Cadiac cycle,ECG,Hypertension

Anatomy of the heart

• Approximately the size of your fist
– Wt. = 250-300 grams
– 4 Chambers 2 atria and 2 ventricals
• Location
– In the mediastinum between the lungs
– Superior surface of diaphragm
– Anterior to the vertebral column, posterior to the sternum
– ⅔’s of it lies to the left of the midsternal line
• External markings
– Apex - pointed inferior region (free)
– Base - upper region (attached)
• The apex reaches to the fifth intercostal space, 7.5
cm to the left of the midline.
– Coronary sulcus
• Indentation that separates atria from ventricles
– Anterior and posterior interventricular sulcus
• Separates right and left ventricles
• Internal divisions
– Atria (superior) and ventricles (inferior)
– Interventricular and interatrial septa
 Right side.
• Vessels
Superior vena cava – head
neck and upper limb
Inferior vena cava- lower parts
Pulmonary artery - Lungs
• Valves
Tricuspid valve
Pulmonary valve
• The pacemaker- Sinoatrial
node.
 Left side
• Vessels
Aorta
Pulmonary vein- Lungs
• Valves
Mitral valve (Bicuspid)
Aortic valve
• Left ventricle –
three times
thicker than right
– Exerts more
pumping force
– Flattens right
ventricle into a
crescent shape

Figure 18.7
 Valves
• Heart valves ensure unidirectional blood
flow through the heart
– Composed of an endocardium with a
connective tissue core
• Two major types
– Atrioventricular valves
– Semilunar valves
 Atrioventricular valves
• Atrioventricular (AV) valves lie between the atria
and the ventricles
– R-AV valve = tricuspid valve
– L-AV valve = bicuspid or mitral valve
• AV valves prevent backflow of blood into the
atria when ventricles contract
• Chordae tendineae anchor AV valves to
papillary muscles of ventricle wall
– Prevent prolapse of valve back into atrium
 Semilunar Heart Valves
• Semilunar valves prevent backflow of
blood into the ventricles from the vessels.
• Have no chordae tendinae attachments
• Aortic semilunar valve lies between the left
ventricle and the aorta
• Pulmonary semilunar valve lies between
the right ventricle and pulmonary trunk
 Fibrous Skeleton
• Surrounds all four valves
– Composed of dense connective tissue
• Functions
– Anchors valve cusps
– Prevents overdilation of valve openings
– Main point of insertion for cardiac muscle
– Blocks direct spread of electrical impulses
 Heart Sounds
• “Lubb” heart sound occurs during the
ventricular contraction when the A-V
valves are closing.
• “Dubb” heart sound occurs during
ventricular relaxation when the pulmonary
and aortic valves are closing.
• A heart murmur is when the heart valves
fail to close completely causing leakage.
Layers of the heart
 Pericardium – outer most layer

1. Outer fibrous layer

Continues as a tunica adventia of blood vessels
Attached to the diaphragm below
Prevents overstretching of heart
2. Inner serous layer
Two layers outer parietal and inner visceral
Space between is pericardial space
Thin film of fluid allowing smooth movement
 Myocardium – Middle layer
• Formed by cardiac muscle cells or fibers
• 3 types of muscle fibers
1. Contractile- Striated muscles
2. Pacemaker- Specialized P cells (SA
node)
3. Conductive system
 Endocardium
• Inner most
• Thin, smooth, glistering
• Lines the inner surface of heart
• Single layer of endothelial cell
• Continues as endothelium of blood
vessels
 Cardiac muscle
• Atrial, ventricular muscle- striated
• Excitatory and conductive muscle
contains few contractile cells
Exhibits rythmicity and varying rates of
conduction
 Physiologic anatomy
• Latticework- dividing,
recombining, spreading.
• Striated
• Myofibrils – actin and
myosin filaments
• Intercalated disc – cell
membrane separating
individual cells.
Syncytium- mass of cell containing
many nuclei
• Electrical resistance through the
intercalated disc is very less compared to
cell membrane.
• Functional point of view – ions move with
ease along long axis. So when one cell is
exited, action potential spreads to all of
them and also through latticework.
• Thus cardiac muscle is syncytium of many
heart cells.
• Heart is composed of two syncytiums
Atrial and ventricular seprated by fibrous
tissue that surrounds the valve
• Action potential is conducted from atria to
ventricles through conductive system
• This allows the atria to contract a short
time ahead of ventricles.
 Physiology of cardiac muscles
• Resting membrane potential -85 to -90mv
• Action potential – rises up to +20mv
(overshoot potential)
• Membrane remains depolarized for about)
0.2 to 0.3 seconds
• Which is shown as plateau
Electrical Properties of Myocardial Fibers
1. Rising phase of action potential
• Due to opening of fast Na+ channels
2. Plateau phase
• Closure of sodium channels
• Opening of calcium channels
3. Repolarization phase
• Calcium channels closed
• Increased K+ permeability
Conducting System
SA node

