Systemic Hypertension

systemic hypertension  Def: •

systemic HTN is diagnosed of the avenge Level of  ≥140/90. SBP is 140 mm Hg DBP is 90 mm Hg or more If SBP is ≥160 mm Hg a single visit for  measurement OR DBP is≥ 105mm Hg sufficient for the diagnosis •

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 Etiology:

1) systolic HTN( SBP ≥ 160 mm Hg with Normal DBP).  A ) ↑increased LT. ventricular stroke volume: 1- aortic reguige 2- thyrotoxicosis & fever  3- A-V fistula 4- P.D.A 5- hypa Kinetic disease  B) ↓decreased aortic compliance aortic atherosclerosis 2) systolic & diastolic HTN a-essential HTN:  Commonest form of systemic HTN (> 90% of  cases)  occurs in middle & late ages. the problem is probably multifactorial multifactorial as  HTN is more common in some ethnic 1. groups - Japanese - American Blacks. in 40-60% is explained by genetic factors 2. 3. important environmental factors:

high salt intake heavy alcohol consumption obesity impaired intrauterine growth b- 2ry HTN (disease or abnormality  Na retention or  Peripheral V.C.) 1- Alcohol 2- Pregnancy (pre-iclampsia) 3- Renal renal vascular syndrome (R.A.S)   parenchymal renal disease : - GN  - chronic pyelonephritis  polycystic kidney   diabetic nephropathy 4- Endocrine Disease:  phaeochromocytoma cons syndrome acromegaly Cushing syndrome hyperparathyroidism & 1ry hypothyroidism thyrotoxicosis cong .adrenal hyperplasia Due to - 11B-hydroxypase deficiency or  - 17 hydroxypase deficiency 5- drugs  oral contraceptive pills anabolic steroids  Corticosteroid    NSAIDs  Sympathomimetic agents. 6- coarctation of aorta. ↑incresed I.C tension 7- Nervous Disease as • •

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8- polycythemia vera.

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C/P A.

uncomplicated HTN:

 symptoms:

1- majority of Pts are Asymptomatic there may be Headache • dizziness vertigo • tinnitus •  palpitation easy fatigability & it may develop of the pt. has been informed about his HTN due to development of amxiety neurosis. 2-

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3-sever HTN occipital Headache which is usually  present when pt. awakes & subsides spontaneously often several hours  signs : 1•

Pulse: ↑ increased pulse volume in systolic HTN

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↓ decreased pulse volume in systolic & diastolic HTN.

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blood pressure: ↑ increased take care of white coat HTN

Severity of HTN: Normal Person

category

*Optimal * Normal Stage 1(mild) Stage 2(Moderate) Stage 3 (sever)

HTN

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Systolic (mmHg) <120 120-139 140-159 160-179 ≥180

Diastolic (mmHg) <80 80-89 90-99 100-109 ≥110

Cardiac Examination : ↑load A2 aortic systolic ejection click. Systolic ejection murmur due to dilatation of aortic ring with the development of Aortic in competence (functional) Earliest clinical sign of cardiac affection is the appearance of a presystolic gallop . •

Note: the majority of deaths due to HTN result from myocardial infarction or  congestive heart failure •

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 investigations :

Chest X-ray  many reveal prominent aortic knock 

) complicated HTN (target organ Damage ) B.

1- cardiac complication: (systolic , Diastolic ) Dysfunction  L A. t. Ventricular hypertrophy of subsequent Lt ventricular  failure Then Rt . sided failure may follow later on Note: 

Lt. ventricular hypertrophy is a major risk factor of   premature cardio vascular: - morbidity. (or) - mortality.  All anti HTN agents reverse the LT ventricular  hypertrophy especially ACEI centrally acting " captopril" B.B CCB B.coronary atherosclerosis which may lead to  is chemic •

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2- Vascular Complications: 1- accelerated atherosclerosis 2- Hge e.g.:- epistaxisis Due to rupture of  -haematouria small vessels . 4- arterial medial hypertrophy & later on fibrinoid degeneration 5- cystic medial necrosis of the aorta  so HTN is implicated in the pathogenesis of : -aortic aneurysm.

