Transcript Physiology of BP

‫فيزيولوجيا القلب‬
‫والضغط الشرياني‬
Epidemiology
Physiology of the heart
• The basic unit of contraction is the sarcomere, which
is aligned to those of adjacent myofibrils.
• Actin filaments are attached and interdigitate with
thicker parallel myosin filaments.
• During contraction, shortening of the sarcomere
results from the interdigitation of the actin and
myosin molecules.
• The force of cardiac muscle contraction, or inotropic
state, is regulated by the influx of calcium ions
through ‘ slow calcium channels’.
Pathophysiology
• Cardiac output depends upon :
1. Preload
2. Afterload
3. Myocardial contractility
Physiology of BP
Two important determinants of B.P.
A. Cardiac output (determined by
stroke volume + Heart rate)
B. Peripheral resistance (determined by
vascular function + v.structure)
Heart Physiology
Physiologic Principles
• More than 90% of cases of hypertension do not have a clear
cause.
• Hypertension clusters in families and results from a complex
interaction of genetic and environmental factors.
• The hypertension-related genes identified to date regulate
renal salt and water handling.
• Major pathophysiologic mechanisms of hypertension include
activation of the sympathetic nervous system and renin–
angiotensin–aldosterone system.
• Endothelial dysfunction, increased vascular reactivity, and
vascular remodeling may be causes, rather than
consequences, of blood pressure elevation; increased vascular
stiffness contributes to isolated systolic hypertension in the
elderly.
Physiologic Principles
• Essential hypertension, or hypertension of unknown
cause, accounts for more than 90% of cases of
hypertension.
• It tends to cluster in families and represents a
collection of genetically based diseases or syndromes
with several resultant inherited biochemical
abnormalities .
• The resulting phenotypes can be modulated by
various environmental factors, thereby altering the
severity of blood pressure elevation and the timing
of hypertension onset.
Physiologic Principles
• Many pathophysiologic factors have been
implicated in the genesis of essential
hypertension: increased sympathetic nervous
system activity, perhaps related to heightened
exposure or response to psychosocial stress;
overproduction of sodium-retaining hormones
and vasoconstrictors; long-term high sodium
intake; inadequate dietary intake of potassium
and calcium
Physiologic Principles
• Increased or inappropriate renin secretion with resultant
increased production of angiotensin II and aldosterone;
deficiencies of vasodilators, such as prostacyclin, nitric
oxide (NO), and the natriuretic peptides; alterations in
expression of the kallikrein–kinin system that affect
vascular tone and renal salt handling; abnormalities of
resistance vessels, including selective lesions in the renal
microvasculature; diabetes mellitus; insulin resistance;
obesity; increased activity of vascular growth factors;
alterations in adrenergic receptors that influence heart
rate, inotropic properties of the heart, and vascular tone;
and altered cellular ion transport
Role of the sympathetic nervous system in the
pathogenesis of cardiovascular diseases.
Physiologic Principles
• The novel concept that structural and
functional abnormalities in the vasculature,
including endothelial dysfunction, increased
oxidative stress, vascular remodeling, and
decreased compliance, may antedate
hypertension and contribute to its
pathogenesis has gained support in recent
years.
Pathophysiologic mechanisms of
hypertension.
Physiologic Principles
• Although several factors clearly contribute to the
pathogenesis and maintenance of blood pressure elevation,
renal mechanisms probably play a primary role, as
hypothesized by Guyton and reinforced by extensive
experimental and clinical data. Other mechanisms amplify (for
example, sympathetic nervous system activity and vascular
remodeling) or buffer (for example, increased natriuretic
peptide or kallikrein– kinin expression) the pressor effects of
renal salt and water retention.
• These interacting pathways play major roles in both increasing
blood pressure and mediating related target organ damage.
Understanding these complex mechanisms has important
implications for the targeting of antihyper-tensive therapy to
achieve benefits beyond lowering blood pressure.
Control of Blood Pressure
• Changes in blood pressure are routinely made in
order to direct appropriate amounts of oxygen and
nutrients to specific parts of the body. For example,
when exercise demands additional supplies of
oxygen to skeletal muscles, blood delivery to these
muscles increases, while blood delivery to the
digestive organs decreases.
• Adjustments in blood pressure are also required
when forces are applied to your body, such as when
starting or stopping in an elevator.
Control of Blood Pressure
• Blood pressure can be adjusted by
producing changes in the following
variables:
• Cardiac output can be altered by changing stroke
volume or heart rate.
