Cardiac Drugs I

Front 1

myocardial contractility

Back 1

the force of contraction

-exercise increases contractility
-sleeping/resting decreases contractility

Front 2

cardiac output

Back 2

the volume of blood expelled by the ventricles of the heart every minute

average=5L/min

Front 3

cardiac output=

Back 3

heart rate X stroke volume

Front 4

stroke volume

Back 4

the volume of blood expelled in one heart beat

-strong contraction= increased SV
-weak contraction= decreased SV

Front 5

3 factors that influence stroke volume

Back 5

1) myocardial contractility: force of contraction
2) after-load: load against which a muscle exerts its force
3) pre-load: amount of tension/stretch applied to muscle PRIOR to contraction

Front 6

after load

Back 6

the resistance against which a muscle exerts its force and the muscle must overcome to contract

Front 7

heart rate

Back 7

heart beats per minute

Front 8

preload

Back 8

amount of tension/stretch applied to a muscle PRIOR to contraction

Front 9

starling's theory

Back 9

the bigger the muscle, the bigger the stretch PRIOR to contraction

Front 10

vasoconstriction will __________________ afterload

Back 10

INCREASE

Front 11

as after load increases, stroke volume _____________

Back 11

DECREASES

Front 12

as preload increases, stroke volume _________________

Back 12

INCREASES

Front 13

arterial pressure=

Back 13

cardiac output X peripheral resistance

Front 14

physiologic regulators of blood pressure (3)

Back 14

sympathetic nervous system, RAAS system, kidneys

Front 15

sympathetic nervous system causes what changes (5)

Back 15

-blood pressure increase
-heart rate increase
-epinephrine and norepineprine are released and cause increased contractility
-bronchodilation
-vasoconstriction of unimportant vessels--that blood gets pushed to muscles and organs needed for fight or flight response

Front 16

RAAS system (5)

Back 16

1-release of renin
2-conversion of angiotensin 1
3-conversion to angiotensin 2 via ACE enzyme
4-causes systemic vasoconstriction
5-causes secretion of aldosterone

Front 17

what does aldosterone do?

Back 17

makes kidneys retain sodium and water

Front 18

when does the RAAS system kick in?

Back 18

whenever there is decreased perfusion of the kidneys; dehydration or stress

Front 19

#1 cause of heart failure

Back 19

uncontrolled HYPERtension

Front 20

cardiac output is determined by (4)

Back 20

-heart rate
-contractility
-blood volume
-venous return

Front 21

pulse rate is determined by

Back 21

arteriolar constriction

Front 22

classes of drugs that REDUCE AFTERLOAD

Back 22

-beta adrenergic blockers
-calcium channel blockers
-vasodilators
-ACE inhibitors
-angiontensin II receptor blockers

Front 23

beta blockers

MOA

Back 23

block beta 1 receptors in cardiac muscle which LOWERS cardiac contractility and LOWERS blood pressure

DIRECT IMPACT ON SYMPATHETIC NERVOUS SYSTEM

Front 24

beta blockers

USES

Back 24

-arrhythmias
-angina
-HYPERtension
-post MI
-early stages of heart failure
-migraines
-stage fright
*athletes can use BB to promote coordination

Front 25

beta blockers

SIDE EFFECTS

Back 25

CARDIAC:
-bradycardia (HR<60)
-fatigue
-HYPOtension
-dizziness

PULMONARY:
-bronchoconstriction
-bronchospasm

ENDOCRINE:
-MASK symptoms of hypoglycemia
-can CAUSE hypoglycemia
*****AVOID FOR ASTHMA/COPD PATIENTS******

NEUROLOGICAL:
-fatigue/malaise
-sexual dysfunction
*depression

Front 26

who SHOULDNT take beta blockers?

