Hyper/Hypotension (Cardio 1) Flashcards
What is the prevalence of HTN in adults?
30%, 58-65 million people
What co-morbidities are associated with HTN?
- coronary artery dz
- left ventricular hypertrophy
- ischemic stroke
- chronic kidney dz
- DM
- peripheral artery dz
Patient Barriers to Effective HTN Tx
- lack of health insurance or regular provider
- nonadherence to therapy: medication cost, complicated regimen, side effects, lack of support, poor physician communication
- advanced age or obesity
Systole
phase of cardiac cycle when ventricles contract
Diastole
phase of cardiac cycle when ventricles relax
Systolic Pressure
maximum arterial pressure during ventricular contraction
Diastolic Pressure
point of lowest arterial pressure
What 2 things determine arterial pressure?
- cardiac output
- peripheral resistance
Cardiac Output
CO = HR + stroke volume
What determines/influences peripheral resistance?
- vascular structure
- vascular function
Normal BP
less than 120/80
Pre-HTN
systolic 120-139
diastolic 80-89
HTN:
- Stage 1
- Stage 2
- systolic 140-159, diastolic 90-99
2. sys 160+, dias 100+
JNC 8 Goal BP Levels
- age 60+: goal < 150/90 (if you’re 60, you can have 150)
2. less than 60 yo: goal < 140/90
Pheochromocytoma
- 5 Ps: pressure, pain, perspiration, palpitation, pallor
- 2% of people with secondary HTN
- paroxysmal secretion of epinephrine, norepi by adrenal or remote tumor
What are some secondary causes of HTN?
- ENDOCRINE: Cushing’s, primary aldosteronism, congenital adrenal hyperplasia, hyper or hypothyroid
- RENAL: renovascular dz, pre-eclampsia
- MECHANICAL: coarctation of aorta, A/V fistula
- MEDICINE: stimulants, corticosteroids, SSRIs, oral contraceptives
White Coat HTN
- falsely elevated BP in clinical setting
- 20-25% of pts will have false, mild elevation of pressure
Malignant HTN
- SBP > 180, DBP > 120
- most often w/ long standing, uncontrolled HTN
- multiple other causes
- can lead to HTN encephalopathy
- risk for seizures/coma if not treated
Reversible/Modifiable Risk Factors for HTN
- smoking
- excessive ETOH intake
- physical inactivity
- renal dz
- obesity (BMI >30)
- dyslipidemia
- DM
Non-reversible Risk Factors for HTN
- age
- family hx: premature CVD in men <65
- race
Metabolic Syndrome
-abdominal obesity: waist >40 inches men, >35 women
-fasting glucose > 110
-BP > 130/85
-triglycerides > 150
-HDL < 40 in men, < 50 in women
++3 or more of these make dx –> increased risk of developing HTN, CVD
Clinical Presentation HTN
- often no specific sxs
- neurological sxs: headache, dizziness, palpitations, fatigue, impotence
- vascular sxs: epistaxis, hematuria, metrorrhagia, blurred vision, weakness, angina
History Pertinent to HTN
- onset and duration of sxs
- past MHx: consider potential target organs affected
- past surgical hx
- family hx of HTN or CVD
- social hx: alcohol, tobacco, caffeine, diet, drugs, exercise
Pertinent Physical Exam Findings in HTN
- Cushingoid appearance (moon face, hirsutism, abdominal/trunk obesity)
- fundoscopy (eye vessels)
- CV exam: displacement of PMI, S3 or S4, carotid bruits
- ab: renal artery bruits, palpation for enlarged kidneys
- peripheral vascular: equality of peripheral pulses, femoral artery bruits
Lab Work Up for HTN
- CBC: anemia, polycythemia
- serum potassium: r/o hyperkalemia
- BUN and creatinine: assess renal fx
- calcium and phosphate (parathyroid dz)
- fasting glucose: DM screen
- fasting lipid profile: assess risk of arteriosclerosis
- TSH
- urinalysis with microscopic UA: protein, blood, glucose
- chest x ray: cardiomegaly
- EKG: evidence of MI, LVH, dysrhythmia
HTN End Organ Damage: Brain
- stoke
- TIA, reversible ischemic neurological deficit
Papilledema
optic nerve swelling
A/V Nicking
compression of retinal veins
Cotton Wool Spots
ischemic regions of retina
HTN End Organ Damage: Eye
- retinopathy
- papilledema: optic nerve swelling
- A/V nicking: compression of retinal veins
- hemorrhage
- exudates: lipid deposits after hemorrhage
- cotton wool spots: ischemic regions of retina
HTN End Organ Damage: LVH
- S4 heart sound = stiff ventricle
- cardiomegaly
- EKG changes: R wave of aVL > 11 mm; S wave of V1 or V2 + R wave of V5 or V6 > 35 mm
HTN End Organ Damage: Kidney
- proteinuria
- renal insufficiency
Peripheral Arterial Dz
- hair loss on legs
- diminished peripheral pulses
- cool extremities
- sluggish cap refill (> 3 secs)
Non-Pharmacological Management of HTN
- lower BP, enhance efficacy of HTN meds
- weight reduction (BMI 18-25)
- diet: DASH (potassium, calcium, fruits, veggies) or low sodium diet (1600mg/day)
- exercise: 30 mins/day
- reduce EtOH intake (1-2 servings/day)
Postural/Orthostatic Hypotension
- significant drop in arterial BP with position change
- represents a defect in vasomotor reflexes
- frequent cause of syncope in elderly
- prominent feature in many ANS disorders
Autonomic NS Disorders that can Cause Orthostatic Hypotension
- multiple sclerosis
- Parkinson’s
- peripheral neuropathy
- Raynaud’s
- reflex sympathetic dystrophy
Causes of Orthostatic Hypotension
- drugs (antihypertensives, antidepressants, vasodilators)
- physical deconditioning
- sympathectomy
- decreased blood volume: GI bleed, dehydration, adrenal insufficiency
- idiopathic/familial postural hypotension
- advanced age
Dx of Orthostatic Hypotension
- measure BP and HR from supine to sitting to standing
- wait 2 mins btw position changes
- SUSTAINED drop of SBP > 20 or DBP > 10
- absence of compensatory HR increase (15 bpm) suggests neurogenic etiology
- compensatory HR increase suggests non-neurogenic
Management of Orthostatic Hypotension
- reduce/eliminate offending drugs
- caution pt on position changes
- elevate head of bed
- compression stockings
- some pts require high sodium diet
- may require drug therapy