• Resistance to blood flow in the blood vessels is most
often altered by changing the diameter of the vessels
(vasodilation or vasoconstriction).
• Changes in blood viscosity (its ability to flow) or in the
length of the blood vessels (which increases with
weight gain) can also alter resistance to blood flow
The following mechanisms help
regulate blood pressure
• The cardiovascular center provides a rapid, neural
mechanism for the regulation of blood pressure
by managing cardiac output or by adjusting blood
vessel diameter. Located in the medulla
oblongata of the brain stem, it consists of three
distinct regions:
• The cardiac center stimulates cardiac output by
increasing heart rate and contractility. These
nerve impulses are transmitted over sympathetic
cardiac nerves.
The following mechanisms help
regulate blood pressure
• The cardiac center inhibits cardiac output by
decreasing heart rate.
• These nerve impulses are transmitted over
parasympathetic vagus nerves.
• The vasomotor center regulates blood vessel
diameter. Nerve impulses transmitted over
sympathetic motor neurons called vasomotor nerves
innervate smooth muscles in arterioles throughout
the body to maintain vasomotor tone, a steady state
of vasoconstriction appropriate to the region.
The cardiovascular center receives
information about the state of the body
through the following sources:
• Baroreceptors are sensory neurons that
monitor arterial blood pressure. Major
baroreceptors are located in the carotid sinus
(an enlarged area of the carotid artery just
above its separation from the aorta), the
aortic arch, and the right atrium.
Chemoreceptors
• Chemoreceptors are sensory neurons that
monitor levels of CO 2 and O 2. These neurons
alert the cardiovascular center when levels of
O 2 drop or levels of CO 2 rise (which result in
a drop in pH).
• Chemoreceptors are found in carotid bodies
and aortic bodies located near the carotid
sinus and aortic arch.
Chemoreceptors
• Higher brain regions, such as the cerebral
cortex, hypothalamus, and limbic system,
signal the cardiovascular center when
conditions (stress, fight‐or‐flight
response, hot or cold temperature)
require adjustments to the blood
pressure.
The kidneys provide a hormonal
mechanism for the regulation of blood
pressure by managing blood volume.
• The renin‐angiotensin‐aldosterone system of the
kidneys regulates blood volume. In response to
rising blood pressure, the juxtaglomerular cells in
the kidneys secrete renin into the blood. Renin
converts the plasma protein angiotensinogen to
angiotensin I, which in turn is converted to
angiotensin II by enzymes from the lungs.
Angiotensin II activates two mechanisms that
raise blood pressure:
The kidneys provide a hormonal
mechanism for the regulation of blood
pressure by managing blood volume.
• Angiotensin II constricts blood vessels
throughout the body (raising blood pressure
by increasing resistance to blood flow).
• Constricted blood vessels reduce the amount
of blood delivered to the kidneys, which
decreases the kidneys' potential to excrete
water (raising blood pressure by increasing
blood volume).
The kidneys provide a hormonal
mechanism for the regulation of blood
pressure by managing blood volume.
• Angiotensin II stimulates the adrenal cortex to
secrete aldosterone, a hormone that reduces
urine output by increasing retention of H 2O
and Na + by the kidneys (raising blood
pressure by increasing blood volume).
Various substances influence blood
pressure. Some important examples
follow:
• Epinephrine and norepinephrine, hormones
secreted by the adrenal medulla, raise blood
pressure by increasing heart rate and the
contractility of the heart muscles and by
causing vasoconstriction of arteries and veins.
These hormones are secreted as part of the
fight‐or flight response.
Various substances influence blood
pressure. Some important examples
follow:
• Antidiuretic hormone (ADH), a hormone
produced by the hypothalamus and released
by the posterior pituitary, raises blood
pressure by stimulating the kidneys to retain
H2O (raising blood pressure by increasing
blood volume).
A pathway for the development of
salt-sensitive hypertension.
Various substances influence blood
pressure. Some important examples
follow:
• Atrial natriuretic peptide (ANP), a hormone
secreted by the atria of the heart, lowers
blood pressure by causing vasodilation and by
stimulating the kidneys to excrete more water
and Na +(lowering blood pressure by reducing
blood volume).
• Nitric oxide (NO), secreted by endothelial
cells, causes vasodilation.
Various substances influence blood
pressure. Some important examples
follow:
• Nicotine in tobacco raises blood pressure by
stimulating sympathetic neurons to increase
vasoconstriction and by stimulating the adrenal
medulla to increase secretion of epinephrine and
norepinephrine.
