CVS

1. Lecture №5. The syndrome of an
arterial hypertension and
pulmonary hypertension.
Systemic hypertension and hypotonia.
Pulmonary hypertension and “Cor
pulmonale”.
1

2. Causes
• Essential hypertension (primary, cause unknown).
~95% of cases.
• Secondary hypertension. ~5% of cases.
Causes include:
• Renal disease:
• glomerulonephritis, polyarteritis nodosa (PAN), systemic
sclerosis, chronic pyelonephritis, or polycystic kidneys.
• Renovascular disease, atheromatous (elderly , cigarette
smokers, eg with peripheral vascular disease) or rarely
fibromuscular dysplasia (young ).
• Endocrine disease: Cushing's and Conn's syndromes,
phaeochromocytoma (p314), acromegaly,
hyperparathyroidism.
• Others: Coarctation, pregnancy , steroids, MAOI, Pill. 2

3. Plate 17
Right
3

4. Plate 18
Left
4

5. Plate 18
Right
5

6. Signs & symptoms
• Usually asymptomatic (except malignant
hypertension, above).
• Always examine the CVS system fully and check for
retinopathy.
• Are there features of an underlying cause
(phaeochromocytoma,), signs of renal disease,
radiofemoral delay, or weak femoral pulses
(coarctation), renal bruits, palpable kidneys, or
Cushing's syndrome?
• Look for end-organ damage: LVH, retinopathy &
proteinuria indicates severity and duration of
hypertension and associated with a poorer
prognosis. 6

7. Investigations
Basic:
• U&E,
• creatinine,
• cholesterol,
• glucose,
• ECG,
• urine analysis (for protein, blood).
• Specific (exclude a secondary cause): renal
ultrasound, renal arteriography, 24-h urinary VMA
Г— 3 (314), urinary free cortisol , renin, and
aldosterone.
• ECHO and 24-h ambulatory BP monitoring may be
helpful in some cases eg white coat or borderline
hypertension. 7

8. Hypertensive retinopathy
Grade
I. Tortuous arteries with thick shiny walls
(silver or copper wiring)
II. A–V nipping (narrowing where arteries
cross veins)
III. Flame haemorrhages and cotton wool
spots
IV. Papilloedema.
8

9. Measuring blood pressure
• Use the correct size cuff. The width of the cuff
should be at least 40% of the arm circumference.
The bladder should be centred over the brachial
artery, and the cuff applied snugly. Support the arm
in a horizontal position at mid-sternal level.
• Inflate the cuff while palpating the brachial artery,
until the pulse disappears. This provides an
estimate of systolic pressure.
• Inflate the cuff until 30mmHg above systolic
pressure, then place stethoscope over the brachial
artery. Deflate the cuff at 2mmHg/s.
9

10. Measuring blood pressure
• Systolic pressure: The appearance of sustained
repetitive tapping sounds (Korotkoff I).
• Diastolic pressure: Usually the disappearance of
sounds (Korotkoff V).
• However, in some individuals (eg pregnant women)
sounds are present until the zero-point.
• In this case, the muffling of sounds, Korotkoff IV,
should be used.
10

11. Papilloedema: swollen, hyperaemic
disc with blurred margins
11

12. Advanced papilloedema with congestion
and oedema of the disc
12

13. Advanced papilloedema:tortuous
and congested veins withoedema
13

14. Papilloedema with completely obscured
disc. Note tortuous veins with dark blood
columns
14

15. Papilloedema with haemorrhages and
exudates(accelerated hypertension)
15

16. THE INFORMATION BLOCK:
• Arterial hypertention - primary (essential
hypertension) or secondary increase of
systolic and/or diastolic arterial (blood)
pressure.
• According to recommendations of the
International Incorporated Committee (1999)
hypertension is defined at adults on level
systolic blood pressure=140 mm Hg and more,
or diastolic blood pressure=90 mm Hg and
more, and are classified further on degrees:
16