Bachman Wenckbach Thorel

AV node

Bundle of His

Purkinje fibers
Normal Impulse Conduction
Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers
Conducting System of Heart
 Conduction of the Heart
• The sinoatrial node in humans is in the shape of a crescent and is about
15 mm long and 5 mm wide.

• The SA nodal cells are self-excitatory, pacemaker cells.

• They generate an action potential at the rate of about 70 per minute.

• From the sinus node, activation propagates throughout the atria, but
cannot propagate directly across the boundary between atria and
ventricles.

• The atrioventricular node (AV node) is located at the boundary between

the atria and ventricles; it has an intrinsic frequency of about
50 pulses/min.

• If the AV node is triggered with a higher pulse frequency, it follows this

higher frequency. In a normal heart, the AV node provides the only
conducting path from the atria to the ventricles.
 Blood supply of heart
• Two main coronary
arteries.
• Right coronary artery
• Left coronary artery
• Both of these arteries
originate from the root
of the aorta,
immediately above the
aortic valve.
 Sympathetic & Parasympathetic
Nervous Systems
• Physical exercise, body temperature, and
concentration of various ions affect heartbeat.
• Branches of sympathetic and parasympathetic
nerve fibers innervate the S-A and A-V nodes.
• Parasympathetic impulses decrease heart
action, sympathetic increases heart action.
• Cardiac center in the medulla oblongata
regulates autonomic impulses to the heart.
 Effects of K+ & Ca2+
• Potassium and calcium are two ions that influence heart
action and are the most important.
• Potassium affects the electrical potential of the cell
membrane.
• Calcium ions are needed more for cardiac muscles
 Conditions
• Hyperkalemia (excessive potassium ions)
decreases the rate and force of cardiac
contractions.
• Very high amounts may block cardiac impulses.
• Hypokalemia is low potassium and can cause an
abnormal arrhythmia.
• Hypercalcemia increases heart action causing a
prolonged contraction.
• Hypocalcemia depresses heart action.
 The cardiovascular system is
divided into two circuits

• Pulmonary circuit
– blood to and from the lungs
• Systemic circuit
– blood to and from the rest of the body
• Vessels carry the blood through the circuits
– Arteries carry blood away from the heart
– Veins carry blood to the heart
– Capillaries permit exchange
 Cardiac cycle.
• Succession of coordinated activities which
take place during every heart beat.
• Events are described in to 2 divisions
systole and diastole.
• Duration is 0.8 seconds
• Systole = 0.27 sec
• Diastole = 0.53 sec
• Systole
Isometric contraction = 0.05
Ejection period = 0.22
• Diastole
Prodiastole = 0.04
Isometric relaxation = 0.08
rapid filling = 0.11
Slow filling = 0.19
Atrial systole = 0.11
ATRIAL SYSTOLE

The end of diastole

ATRIAL SYSTOLE - Heart

• Prior to atrial systole, blood has

been flowing passively from the
atrium into the ventricle through
the open AV valve.
• During atrial systole the atrium
contracts and tops off the volume
in the ventricle with only a small
amount of blood (10%). Atrial
contraction is complete before the
ventricle begins to contract.
ISOVOLUMETRIC
CONTRACTION

The Beginning of
systole
 ISOVOLUMETRIC CONTRACTION
Heart
The atrioventricular (AV) valves close at the
beginning of this phase.
Mechanically, the interval between the closing
of the AV valves and the opening of the
semilunar valves
Venticals contract without change in the
volume of chamber or length of the muscle
fibers.
Pressure increases sharply.
 EJECTION

The end of systole

• Blood is ejected out of ventricles due to
opening of semilunar valve
• 2 stages Rapid ejection period
Slow ejection period
ISOVOLUMETRIC
RELAXATION