Back 26

diabetics, because glycogenolysis is mediated by beta receptors

ASTHMA/COPD PATIENTS

Front 27

ending of most beta blockers

Back 27

-OLOL

Front 28

generations of beta blockers (3)

Back 28

FIRST:
non-selective block b1 and b2 receptors (propranOLOL)

SECOND:
cardio-selective produce selective blockade of b1 receptors (metoprOLOL & atenOLOL)

THIRD:
vasodilating which act on blood vessels to cause dilation, but may produce nonselective or cardioselective beta blockade (carvediLOL)

Front 29

beta blockers

DRUG INTERACTIONS

Back 29

-any drug that lowers blood pressure- risk of HYPOtension
-calcium channel blockers + BB= bradycardia
-insulin+BB= hypoglycemia

Front 30

calcium channel blockers

MOA

Back 30

agents that act mainly on vascular smooth muscle

-significantly blocks calcium channels and cause VASODILATION= lowers blood pressure

Front 31

calcium channel blockers: family

dihydropyridine

DRUGS AND MOA

Back 31

DRUGS: amlodipine & nifedipine (ENDS IN -PINE)

agents that act on vascular smooth muscle by causing VASODILATION

Front 32

calcium channel blockers: family

dihydropyridine

SIDE EFFECTS

Back 32

-HYPOtension
***-REFLEX TACHYCARDIA
-flushing
-headache
-dizziness
-peripheral EDEMA

Front 33

calcium channel blockers: family

dihydropyridine

DRUG INTERACTIONS

Back 33

-any drug that lowers BP= HYPOtensin

-CCB+BB= control reflex tachycardia (can add diuretic if edema is present)
-CCB+DIURETIC= control edema

Front 34

calcium channel blockers: other 2 drugs

DRUG NAMES AND MOA

Back 34

DRUGS: verapamil & diltiazem

MOA: agents that act on vascular smooth AND the heart [VASODILATION] (affinity to cardiac muscle)

contractility DECREASES, heart rate DECREASES

BLOCK CALCIUM CHANNELS IN VSM AND HEART

Front 35

calcium channel blockers: verapamil & diltiazem

USES

Back 35

-angina
-anti arrhythmias

Front 36

calcium channel blockers: verapamil & diltiazem

SIDE EFFECTS

Back 36

-HYPOtension
**-bradycardia
-flushing
-headache
-dizziness
-constipation
-peripheral edema

Front 37

calcium channel blockers: verapamil & diltiazem

DRUG INTERACTIONS

Back 37

-any drug that lowers BP= risk of HYPOtension
-BB+ V/D= extensive drop in heart rate
****-digoxin+verapamil= risk for digoxin toxicity

Front 38

vasodilators: DIRECT ACTING

MOA

Back 38

relax vascular smooth muscle and cause VASODILATION

**REDUCE CARDIAC WORKLOAD**

Front 39

vasodilators: DIRECT ACTING

SIDE EFFECTS

Back 39

-orthostatic HYPOtension
-reflex tachycardia= increases workload (BAD)
-increase blood volume and edema/ fluid retention= activate RAAS system

**WHEN GIVEN ALONE EXPECT TO SEE REFLEX TACHYCARDIA**

Front 40

vasodilators: DIRECT ACTING

DRUG INTERACTIONS

Back 40

-any drug that lowers BP= risk of HYPOtension

-vasodilators+BB= reduce/block reflex tachycardia
-vasodilators+diuretic=reduce edema

Front 41

drugs acting on the RAAS system

Back 41

ACE inhibitors & angiotensin II receptor blockers

Front 42

physiological action of angiotensin II

Back 42

-systemic vasoconstriction= INCREASES BP (to push blood out of kidneys)
-makes body secrete aldosterone (retention of NA and water)= INCREASED blood volume, INCREASED blood pressure

Front 43

why do we block RAAS?

Back 43

to DECREASE blood pressure and DECREASE fluid retention

Front 44

ACE inhibitors

MOA & COMMON ENDING

Back 44

inhibiting/blocking ACE enzyme causing a reduction in angiotensin II

**inhibiting ACE results in VASODILATION (reduce blood volume/sodium retention/water retention)**

ENDS IN -opril
(lisinopril)

Front 45

ACE inhibitors

USES

Back 45

-HYPERtension
-heart failure- because they reduce after load to give heart a 'rest'
-post MI- reduce mortality after MI
-decrease proteinuria and slow development of nephropathy in diabetic patients

Front 46

ACE inhibitors

SIDE EFFECTS

Back 46

1) HYPOtension
2) COUGH****
3) HYPERkalemia
4) fetal injury
5) angioedema
------------
-decrease vascular/cardiac remodeling [GOOD]