17. • Table 1.
Category the blood pressure The systolic (mm.
Hg)
The diastolic (mm. Hg)
The optimum <120 <80
The normal 120-129 80-84
High-normal 130-139 85-89
I degree of hypertension (mild) 140-159 90-99
II degree of hypertension (moderate) 160-179 100-109
III degree of hypertension (severe) 180 and more 110 and more
Isolated systolic hypertension It is more then 140 It is less then 90
The boundary systolic hypertension 140-140 It is less then90
17

18. The causes: the сause of the essential АH or primary
АH is not known; symptomatic АH have a known
etiology (parenhematous renal diseases, diseases of
renal vessels, diseases of adrenal glands, anomalies
of vessels, aortic regurgitation, etc.).
Undoubtedly, there is a genetic predisposition to the
hypertensia; apparently, environment factors
(quantity of sodium in food, character of a food and
the lives, promoting adiposity, and stress, smoking,
a diabetes mellitus) have the an effect only on
genetically predisposed individuals.
.
18

19. Risk factors
Thus, at the analysis of risk factors began to consider of
next criteria:
1. Level the blood pressure (in mm. Hg.)
2. Major risk factors:
. Levels the systolic blood pressure and diastolic blood
pressure (1-3 degrees)
. Age of men> 55 years
. Age of women> 65 years
. Smoking
. Cholesterol level> 6,5 mmol/l (250 ml/dl)
. A diabetes
. Cardiovascular diseases and their complications at
relatives: at women till 65 years, at men - till 55 years.
19

20. 3. Other risk factors negatively influencing the forecast
. Decrease of level of high density lipoproteids
. Increase of of low density lipoproteids
. Microalbuminuria at a diabetes
. Infringement of tolerance to glucose
. Adiposity
. A sedentary life
. Increase of concentration fibrinogen in blood
. An accessory to socially-ethnic groups of high risk (for
example, in the USA representatives of black race)
. The geographical environment promoting to high risk
20

21. 4.Damage of targets-organs-
. Left ventricular hypertrophy (according to
an electrocardiogram, ultrasound and-or X-
ary investigation).
.Proteinuria and-or passing increase of
creatinine in blood (1,2-2,0 mg/dl)
. Initial displays of an atherosclerosis of an
aorta and peripheral arteries (carotid,
femoral) according to ultrasonic or X-ray
investigations
.General or local narrowing of arteries of a
retina of an eye 21

22. 5. Accompanying cardiovascular illnesses
and pathological conditions
. Cerebrovascular (an ischemic stroke,
hemorrhages in a brain)
.Cardiac (a myocardium infarction, a stenocardia,
coronary revasculirization, cardiac failure)
.Renal (diabetic nephropathy, renal failure - level
of creatinine more than 2 mg %)
.Vascular (stratifying aneurysm) symptomatic
illnesses of vessels
.Obvious hypertensive retinopathy (hemorrage or
exudate in retina, a hypostasis of an optic nerve)
22

23. Arterial blood pressure (mm. Hg.)
Other risk factors,
except of high
blood pressure; and
life hystory
The mild
hypertension
(SBP 140-159
or DBP 90-99)
The moderated
hypertension
(SBP 160-179 or
DBP 100-109)
The severe
hypertension
(SBP>=180
or DBP=110
I There are no other
risk factors
Low risk Moderate risk High risk
II 1-2 risk factors Moderate risk Moderate risk Very high
risk
III 3 and more risk
factors or damage
of bodies-targets or
diabetes
High risk High risk Very high
risk
IV The accompanying
the clinical
conditions.
Very high risk Very high risk Very high
risk
23

24. Pathogenesis
Exact mechanism unknown. Following are the
suggestions.
• B.P = Cardiac output X Peripheral resistance
In the beginning of the essential hypertension, the
increase of blood pressure is due to a small increase
in cardiac output. This could be due to sympathetic
overactivity. Later in the disease, the cardiac output
induces vascular changes (increased peripheral
resistance) that increase the blood pressure.
24