The beginning of
Diastole
• All valve are closed
• Ventricles relax without change in volume
and or length of the fibers
• Sharp fall in the pressure
• Responsible for opening of the AV valves
VENTRICULAR FILLING
• Rapid filling – Blood accumulates in atria
during diastole, when AV valves are
opened there is sudden rush of blood in
the ventricles (70% of filling)
• Slow filling – Followed by sudden filling
also called as diastasis (20% of filling)
Pressure changes
 Cardiac output
• Cardiac output is the volume of blood pumped
by the heart per minute (mL blood/min).
• Cardiac output is a function of heart rate and
stroke volume.
• Theheart rate is simply the number of heart
beats per minute. The stroke volume is the
volume of blood, in milliliters (mL), pumped out
of the heart with each beat.
• Increasing either heart rate or stroke volume
increases cardiac output.
• Cardiac Output in mL/min = heart rate
(beats/min) X stroke volume (mL/beat)
• Cardiac Output = 70 (beats/min) X 70 (mL/beat)
= 4900 mL/minute.
• The total volume of blood in the circulatory
system of an average person is about 5 liters
(5000 mL).
• During vigorous exercise, the cardiac output can
increase up to 7 fold (35 liters/minute)
 Control of Heart Rate
• Under conditions of rest the parasympathetic fibers
release acetylcholine, which acts to slow the pacemaker
potential of the SA node and thus reduce heart rate.

• Under conditions of physical or emotional activity

sympathetic nerve fibers release norepinephrine, which
acts to speed up the pacemaker potential of the SA node
thus increasing heart rate.

• Sympathetic nervous system activity also causes the

release of epinephrine from the adrenal medulla. -
increase in heart rate.
 Control of Stroke Volume
• Stroke volume is increased by 2
mechanisms:
• increase in end-diastolic volume
• increase in sympathetic system activity
 End-diastolic Volume
• An increase in venous return of blood to the heart will
result in greater filling of the ventricles during diastole.
• Consequently the volume of blood in the ventricles at the
end of diastole, called end-diastolic volume, will be
increased.- stretch
• Stretch of the sinus node will increase heart rate by 10 –
15 %
• Bainbridge reflex- stretched right atrium.
It passes to vasomotor center in brain and back to heart
through sympathetic nerve causing in heart rate
Frank Starling Law of the Heart
• The more cardiac muscle is stretched within
physiological limits, the more forcibly it will
contract.
• Rubber band analogy
• Increasing volumes of blood in ventricles
increase the stretch & thus the force
generated by ventricular wall contraction.
• Greater stretch means more blood volume is
pumped out, up to physical limits.
 Frank Starling Law of the Heart

Increased blood volume = Increased force to pump blood

increased stretch of myocardium out.
 ECG
• During the late 1800's and early 1900's, Dutch physiologist
Willem Einthoven developed the electrocardiogram.He won
the Nobel prize for its invention in 1924.

• Hubert Mann first uses the electrocardiogram to describe

electrocardiographic changes associated with a heart attack in
1920.

• The science of electrocardiography is not exact. The

sensitivity and specificity of the tool in relation to various
diagnoses are relatively low
• The ECG records the electrical signal of the
heart as the muscle cells depolarize (contract)
and repolarize.
• Normally, the SA Node generates the initial
electrical impulse and begins the cascade of
events that results in a heart beat.
• Recall that cells resting have a negative
charge with respect to exterior and
depolarization consists of positive ions
rushing into the cell
ELECTROCARDIOGRAM

It is a graphic recording of changes of total electromotive

force of heart during spreading excitation wave in the heart

Functions of myocardium that can be

evaluated by the electrocardiography:

functions of automaticity, conductibility, excitability.

But not myocardial contractility!

AUTOMATICITY

It is ability of heart to initiate electric impulses in the absence

of exogenous irritants.

Pacemakers:
1. Pacemaker of the first order – sinoatrial node (60-80 electric impulses per minute)
2. Pacemaker of the second order – atrioventricular joint (march between AV node
and initial part of His bundle) (40-60 electric impulses per minute)
3. Pacemaker of the third order – finite part of His bundle, its branches and
hemifascicles (25-40 electric impulses per minute)

In health only pacemaker is sinoatrial node which suppresses

activity of the rest of ectopic pacemakers!
CONDUCTIBILITY

It is ability of specialized conducting tissue and ordinary

muscles to conduct the activation.

