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62 Cards in this Set
- Front
- Back
Factors affecting blood pressure
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BP = [LVEDV - LVESV] * HR * SVR
How full is the heart at the end of diastole? How empty is the heart after systole? How fast is the heart beating? How much peripheral resistance is there? |
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Types of receptors affecting blood pressure
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Alpha 1
Alpha 2 Beta 1 Beta 2 Dopamine Vasopressin |
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Alpha 1 receptors: Locations and effects
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Locations: peripheral and splanchnic vasculature.
Action: causes vasoconstriction |
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Alpha 2 receptors: Locations and effects
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Location: Peripheral and splanchnic vasculature, CNS.
Action: causes vascular constriction, roles in pain and sedation. *Pre-synaptic receptors cause negative feedback: next stimulation will not be as strong. |
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Beta 1 receptors: Locations and effects
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Location: cardiac tissue, peripheral vasculature.
Action: Inotropic, chronotropic, lusitropic effects on cardiac tissue. Vasodilation in peripheral vasculature. *presynaptic receptors cause positive feedback. |
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Beta 2 receptors: Locations and effects
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Location: Cardiac tissue, peripheral vasculature, bronchial smooth muscle.
Effects: Inotropic, chronotropic, lusitropic effects in cardiac tissue (same as B1). Vasodilation in peripheral vasculature. Relaxation/dilation in bronchial smooth muscle. |
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B1/B2 receptor ratio in the heart (normal and in chronic CHF)
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Normally B1:B2 is 4-6:1.
In chronic CHF, receptors are downregulated by epi stimulation. CHF ratio is 1-1.5:1 |
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Dopamine receptors: Locations and effects
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Locations: cardiac tissue (2 types), peripheral vasculature, splanchnic vasculature, renal, CNS.
Actions: Inotropic and chronotropic effects in the heart. Vasodilation in splanchnic vasculature (improves renal blood flow). Growing use in neurology, fading in CV. |
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Vasopressin receptors: Locations and effects
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Locations: peripheral vasculature, splanchnic vasculature.
Action: MARKED vasoconstriction. |
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Stereotypic effects of receptors: alpha, beta, DA, Vasopressin
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Alpha receptors: cause vasoconstriction (increase afterload)
Beta receptors: increase inotropy, chronotropy, vasodilation, bronchodilation. DA receptors: Splanchnic/renal vasodilation. Vasopressin receptors: vasoconstriction. |
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Beta adrenergic receptor complex: basic mechanism.
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Epi or adrenaline stimulates the receptor (usually a G-protein receptor). The receptor is coupled with adenylyl cyclase, which converts ATP into cAMP. cAMP is the biggest intracellular mediator (signal). cAMP causes phosphorylation of calcium channel. Next time a stimulation comes, Ca enters and interacts with SR - causes Ca release that interacts with actin and myosin (muscle contraction).
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Affecting LVEDV
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LVEDV: preload, or how full the heart gets before it contracts.
Treatment: Fluids (major), alpha agonists (minor). |
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Affecting LVESV
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LVESV: Afterload (how empty the heart gets after systole) and contractility (ability of the heart to pump against pressure).
Treatment: Affect afterload with vasodilators, ACE inhibitors, nitroprusside, PDE inhibitors. Affect contractility with inotropes, B adrenergic agents, PDE inhibitors. |
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Affecting HR
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Heart rate = chronotropy = pulse.
Treatment: chronotropes (b adrenergic agents, atropine, pacemaker) |
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Affecting SVR
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SVR: systemic vascular resistance.
Treatment: vasoconstrictors (alpha adrenergic agents) |
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Cardiovascular drugs
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Epinephrine
Dobutamine Norepinephrine Phenylephrine Dopamine Vasopressin Phosphodiesterase inhibitors |
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Epinephrine
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Adrenaline: "God's inotrope"
B effects at low doses. A effects at high doses. Inotopic and chronotropic. Indications: sepsis, cardiogenic shock, post-CABG (coronary artery bypass graft). |
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Dobutamine
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Inotrope, chronotrope, vasodilating effects. Increases contractility and heart rate. Vasodilates, reduces afterload.
