggregation
 Vasodilation – prostacyclin
 Endothelin (ET) potent vasoconstrictor
Endothelial dysfunction may contribute to atherosclerosis &
primary hypertension

Renal System
 Control Na+ excretion & extracellular fluid volume
 Renal - Renin-angiotensin-aldosterone
 Renin converts angiotensinogen to angiotensin I
 Angiotensin-converting enzyme (ACE) converts I into
angiotensin II
 Immediate: Vasoconstrictor – increased systemic vascular
resistance
 Prolonged: Stimulates the adrenal cortex to secret
Aldosterone – Na+ and Water retention
 Renal Medulla - Prostaglandins - vasodilator effect
Hypertension
Renin-Angiotensin
Hypertension
Renin-Angiotensin System

Endocrine System
 Stimulates the SNS with
 Epinephrine – increases HR and contractility
 Activates B2-adrenergic receptors in peripheral arterioles
of skeletal muscle = vasodilation
 Activates A1-adrenergic receptors in peripheral arterioles
of skin and kidneys = vasoconstiction
 Adrenal Cortex – Aldosterone – stimulates kidneys to
retain Na+
 Increased Na+ stimulates posterior pituitary – ADH –
reabsorbs ECF/water
Aldosterone Mechanism
Increased Aldosterone
 Increases sodium reabsorption
 Increases water reabsorption
 Increases blood volume
 Increases cardiac output
MI , HF
Renal
stroke
dx
Hyper
tension
Pre hypertension
SBP -- 120 to 139 mmhg
DBP -- 80 to 89 mmhg
epidemiology
Before age of 55yrs – common in men
After age of 55yrs – common in women
Men with HTN is more chance of MI than
stroke
Women with HTN is more chance of
stroke than MI
classification
TYPE
SBP
DBP
NORMAL
< 120 mmhg
< 80 mmhg
PRE HTN
120 – 19 mmhg
80 – 89 mmhg
HTN stage I
140 – 159 mmhg
90 – 99 mmhg
HTN stage II
> 160 mmhg
> 100 mmhg
Category
Optimal
Normal
High normal
Systolic blood pressure
Diastolic
< 120
< 80
< 130
< 85
130-139
85-89
Hypertension
Grade I (mild )
140-159
90-99
Grade 2 (moderate)
160-179
100-109
Grade 3 (severe)
≥180
≥110
Grade 1
140-149
< 90
Grade 2
≥160
<90
Isolated
subtypes
Isolated
Pseudo
Isolated hypertension
SBP greater than or equal to 140mmhg with
average DBP less than 90 mmhg
SBP = increases with aging
DBP = increases untill 50 yrs and then
declines
Pseudo hypertension
occur with advanced atherosclerosis
sclerotic arteries don't collapse when cuff is fully
inflated
presenting high cuff pressures than actually
exist within vessels
OSLER SIGN
Etiology
Primary HTN – essential
/ idiopathic
Elevated BP without
identified cause
Contributing factors
Secondary HTN – elevated BP with
specific cause
Medications =
Pheochromocytoma
Cirrhosis
Endocrine
disorders
COA =
PIH
Renal dx
Risk factors
Age
Life
style
stress
DM
obesity
Gender
alcohol
Socio
economicity
smoking
genetic
Sr.lipids
diet
White-coat hypertension
blood pressure measurements taken in a doctor's
office may not correctly characterize their typical
blood pressure.In up to 25% of patients, the
office measurement is higher than their typical
blood pressure
Cardiovascular
 Heart
- Increased workload on left ventricle
 Left ventricular hypertrophy
 left ventricular failure.
- Greater thickness of left ventricle
 decreased perfusion and ischemia of
subendocardial region of myocardium.

Arteries
- Accelerated atherogenesis.
-  risk of developing aortic dissecting aneurism.
 Arterioles: Arteriolosclerosis
-
Benign HT:
Deposition of eosinophilic (‘hyaline’) material in vessel
walls due to influx of plasma proteins.
-
Malignant HT:
Thickening of intima.
Necrosis of vessel walls ('fibrinoid' necrosis) and
formation of micro-aneurisms (of Bouchard) in brain.
CNS
- Rupture of micro-aneurisms of small penetrating
arteries  Intracerebral haemorrhage.
-  Risk of cerebral infarction due to atherosclerosis
of circle of Willis.
- Acute malignant HT: ‘Hypertensive
encephalopathy’
due to cerebral oedema (headache, nausea and
vomiting,
visual disturbances, seizures and disturbances of
consciousness).
Renal complications
Arteriolosclerosis
 Ischemic sclerosis of glomeruli and
tubular atrophy.
Proteinuria and microscopic haematuria,
especially in malignant HT .
Clinical features
CARDIAC
RENAL
EYE
LVF
Proteinuria
Retinopathy
MI , angina
Microalbuminuria
Papiledema
CAD
Nephrosclerosis
HF
> sr.creatinine –
1.5mg
palpitation
PERIPHERAL VASCULAR
CEREBRO VASCULAR
Aneurysm
TIA
Claudication
stroke
Bruit / thrill
Decreased or absent PP
Nose bleed
Headache , dizziness
Decreased activity
tolerance
Hypertensive Retinopathy:




