HYPERTENSION
Wahyu Febrianto
Hypertension
Hypertension (HTN) affects approximately 75
million adults in the United States.
Hypertension is major risk factor for stroke,
myocardial infarction, vascular disease, and
chronis kidney disease
Definition
A systolic blood pressure (SBP) of 140
mmHg or more.
A diastolic blood pressure (DBP) of 90
mmHg or more.
On each of two or more office visits.
Blood pressure = Cardiac output x Peripheral resistance
Hypertension = Increased CO and/or Increased PR
Vasoconstriction
Preload Contractility
Heart rate
Fluid volume
Sympathetic Renin-
nervous system angiotensin-
Renal sodium aldosterone
retention system
Excess Genetic
sodium factors
intake
Kaplan (1994)
Hypertension
Cardiac Systemic Vascular
Output Resistance
Hypervolemia Stress
- Renal artery stenosis - Sympathetic activation
- Renal disease Atherosclerosis
- Hyperaldosteronism Renal artery disease
- Aortic coarctation - Increased Ang II
Stress Pheochromocytoma
- Sympathetic activation - Increased cathecholamine
Pheochromocytoma Thyroid dysfunction
- Increased Diabetes
cathecholamines Cerebral ischemia
Types of Hypertension
Primary HTN: Secondary HTN:
also known as less common cause
essential HTN. of HTN ( 5%).
accounts for 95% secondary to other
cases of HTN. potentially rectifiable
no universally causes.
established cause
known.
Primary or “Essential” Hypertension
1. Etiology - unknown
2. Accounts for approximately 90% of hypertension
3. Onset typically in the fifth or sixth decade of life
4. Strong family history - 70-80% positive family history
BP correlations are stronger among parent and child than
between spouses, suggesting that environmental factors
are less important than genetic ones
Certain races (e.g. African Americans) are at much
higher risk of HT
Risk factors
Race (More common and more severe in blacks)
Age > 60 years
Sex (men and postmenopausal women)
Family history of CVD
Smoking
High cholesterol diet
Co-existing disorders such as diabetes, obesity and
hyperlipidemia
Sodium intake
High intake of alcohol
Sedentary life style
Secondary Hypertension
1. Identifiable underlying cause:
kidney disease
renal artery stenosis
hyperaldosteronism
pheochromocytoma
2. Represents approximately 10% of all hypertension
3. Has specific therapy, and is potentially curable
4. Often distinguishable from essential hypertension on
clinical grounds
Endocrine hypertension
Secondary hypertension 6-8%
Renal 4-5%
Miscellaneous ~2%
Endocrine 1-2%
Primary hyperaldosteronism 0.3%
Cushing’s syndrome <0.1%
Pheochromocytoma <0.1%
The risks of hypertension
The risks of hypertension are well recognised
Cerebrovascular disease: Thromboembolic, Intra
cranial bleed, TIA
Cardiovascular disease: MI, HF, CAD
LVH -- enhanced incidence of HF, ventricular
arrhythmias, death following MI, and sudden
cardiac death.
Peripheral vascular disease
Renal failure
Target Organs
CVS (Heart and Blood Vessels)
The kidneys
Nervous system
The Eyes
Diagnosis
Based upon the average of > 2 properly
measured readings at each of > 2 visits (at least
3 to 6 visits, spaced over a period of weeks to
months)
Apply to adults on no antihypertensive
medications and who are not acutely ill.
If there is a disparity in category between the
systolic and diastolic pressures, the higher value
determines the severity of the hypertension.
Classification
[Link]
Evaluation - Aim
To determine the extent of target organ
damage.
To assess the patient's overall
cardiovascular risk status.
To rule out identifiable and often curable
causes of hypertension
Follow-up based on initial BP
measurements for adults*
[Link] *Without acute end-organ damage
TREATMENT
Lifestyle modifications
[Link]
Antihypertensive drug strategies
• Reduce cardiac output
– -adrenergic blockers
– Ca2+ Channel blockers
• Dilate resistance vessels
– Ca2+ Channel blockers
– Renin-angiotensin system blockers
– 1 adrenoceptor blockers
– Nitrates
• Reduce vascular volume
– Diuretics
– Direct vasodilators
Anti-Hypertensive Drugs: Sites of Action
Symphatetic
Renin inhibitors Activity
Renin
β BLOCKERS
Cardiac
Output
Thiazids
ACE-i
ARBs
Calsium Antagonist+
α BLOCKERS
PERIPHERAL
HYDRALAZINE VASCULAR
RESISTENCE
Choosing the right antihypertensive
Condition Preferred drugs Other drugs that can be Drugs to be
used avoided
Asthma CCBs a-blockers/ARB/Diuretics/ b-blockers
ACE-i
Diabetes a-blockers/ACE-i/ CCBs Diuretics/
mellitus ARB b-blockers
High a-blockers ACE-i/ARB/ CCB b-blockers/
cholesterol Diuretics
levels
Elderly CCBs -blockers/ACE-i/
patients ARB/- blockers
BPH - blockers b-blockers/ ACE-i/ ARB/
Diuretics/ CCBs
Antihypertensive: Side-effects and Contraindications
Class of drugs Main side-effects Contraindications/
Special Precautions
Diuretics (e.g. Electrolyte Hypersensitivity, Anuria
HCT) imbalance, level of
total and C-LDL,
glucose levels, UC,
↓C-HDL
b-blockers (e.g. Impotence, Hypersensitivity, Bradycardia,
atenolol) Bradycardia, fatique Conduction disturbances,
Diabetes, Asthma, Severe cardiac
failure
Antihypertensive: Side-effects and Contraindications
Class of drugs Main side-effects Contraindications/
Special Precautions
CCB (e.g. Pedal edema, Non-DHP CCBs (e.g diltiazem)–
Amlodipine, Headache Hypersensitivity, Bradycardia,
Diltiazem) Conduction disturbances, CHF, LV
dysfunction.