B effects. Indications: acute MI, mild cardiogenic shock. |
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Norepinephrine
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Levophed: "God's pressor."
POTENT VASOCONSTRICTOR A effects predominate. B effects are present (maintain contractility against more afterload) Vasoconstriction and increased SVR. Indications: sepsis, distributive shock with good CO. |
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Phenylephrine (Neosynephrine)
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Pure alpha agonist.
Vasoconstriction and increased SVR. Indications: Mild sepsis, hypotension with good CO. |
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Dopamine (Intropin)
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Dose dependent:
B effects at low doses A effects at high doses Not used much. |
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Vasopressin (Pitressin)
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Intense vasocontriction though vasopressin receptors.
Non-adrenergic, no direct cardiac effects. Beware: splanchnic vasoconstriction and ischemia. Indications: raise MAP during cardiac arrest, ACLS, severe shock, CABG (on ACEI) |
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Phosphodiesterase inhibitors (PDEI)
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Milrinone & amrinone
Vasodilators and inotropes Augments B adrenergic stimulation, causes smooth muscle relaxation (hypotension). Indications: CABG, vasoconstricted with low CO. |
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Drugs that act on alpha receptors
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NE, phenylephrine, epi, DA
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Drugs that act on beta receptors
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Isoprotenerol, Epi, Dobutamine, Norepi, DA, Dopexamine
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Drugs that act on PDE
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Milrinone,amrinone: PDE inhibitors
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General drug classes for the treatment of hypertension
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Diuretics
Beta blockers ACE inhibitors Calcium channel blockers Vasodilators Centrally acting agents |
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Diuretics: 3 types and mechanism of action
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Thiazide diuretics: inhibit Na+ absorption at distal tubule
Loop diuretics: Inhibit Na/Cl absorption at ascending loop of Henle Potassium sparing diuretics: K+ exchange at distant renal tubule (inhibit aldosterone) |
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Thiazide diuretics: drugs
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Hydrochlorothiazide (HCTZ)
Chlorthalidone (Hygroton) Metolazone (Zaroxolyn) Indapamide (Lozol) |
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Thiazide diuretics: dosing and indications
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Oral agents, taken 1/day, good for long term management of HTN. Takes 1-2 hours before effects are seen (urine output increases).
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Thiazide diuretics: Side effects.
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Electrolyte wasting
(ESPECIALLY potassium, magnesium), sodium. Hyperglycemia Gout Dehydration RASH (due to sulfur) HCTZ overdose: electrolyte wasting without any more blood volume reduction (>25mg). |
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Hydrochlorothiazide
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HCTZ
Most commonly used Thiazide diuretic |
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Loop diuretics: drugs
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Furosemide (Lasix)
Bumetanide (Bumex) Torsemide (Demadex) Ethacrynic acid (Edecrin) |
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Loop diuretics: dosing and indications
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Taken 3x/day - for patients with decompensated heart failure, compromised renal function (works higher in the nephron). Duration: 4-6 hours. Onset: 30 minutes - use these when you want to get fluid off in a hurry.
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Loop diuretics: side effects
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Electrolyte wasting (ESPECIALLY potassium, magnesium), sodium
Hyperglycemia Gout Dehydration Rash ***ALL GIVE RASH EXCEPT ETHACRYNIC ACID (no sulfur moiety) |
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Furosemide
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Lasix
Gold Standard of Loop Diuretics |
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Potassium sparing diuretics: drugs
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Spirinolactone (Aldactone)
Eplerenon (Inspra) Triamterene Amiloride |
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Potassium sparing diuretics: usage and indications
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Dosing: given 1x/day. Slow onset of action (hours-days) because you're inhibiting a hormone (aldosterone). Duration is about 1 day.
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Potassium sparing diuretics: Side effects
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Hyperkalemia
***Spirinolactone causes gynecomastia |
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ACE inhibitors and ARB's: mechanism of action
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Hypertension drugs
ACE inhibitors block angiotensin-converting enzyme (which converts aI to aII). ARB's block angiotensin II receptors. |
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ACE inhibitors and ARB's: side effects
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Both ACEI and ARB's cause hyperkalemia, increased serum creatinine, acute renal failure, angioedema. CONTRAINDICATED FOR PREGNANCY.