Grade I – Thickening of
arterioles.
Grade II – Focal
Arteriolar spasms. Vein
constriction.
Grade III –
Hemorrhages (Flame
shape), dot-blot and
Cotton wool and hard
waxy exudates.
Grade IV Papilloedema
EXAMINATION

Elevated blood pressure is usually the only
abnormal sign.

Signs of an underlying cause should be sought,
such as renal artery bruits in renovascular
hypertension, or radiofemoral delay in coarctation
of the aorta.

The cardiac examination may also reveal features
of left ventricular hypertrophy and a loud aortic
second sound. If cardiac failure develops, there
may be a sinus tachycardia and a third heart
sound.
Drug therapy
DIURETICS – inhibit Nacl reabsorption
Eg …
metalazone , hydrochlorthiazide(thiazide)
torsemide (loop)
amiloride (k spar)
spirinolactone , eplerenone(aldos recep
block) – C/I in ?
DIRECT VASODILATORS
Hydralazine : minoxidil ( C/I in pheo) =
direct arterial vasodilatation
NTG = relax arterial , venous smooth muscle
SNP = direct arterial vasodilatation ,
reduce SVR , BP ,, thiocynate toxicity
GANGLIONIC BLOCKERS
Interrupt adrenergic control of artery trimethapan
ACE INHIBITORS
Inhibit ACE and
prevent conversion of
A I to A II
C/I in renal
imparement , reno
vascular dx
Eg : captopril,
enalpril, lisnopril
vasotec
A/E – inc K ,
angioedema, cough
ANGIOTENSIN
RECEPTOR BLOCKERS II
Prevent the action of A
II and vasodilating
effect and sodium ,
water reabsorption
Eg : losartan, valsartan,
telmisartan, olmesartan
ADRENERGIC INHIBITORS
Centrally acting alpha adrenergic antagonist =
decrease the sympathetic outflow from CNS ..(clonidine , methyl
dopa)
Peripherally acting – prevent release of nor
epinephrine - resperine
Alpha adrenergic blockers – block alpha 1
receptors – (prazosin , terazosin)
Beta adrenergic blockers – block beta 1,2 receptor ,
decrease renin release, bronchospasm ,
conduction block.
Combined alpha , beta adrenergic blockers carvidelol
CALCIUM CHANNEL BLOCKERS
Non dihydropyridines – diltiazem , verapamil
Dihydropyridines – amlodipine , nife and
nicardipine
Blocks the extracellular calcium movement
into the cells – dec H.R , Contractility , SVR,
vaso dilating effect
C/I – sick sinus syndrome, HF, AV block
COMBINATION THERAPY
ACEI + DIURETICS
ARB + DIURETICS
BETA ADRENERGIC BLOCKERS + DIURETICS
CENTRALLY ACTING DRUGS + DIURETICS
DIURETICS + DIURETICS
ACEI + CALCIUM CHANNEL BLOCKERS
DASH DIET = DIETARY
APPROACH TO STOP
HYPERTENSION
HYPERTENSIVE CRISIS
Severe abrupt elevation of BP , esp DBP > 140mmhg
RISK FACTORS
Exacerbation of chronic hypertension
Renovascular hypertension
Pre eclampsia / Eclampsia
Pheochromocytoma , coccine use
Rebound Htn , head injury
Aortic dissection
HYPERTENSIVE EMERGENCY
HYPERTENSIVE URGENCY
Developed over hours to
day
Over days to weeks in
Patient BP severely
elevated ( > 180 / > 120
mmhg) with evidence of
acute organ damage of
esp. CNS
severely but no evidence of
Encephalopathy , CNS
hemorrhage , acute LVF
with pulmonary edema , MI
, renal failure , dissecting
aneurysm
which patient BP is elevated
organ damage
GOAL
TO DECREASE MAP BY NO MORE THAN
25% IN ONE HOUR
BP = 160 / 100 mmhg over 2 – 6 hrs
I.V – SNP ,NTG , Labetolol, esmolol ,
vasotec
Life style modifications
BP REDUCE BY
WEIGHT REDUCTION
BMI : 18.5 – 24.9/kg/m2
5 – 20 mm / 10 Kg
ADOPT DASH
Fruit , vegetables , low
fat ,dietary products
8 – 14 mmhg
DIET SODIUM
RESTRICTION
100 mmol / day
2 -8 mmhg
PHYSICAL ACTIVITY
Aerobic – 30 mn /day
4 – 9 mmhg
Summary
• Hypertension is the commonest cause of major morbidity,
but less than a quarter of patients are adequately treated.
• A reduction in cardiovascular disease mortality and
morbidity can be achieved through improved treatment and
control of hypertension.
• A greater choice of drugs are available for hypertension
than for other chronic diseases.