• Alcohol lowers blood pressure by inhibiting the
vasomotor center (causing vasodilation) and by
inhibiting the release of ADH (increasing H 2O
output, which decreases blood volume).
Endothelial function in the normal
vasculature and in the hypertensive
vasculature.
Cardiovascular Risk Factors
BMI In Worldwide
Normal pressure values
(Left Side)- mm
•
•
•
•
•
•
Arterial Peak Systolic 90-140
Arterial end-diastolic
60-90
Arterial mean
70-105
LV Peak Systolic
90-140
LV End diastolic
4-12
LA - mean
4-12
Normal pressure values
(Right side) - mm
•
•
•
•
•
•
Pulm.Art.Peak Systolic
Pulm.Art.End Diastolic
Pulm.Art.Mean
RV Peak Systolic
RV End Diastolic
RA Mean
15-30
5-15
10-20
15-30
0-5
0-5
Risk Factors for
Atherosclerosis
• Age & Sex
* Family History
• Smoking
• Hypertension
• Hypercholesterolemia
Hypertension and Obesity
Undiagnosed Hypertension, DM and
Hypercholesterolemia
Risk Factors ( Cont.)
•
•
•
•
•
DM
Physical inactivity
Obesity
Diet & alcohol
Personality & Social factors
Hypertension and Location
Endothelial Function
• Vasodilators
Nitric Oxide
Prostacyclin
Endothelium derived Hyperpolar
Factor
• Vasoconstrictors
Endothelin – l
Angiotensin – ll
* Formation & Disolution of Thrombus
BLOOD PRESSURE
• → Rest the patient for five minutes
• → In ambulant patients, measurements are normally made with the patient
seated. Either arm can be used.
• → Support the patient's arm comfortably at about heart level.
• → Apply the cuff to the upper arm with the centre of the bladder over the brachial
artery.
• → Palpate the brachial pulse.
• → Inflate the cuff until the pulse is impalpable. Note the pressure on the
manometer. This is a rough estimate of systolic pressure.
• → Now inflate the cuff another 10 mmHg and listen through the stethoscope over
the brachial artery.
• → Deflate the cuff slowly until regular sounds are first heard. Note
the reading to the nearest 2 mmHg. This is the systolic pressure.
• → Continue to deflate the cuff slowly until the sounds disappear.
• → Record the pressure at which the sounds completely disappear as
diastolic pressure. Occasionally muffled sounds persist and do not
disappear, in which case the point of muffling is the best guide to the
diastolic pressure
Notes on BP measurement
• Take BP after 5 minutes rest & ask patient
not to take coffee or to smoke 30 minutes
before measuring BP. One reading of high BP
does not mean HT except when very high.
• Always start with BP measurement by
palpation.
Notes on BP measurement
• Pay attention to placement of cuff &
stethoscope
• Inflation & deflation should not be very
slow or fast
• For the 1st time measure in both arm & in
arm and leg ( Coaractation )
Notes on BP measurement
• BP is variable. It is lower at night. Absence of this
dip (non dipper) is associated with high risk of CV
complication especially thrombotic stroke.
• Blood Pressure tends to be higher in early
morning hours…People with accentuation
of this rise have higher incidence of cerebral
haemorrhage.
MEASUREMENT OF BLOOD PRESSURE
•Use a machine that has been validated, well maintained and
properly calibrated
•Measure sitting BP routinely, with additional standing BP in
elderly and diabetic patients and those with possible postural
hypotension
•Remove tight clothing from the arm
•Support the arm at the level of the heart
•Use a cuff of appropriate size (the bladder must encompass >
two-thirds of the arm)
•Lower the mercury slowly (2 mm per second)
•Read the BP to the nearest 2 mmHg
•Use phase V (disappearance of sounds) to measure diastolic
BP
•Take two measurements at each visit
Ventricular Enlargement - LVH
1. Voltage Criteria (SV1+RV5 or RV6) = 35
mm or more
2. ST depression + T inversion
(Strain pattern)
** Voltage criteria is seen in volume load
conditions while strain pattern is seen in
pressure load
LVH with Strain pattern
Bundle Branch Block - LBBB
4.Echocardiography
• 2D Echo (chamber, valve, pericardium &
great vessels)
• Doppler Echo (flow across valve & vessels) &
coloured doppler (shunt)
• TEE (posterior structure of the heart
(left atrium, mitral valve & aorta..Useful in
dissecting aneurysm).