DHP CCBs–Hypersensitivity
a-blockers (e.g. Postural hypotension Hypersensitivity
Doxazosin)
ACE-inhibitors Cough, Hypertension, Hypersensitivity, Pregnancy,
(e.g. Lisinopril) Angioneurotic edema Bilateral renal artery stenosis
A-II RB Headache, Dizziness Hypersensitivity, Pregnancy,
Bilateral renal artery stenosis
Hypertensive Crises
Definitions:
Acute life-threatening increase in BP
Hypertensive urgency: severe
hypertension (usually SBP > 180 and DBP
> 120 mmHg) without acute target organ
damage (TOD)
Hypertensive emergency : severe HTN +
TOD
Pathogenesis
• Untreated essential hypertension
• Sudden withdrawal / non-adherence to
antihypertensive drug therapy
• Increase in sympathetic tone (stress, drugs)
• Renovascular hypertension, renal parenchymal
diseases, pheochromocytoma, or primary
hyperaldosteronism.
• Pressure damages vascular endothelium
• Platelets and fibrin activate
Clinical Manifestations
Encephalopathy
AMI/USA
Nephropathy
Aortic dissection
LV failure/cardiac decompensation
Eclampsia
Patient evaluation
Medical history
Physical examination
Laboratory evaluation
serum
urine
Medication profile
Drug use
Fundoscopy
EKG, CXR, head CT, echo
Laboratory evaluation
Urinalysis: protein, RBC, casts
Cardiac enzymes- CKMB, troponins
Electrolytes, BUN, creatinine
Toxicology screen
EKG, echo, angiography, X-ray
Thyroid, cortisol, BG
LFTs
Therapeutic approach
Time frame - consider risk level
BP goal
Urgency: gradual; DBP to 110 in 24-48 hours
Emergency: MAP < 20 to 25% in 1 to 2 hours
Drug selection
Route
Complications of rapid BP reduction in
severe hypertension
Widening neurologic deficits
Retinal ischemia: blindness
Acute myocardial infarction
Deteriorating renal function
Drug treatment of
hypertensive emergencies
Nitroprusside
Potent arterial and venous dilator
Onset seconds, duration 1-2 minutes
Immediate rebound
ADR:
coronary “steal”
cyanide toxicity
• Hepatic conversion to thiocyanate
• Less toxic
• Cleared renally
• Na thiosulfate antidote
ototoxicity, encephalopathy, seizures
Increase mortality post MI
May drop cerebral blood flow
May increase intracranial pressure
Recommended vs. toxic dose!
Approved dose max 10mcg/kg/min
Toxic at 4mcg/kg/min for 2-3 hrs
Protect from light
Nicardipine
Water soluble DHP CCB
IV infusion, titratable effects
As effective as nitroprusside
Onset 5-15min, dur 4-6h
Dose independent of pt wt (5-15mg/h)
Parenteral drugs for treatment of hypertensive emergencies
Parenteral drugs for treatment of hypertensive emergencies
Nifedipine
Given SL, absorbed PO
onset 5min, peak 30-60, duration 6h
direct arterial dilation, decrease PVR
unpredictable BP lowering
cerebral, renal, cardiac ischemia- fatal!
Elderly most prone to ADR
Do not use!
Oral agents
Limitation: slower onset of action and an inability to control
the degree of BP reduction.
May be useful when there is no rapid access to the
parenteral medications.
Nifedipine SL (10 mg) and captopril SL (25 mg) lower the
BP within 10 to 30 minutes in many patients.
Major risk with these drugs is ischemic symptoms (eg, AP,
MI, or stroke) due to an excessive and uncontrolled
hypotensive response.
Should be avoided if more controllable drugs are available.
Terima Kasih