Ordinary muscles conduct impulses at a velocity much lower than

intraventricular specialized conducting tissue (the His-Purkinje system),
but considerably faster than AV node.
EXCITABILITY

It is ability of specialized conducting tissue cells and ordinary

muscle fibers to become excited under the influence
exogenous electric impulses.

Ordinary muscles conduct impulses at a velocity much lower than

intraventricular specialized conducting tissue (the His-Purkinje system),
but considerably faster than AV node.
 COMPONENTS USED IN THE RECORDING AND
PROCESSING OF AN ELECTROCARDIOGRAM

(1) electrodes, which are attached to the body of the patient to pick up the potential
differences that arise during excitation of the heart muscle, and lead wires; (2)
amplifiers, which amplify the minutest voltage of e.m.f. (1-2 mV) to the level that can be
recorded; (3) a galvanometer to measure the voltage; (4) a recording instrument,
including a traction mechanism and a time marker; and (5) a power unit
 ECG paper
-ECG paper: contains small and large squares.
-Each small square is 1 mm and large square is 5mm
-Time is measured along horizontal line and each small
square is 0.04 sec and each large square is 0.2 sec. so 1
inch is equal to 1 second
-Voltage is measured along vertical line and 10 mm is equal
to 1 mV
-ECG paper moves at 25 mm/s speed, i.e. 1500
squares/min
 ECG leads
2 types of lead Bipolar
Unipolar
Bipolar
Lead I – Ra and La
Lead II – Ra and Ll
Lead III – La and Ll
 Placement of leads
Unipolar
Augmented leads:
aVR: right arm
aVL: left arm
aVF: left foot

Chest leads
V1: in 4th ICS at right sternal border
V2: in 4th ICS at lft sternal border
V3: midway between V2 and V4
V4: 5th ICS in lft MCL
V5: anterior axillary line in 5th ICS
V6: mid axillary line in 5th ICs
 MAKING A RECORDING

1. The patient must lie down and relax (to prevent muscle
tremor)
2. Connect up the limb electrodes, making certain that they
are applied to the correct limb
3. Calibrate the record with the 1 mV signal
4. Record the six standard leads – three or four complexes
are sufficient for each
 THE NORMAL ELECTROCARDIOGRAM

The P wave is generated by activation of the atria,

the PR segment represents the duration of atrioventricular (AV) conduction,
the QRS complex is produced by activation of both ventricles,
the ST-T wave reflects ventricular recovery.
 THE ECG WAVES
R

T
P

Q
S

The P wave represents the electrical activation (depolarization) of both atria;

the Q wave corresponds to excitation of the interventricular septum (beginning
of ventricular depolarization);
the R wave displays the subsequent spreading of excitation of right and left
ventricular myocardium;
the S wave represents the completion of ventricular depolarisation (excitation
of the basal areas of interventricular septum);
the T wave corresponds to the process of rapid late repolarization of the
ventricular myocardium.
 THE ECG INTERVALS
RR

PQ QT TP

The PQ interval represents the time required for impulse to pass from SA node
through the atrial internodal tracts, atrioventricular node, His’ bundle, bundle
branches, Purkinje fibers to the working muscle fibers (normal duration of PQ
interval is 0.12-0.20 sec);
the RR interval represents the duration of one cardiac cycle;
the QT interval shows the duration of electric systole of ventricles;
the interval TP displays the duration electric diastole of ventricles.
Atrial Depolarization and the Inscription of the P-wave