• Rational choice of single and combination drugs facilitated
by understanding their effects on the renin system, but
systematic trial and error may still be necessary.
A client is scheduled for a cardiac catherization
using a radiopaque dye. Which of the following
assessments is most critical before the
procedure?
Intake and output
Baseline peripheral pulse rates
Height and weight
Allergy to iodine or shellfish
A client is wearing a continuous cardiac monitor,
which begins to sound its alarm. A nurse sees no
electrocardiogram complexes on the screen. The
first action of the nurse is to:
Check the client status and lead placement
Press the recorder button on the
electrocardiogram console.
Call the physician
Call a code blue
A client who has been receiving heparin therapy also is
started on warfarin. The client asks a nurse why both
medications are being administered. In formulating a
response, the nurse incorporates the understanding that
warfarin:
Stimulates the breakdown of specific clotting factors by the liver,
and it takes 2-3 days for this to exert an anticoagulant effect.
Inhibits synthesis of specific clotting factors in the liver, and it takes 34 days for this medication to exert an anticoagulant effect.
Stimulates production of the body’s own thrombolytic substances,
but it takes 2-4 days for this to begin.
Has the same mechanism of action as Heparin, and the crossover
time is needed for the serum level of warfarin to be therapeutic.
2. Warfarin works in the liver
and inhibits synthesis of four
vitamin K-dependent
clotting factors (X, IX, VII,
and II), but it takes 3 to 4
days before the
therapeutic effect of
warfarin is exhibited.
A 60-year-old male client comes into the emergency
department with complaints of crushing chest pain that
radiates to his shoulder and left arm. The admitting
diagnosis is acute myocardial infarction. Immediate
admission orders include oxygen by NC at 4L/minute,
blood work, chest x-ray, an ECG, and 2mg of morphine
given intravenously. The nurse should first:
Administer the morphine
Obtain a 12-lead ECG
Obtain the lab work
Order the chest x-ray
1. Although obtaining the ECG,
chest x-ray, and blood work are
all important, the nurse’s priority
action would be to relieve the
crushing chest pain.
The nurse teaches the client with angina about
the common expected side effects of
nitroglycerin, including:
Headache
High blood pressure
Shortness of breath
Stomach cramps
1. Because of the widespread
vasodilating effects, nitroglycerin often
produces such side effects as
headache, hypotension, and dizziness.
The client should lie or shit down to avoid
fainting. Nitro does not cause shortness
of breath or stomach cramps.
Which of the following arteries primarily
feeds the anterior wall of the heart?
Circumflex artery
Internal mammary artery
Left anterior descending artery
Right coronary artery
3. The left anterior descending artery
is the primary source of blood flow for
the anterior wall of the heart. The
circumflex artery supplies the lateral
wall, the internal mammary supplies
the mammary, and the right
coronary artery supplies the inferior
wall of the heart.
When do coronary arteries
primarily receive blood
flow?
During inspiration
During diastolic
During expiration
During systole
Although the coronary arteries
may receive a minute portion of
blood during systole, most of the
blood flow to coronary arteries is
supplied during diastole.
Breathing patterns are irrelevant
to blood flow
Which of the following parameters is the
major determinate of diastolic blood
pressure?
Baroreceptors
Cardiac output
Renal function
Vascular resistance
Vascular resistance is the
impedance of blood flow by
the arterioles that most
predominantly affects the
diastolic pressure. Cardiac
output determines systolic
blood pressure.