2041863_HTA eng noua.p hypertension ppdf

Hypertension

1. Hypertension
Dr. Tcaciuc Angela

2. Blood pressure is the pressure exerted by circulating
blood on the walls of the arteries.
❑Blood pressure is determined by the
•cardiac output and
•peripherial resistense
❑Blood pressure dependson
•the heart
•blood vesssels
•extracellular fluid volume
•the central and peripherial nervous system
•kidneys
•circulating humoral factors

3. Blood pressure
Blood
pressure
Cardiac
output
Stroke
volume
Heart rate
Peripherial
resistance
vascular
structure
Endothelial
factors

4. ❑Stroke volume (L/min)
depends on
➢intravascular volum
➢myocardial contraction
➢preload
➢afterload
➢contractility

5. Miocardial contraction
❑is a complex process and depends on:
•the intrinsic cardiac condaction system
•membrane transport
•cellular events, including influx of calcium
•effects of humoral substances, such as
catecholamines and thyroxine
•sympathetic and parasympaphetic regulation of
heart rate

6. The peripherial resistens
❑depends on a number of factors:
•neurohumoral substance
•baroreflexes
•sympathetic nervous system
•endothelial factors
•electolytes (sodium, potassium, calcium)
•volume
•intracellular events mediated by receptors and
signal transduction

7. Definition
❑Hypertension-persistent increase of blood
pressure ≥140 mmHg systolic and ≥90mmHg
diastolic blood pressure in untreated patient

8. Classification of hypertension
❑Essential or primary hypertension-
hypertension with unknown cause, but its appearance
contributes to a number of mechanisms,whichcause increased
cardiac output or peripheral vascular resistance.
•pathophysiologicalessential hypertension is a heterogeneous
disease.
•The factors are:genetic, neurogenic, environmental, hormonal,
hemodynamic.
•The prevalence of essential hypertension is over 95%
❑Secondary hypertension-
has an identifiable, potentially treatable cause.

9. Etiopathogenesisof essential hypertension
•The mechanisms underlying its occurrence are:
❖genetic predisposition - at least 10 monogenic pathologies
responsible for hypertension. In all monogenic hypertensive pathologies the
final common pathway was increased sodium absorption and hydrosaline
retention. Liddle syndrome, the most studied form of monogenic hypertension,
has mutations in the β and γ subunits of the sodium channel in the renal
epithelial cells and in the collecting duct, resulting in hydrosaline retention,
monogenic hypertension is rare and constitutes <1% of hypertension.
❖sodium and water retention - refers to the acquired or inherited
impairment of the kidney's ability to eliminate excess salt from the diet. Salt
retention leads to increased volume and subsequent cardiac output, resulting in
mechanisms that increase systemic vascular resistance.

10. Etiopathogenesis of essential hypertension
❖vascular remodeling
•endothelial dysfunction
•vascular remodeling
•arterial stiffness
❖ sympathetic nervous system hyperactivity - in young
adults with hypertension the mechanisms involved are
• increased heart rate and cardiac output
•plasma and urinary norepinephrine levels
• peripheral sympathetic nervous hyperactivity
oIn patients with sleep apnea, repeated episodes of hypoxemia
and hypercapnia increase sympathetic tone by activating
arterial chemoreceptors The signals transmitted from the
chemoreceptors excite the vasomotor center, which controls
the increase in blood pressure.

11. Etiopathogenesis of essential hypertension
❖hyperactivity of the renin-angiotensin-aldosterone system -
plays a central role in the pathogenesis of essential hypertension. RAAS
contributes to the regulation of blood pressure by the vasoconstrictor
properties of angiotensin II and by the sodium retention produced by
aldosterone. Angiotensin II is a potent vasoconstrictor- increasing total
peripheral resistance and, implicitly, blood pressure.
❖hyperisulinemia or insulin resistance.the following mechanisms:
•1. Renal sodium retention
•2. Increasing sympathetic activity
•3. Smooth muscle hypertrophy of the vascular wall under the mitogenic
action of 'insulin'
•4. Modification of transmembrane ion transport, which increases the
concentration of calcium in the cytosol