* Stress Echo
European Society of Ht
classification
Optimal
Normal
High Normal
HT ( grade 1)
HT ( grade 2 )
HT ( grade 3)
Systolic
Diastolic
120
80
129
85
130-139
85-89
140-159
90-99
160-179 100-109
180 +
110+
Epidemiology of HT
• 10-30% of adult population are Hypertensive.
The figure is more than that in certain
ethnic groups.
* 50% of people above 60 are hypertensive
* 95% of hypertensive have primary HT.
Pathogenesis of HT
1.
2.
3.
4.
5.
5.
Genetic Factors
Sympathetic System
Blood vessel elasticity
Renin-Angiotensin
Defect in natriuresis
Intracellular Na & Ca
Exacerbating factors
1.
2.
3.
4.
5.
6.
7.
8.
Obesity
Excessive Na intake
Excessive alcohol
Smoking
Lack of exercise
Polycythemia
Low K intake
Drugs (NSAID)
The objectives of the initial evaluation of a
patient with high blood pressure reading are
1. To obtain accurate and representative
measurements of blood pressure.
2. To identify contributory factors and any
underlying cause.
3. To assess other risk factors and quantify
cardiovascular risk.
4. To detect any complications( target organ
damage) that are already present.
5. To identify comorbidity that may influence the
choice of antihypertensive therapy.
Secondary HT
• Secondary hypertension should be suspected
when HT is diagnosed before the age of 20
* Secondary cause should be suspected when a
well controlled Ht becomes uncontrollable.
Examine patient with high blood pressure
1. Check the pulse rate-irregularly irregular suggests atrial
Fibrillation.
2. Measure the blood pressure in both arms.
3. Check for radiofemoral delay (coarctation of the aorta).
4. Examine the optic fundi for hypertensive retinopathy.
5. Look for features of Cushing’s syndrome or virillization.
6. Examine the heart for the heave of LVH and for fourth
Heart sound.
7. Look for evidence of heart failure.
8. Palpate the abdomen for renal enlargement and
abnormal pulsation of an abdominal aortic aneurysm.
9. Listen for bruits over the renal arteries(R.artery stenosis)
Causes of secondary HT
1. Chronic Renal Disease
2. Obstructive uropathy
3. Reno-vascular
4. Coaractation of the aorta
5.
6.
7.
8.
Cushing disease & acromegaly
Pheochromocytoma
Primary aldosteronism
Thyroid and Parathyroid disease
9. Sleep apnea
10. Hypercalcemia (all causes)
11. Drug induced hypertension (estrogen, NSAID, cyclosporine)
Investigations
Routine Investigations
1. General urine examination
2. Biochemical (BU, Creatinine, electrolytes FBS, Lipid profile )
3. ECG , Chest x-ray , Echo
Specific Tests
Cortisol , Aldosterone/ Renin, Renal ultra-sound,
CT scan, MRI, Renal angiography, Aortogram,
Catecholamines….
HYPERTENSION: INVESTIGATION OF SELECTED PATIENTS
•Chest X-ray: to detect cardiomegaly, heart failure, coarctation of
the aorta
•Ambulatory BP recording: to assess borderline or 'white coat'
hypertension
•Echocardiogram: to detect or quantify left ventricular
hypertrophy
•Renal ultrasound: to detect possible renal disease
•Renal angiography: to detect or confirm presence of renal artery
stenosis
•Urinary catecholamines: to detect possible
phaeochromocytoma
•Urinary cortisol and dexamethasone suppression test: to detect
possible Cushing's syndrome
•Plasma renin activity and aldosterone: to detect possible
primary aldosteronism
Drugs that may cause resistant HT
1.
2.
3.
4.
5.
6.
7.
8.
NSAID
Decongestant
Diet pills
Cocaine
Amphetamine
Oral contraceptive pills
Cyclosporine
Steroids
Special types of HT
1. White coat HT
2. Systolic HT (elderly)
3.
Paroxysmal HT (Pheochromocytoma)
4. Malignant HT ( encephalopathy or
nephropathy + papilloedema)
Common Mistakes (patients)
1. Non-compliance to drug therapy
2. Wrong concept that drug can be
discontinued once BP is normal
3. Patient thinks that his BP is normal as
long as there is no headache
4. Poor follow-up
5. Fear of diuretics
Common mistakes (physician)
1. Not enough time for patient’s education.
2. Withdraw drugs once BP is normal.
3. Prescribes drugs with small dose or wrong
frequency of use.
4. Prescribes two drugs of the same mode of
action.
Drug Therapy