cardio and renal Flashcards
staging and treatment of heart failure
- used to aid drug choice
- stage A: no evidence of CAD, no symptoms, no limitations to ADLs-ACE inhibitors or ARBS
- stage B: minimal CAD, mild symptoms, slight limitations to ADLs, comfortable at rest-ACE, beta blockers
- stage C: moderate/severe CAD, marked limitation on ADLs, comfortable only at rest-ACE, beta blockers, diuretic, digoxin
- stage D: severe CAD, severe limitations, symptoms even at rest-dubutamine, LVAD, transplant list, hospice
pharmacodynamics of ACE inhibitors
- decrease angiotensin II and aldosterone by decreasing angiotensinogen
- lowers vascular resistance without decreasing CO or GFR-no reflexive tachycardia
- increases o2 to heart muscle and reduces remodeling after MI
- improves insulin sensitivity or affect glucose metabolism
- doesn’t raise lipid levels
ACE on special pt groups
- Use with young Caucasians with angina, DM pts, or HF pts
- Not as effective on African Americans but if in combo with diuretic ethnicity doesn’t matter
- African and Asian Americans greater risk of angioedema
- category D-not to be used if pregnant
ADRs for ACE
- dry cough (more likely in older pt)
- angioedema
- decreased K+
- pancreatitis, renal failure
- rash
- orthostasis (within 1 hr of first dose)
pharmocodynamics of ARBs
- inhibits RAAS system by blocking angiotensin II receptors (on kidneys, brain, heart, and arterial wall)
- use in kidney dz-not renal protective unless late stage of renal failure
- an alternative to ACE inhibitors
- many combined with HCTZ
pharmacokinetics of ARBs
-extensive 1st pass-only
ADRs of ARBs
decreased BP, angioedema, increased K+, renal failure
- food doesn’t effect it
- cat D-don’t use in pregnancy
direct renin inhibitors-Alsikiren (Tekturna)
- works on RAAS system-blocks conversion of antiotensinogen to angiotensin I
- not same renal protective qualities
- cat D-don’t take during pregnancy
- high fat diet decreases absorption
- effect takes 2 weeks to be seen
- ADR: increased K+
pharmacodynamics of calcium channel blockers
-act as vasodilators by lowering Ca++ into smooth muscles
-2 classes: type 1 NDHP: diltiazem, verapamil-strong inotropic effect avoid using with HF pts
type 2 DHP: amlodipine, nicardipine
-DHP has no chronotropic effect
-NDHP: effects conduction through AV node and therefore decreases chronotropic effect and decreases HR
pharmacokinetics of calcium channel blockers
- metabolized by liver CYP450 3A4
- ADRs: contipation, dizziness, headache, edema, rash, gingival hyperplasia-encourage oral care
- using CCB with ACE decreases peripheral edema by 50% rather than increasing dose of CCB alone
- if pt has GERD-symptoms may be worse due to decrease of esophageal tone
- pt avoid NSAIDS, ETOH, alone in jacuzzi
- pregnancy cat C
Digoxin
- highly selective ATP inhibitor-leads to increased contractility (increased inotropy) and decreased chromotropy
- seruim concentrations> 1 mg/mL increase mortality (higher risk in women general)–initiate treatment at lowest dose
- best used for severe HF, enlarged hrt, 3rd heart tone, pt who have tried ACE and beta blockers
- steady state achieved in about 1 wk.
- not heavily metabolized–excreted unchanged by kidneys
- half-life 36-48 hrs
- drug interactions with amiodorone, diltiazem, verapamil
ADRs of digoxin
-GI: n/v/d, anorexia
CNS: fatigue, DPN
toxicity: yellow vision, green halos, hallucinations
cardiac: bradycardia d/t blocking AV junction
-needs to be monitored clinically and with labs (toxicity serum>2 mg/ml-consider giving K+)
arrhythmias
-caused by physiological/and or anatomical consequences to prevent normal cardiac action potential
normal HR
-depends on intrinsic electrical impulses initiated at SA node and conducted to AV node and over ventricles
absolute refractory period
-cell not depolarizing no matter how strong the stimuli
relative refractory period
-stronger than normal stimuli can induce depolariztion
refractoriness
- state of cell that determines polarization
- damaged cell could keep constant of refractions or none at all
spontaneous depolarizing cells
- AV and SA node
- purkinje fibers
automaticity
-ability of heart cell to depolarize and action potential
re-entry phenomena
- paroxysmal tachycardia d/t altered, enhanced,damaged cell, biochemical disturbances
- 2 types: anatomical and physiological impulses
- alternate pathways lead to firing upon itself possibly leading to vtach and SVT
class I antiarrhythmic drugs
sodium channel blockers (membrane stabilizing agents)
IA: lengthens duration of action potential; reduce rate of rapid firing, reduce speed of conduction by increasing effective refractory period; increase conduction rate at AV node; (i.e.procainamide, quinidine)
IB: shortens duration of action potential-eliminating unindirectional blocks but may trigger reentry arrhythmias; rapidly acts with Na+ channels-blocks active and inactive channels, does not affect automaticity of AV or SA node; reserved for severe vtach pts whom other drugs have not worked (i.e. lidocaine, phenytoin)
IC: no effect on action potential (or minimally); slowly acts with sodium channels (i.e. encainide, iorcanide)
class II antiarrhythmic drugs
beta blockers
- reduce andrenergic activity in hrt
- increase threshold and prolong effective refractory period–decrease hr and conduction velocity
- produce negative inotropic effect
- i.e. sotalol, metoprolol, propanolol
class III antiarrhythmic drugs
potassium channel blockers
- prolong effective refractory period by blocking potassium channels–decreases rate of automaticity of ventricular ectopic beats
- little effect on depolarization
- i.e. amiodarone, bretylium
class IV antiarrhythmic drugs
calcium channel blockers
- vasodilator lowering calcium influx into smooth muscle
i. e. verapamil, diltiazem, beptidil