12. Hyperinsulinemia
adrenergic↑
activity
Aldosteron↑
Hypertrophy of
smooth muscles in the
vascular wall
Distribution activation
Na⁺/K⁺
↑Blood pressure
↑ Peripherial resistance
Absorption ↑Na⁺
↑ Intravascularvolume
↑ Cardiac output

13. Etiopathogenesis of essential hypertension
❖The additional action of environmental factors
•obesity - is a major cause in essential hypertension. The
mechanisms involved are: increased activity of the SNS,
activation of theRAAS, compression of the kidneys with the
fat accumulated around them.
•sedentary lifestyle - hypodynamics leads to obesity
• alcohol consumption in high doses - 50% of alcohol addicts
have high blood pressure
•increased salt intake - leads to fluid retention and volume
expansion
• stress - in response to stress there is excessive sympathetic
stimulation
•smoking - tobacco increases the release of norepinephrine,
which contributes to increased BP, stimulates atherosclerosis
•familiar eating habits - increased intake of carbohydrates,
saturated fats

14. Diagnostic plan:
1.Symptoms
2.Historyof disease
3. Physical examination
4. Repeated measurements of BP values
5. Paraclinical investigations

15. Symptoms collection
• Typical symptomsin hypertension: fronto-
occipital headache with constrictive character,
often morning.
• Neurological manifestations: irritability,
anxiety, asthenia, depression, instability in
walking and balance.
• Vision and hearing disorders: tinnitus,
dizziness, foggy vision, phosphenes.

16. •Determining the duration of increased BP values and its
levels, the anti-hypertensive treatment previously
prescribed and its effectiveness.
•Possible iatrogenic causes: contraceptive medication,
corticosteroid, nonsteroidal anti-inflammatory drugs,
vasoconstrictordrugs
•Lifestyle: eating habits (increased intake of salt, alcohol,
saturated fat, carbohydrates ..). Psycho-emotional stress,
smoking.
•Personal pathological history: diseases with
cardiovascular impact - diabetes, hypercholesterolemia,
kidney disease, Hypertention complications (stroke,
angina, myocardial infarction)
History of disease

17. Physical examination
General exam:
• Frequently hyperstenic constitutional type, obese
android picnic
• Facies: pletoric (frequent) in essential hypertention;
pale - in renal and essentially hypertention
• Determine the body mass index (BMI)
• Waist circumference Comparatively of weight, this
parameter indicates metabolic syndrome or the risk of
developing diabetestype 2.
In men ˃94 cm, in women ˃80 cm it indicates
abdominal obesity.
• The presence of oedema is determined (evidence of
biventricular decompensation)

20. Examination of peripheral vessels
• Enlargement of the jugular veins in the
hypertensive patient attests to biventricular
decompensation
• Palpation and auscultation of the carotid arteries -
murmur in case of atheromatous stenosis
• Palpation and auscultation of the aorta useful in
aneurysm ± aortic dissection; aortic coarctation +
palpation and auscultation of the murmurs on the
thoracic collateral
• Palpation and auscultation of the abdominal aorta
and renal arteries - systolic-diastolic (continuous)
murmurs in case of local stenoses of various
etiologies

22. BP values can be measured:
❑in office
•by the medical staff
❑out-of-office
• by the patient at home-HBPM
• automatic -ABPM (Holter) for
a period of 24/h