Front 47

ACE inhibitors

DRUG INTERACTIONS

Back 47

-any drug that lowers BP= risk of HYPOtension
-any drug that raises K= HYPERkalemia
-diuretics= FIRST DOSE HYPOTENSION

Front 48

cardiac remodeling

Back 48

the process where ventricles dilate (MORE CONTRACTILITY), hypertrophy (WALL THICKNESS INCREASES), and become more spherical


BAD

Front 49

ACE inhibitors effect on heart

Back 49

PREVENT or REVERSE remodeling in cardiac muscle and blood vessel walls in heart disease

Front 50

ACE inhibitors effect on kidneys

Back 50

DECREASE proteinuria and slow development of kidney disease/failure in DIABETICS

Front 51

angiotensin II receptor blockers

MOA AND COMMON ENDING

Back 51

DIRECTLY block angiotensin II receptors which results in blocking the effects of angiotensin II= VASODILATION and DECREASE in sodium and water retention

ENDS IN -sartan
(losartan)

Front 52

angiotensin II receptor blockers (ARBs)

USES

Back 52

-HYPERtension
-heart failure
-post MI
-reduce kidney problems

Front 53

angiotensin II receptor blockers

SIDE EFFECTS

Back 53

-HYPOtension
-fetal injury
-angioedema (RARE)

Front 54

angiotensin II receptor blockers

DRUG INTERACTIONS

Back 54

-ACE inhibitors+ARBs= SHOULD NOT BE USED TOGETHER
-any drug that lowers BP= risk of HYPOtension

Front 55

cardiac glycosides: digoxin

MOA

Back 55

INCREASE force of contractility by inhibiting enzyme SODIUM POTASSIUM ATPase
-when you inhibit this you promote calcium to accumulate inside the cell= increases contractile force [cardiac output increases]

**VERY NARROW THERAPEUTIC INDEX**

Front 56

cardiac glycosides: digoxin

SIDE EFFECTS/SIGNS OF TOXICITY

Back 56

GI:
-nauseous
-vomiting
-anorexia

CARDIAC:
-cause arrhythmias (check APICAL pulse BEFORE you give digoxin to assess for abnormalities)

CNS:
-visual changes (blurred vision, 'halos')
-mental status change (delirium/confusion)

ANTIDOTE:
-digoxin immune fab 'digibind'

Front 57

stages of heart failure (4)

Back 57

A: at high risk for heart failure but WITHOUT structural heart disease or symptoms of heart failure
-GIVE ACE INHIBITOR

B: structural heart disease but WITHOUT symptoms of heart failure
-ACE INHIBITOR= reduce remodeling; BETA BLOCKER= reduce SNS

C: structural heart disease WITH prior or current symptoms of heart failure
-DIURETIC; ACE INHIBITOR; BETA BLOCKER

D: ADVANCED structural heart disease with marked symptoms of heart failure AT REST and requiring special interventions
-DO NOT GIVE BETA BLOCKER

Front 58

heart failure is characterized by:

Back 58

-ventricular dysfunction
-REDUCED cardiac output
-signs of fluid retention
-INCREASED heart rate
-INCREASED contractility

Front 59

cardiac contractility is affected by:

Back 59

-stress
-activity
-anxiety
-heart failure

Front 60

drugs used to treat heart failure

#1

Back 60

DIURETICS:
-1st line drugs for patients with signs of volume overload
-REDUCES BLOOD VOLUME
-does not prolong survival/symptom control

Front 61

drugs used to treat heart failure

#2

Back 61

AGENTS INHIBITING RAAS
---------
ACE INHIBITORS:
-improve functional status
-prolong life
-improve hemodynamics and alter cardiac remodeling
------
ARBs

Front 62

drugs used to treat heart failure

#3

Back 62

BETA-BLOCKERS:
-can improve patient status
-need to be controlled carefully
-protects heart from excessive sympathetic stimulation
-PROTECTS AGAINST DYSRHYTHMIAS

Front 63

drugs used to treat heart failure

#4

Back 63

DIGOXIN:
-positive inotropic agent (impacts contractility, increases force of contraction, increases workload)
-improves muscle contraction

Front 64

Nursing responsibilities

Back 64

-monitor digoxin levels
-monitor potassium levels
-check apical pulse for one minute to assess for abnormalities
-assess 'halos' if present