SA
node

Lead II electrode:
AV 60 downward rotation
node from the horizontal 0

Delay (no electrical

0 activity) before the
beginning of ventricular
depolarization due to
90 AV node function
Ventricular Depolarization and the Inscription of the QRS complex
N o t e : c o m p a
t h e le f t v e n t r ic
r i g h t v e n t r ic l e
s m a l le r a n d c
li t t l e t o t h e o v
1 . T s he ep t u m d e p o l a r iz e s v f e r oc t mo r to h f ed e p o
in s i d e o u t a n d t h e r e s u l t i n g
o
d e p o la r i z a t io n w a v e m 6 o0 v e sL o e a d I I e l e c
a w a y f r o m t h e e l e c t r o d e 6 0 d o w n w
r o t a t i o n a on g
r e c o r d i n g L e a d I I f r o m t h e h o
2 . T h e r le e s f tt vo ef nt h t re i c l e
d e p o la r i z e s c o u n t e r - c lo c k w i s e
f r o m t h e i n s id e o u t a n d c r e a t e s
mt h ae i n c a r d i a c v e c t o r ( l a r g e a r r o w
w h i c h i s e s s e n t i a ll y , t h e a l g e b r a i c
s u m o f a l l o f t h e s m a l l d e p o la r i z a t io n
v e c t o r s ( i n c lu d in g t h e s m a l l
c o n t r i b u r t i og nh t f rv o e m n t rt hi ce l e
. I n a n o r m a l h e a r t , t h is v e c t o r
is a l w a y s m o v i n g d i r e c t l y
t o w a r d L e a d I I , g e n e r a t in g a
m o s t l y p o s i t i v e Q R S c o m p l e x
Ventricular Repolarization and the Inscription of the T-wave
 THE ORDER ECG INTERPRETATION

1. Regularity of heart beats (regular, irregular)

2. Rhythm (sinus or other)
3. Heart rate
4. Cardiac axis
5. A description of the P wave
6. Conduction intervals
7. A description of the QRS complexes
8. A description of the ST segments and T waves
9. A description of the QT interval
10. ECG report.
 THE ECG REPORT

1. Rhythm (sinus or other)

2. Regularity of cardiac rhythm (regular, irregular)
3. Heart rate
4. Cardiac axis
5. ECG abnormalities of:
- rhythm
- conduction
- hypertrophy of myocardium of ventricles or atria
- myocardial damage (ischaemia, injury, necrosis, scar)
 Uses of ECG
1. Aids diagnosis, prognosis and treatment
2. Gives information regarding functioning
of atria and ventricles
3. Identify damage to heart (infarction)
4. Identify abnormal rhythm and rate
5. Identify change in size of chambers of
heart
Some Abnormalities in ECG
P wave:
a) p wave wide and notched (p-mitral)-left atrial hypertrophy
b) p wave tall and peaked ( p-pulmonale) –right atrial hypertrophy

QRS complex:
Tall QRS- ventricular hypertrophy
Tall peaked T wave- hyperkalemia
Low or inverted T wave- myocardial ischemia

U wave:
Prominent U wave- hypokalemia

ST segment:
Elevated with convexity upward-myocardial infaction
Depressed- angina pectoris
PR interval:
Increased PR interval -Bradycardia
Decreased PR interval- tachycardia
No PR interval- complete heart block
• Q wave duration of more than 0.04
seconds
• Q wave depth of more than 25% of
ensuing r wave
• ST elevation in leads facing infarct (or
depression in opposite leads)
• Deep T wave inversion overlying and
adjacent to infarct
• Cardiac arrhythmias
NORMAL SINUS RHYTHM
Tachycardia
Impuses originate at S-A node at normal rate

SINUS TACHYCARDIA
Impuses originate at S-A node at rapid rate

All complexes normal, evenly spaced

• Sinus rhythm features are present in each cardiac cycleRate > 100/min

• Impulse formation beginning in the sinus node is

accelerated (between 91 and 160 (180) beats/min,);
• The RR interval is shortened.
 ECG CRITERIA OF ATRIAL FLUTTER

Rapid, regular, coordinated, ectopic atrial rhythm at a rate of 220 to 350

beats/min, accompanied by regular or irregular ventricular contractions
of various frequency.

• the P wave is absent in all leads;

• regular multiple high equiform waves ‘F’ (flutter) are recorded
instead of P waves QRS complex is not changed;
• ST segment and T wave are deformed due to superposition of
F waves;
 ECG CRITERIA OF ATRIAL FIBRILLATION
Chaotic, disorganized excitation and contractions of separate atrial fibers
(rapid irregular twitchings ) at a rate of 350 to 600 beats/min (without
effective atrial contraction), the ventricles respond to the dysrhythmic
bombardment from the atria irregularly (absolute arrhythmia of ventricular
contractions).

• P waves is absent in all leads;

• multiple oscillating baseline waves ‘f’ (fibrillation) of various
amplitude and shape are recorded instead of P waves .RR
intervals are of various duration (irregular ventricular rhythm);
• QRS complexes are not changed.
 Cardiac Rhythm: Ventricular
Most serious of all cardiac arrthyemias.- fatal if not treated
Results from irregular cardiac impulse in all of ventricular mass
causing relaxation and contraction in different parts of the ventricle.
There is negligible amount of blood flow.