24. Patients should be seated comfortably in a quiet environment for 5 min before beginning BP measurements.
Three BP measurements should be recorded, 1–2 min apart, and additional measurements only if the first two
readings differ by >10 mmHg. BP is recorded as the average of the last two BP readings.
Additional measurements may have to be performed in patients with unstable BP values due to arrhythmias, such
as in patents with AF, in whom manual auscultatory methods should be used as most automated devices have not
been validated for BP measurement in patients with AF.
Use a standard bladder cuff (12–13 cm wide and 35 cm long) for most patients, but have larger and smaller cuffs
available for larger (arm circumference >32 cm) and thinner arms, respectively.
The cuff should be positioned at the level of the heart, with the back and arm supported to avoid muscle
contraction and isometric exercise-dependant increases in BP.
When using auscultatory methods, use phase I and V (sudden reduction/disappearance) Korotkoff sounds to
identify SBP and DBP, respectively.
Measure BP in both arms at the first visit to detect possible between-arm differences. Use the arm with the
higher value as the reference.
Measure BP 1 min and 3 min after standing from a seated position in all patients at the first measurement to
exclude orthostatic hypotension. Lying and standing BP measurements should also be considered in subsequent
visits in older people, people with diabetes, and people with other conditions in which orthostatic hypotension
may frequently occur.
Record heart rate and use pulse palpation to exclude arrhythmia
Office blood pressure measurement

26. White-coat hypertension
•White-coat hypertension refers to the untreated condition in which BP is
elevated in the office, but is normal by ABPM, HBPM, or both.
•‘white-coat effect’, reflect the pressor response to an alerting reaction
elicited by office BP measurements
•the prevalence varies between studies, can account for up to 30 − 40% of
people (and >50% in the very old).
•It is more common with increasing age, in women, and in non-smokers.
•Its prevalence is lower in patients with HMOD, when office BP is based on
repeated measurements, or when a doctor is not involved in the BP
measurement.
• A significant white-coat effect can be seen at all grades of hypertension
(including resistant hypertension), but the prevalence of white-coat
hypertension is greatest in grade 1 hypertension.

27. Masked hypertension
•Masked hypertension refers to untreated patients in whom the BP is normal
in the office, but is elevated when measured by HBPM or ABPM.
•Can be found in approximately 15% of patients with a normal office BP
•The prevalence is greater in younger people, men, smokers, and those with
higher levels of physical activity, alcohol consumption, anxiety, and job
stress.
•Obesity, diabetes, CKD, family history of hypertension, and high–normal
office BP are also associated with an increased prevalence of masked
hypertension.
•Masked hypertensionis associated with dyslipidaemia and dysglycaemia,
HMOD,adrenergic activation, and increased risk of developing diabetes
and sustained hypertension.
•Masked hypertension increase the risk of CV and renal events in diabetes,
especially when the BP elevation occurs during the night.

28. Hypertension and total
cardiovascular risk assessment
❑Hypertension rarely occurs in isolation, and often clusters with other CV
risk factors such as dyslipidaemia and glucose intolerance.
•This metabolic risk factor clustering has a multiplicative effect on CV risk.
•Quantification of total CV risk (i.e. the likelihood of a person developing a
CV event over a defined period) is an important part of the risk stratification
process for patients with hypertension.
•The SCORE system estimates the 10 year risk of a first fatal atherosclerotic
event, in relation to age, sex, smoking habits, total cholesterol level, and
SBP(sistolicbloodpresure).

30. Hypertension-mediated organ damage
•HMOD refers to structural or functional changes in
arteries or end organs
•Heart
•Blood vessels
•Brain
•Eyes
•Kidney
caused by an elevated BP
•HMOD is common in severe or longstanding
hypertension

32. Factors influencing cardiovascular risk in patients with
hypertension
•Demographic characteristics and laboratory parameters
•Sex(men >women)
•Age
•Smoking (current or past history)
•Total cholesteroland HDL-C
•Uric acid
•Diabetes
•Overweight or obesity
•Family history of premature CVD (men aged <55 years and women
aged <65 years)
•Family or parental history of early-onset hypertension
•Early-onset menopause
•Sedentary lifestyle
•Psychosocial and socioeconomic factors
•Heart rate (resting values >80 beats/min)