25. • In regulation of the pressure of blood volume of
participates juxtaglomerular apparatus (JGA). Formed
in granulus cells of JGA the proteolytic enzyme rhenine
cataliziratat the transformation of angiotenzine (one of
protein of plasma) in decapeptidis angiotensin I which
is split by enzyme (mainly in lungs, but also in kidneys
and a brain) till ocapeptidis angiotensin II which
operates as powerful vasoconstrictor, and also
stimulates liberation aldosterone.
• Besides, in blood is available not containing of
aspoginate acids hectapeptidis (angiotensin III) which
stimulates liberation аldosterone, as well as angiotensin
II, but possesses with much smaller pressor activity.
• The aldosterone conducts to a sodium delay in an
organism; surplus of endocellular sodium raises
sensitivity of smooth muscles of vessels to sympathetic
stimulation. 25

26. Secretion of renine is regulated, at least, by 4 mechanisms which are
not mutually exclusive:
1) With receptors of renal vessels, which, obviously, react to changes of
pressure of walls bringing аrterioles
2) With receptors macula densa, which, apparently, are sensitive to
changes of speed receipts or concentration NaCI in distal tubes
3) With negative feedback between concentration in blood of
angiotensin and secretion of renine and
4) With sympathetic nervous system, stimulating secretion of renine as
a result of activation of B-adrenoreceptions of renal nerve.
As a result of a long hypertensia there are structural changes of
arteriols, their gleam decreases, that conducts to increase of
common peripheral resistanceof vessels.
• The hypertensia can develop as a result of deficiency of vasodilating
substances. Their reduction or the absence caused by damage of ren
promotes increase the arterial blood pressure. 26

27. Complaints:
To headaches, mainly in suboccipital area, sometimes in
temporal areas, frontal area, often arise at stress, bad
weather, abusing salty food, weight in a head, dizziness,
palpitation, nasal bleedings, nervousness, fatigue. In 25
% of cases primary АH can be asymptomatic, until
complications will develop.
The clinical picture nonspecific also is defined by defeat of
bodies-targets.
Hypertensia complications concern: left ventricular failure,
ischemia, hemorrhages, exudates and a hypostasis of a
nipple of an optic nerve, and acute vascular
infringements in a retina; damage of brain blood
circulation with a stroke or without it; renal failure.
Then there is a dyspnea, sight deterioration, working
capacity decrease, «flashing of front sights» before eyes.27

28. Survey:
• Hyperemia of face, the expressed temporal arteries, a
symptom of "worm". Depending on causes: puffiness of
the face- at renal АH, moonface- at Ikushing’s syndrome,
аssymetry trunks: the developed superior part, in
comparison with inferior part- at aortic coarctation, etc.
Palpation:
• The apex beat is strengthened, displaced to the left,
pulse - firm, full, strained.
Percussion:
• Displacement to the left the left border of relative
dullness of heart.
Auscultation:
• Sounds are strengthened, accent II sound over an aorta
in 2 intercostals space on the right, can be functional
systolic murmur on an apex.
28

29. Laboratory and instrumental
investigations:
• Chest x-ray: aortic configuration of the heart, an
aorta is condensed, expanded.
• Electrocardiogram: high R in I, displacement of
segment SТ, lowered, negative or diphasic wave
Tin I, II, V5-V6; at II-III stages of hypertension
disease - signs of left ventricular hypertrophy.
• Echo CG: at II-III stages of hypertension disease - a
thickness of a back wall and intraventricular sept
more than 1,2 sm the.
• Eye : hypertensive retinopathy I, II, III, IV degrees.
29

30. Laboratory and biochemical
investigations
Common blood count, urine analysis (at disease progressing -
microalbuminuria and proteinuria), definition of sodium and calium ,
creatinine, blood glucose on an empty stomach, the common
cholesterol (HS) and high density lipoproteids cholesterol.
Late displays of arteriolonephrosclerosis-polyuria, nicturia, reduction the
concentration function of kidneys, proteiuria, microhematuria,
cylindruria and a nitrogen delay.
• Symptomatic AH owing by hyperkatecholemy, the caused tumour of
chromaffine cells of adrenal glands (pheochromacytoma), besides
increase the blood pressure usually causes symptoms (the headaches,
the expressed palpitation, arrhytmias a tachycardia, эectopic beats,
paroxysmal tachycardia, increase of sweating , tremor and pallor of
skin), allowing to suspect this АH.
• The diagnosis leans against revealing in urine or in plasma of blood the
raised concentration in urine their metabolytes- methanephrines and
vaninilmindal acids.
30

