CV drugs Flashcards
2 main causes of arrhthmias
- abberant pulse generations
2. defection in conduction system
what is cardiac output
SV x HR
what determines CO (3)
- preload
- afterload
- contractility
3 major determinants of myocardial O2 demand
- HR
- contractility
- ventricular wall stess
what is formula for ABP
HRxSVxTPR
2 ways Ca is involved in contraction
- influx from channels in sarcolemma
2. release of intracellular Ca from sarco reticulum
pathway of vasocontriction
depolarization>Ca in>activates calmodulin>activates MLCK>binds with actin
pathway of vasodilation
bind to GCPR>activate guanylate cyclase>cGMP>activates PKA>phosphoylates MLCphosphotase>no action
2 targets for hypertension
- CO
2. peripheral resistance
3 aspects of hypertension
- inceased vascular tone
- increase resistance
- lower venous capacitance
(see chart)
classes of antihypertensives
- diuretics
- B blockers
- ACEi
- ARBs
- Ca channel blockers
- vasodilators
4 diuretics in order of use and mechanism
- thiazides - Na/Cl inhibition
- loops - Na/K/2Cl inhibition
- spironolatone - aldosterone antag
- amiloride - Na channel antag
2 antihypertensive functions of B-blockers
- lower HR/contractility
2. lower renin
how do ACEi help (2)
- inhib. Ang2 which is a vasoconstrictor
2. less Na retention by blocking aldo
how do ARBs help
same as ACE, but by blocking the Ang2 receptor
how do CCBs work
inhibit Ca influx for heart can’t contract and smooth muscle can’t constrict
other effects of CCBs (2)
- dilate coronary arteries, which improves flow
2. cardiac myocyte decreased action
3 binding site of Ca channel and drug that work on them
N - nifedipine
D - diltiazem
V - verapamil
which has less heart action and most vasculr
N - nifidepine
what is sodium nitroprusside
liberates NO which dilates both Art and veins
- stimulates RAAS
2 actions of NO
- activates guanylate cyclase> cGMP>MLCphosphoatse
2. activates Ca dependent K channel which hyperpolarizes the cells - less active
what is angina pectoris
sudden sever crushing pain due to heart iscemia due to increased heart demand or supply of oxygen
how to help angina
lower o2 demand via BP, venous return, HR, contractility
3 agents for angina
- nitrates
- B blocker
- CCBs
what do nitrates predominantly dilate
venous system
pathway of nitrate actions
venous dilation>less R heart blood>lower EDP in vents>less preload>less O2 demand
nitrates for chronic and acute angina
acute: nitroglycerine under the tongue
chronic: isosorbide dinitrate or patch – longer half-life
nitrate limitations
- tolerance to antianginal effects
- many contraindications
2 aspects of heart failure
- can’t fill heart
2. can’t pump blood out
2 types of congestive heart failure
- pulmonary congestion - Left heart failure
2. peripheral edema - Right heart failure
best treatment for heart failure
digoxin+diuretic+ACEi
digoxin mech
inhibitits Na/K exchanger>high intracellular Na> slows the Na/Ca exchanger>more Ca in cell
