Week 3 (Hypertension, Hypertrophy and Heart Failure) Flashcards
(136 cards)
Mechanisms of regulation of blood pressure
Renal
Hormonal
Neural
Vascular
Initial evaluation of patient with hypertension
1) Accurately stage BP
2) Assess overall cardiovascular risk
3) Seek clues for rare secondary causes
Staging BP
Normal: <120/80
Prehypertension: <140/90 (2x as likely to progress to HTN, but not known if treating this helps morbidity/mortality)
Stage 1 hypertension: <160/100
Stage 2 hypertension: >160/100
When do you take additional BP measurements?
Take 2nd measurement if clinic BP >140/90
Take 3rd measurement if BPs differ
Record lower of last 2 as clinic BP
White coat reaction
White coat (office-only) HTN: BP is only high in doctor’s office but otherwise completely normal in daily life
White coat aggravation: BP higher in doctor’s office but still not normal in daily life (alerting reaction superimposed on fixed HTN)
Masked HTN
BP is only normal in doctor’s office, masking the diagnosis of hypertension
This happens if stress of daily life (but more relaxed in doctor’s office)
Normative cutoff values for 24 hour ambulatory BP monitor
Awake average: <135/85
24 hour average: <130/80
Sleep BP: <120/70
Home BP measurement
Measure BP in AM and PM daily x 7 days (though 4 is probably fine)
Discard first day’s BPs and average all the rest
Normative cutoff value <135/85
Isolated systolic hypertension
Systolic >140
Diastolic <90 (normal)
This is the kind of HTN people over 50 have
Primary fault is decreased distensibility of large arteries (aorta stiff) because collagen replaces elastin in elastic lamina of aorta, which is age-dependent process accelerated by atherosclerosis and HTN
Cardiovascular risk here is related to pulsatility, repetitive pounding of blood vessels with each cardiac cycle and more rapid return of arterial pulse wave from periphery, both causing more systolic HTN
Higher risk for fatal MI than combined sys/diast HTN
Overall cardiovascular risk of HTN
Severity of HTN
Target organ damage from HTN
Other CV risk factors (age, family hx premature heart disease, dyslipidemia, DM, CKD, cigarette smoking, obesity, physical inactivity, dietary sodium)
HTN target organ disease
Neuro: stroke, TIA, dementia, retinopathy
Cardiac: atrial fibrilation, heart failure
Renal: CKD
Vascular: angina, MI, coronary revascularization, aortic aneurysm, peripheral vascular disease (PVD)
Hypertension physical exam
Neurologic exam
Fundoscopy
Neck: palpation and auscultation of carotids, thyroid
Lungs: rhonchi, rales
Heart: size, rhythm, sounds
Accurate BP measurement
Abdomen: renal masses, bruits over aorta or renal arteries, femoral pulses
Extremities: peripheral pulses, edema
Hypertension standard labs
Blood chemistries: electrolytes, serum creatinine, glucose, lipid profile
Spot urinalysis: albumin
ECG: left ventricular hypertrophy (uncontrolled HTN), atrial fib, coronary disease
Hypertensive emergency vs. urgency
Both are BP >160/100
Hypertensive urgency: stable or no target organ damage –> give oral Rx in ER and clinic appt 72h later
Hypertensive emergency: rapidly progressive target organ damage (aortic dissection, post-CABG hypertension, acute MI, unstable angina, eclampsia, head trauma, body burns, postop bleeding from vascular suture lines) –> parenteral Rx, admit to ICU for hemodynamic monitoring and IV therapy
Multi-factorial causes of primary HTN
Genetics: cell membrane alteration
Obesity: insulin
Endothelial factors: structural changes effect RAAS
Stress: activation of SNS
Diet: sodium retention causes increased fluid volume
Kidney disease: sodium retention causes increased fluid volume
Treatment of primary vs. secondary HTN
Primary HTN can be managed with medication but not cured
Secondary HTN, if diagnosed, can lead to definitive cure
Secondary HTN
RAAS:
CKD: elevated serum creatinine or abnormal UA
Renovascular HTN: elevated serum creatinine (esp after ACEI or ARB), refractory HTN, flash pulmonary edema, abdominal bruit
Coarctation of aorta: arm pulses > leg pulses, arm BP > leg BP, chest bruits, rib notching on CXR
