CV drugs Flashcards

1
Q

2 main causes of arrhthmias

A
  1. abberant pulse generations

2. defection in conduction system

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2
Q

what is cardiac output

A

SV x HR

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3
Q

what determines CO (3)

A
  1. preload
  2. afterload
  3. contractility
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4
Q

3 major determinants of myocardial O2 demand

A
  1. HR
  2. contractility
  3. ventricular wall stess
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5
Q

what is formula for ABP

A

HRxSVxTPR

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6
Q

2 ways Ca is involved in contraction

A
  1. influx from channels in sarcolemma

2. release of intracellular Ca from sarco reticulum

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7
Q

pathway of vasocontriction

A

depolarization>Ca in>activates calmodulin>activates MLCK>binds with actin

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8
Q

pathway of vasodilation

A

bind to GCPR>activate guanylate cyclase>cGMP>activates PKA>phosphoylates MLCphosphotase>no action

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9
Q

2 targets for hypertension

A
  1. CO

2. peripheral resistance

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10
Q

3 aspects of hypertension

A
  1. inceased vascular tone
  2. increase resistance
  3. lower venous capacitance
    (see chart)
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11
Q

classes of antihypertensives

A
  1. diuretics
  2. B blockers
  3. ACEi
  4. ARBs
  5. Ca channel blockers
  6. vasodilators
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12
Q

4 diuretics in order of use and mechanism

A
  1. thiazides - Na/Cl inhibition
  2. loops - Na/K/2Cl inhibition
  3. spironolatone - aldosterone antag
  4. amiloride - Na channel antag
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13
Q

2 antihypertensive functions of B-blockers

A
  1. lower HR/contractility

2. lower renin

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14
Q

how do ACEi help (2)

A
  1. inhib. Ang2 which is a vasoconstrictor

2. less Na retention by blocking aldo

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15
Q

how do ARBs help

A

same as ACE, but by blocking the Ang2 receptor

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16
Q

how do CCBs work

A

inhibit Ca influx for heart can’t contract and smooth muscle can’t constrict

17
Q

other effects of CCBs (2)

A
  1. dilate coronary arteries, which improves flow

2. cardiac myocyte decreased action

18
Q

3 binding site of Ca channel and drug that work on them

A

N - nifedipine
D - diltiazem
V - verapamil

19
Q

which has less heart action and most vasculr

A

N - nifidepine

20
Q

what is sodium nitroprusside

A

liberates NO which dilates both Art and veins

- stimulates RAAS

21
Q

2 actions of NO

A
  1. activates guanylate cyclase> cGMP>MLCphosphoatse

2. activates Ca dependent K channel which hyperpolarizes the cells - less active

22
Q

what is angina pectoris

A

sudden sever crushing pain due to heart iscemia due to increased heart demand or supply of oxygen

23
Q

how to help angina

A

lower o2 demand via BP, venous return, HR, contractility

24
Q

3 agents for angina

A
  1. nitrates
  2. B blocker
  3. CCBs
25
Q

what do nitrates predominantly dilate

A

venous system

26
Q

pathway of nitrate actions

A

venous dilation>less R heart blood>lower EDP in vents>less preload>less O2 demand

27
Q

nitrates for chronic and acute angina

A

acute: nitroglycerine under the tongue
chronic: isosorbide dinitrate or patch – longer half-life

28
Q

nitrate limitations

A
  • tolerance to antianginal effects

- many contraindications

29
Q

2 aspects of heart failure

A
  1. can’t fill heart

2. can’t pump blood out

30
Q

2 types of congestive heart failure

A
  1. pulmonary congestion - Left heart failure

2. peripheral edema - Right heart failure

31
Q

best treatment for heart failure

A

digoxin+diuretic+ACEi

32
Q

digoxin mech

A

inhibitits Na/K exchanger>high intracellular Na> slows the Na/Ca exchanger>more Ca in cell