Bizarre, no rhythm of any type

VENTRICULAR FIBRILLATION
Chaotic ventricular depolarization – ineffective at pumping blood – death within minutes
 Atrioventricular block
• Ischemia
• Compression of AV bundle – scar tissue
,calcification
• Inflamation of AV node
 1 degree block
st

• Delay of conduction from atria to ventricles

but not actual blockage.
• Prolonged PR interval – (> 0.2 sec) ( N
0.16 sec)
 Second degree block
• Sometimes strength of action potential is
not enough to cross AV node to ventricles
• So atria beats faster than ventricles and is
is said that there are dropped beats
 Complete block
• P waves are dissociated from QRS
complex because ventricles have
“escaped” from control by atria and
beating on there own
 Hypertension- Etiology
Essential hypertension.- (95%) of cases, a specific underlying cause of hypertension cannot be
found.
• SECONDARY HYPERTENSION
• Alcohol,Obesity
• Renal disease
• Renal vascular disease
• Parenchymal renal disease, particularly glomerulonephritis
• Polycystic kidney disease
• Endocrine disease
• Phaeochromocytoma (excess adrenalin)
• Cushing's syndrome (excess coeticosteroids)
• Primary hyperaldosteronism (Conn's syndrome) (excess aldosteron)
• Hyperparathyroidism
• Acromegaly
• Primary hypothyroidism
• Thyrotoxicosis
• Congenital adrenal hyperplasia
• Drugs
• e.g. Oral contraceptives containing oestrogens, anabolic steroids, corticosteroids, non-steroidal
anti-inflammatory drugs, carbenoxolone sympathomimetic agents
Measurement of blood pressure
• Measurements should be made to the
nearest 2 mmHg, in the sitting position
with the arm supported, and repeated after
5 minutes' rest if the first recording is high
• To avoid spuriously high recordings in
obese subjects, the cuff should contain a
bladder that encompasses at least two-
thirds of the circumference of the arm
 MEASUREMENT OF BLOOD
PRESSURE (contd)
• 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
 DEFINITION OF HYPERTENSION
-The British Hypertension Society
Category Systolic blood Diastolic blood
pressure pressure
Optimal < 120 < 80

Normal < 130 < 85

High normal 130-139 85-89

Hypertension

Grade 1(mild) 140-159 90-99

Grade 2 160-179 100-109

(moderate)

