Hypertension Update Flashcards
HTN =
High BP defined as SBP >140 or DBP >90
Having been told at least 2 times by health care provider that one has HBP
PreHTN
Gray area of 120-139/80-89
Develops into HTN in 50% of population within 4 yrs
Should be monitored annually
Benefit of lowering BP
Reduction in incidence of stroke, MI, HF
Mechanisms for development of HTN
Complex interplay of individual’s heart and BP
Major Players: CNS, kidneys, Local endothelial factors, genetic, lifestyle
Pathophysiology
In some cases, the arteriolar constriction may be due to some secondary underlying disorder.
CNS and ANS regulate blood pressure through stimulation of alpha and beta receptors on the arterioles and venules.
Kidneys also provide humeral response to maintain blood pressure in the presence of decreased blood flow to the kidneys - results in the release of renin and its subsequent vasoconstrictors, angiotnesin and aldosterone.
Pathologic disruption in any of these systems can lead to hypertension.
Classification
Classification SBP DBP
Normal 160 OR >100
CVD Risk Factors
Hypertension*
Cigarette smoking
Obesity* (BMI >30 kg/m2)
Physical inactivity
Dyslipidemia*
Diabetes mellitus*
Microalbuminuria or estimated GFR <60 ml/min
Age (older than 55 for men, 65 for women)
Family history of premature CVD
(men under age 55 or women under age 65)
*components of metabolic syndrome
Factors that Increase Susceptibility to HTN
Age Ethnicity Less educated Lower socioeconomic status Cigarette smoking Sedentary lifestyle Obesity
Protective Factors Against HTN
Not smoking
Low-fat, low sodium diet
Genetics
Objectives for Eval of pts with Documented HTN
- Assess lifestyle and identify other CV risk factors or concomitant disorders that affects prognosis and guides treatment.
- Reveal identifiable causes of high BP.
- Assess the presence or absence of target organ damage and CVD.
Target Organ Damage
Heart Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart failure Brain Stroke or transient ischemic attack Chronic kidney disease Peripheral arterial disease Retinopathy
Symptoms of early HTN
May be asymptomatic
Blurred vision Chest pain Dizziness Dyspnea Fatigue Flushing Headaches Hematuria Muscle cramps Palpitations
Identifiable/secondary Causes of HTN
Sleep apnea Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushing’s syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease Gout Toxemia of Pregnancy
Drug-induced causes of HTN
Oral contraceptives Steroids NSAIDs Nasal decongestants/cold remedies Appetite Suppressants Sodium bicarbonate products (antacids) Licorice Tricyclic antidepressants Monamine oxidase inhibitors Cyclosporine Erythropoietin
Fam Hx
There is a higher incidence in children who exhibit other risk factors for cardiovascular disease or have hypertensive parents Ask Fam Hx of: Premature Coronary artery disease Peripheral vascular disease Diabetes mellitus Hypertension Stroke, TIA, or seizures Renal disease Dyslipidemia
Dietary History, especially Sodium Cholesterol Fat Alcohol use
Ambulatory BP Monitoring
ABPM is warranted for evaluation of “white-coat” HTN in the absence of target organ injury.
ABPM values are usually lower than clinic readings.
Awake, individuals with hypertension have an average BP of >135/85 mmHg and during sleep >120/75 mmHg.
BP drops by 10 to 20% during the night; if not, consider renal disease or LVH.
Self-Measurement of BP
Provides information on:
Response to antihypertensive therapy
Improving adherence with therapy
Evaluating white-coat HTN
Home measurement of >135/85 mmHg is generally considered to be hypertensive.
Home measurement devices should be checked regularly. Bring to office and compare with office BP measurement.
PE
Record height and weight –BMI!
Funduscopic examination
Examine neck - carotid bruits, distended veins, thyromegaly
Heart - increased rate, size, precordial heave, clicks, murmurs, arrhythmias, and S3 or S4
Abdomen - bruits, enlarged kidneys, masses, abnormal aortic pulsations
Extremities - decreased or absent pulses, bruits, or edema
Neurologic assessment
Labs
Routine Tests
Electrocardiogram
Urinalysis
Blood glucose, and hematocrit or complete blood count (CBC)
Comprehensive metabolic panel
Serum potassium, creatinine, or the corresponding estimated GFR
Lipid profile, after 9- to 12-hour fast, that includes high-density and low-density lipoprotein cholesterol, and triglycerides
Thyroid –stimulating hormone (TSH)
Optional Tests
Measurement of urinary albumin excretion or albumin/creatinine ratio
DD
Differentiate b/t Primary, Pseudo-, and Secondary HTN
PseudoHTN caused by faulty BP reading
Suspect secondary hypertension
Drug therapy ineffective
Elevate blood pressure < age 25 or >60 years
Associated symptoms are present
Goals of Tx
Reduce CVD and renal morbidity and mortality.
BP targets <130/80 in pts with CRD or DM
Lifestyle Modifications
Wt loss Adopt DASH eating plan Dietary Na reduction Physical activity Moderation of ETOH comsumption
Management for each classification
Normal: Lifestyle modification
PreHTN: Lifestyle modification. Only initiate meds if there is a compelling indication
Stage 1: Lifestyle mod. and initiate Thyazide-type diuretic. Consider ACE-I, ARB, BB, CCB
Stage 2: Lifestyle mod and 2 drug tx
Diuretics
Thiazides - hydrodiuril
Loop - Ethacrynic acid
Potassium-sparing agents: spironolactone
First-line therapy for systolic hypertension and essential hypertension