31. In primary hyperaldosteronism maybe hypokaliemia not caused
reception diuretics.
Detection in urine at an early stage of a hypertensia of protein
and cylinders, and also microhematuria (with a delay of
nitrogen or without it) serves as the weighty proof of primary
damage of kidneys.
Absence or considerable reduction and delay of a pulsation of a
femora artery at sick of a hypertensia is younger 30 years
usually specifies for aortic coarctation.
The suspicion on a reno-vascular hypertension should arise, if
• increase the arterial pressure develops for the first time at
persons before 30 years or is more senior 55 years, or
suddenly rogresses before stable АH
• fast development malignant АH(during 6 month from the
disease beginning)
• systolo-diastolic murmur in epigastric areas
• usually assymtomatic
31

32. Hypertensive crisis
• The hypertensive crisis is the syndrome characterised by acute
lifting the arterial pressure (as a rule, diastolic blood pressure
exceeds 120 mm hg) and symptoms of infringement of regional
blood circulation, more often the brain.
The causes of a hypertensive crisis:
• Inadequately treatment of essential hypertension
• Renovascular hypertension
• Diseases of kidneys, acute glomerulonephritis
• Pheochromocytoma
• Sclerodermia and other diseases of a connecting tissues
• Use sympathomimethic means (cocaine, etc.)
• A cancellation syndrome (Clonidine, beta-blockers)
• Eklampsya
• Head traumas
• renin- and aldosteron secreting tumours
• vasculitis
32

33. Now allocate crises of 2 types: I type (emergency) - demands emergency
treatment, when it is necessary to achieve decrease the arterial pressure
during 1 hour to reduce danger of development of irreversible infringements
and death of the patient; hypertensive crises of this type concern:
– A hypertensive encephalopathy
– An intracranial hemorrhage
– A stroke
– A hypostasis of lungs
– A myocardial infarction
– Pheochromosytomic crisis
– Stratifying an aorta aneurysm
– eklampsy (pregnancy nephropathy)
II types (uгgency) - demand urgent treatment. The arterial pressure should be
lowered during 12-24 hours; them concern:
– A malignant hypertensia
– An unstable angina pectoris
– Left ventricular failure (cardiac asthma)
– A hypertensia in pre-and the postoperational period
– Preeklampsy.
33

34. • CLINIC
At a hypertensive encephalopathy the acute
headache, a nausea, vomiting, visual
frustration is marked. Usually the blood
pressure very high, symptoms accrue
imperceptibly during 48-72 частов (unlike an
intracranial hemorrhage).
34

35. Complications of hypertension
The adverse effects of hypertension principally
involve the CNS, retina, heart and kidneys.
• CNS
Stroke: It results from cerebral hemorrhage or
infarction mostly as a complication of
hypertension.
Hypertensive encephalopathy:It is characterized by
severe hypertension with neurological symptoms
e.g. transient disturbance of speech or vision,
disorientation, fits and unconsciousness.
Subarachnoid hemorrhage: It is also more common
in hypertensive patients.
Multi-infarct dementia.
35

36. • RETINA
Retinal changes are graded as following:
Grade I: tortuosity of the retinal arteries with increased
reflectiveness (silver wiring).
Grade II: Grade I plus appearance of arteriovenous nipping
produced when thickened retinal arteries pass over the retinal
vein.
Grade III: grade II plus flame-haped hemorrhages and soft "cotton
wool" exudates due to small infarcts.
Grade IV: Grade III plus papilledema (blurring of the margins of the
optic disc).
• HEART
Left ventricujar hypertrophy and ultimately left ventricular failure.
Ischemic heart disease.
Aortic dissection
• KIDNEYS
• Long stending hypertension may cause nephrosclerosis
(hypertensive nephropathy – proteinuria and progressive renal
feilure). 36