Grade 3 (severe) ≥180 ≥110

• sphygmomanometry, particularly when
performed by a doctor, can cause an
unrepresentative surge in BP which has
been termed 'white coat' hypertension,
and as many as 20% of patients with
apparent hypertension in the clinic may
have a 'normal BP' when it is recorded by
automated devices used in their own
home.
 Target organ damage
• The adverse effects of hypertension
principally involve the blood vessels,
central nervous system, retina, heart and
kidneys, and can often be detected
clinically
 Blood vessels
• In larger arteries (over 1 mm in diameter) the
internal elastic lamina is thickened, smooth
muscle is hypertrophied and fibrous tissue is
deposited. The vessels dilate and become
tortuous and their walls become less compliant.
• In smaller arteries (under 1 mm) hyaline
arteriosclerosis occurs in the wall, the lumen
narrows and aneurysms may develop.
• These structural changes in the vasculature
often aggravate hypertension by increasing
peripheral vascular resistance and reducing
renal function.
 Central nervous system
• Stroke is a common complication of hypertension and
may be due to cerebral haemorrhage or cerebral
infarction.
• Carotid atheroma and transient cerebral ischaemic
attacks are more common in hypertensive patients.
• Hypertensive encephalopathy is a rare condition
characterised by high blood pressure and neurological
symptoms, including transient disturbances of speech or
vision, paraesthesiae, disorientation, fits and loss of
consciousness.
• Papilloedema is common. A CT scan of the brain often
shows haemorrhage in and around the basal ganglia.
 Retina
• The optic fundi reveal a gradation of changes
linked to the severity of hypertension
• Grade 1 Arteriolar thickening, tortuosity and
increased reflectiveness ('silver wiring')
• Grade 2 Grade 1 plus constriction of veins at
arterial crossings ('arteriovenous nipping')
• Grade 3 Grade 2 plus evidence of retinal
ischaemia (flame-shaped or blot haemorrhages
and 'cotton wool' exudates)
• Grade 4 Grade 3 plus papilloedema
 Heart
• High blood pressure places a pressure load on the heart
and may lead to left ventricular hypertrophy with a
forceful apex beat and fourth heart sound.
• ECG - useful in risk assessment
• Atrial fibrillation is common and may be due to diastolic
dysfunction caused by left ventricular hypertrophy.
• Severe hypertension can cause left ventricular failure in
the absence of coronary artery disease, particularly
when renal function, and therefore sodium excretion, is
impaired.
 Kidneys
• Long-standing hypertension may cause
proteinuria and progressive renal failure
by damaging the renal vasculature.
 Malignant or 'accelerated' phase
hypertension
• This rare condition may complicate hypertension
of any aetiology and is characterised by
accelerated microvascular damage with necrosis
in the walls of small arteries and arterioles and
by intravascular thrombosis.
• The diagnosis is based on evidence of high
blood pressure and rapidly progressive end
organ damage such as retinopathy (grade 3 or
4), renal dysfunction (especially proteinuria)
and/or hypertensive encephalopathy Left
ventricular failure may occur and, if this is
untreated, death occurs within months.
 HYPERTENSION:
INVESTIGATION PATIENTS
• Urinalysis for blood, protein and glucose
• Blood urea, electrolytes and creatinine
• Blood glucose
• Serum total and high-density lipoprotein
(HDL) cholesterol
• 12-lead ECG (left ventricular hypertrophy,
coronary artery disease)
 HYPERTENSION:
INVESTIGATION OF SELECTED
•
PATIENTS
Chest X-ray: to detect cardiomegaly, heart failure,
coarctation of the aorta
• Echocardiogram: to detect or quantify left ventricular
hypertrophy
• Renal ultrasound: to detect possible renal disease
• 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
 Non-drug therapy
• Appropriate lifestyle measures may obviate the
need for drug therapy in patients with borderline
hypertension, reduce the dose and/or the
number of drugs required in patients with
established hypertension, and directly reduce
cardiovascular risk.
• Correcting obesity, reducing alcohol intake,
restricting salt intake, taking regular physical
exercise and increasing consumption of fruit and
vegetables
• DASH diet (Dietary Approach to Stop
Hypertension)
 Antihypertensive drugs
• Diuretics....
• Help by sodium diuresis and volume
reduction
• Eg Thiazides
Furosemide
spironolactone
 β-blockers

• Eg Metoprolol (100-200 mg daily)

• atenolol (50-100 mg daily)
• bisoprolol (5-10 mg daily)
• Blocks the smpathetic effects on heart-
reduced cadiac output and arterial presure
• Used as first line drug
• cardioselective and therefore preferentially
block the cardiac β1-adrenoceptors
 Angiotensin-converting enzyme
(ACE) inhibitors
• (e.g. enalapril 20 mg daily, ramipril 5-10
mg daily)
• inhibit the conversion of angiotensin I to
angiotensin II
• They should be used with particular care
in patients with impaired renal function or
renal artery stenosis because they can
reduce the filtration pressure in the
glomeruli and precipitate renal failure
 Angiotensin receptor blockers.
• (e.g. losartan 50-100 mg daily, valsartan
40-160 mg daily)
• block the angiotensin II type I receptor and
have similar effects to ACE inhibitors
 Calcium channel blocker
• Calcium antagonists
• Phenylalkline derivatives (vermapril)
dihydropyridines (Nifedipin,amelodipine)
Benzothiazines (Diltiazem)
• Inhibits influx of calcium in cardiac and smooth
muscle – reduced muscle contraction, vasoldialtion
• effective and usually well-tolerated antihypertensive
drugs that are particularly useful in the elderly.
 Adjuvant drug therapy
• Aspirin. Antiplatelet therapy is a powerful means
of reducing cardiovascular risk but may cause
bleeding, particularly intracerebral haemorrhage,
• Statins. Treating hyperlipidaemia can also
produce a substantial reduction in cardiovascular
risk. These drugs are strongly indicated in
patients who have established vascular disease,
or hypertension with a high risk of developing
coronary heart disease