33. Asymptomatic HMOD
❑Arterial stiffening:
•Pulse pressure (in older people) ≥60 mmHg. Carotid–femoral PWV >10 m/s
❑ECG LVH (Sokolow–Lyon index >35 mm, or R in aVL ≥11mm; Cornell voltage duration
product >2440 mm.ms, or Cornell voltage >28 mm in men or >20 mm in women)
❑Echocardiographic LVH [LV mass index: men >50 g/m
2
; women >47 g/m
2.
(height in
indexation for BSA(body surface area); may be used in normal-weight patients; LV
mass/BSA g/m
2
>115 (men) and >95 (women)]
❑Microalbuminuria (30–300 mg/24 h), or elevated albumin–creatinine ratio (30–300 mg/g;
3.4–34 mg/mmol) (preferentially on morning spot urine)Moderate CKD with eGFR >30–59
mL/min/1.73 m
2
(BSA) or severe CKD eGFR <30 mL/min/1.73 m
❑Ankle−brachial index <0.9
❑Advanced retinopathy: haemorrhages or exudates, papilloedema

34. Established CV or renal disease(Symptomatic HMOD)
❑CAD(coronary artery disease): myocardial infarction,
angina, myocardial revascularization
❑ Presence of atheromatous plaque on imaging
❑ Heart failure, including HFpEF
❑ Peripheral artery disease
❑Atrial fibrillation
❑ Cerebrovascular disease: ischaemic stroke, cerebral
haemorrhage, TIA

36. The brain in hypertension
Asymtomatic phase – MRI can detect brain damage as:
•white matter hyperintensities
•silent microinfarcts, (most of which are small and deep, i.e.
lacunar infarctions)
•microbleeds
• brain atrophy
❖White matter hyperintensities and silent infarcts are associated with an
increased risk of stroke and cognitive decline due to degenerative and
vascular dementia
Symtomatic phase
•TIA
•Ischaemic stroke
•Cerebral haemorrhage

37. The blood vessels in hypertension
•Asymtomatic phase –
Arterial stiffening:
1.Pulse pressure (in older people) >60 mmHg
2.Carotid intima-media thicknes (IMT) > 0,9 mm
3.Carotid –femoral pulse wave velocity (PWV) >10 m/s
4. Ankle-brachial index (ABI) < 0,9, indicates lower extremity artery
disease (LEAD), is usualy indicative of advanced artherosclerosis, and
has predictive value for CV events.
•Symtomatic phase -
1.Symtomatic lower extremities peripheral artery disease

38. The heart in hypertension
➢Chronically increased left ventricular workload in
hypertensive patients can result in:
• LVH
• impaired LV relaxation
•left atrial enlargement, an increased risk of arrhythmias,
especially AF.
• heart failure with preserved ejection fraction (HFpEF)
• heart failure with reduced ejection fraction (HFrEF).

39. ECG left ventricular hypertrophy
ECG voltage criteria Criteria for LVH
SV1+RV5(Sokolow–Lyon
criterion)
>35 mm
R wave in aVL ≥11 mm
SV3+RaVL(Cornell
voltage)
a
Cornell duration
product
b
>28 mm (men)
>20 mm (women)
>2440 mm.ms

40. ECG left ventricular hypertrophy

41. Transthoracic echocardiography in hypertension
➢Provides information about: LV geometry, left atrial volume, aortic
root dimensions,LV systolic and diastolic function, pump
performance, output impedance.
• Left ventricular hypertrophy – LV mass/BSA g/m2
>115 (men) and >95 (women)
• SIV >11 mm (N 6-11 mm)
• Posterior wall of the LV> 11 mm (N 6 -11 mm)

42. Routine laboratory tests
Haemoglobin and/or haematocrit
Fasting blood glucose and glycated HbA1c
Blood lipids: total cholesterol, LDL cholesterol, HDL cholesterol
Blood triglycerides
Blood potassium and sodium
Blood uric acid
Blood creatinine and eGFR
Blood liver function tests
Urine analysis: microscopic examination; urinary protein by dipstick test or,
ideally, albumin:creatinine ratio
12-lead ECG

43. Asssessment of HMOD

44. Lifestyle interventions for patients with HTA

45. Blood pressure treatment

50. Treatment for uncomplicated hypertension