-aortic dissection 3-

cerebral complications: 1- transient ischemic attacks 2- cerebral thrombosis 3cerebral hge (due to rupture of vascular microaneurysm) 4subarachnoid hge 5Hypertensive encephalopathy (mean bp↑>180 mmhg) Disturbed consciousness Retinopathy with papilloedema ↑ I.C.P & seizres focal neurological signs. E.g. Transient disturbances of (speech & rision ) •

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4- Renal complications: Protein urea & Haematouria Due to glomerular injury atherosclerosis of the afferent & efferent arterioles of glomerular capillaries  Note. Nephrosclerosis : disturbed glomerular filtration, Tubular dysfunction, Followed by R.F in 10-20 % of pts •

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5) Retina → Hypertensive retinopathy . Grade 1: 1- arteriolar thickening 2- touristy 3- ↑increased reflectivness (silver wiring). Grade 2: 1+ construction of vien's at arterial crossing (A-V nipping).

Grade 3: 2+ evidence of retinal ischemia - flame shaped or blot Hges. - cotton wool exudates. Garde 4: 3+ papilloedema.

Malignant or accelerated phase HTN:

This rare condition may complicate HTN of any etiology. •

It ccc by accelerated micro vascular damage with → necrosis in the wall of small arteries & arterioles (fibrinoid necrosis).  intravascular thrombosis. •

The diagnosis is based on evidence of  1high BP 2- rapidly progressive 3end – organ damage as-retinopathy [grade 3,4] -renal failure -HTN encephalopathy. Lt. ventricular failure may Occur & if untreated → death within months. •

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 Investigations:

1) Basic (investigations of all pts): 1- urine analysis for: → blood (haematuria). → proteinuria → glucose → glucoseuria. 2- plasma urea & electrolytes  Note: hypokalemia alkalosis may indicate Conns but usually due to diuretics. 3- plasma creatinine. 4- plasma cholesterol. 5- ECG: → to detect LT. vent. Hypertrophy. Or  → evidence of coronary artery D. 2) Investigations of selected PTS: 1- chest X-ray → to detect : - cardiomegaly. - heart failure. - coarctation of aorta. 2- ambulatory blood pressure recording → to assess borderline or white coat HTN. 3- Echocardiogram → to detect LT. vent. Hypertrophy.

4- renal U/S → to detect possible renal D. 5- renal angiography → to detect R.A.S 6- urinary catecholamines → to detect  phaeochromocytoma. 7- urinary cortisol & dexa methasone suppression test → for possible cushing $. 8- plasma rennin activity & aldosterone for conn's $. 9- T3 & T4 & TSH → for hypo & hyperthyroidism.

 Treatment 

1- life style modification [non pharmacological therapy]  Avoidance of smoking. Wt. reduction in over wt. PTs. • Restriction of alcohol intake. • Regular physical activity & relaxation. • Moderation of dietary Na to < 6 gm /d (salt restriction). •

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2- pharmacological therapy:   for stage 1 & 2 HTN:

if BP remains> 140/90 for 3-6 months despite life style modification. Anti Hypertensive drug's should be started with a  single drug (monotherapy). Since → B.B. & Diuretics can ↓decrease  cardiovascular morbidity & mortality. they are proferred far initial drug therapy  if ineffective:  ACEI & CCB or αblocker, α b blocker  

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The lowest doses of the selected drug to avoid their side effects if blood pressure remains uncontrolled for several  wks → ↑ dose gradually if after 1-3 months & the response is still  inadequate 3 options: 1) ↑ dose of the initial drug to maximal levels. 2) Substitute an agent for another. 3) Add a 2nd drug from another class.

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 for stage 3 HTN:  as above but it's often necessary to add: -

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a 2nd or 3rd agent after short interval. The maximum dose of 1 drug may be needed.

 for resistant HTN: def.: blood pressure can't be ↓ ed to <160/100 (if it was > 180/115) or 140/90 (if it was < 180/115). despite appropriate, triple drug therapy is nearly maximum doses. the drug therapy should include at least 3 different  pharmacological agents including a diuretic consider 2ry HTN → ttt of the cause e.g..: repair of renal artery stenosis either by surgically or angioplasty.  for HTN emergencies: "acute HTive crises" If severe rise of Bl pressure with symp & sign's of acute severe target organ damage which must be reduced within minutes (typically using parenteral therapy). •

If sever rise in Bl pressure with mild or no acute target organ damage which must be reduced within hours (typically with oral therapy). •

It includes:

Acute HTive encephalopathy. 2) Acute pul. Oedema → due to HTive LT. ventricular failure 3) Malignant HTN. Acute dissecting aneurysm of aorta. 4) Eclampsia & Hgic strokewz marked 5) elevation of Bl. Pressure. 1)

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In these cases the blood pressure should be lowered only to levels that relieve the immediate crisis Ex.: 160/100 & not more.

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If the Bl. Pressure must be lowered immediately then I.V. in fusion of sodium nitroprusside is the first choice & alternative drugs →are nitroglycerin I.V. & Diazoxide.