Question | Answer |
Prevelance of cardiovascular disease | 33% without or 66% with perhypertensives |
Effects of htn | kidney failure, stroke, heart failure, or any end organ failure |
secondary htn | from underlying curable disease; primary hyperaldosteronism, renal vascular stenosis, pheochromocytoma; can be cured |
essential htn | unknown cause; lifestyle contributions - obesity, sedentary, diet high in Na and fat; only controlled but no cure; goal is control of htn |
Risk factors of primary htn | older male, AA women before and after menopause, menopausal women |
Normal bp | Less than 80 dbp
Less than 120 sbp |
prehypertension | 80-89 dbp
120-139 sbp |
stage 1 | 90-99 dbp
140-159 sbp |
stage 2 | greater than or equal to 100 dbp
greater than or equal to 160 sbp |
Risk doubles with each | 20mmHg increase sbp
10mmHg increase dbp |
Goal bp | different based on patient population |
goal if tolerated | <140/<90 |
goal in diabetics | <130/<80 |
goal in cardiac failure | <130/<85 |
goal in renal failure | <130/<85 |
goal in renal failure with proteinuria >1.0 g/24hr | <125/<75 |
bp reduction of 2mmHg = | reduces risk up to 10% in stroke and 7% in CHD |
normal bmi | less than 25 kg/m2 |
DASH eating plan
Dietary approach to stop htn | reduces bp 8-14mmHg |
Dietary intake suggestions | decrease alcohol; increase fruit, mg2, k, ca, vegetables, whole grains, fish, nuts, poultry |
DASH restrictions | Low salt, low fat dairy, reduced red meat, sugar, fat, and choleserol |
Systems affecting blood pressure | Volume, CNS, PNS, renal, cardiac, adrenal, vasodilators, vasoconstrictors |
Mean arterial pressure = | CO x TPR |
Cardiac output = | stroke volume x heart rate |
TPR = | vascular structure + vascular tone + blood volume |
Baroreflex | Aortic depressor nerve in aortic arch and carotid tells brain either to release or not release NE based on blood pressure |
Renal mechanisms | secretion of renin in glomerulous and the formation of angiotensin II |
Non-renal mechanisms | Baroreflex and hormone system (NO vs endothelium) |
Malignant hypertension cycle | |
Classification of htn drugs | diuretics, agents affecting adrenergic function, vasodilators, RAAS agents |
Thiazides | work on descending loop where 67% of water reabsorption takes place; lose potassium |
Loop diuretics | potassium wasting; work on ascending loop and renal tubule |
Potassium sparing | want to combing these with thiazides to not only increase water excretion but also prevent some of the potassium loss from the thiazides |
Agents affecting adrenergic function | reserpine, guanethedine, guanadrel; prevent release of NE to vasculature or heart |
Reserpine | Depletes neurotransmitter in nerve endings by flushing NE out of intraneuronal vesicles and replacing it with itself which is released instead |
Reserpine effects | Depresses sympathetic function peripherally and centrally; decrease HR, contractility, PVR; depression, insomnia, nightmares, diarrhea, cramps, orthostatic hypotension, dry mouth, impotence |
Guanethedine | Depletes NE from nerve vesicles peripherally only and not centrally but still have orthostatic hypotension |
Guanadrel | Depletes NE from nerve vesicles peripherally; less orthostatic hypotension, diarrhea, and impotence than guanethadine |
Prazosin | A1 blocker used in combination with diuretic and B-blocker; good for lipid profile |
1st dose phenomenon | first time you take A1 blocker it drops blood pressure severely; patient should take half dose for first week |
Prazosin adverse effects | 1st dose phenomenon, fluid retention, dizziness, headache |
Non-selective beta blockers | b1 and b2 |
Intrinsic beta blocker | block betas but stimulate alphas; maintain some sympathetic tone |
cardio-selective beta blockers | b1 blocker |
effects of blocking b1 | decrease renin release, contractility, and heart rate |
beta blocker risks | asthma, a/v block if taking calcium channel blockers |
Propranolol | b1 and b2 blocker |
Labetolol | b1 and b2 blocker; a1 activator; can be given IV |
A2 receptor location | presynaptic terminals; part of negative feedback mechanism; a2 is located peripherally on vasculature |
A2 presynaptic effects | NE binds to them and inhibits future NE release |
Clonidine | A2 agonist; work on presynaptic receptors; can cause rebound hypertension when you stop taking it suddenly (opposite of first dose phenomenon); limited use because of sedation and CNS effects |
Calcium channel blockers | reduce intracellular calcium concentration-relaxing arteriolar smooth muscle-reducing PVR |
Potassium channel openers | hyperpolarize the heart-increasing refractory period and reducing heart rate; hyperpolarize smooth muscle cells in vessels preventing contraction; reflex tach, Na and fluid retention |
Direct acting vasodilators | Nitric oxide donors |
2 groups of calcium channel blockers | phenylalkylamines and benzothiazepines-block vasculature and heart-no reflex tach but promote fluid retention; dihydropyridines-block vascular calcium channels |
Nifedipine | dihydropyridine; main side effect is reflex tachycardia |
Verapamil | phenylalkylamine; ccb on vasculature and heart; no reflex tach |
Diltiazem | benzothiazepine; ccb on vasculature and heart; no reflex tach |
Minoxidil | K channel opener; hirsutism (hair growth) is side effect |
Diazoxide IV | K channel opener; for hypertensive emergency |
Pinacidil | K channel opener |
Sodium nitroprusside | Nitric oxide donor; direct acting vasodilator; side effect is cyanide poisoning and reflex tachycardia; used for hypertensive emergency |
Hydralazine | direct acting vasodilator; reflex tachycardia |
2 types of agents affecting RAS | angiotension converting enzyme inhibitors; angiotensin II receptor blockers |
Captopril | ACE inhibitor |
Enalapril | ACE inhibitor |
Lisinopril | ACE inhibitor |
Losartan | Ang II receptor blocker |
Valsartan | Ang II receptor blocker |
Irbesartan | Ang II receptor blocker |
Ramipril | ACE inhibitor |
Aliskiren | Renin inhibitor; dont have to remember this one |
Clinically important consequence of htn | Damages large and small vessels, leads to left-ventricular hypertrophy, and end organ damage |
First medications tried for hypertension | diuretics |
How does RAS work? | Kidney releases renin-converts angiotensinogen from liver into angio I (inactive)-converted in lung by ACE to angio II (vasoconstrictor) increases sympathetic drive, Na reabsorption, aldosterone release, vasopressin (ADH) release |
3 ways to block angiotensin II | block renin secretion; block conversion of ang I to ang II; block ang II receptor |
effects of ACE | converts ang I to ang II; breaks down bradykinin (too much makes you cough) |
side effects of ACE inhibitor | dry cough due to accumulation of bradykinin; hyperkalemia |
side effects of ARBs | hyperkalemia because of reduced aldosterone; but no cough because ACE is still free to break down bradykinin |
effects of renin inhibitors | binds to renin and blocks its activity so there is no conversion of angiotensinogen to ang I |
side effects of renin inhibitors | hyperkalemia; hypotension; fluid retention (angiodema) |