37. Hypotonia
• Arterial hypotonia characterized by decreases the blood pressure less
then 100/60 mm.Hg. for the persons till 25 age and less then 105/65
mm.Hg. for the persons more then 30 age.
Physiological arterial hypotonia: causes-the constitutional and genetic
factors, are found at healthy persons and no accompanied with
pathological chandes (adaptationaly hypotonia).
Patological hypotonia may be primary and secondary ( symptomatic).
Secondary may be acute and chronic. Causes: primary hypotonic
disease due to infrigement central and vegetative neurological system
with infrigement of regulation of the vessel tone. Causes of secondary
hypotonia – acute and chronic failure of renal gland, hypothyreosis.
At an acute vessels failure ( collapse, syncope) can be sharp collapse of
vessels tone and develop decrease of inflow of the blood to the heart,
decrease of cardiac output and of volume of blood circulation.
37

38. • Clinically: fatuge, confusion, syncope,
vomiting, palpitation, dyspnea, pallor of skin,
sweating, decreases systolic and diastolic
blood pressure. Pulse are threadly.
• Survey: hyperhydrosis, tremor of fingers.
• Border of the heart is normal, cardiac sound is
weakened.
• ECG: decrease of voltage.
• Laboratory and instrumental investigation is
normal.
38

39. Pulmonary arterial hypertension and “cor”
pulmonale.
• PH is characterized by decrease if moderate pressure in pulmonary
arteries in rest more then 25 mm.Hg.( normal-9-16 mm. Hg.) PH
decreased loading right part of heart, lead to develop of the
pulmonary heart9 cor pulmonale). Cor pulmonale its RVH due to
disease, which damage of function and structure of lungs, pulmonary
vessels.
• Causes: disease of broncho-pulmonary apparats and intrapulmonary
airways, kyphoscolyosis, neuro-muscular diseases, primary pulmonary
hypertensia. thrombosis., emboli, arteriitis and ect.
• Clinically: symptoms of basic diseases, pulmonary failure, pulmonary
arterial hypertension, HRV, right ventricular cardiac failure.
• Complaints: dyspnea, cough with sputum and another symptoms of
basic diseases. May be syncope, chestpaine due to anlarged of the
truncus of pulmonary artery and increased of pulmonary pressure,
palpitation, edema, olygouria.
39

40. • Survey: tachypnea, diffuse cyanosis, swelling of neck veins at expirate,
pulsation in left on the II intercostal space, accent II sound over pulmonary
artery, HRV ( increase of border of the heart to right, precardial pulsation,
epigastrical pulsation). The signs of right ventricular cardiac failure consist
swelling of neck veins in breath, increase of right border of the heart,
weakned I sound, systolic murmur over pulmonary artery, diastolic
Grehem- Still’s noise, arrhytmias, hepatomegaly, acytes, edema of feet.
• X-ray: strenfthening of pulmonary roots, pulsation of vessels and increase
of diameter of the right pulmonary artery ( norma-14-16 mm), RVH.
• ECG: axis deviation to right, P-pulmonale, HRV.
• EchoCG: increase pulmonary arterial pressure (N-diastolic less then
12mm.Hg systolic more then 30 mm. Hg., moderate less then 25 mm. Hg.),
increase of anterio-posterior size of right ventricule and tickening of
anterior wall of right ventricule ( more then 5mm).
• Peak expiratory flow rate: sharp expressed infringement by obstruction
type (forced inspiratory volume more then 1Iitre), restriction type ( vital
capacity less then 50%).
• Arterial blood- gas analysis: P O2 less then 87%(N- more then 95%).
• Heart catheterization: level of pulmonary pressure.
• May be investigation-pulmonary angyography, byopsy and morphological
investigation.
40