Cardiovascular Pharm-1

Question 1

Excitability

Answer 1

The ability for a cell to respond to an external electrical stimulus (usually in the form of an action potential)

Question 2

Automaticity

Answer 2

The ability for a cell or region of cells to initiate an action potential (SA nodes etc, pacemaker shit same as excite )

Question 3

Conductivity

Answer 3

ability to receive n transmit AP (all cardiac tissue can conduct AP but some more specialized, mean SA node go thru inter atrial conductive path to av node to his n spreading out in right n left branches, other areas cardiac muscle can also conduct but usually conductivity here less, if scar, ishemia, some areas muscle can become more conductive rep phys or functional conduct pathway not previous present can lead to arrythmia generation and propogation)

Question 4

Dromotropism

Answer 4

The ability to alter the rate of electrical conduction (most drugs we use have neg dromo, dec conduction velocity through AV node)

Question 5

Refractoriness

Answer 5

The inability of a cell to receive and transmit an action potential

Question 6

Drugs that block K+ channel

Answer 6

prolong phase 3 AP longer duration, k+ cant leave cell to repolarize it

Question 7

What happens when drugs block second conformation of the NA+ channel (activated state activation gate and inactivation gate open)

Answer 7

Slow down upslope, DECREASE v max of pahse 0 -due to fast na channel

Question 8

What happens when drugs block third conformation (inactivated closed) of the NA+ channel (inactivation gate closed activation gate open) (late slow inactivated currents)

Answer 8

shorten the AP. Important in CVD and ichemia b/c in these conditions AP is prolonged (bad)

Question 9

Conditions that cause increased late NA+ chennel activity (and thus inceased intra cell CA and early depol arrythmias etc)

Answer 9

Ishcemic heart disease
Heart faiure (diastolic)
Aryythmias (atrial fib and ventricuklar)
PAD

neuromuscuklar: seisures and neuropathic pain,myotonnia muscle paralysisq

Question 10

consequence of increased later na+ channels

Answer 10

increased intacell NA
Na+ exit with Ca2+ entry (NCX\
increased intracell CA+
cellular Ca+ overload

Question 11

cellular Ca overload consequences

Answer 11

Electrical instability
After-depolarizations
Arrhythmias

Mechanical dysfunction
Abnormal contraction & relaxation
(e.g.,  diastolic tension)

Question 12

• Differences between cardiac conduction tissues (nodal) and cardiac muscle:

Answer 12

Phase 0 of AP in nodal
tissues is controlled by
Ca2+ entry
- Phase 0 of AP in non-
nodal cardiac tissue is
controlled by Na+ entry
This difference is of importance in pharmacological handing of arrhythmias originating from these different tissues.

Question 13

Drugs that affect CA affect what most?

Answer 13

Nodal tissue manifests in decrease HR

Question 14

Drugs that block NA channels

Answer 14

target arrthymias that involve ventricular muscle

Question 15

ERP/APD ratio

Answer 15

ERP (normally 0-3 phase 0 repsonse to stimulus)
smaller the ratio greater chance for depol and arryhtmia, cuz ERP is less so can depol more often
many drugs increase ERP/APD ratio makes tissue less repsonsive to abnormal imoulses

Question 16

RRP

Answer 16

after pase 3 can repsond to sufficient stimulus

Question 17

Disorders of Impulse Formation

Answer 17

no change in original pacemaker site (ex all originate from same location like SA NODE)
change in original pacemaker site (ectopic foci) (Af, AF, …)
early and delayed after-depolarizations
*Most common site of generation is SA node

Question 18

Disorders impulse conduction

Answer 18

AV Nodal Block
Ventricular Re-entry
AV Nodal Re-entry (PSVT, PAT, WPW)

Question 19

No change in original pacemaker site

Answer 19

ex sinus tachacardia, originate in SA node, all P waves followed by QRS

Question 20

Change in original pacemaker site

Answer 20

ex ectopic foci, ex premature beats, atrial tachycardia,
atrial fibrillation, etc., not all P waves followed by QRS in atrial tach since depol occurs during qrs repol still refract

Question 21

EAD

Answer 21

The key abnormality if the marked prolongation of the cardiac AP, such as occurs as a result of slow heart rate, hypokalemia or drugs that prolong APD.
 When this occurs, phase 3 repolarization may be interrupted by an early
afterdepolarization.

Question 22

Triggered activities

Answer 22

abnormal upstrokes only occur after an initial normal, or “triggering” upstroke, and so are termed triggered rhythms. includes EAD and DAD

Question 23

where are EAD most common?

Answer 23

EADs are induced more readily in Purkinje cells than in epicardial or endocardial cells. can pccur from MI pr ischemia

Question 24

torsades de pointes (TdP) relationship to EAD

Answer 24

EADs triggering functional reentry across the ventricular wall (transmural re-entry) causes torsades de pointes (TdP), a common polymorphic ventricular tachycardia seen commonly as a result of long QT interval (congenital or acquired). associated with hypokalemia. type of vent tach

Question 25

Which conditions can result in DAD?

Answer 25

myocardial ischemia, adrenergic stress, digitalis intoxication,heart failure

Question 26

DAD

Answer 26

Under conditions of intracellular or sarcoplasmic reticulum Ca2+ overload, a normal action potential may be followed by a delayed afterdepolarization (DAD). If this DAD reaches threshold, a secondary triggered beat or beats may occur.  DAD-mediated triggered beats are more frequent when the underlying heart rate is rapid.

Question 27

primary AV block

Answer 27

increased P-R interval more than 200ms or .2 s but symetric all p waves equally prolonged, #p waves= #qrs

Question 28

secondary av block

Answer 28

progressively longer P-R interval until finally P wave not followed by QRS

Question 29

tertiary AV block

Answer 29

AV dissociation, atria and vent beat according to own rhytmm. have impulses from atria that dont pass through AV node, more P waves than QRS, enlarged QRS slow so think originating from ventricled

Question 30

reentry

Answer 30

reentry represents one of the most common mechanisms of tachycardias. The condition for this mechanism is the existence of conduction routes with different conduction velocity. This difference may be functional or organic.

Question 31

MOA re entry

Answer 31

A premature atrial impulse finds the fast pathway refractory, allowing conduction only down the slow pathway (left). By the time the impulse reaches the His bundle, the fast pathway may have recovered, allowing retrograde conduction back up to the atria—the resultant “circus movement” gives rise to slow-fast atrioventricular nodal re-entrant tachycardia (right).

Question 32

consequences of arrythmias

Answer 32

Compromise of Mechanical Performance dec efficiency = dec SV = decCO Proarrhythmic/Arrhythmogenic e.g. conversion of v. tachycardia to v. fibrillation Thrombogenesis atrial flutter and fibrillation contribute to increased stroke incidence

Question 33

atrial flutter (ex reentry)

Answer 33

t