Primary hyperaldosteronism: hypokalemia, refractory HTN
Other mineralcorticoid excess (Cushing’s where cortisol stim aldosterone receptor): truncal obesity, purple striae, muscle weakness
NSAIDs: block renal prostaglandins, causing salt-dependent HTN in some patients
SNS:
Pheochromocytoma: spells of tachycardia, headache, diaphoresis, pallor and anxiety = paroxysmal HTN, pain in the head, palpitations, pallor, perspiration (check metanephrine and normetanephrine, adrenal CT)
OSA: loud snoring, daytime somnolence, obesity (do sleep study)
Other: sympathomimetics, cyclosporine A, baroreflex failure, thyroid disease
Combined systolic and diastolic hypertension
Both systolic and diastolic BP elevated (>140/90)
More common in those under age 50
Main fault is vasoconstriction at level of resistance arterioles
Hypertension in African Americans
HTN more common in AAs (1/3 compared to 1/4 or 1/5 in whites/Mexicans), even those with access to healthcare
This is definitely a problem of environment since Africans in Africa do not have increased rates of HTN (remember salt-retention theory of slaves coming to US from Africa)
Starts at a younger age
More severe
More target organ damage
High-risk hypertensive patients
Diabetes
CKD
Established CAD (secondary prevention)
Atherosclerotic disease of other arteries: carotids (bruits), abdominals (aneurysm), peripheral artery disease (PAD)
High risk for CAD (primary prevention)
Heart failure
What do diuretics do?
Diuretics increase renal Na+ excretion (“natriuresis”) which leads to negative Na+ balance
Patients have natriuresis (excretion of salt) for about a week, then get to new steady state where Na input = Na output, but this is at a lower body volume (weight) than before diuretic
Factors that limit natriuresis and counteract diuretic induced volume depletion
Increase AT II and NE stimulates proimal Na+ reabsorption and passive H2O reabsorption
Increase aldosterone which increases collecting duct Na+ reabsorption
Increase ADH stimulates H2O reabsorption at collecting tubule
Counter-regulatory responses limit Na+ wasting induced by fixed diuretic does
All net Na+ losses occur within the first week on fixed dose of diuretic and dietary salt intake
Carbonic anhydrase inhibitors
Acetazolamide
Absorbed orally, excreted by kidney
Acts on PCT to inhibit NaHCO3 reabsorption (so you excrete more HCO3)
Mimics RTA type 2 because inhibits reabsorption of HCO3
By increasing distal Na+ and HCO3- delivery, K+ secretion increased –> hypokalemia
CA inhibitors are “weak” diuretics because Na+ absorption occurs along more distal portions of nephron to “pick up the slack”
Specific uses of CA inhibitors: refractory metabolic alkalosis esp if volume overload and CO2 retention needs to be avoided (because furosemide alone worsens metabolic alkalosis but CA inhibitor induces metabolic acidosis), prophylaxis/tx of high altitude sickness, alkalinization of urine, glaucoma
Don’t give if GFR <10 or liver failure (disruption of urea cycle) or metabolic acidosis (because not much HCO3 filtered, so won’t work well)
Loop diuretics
Bumetanide, furosemide (short-acting), torsemide (long-acting), ethacrynic acid
Block Na/K/2Cl co-transporter in TALH
Used in edematous states (CHF, cirrhosis, nephrotic syndrome), HTN (esp in setting of CKD or high Na+ retention states), relative hypervolemic hyponatremia (because can’t reabsorb water), SIADH hyponatremia, hypercalcemia (prevents reabsorption of Ca2+!)
Increased distal delivery of Na+ –> hypokalemia and metabolic alkalosis
Reduced NaCl reabsorption in TALH leads to reduction in medullary tonicity –> suboptimal free water reabsorption at collecting duct
Adverse effects: volume depletion, volume depletion-mediated AKI (esp with ACEI, ARB, NSAIDs), hypokalemia, hypomagnesemia, metabolic alkalosis, ototoxicity, glucose intolerance with hypokalemia (because need K+ in order to allow insulin to bring glucose into cells)
Excreted in kidney via organic anion transporter into lumen
Effective with reduced GFR