ACE inhibitors also cause a buildup of bradykinins in the lungs (due to ACE inhibition) and cause irritation and cough. |
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ACE inhibitors: Drugs
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Captopril (Capoten)
Enalapril (Vasotec) Lisinopril (Zestril, Privinil) Ramipril (Altace) Benazepril (Lotensin) |
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Enalapril
Lisinopril |
Hypertension drugs, ACEI's. Most commonly used, tested, trusted.
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ACEI's: dosage and indications
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Captopril is given 3 times per day, onset 15 minutes, duration 6 hours. Best for inpatients.
Enalapril, Lisonopril, Ramipril, Benazepril are given 1x/day, onset 1 hour, duration 24 hours, best for otupatients. |
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ARB's: Drugs
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Losartan (Cozaar)
Valsartan (Diovan) Irbesartan (Avapro) Candesartan (Atacand) Olmesartan (Benicar) Telmisartan (Micardis) |
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ARB's: dosage and indications
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Given 1x/day. Onset 1-2 hours, duration 24 hours.
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Beta blockers: drugs
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Atenolol (Tenormin)
Metaprolol (Lopressor, Toprol XL) Propanolol (Inderal, Inderal LA) Labetalol (Trandate, Normodyne) Carvedilol (Coreg) |
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Side effects of beta blockers
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CNS: Drowsiness, lethargy, confusion (Higher lipid solubility = more CNS side effects)
Bronchoreactive events (those that also work on B2 receptors) AV nodal blockade |
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Atenolol
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Beta blocker
Low lipid solubility B1 selective |
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Beta blockers: B1 selective vs non-selective drugs
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B1 receptors are located on the heart. B2 receptors are located peripherally in vessels and lungs. Selective B1 blockers are cardioselective and do not have pulmonary effects (such as bronchospasm).
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Beta blockers: mechanism of action
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By blocking beta receptors, they cause decreased HR, contractility, and CO. They also block renin release from the kidney and indirectly lower BP.
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Metaprolol
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Beta blocker
Moderate lipid solubility B1 selective |
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Propanolol
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Beta blocker
High lipid solubility (so CNS side effects are higher) NOT B1 selective - DO NOT GIVE TO A PERSON WITH ASTHMA. |
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Labetalol, Carvedilol
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Beta blockers.
Moderate lipid solubility Block A1, B1, and B2 receptors. So they decrease CO and also inhibit vasoconstriction. |
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Calcium channel blockers: drugs
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Verapamil
Diltiazem Nifedipine Nicardipine Isradipine Nisoldipine |
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Calcium channel blockers: mechanism of action
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For control of HTN.
These drugs decrease Cardiac contractility, heart rate, and peripheral vascular resistance. |
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Calcium channel blockers: Tissue specificity
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Vasodilators: block dihydropyridine channels (all end in -pine), cause reflex tachycardia.
Nifedipine Nicardipine Isradipine Nisoldipine Felodipine Amlodipine Negative inotropes and chronotropes: verapamil, diltiazem. **Diltazem works on both. |
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Best calcium channel blocker drugs
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Amlodipine - due to long duration of action
Diltiazem - both vasodilator and negative inotrope/chronotrope |
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HTN drugs: Peripheral A1 receptor blockers
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Terazosin, Doxazosin, Prazosin. Cause inhbition of vasoconstriction. Reserved for males with benign prostatic hypertrophy. INCREASE in cardiac events when used as the only therapy.
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HTN drugs: Peripheral A2 receptor agonists
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Clonidine, methyldopa. Cause increased vasodilation. Use as add-on therapy with a diuretic.
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HTN drugs: Vasodilators
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Hydralazine, Minoxidil. Cause major blood pressure decreases. Bad side effect profiles. Use with diuretic and beta blocker to counteract compensatory changes.
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Drugs that cause refractory hypertension
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NSAIDs, COX 2 inhibitors
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