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BIOM 3090 > Unit 04: Treatment of Angina > Flashcards

Unit 04: Treatment of Angina Flashcards

1
Q

what is angina

A
  • angina pectoris
  • refers to chest pain due to ischemia (restiriction of blood supply to tissues) of heart muscle
  • typically due to obstruction of coronary arteries resulting in insufficient coronary blood flow
  • oxygen deprivation decreases muscle strength, leading to chest pain (angina)

*caused by imbalance between the eharts oxygen supply and demand

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2
Q

what are the 3 types of angina, describe them

A

Atherosclerotic angina

  • most common
  • due to irreversible atherosclerotic obstruction of coronary arteries
  • precipitated by exertion

Vasospastic angina

  • occurs following spasm of part of the coronary vessel (often at site of atherosclerotic plaque)
  • can occur at any time

Unstable angina

  • product of an atherosclerotic plaque combines with platelet aggregation and vasospasm (precursor of myocardial infraction
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3
Q

what is coronary blood flow

A
  • blood flow provides heart with oxygen and nutrients and local blood flow is regulated by the needs of the heart of oxygen demand
  • during exercise the heart increases work load and oxygen consumption
  • coronary blood flow increases to supply the heart via vasodilation of coronary arteries
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4
Q

what determines mayocardial O2 supply

A
  • determine dby perfsion of the heart - thats determined by vascular tone of coronary arteries
  • major coronary arteries are depicted on epicardial surface of the heart
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5
Q

what is myocardial demand determined by

A
  • ventricular wall stress - function of both preload (venous tone) and afterload (arteriolar tone)
  • venous tone determines myocardial O2 demand by regulating the amount of blood returning to the heart - determiens the end-diastolic ventricular wall stress
  • artial tone determines myocardial O2 demand by regulating systemic vascular resistance (SVR) - the pressue against which the heart muscles contract *determines systolic ventircular wall stress
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6
Q

what is the goal for angina treatment? what is angina the result of?

A
  • goal is to restore the balance between oxygen supply and demand
  • angina is the result of decrease oxygen supply following an increase in demand - often result from an increase in heart rate/cardiac output and/or PVR

*oxygen supply needs to be increased - achieved by increasing coronary blood flow or demand needs to be reduced by decreasing HR and/or PVR

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7
Q

what is nitroglycerin

A
  • vadodilator used to treat angina
  • metabolized by the liver so oral bioavailablity is low - comes in multiple forms
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8
Q

what is the mechanism fo action of nitroglycerin

A
  • mechanism of action of a vasodilator
  • conversation of nitrate -> nitrite groups -> nitric oxide
  • this increases cGMP and results in relaxation of smooth muscle cells in blood vessels (vasodilation)
  • nitrates preferentially affect veins and coronary arteries - can also ahve activity on smooth muscle in other tissues (bronchioles)
  • effect is a decrease in venous return and PVR and dilation of coronary arteries

*overall oxygen requirement decreases and delivery of oxygen increases

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9
Q

what are the toxicities associated with nitrates

A
  • hypotension - tachycardia (reflex increases in SNS activity)
  • tolerance - reduced effictiveness of same dose following exposure to long acting nitrates might also occur
  • mechanism is not clear but it likely involves systemic compensation such as an increase in SNS activty or salt and water retention
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10
Q

what is sildenafil

A
  • viagra
  • inhibits phosphodiesterase and prevents breakdown of cGMP causing relaxation of smooth muscle
  • initially developed as a treatment for angina pectoris - but better suited for erectile dysfunction
  • can result in severe hypotension which can be dangerous and evn fatal if it results in myocardial infraction

*should wait 24 hrs between ingestion of sildenafil and nitrates

side effect: inhibition of phosphodiesterase increases sensitivity of rod cells in the eye - these are calls that are most effective at detecting blue light (causes altered vision

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11
Q

what is verapamil

A
  • vasodilator - calcium channel blocker
  • inhibits calcium influx into blood vessel smooth muscle cells and causes dilation
  • also inhibits calcium influx into cardiac muscle cells and decreases cardiac contractility
  • Overall: effects on smooth muscle and the heart decrease oxygen requirements
  • toxicities associated include: cardiac depression leading to bradycardia, ehart failure and cardiac arrest
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12
Q

describe the mechansims of vascular smooth muscle cell contraction

A
  • controlled by coordinated action of several intracellular signalling mediators

Contraction:

Ca2+ entry thoguh L type voltage gated Ca2+ channels = initial stimulus for contraction

Ca+ entry into the cell activates calmodulim CaM

Ca2+-CaM complex activates myosin light chain kinase (MLCK) to phosphrylate myosin light chain

phosphrylated myosin LC interacts with actin to forma ctin-myosin corss bridges - process that initiates vascular smooth muscle

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13
Q

describe the mechanism of vascular smooth muscle cell relaxation

A
  • relaxation is a coordinated series of steps that act to dephosphrylate (hence inactivate) myosin LC
  • NO diffuses into cell and activates duanylyl cyclase
  • activated guanylyl cyclase catalyzes the conversation of guanosine triphosphate (GTP) to guanosine 3′,5′-cyclic monophosphate (cGMP)
  • cGMP stimulates cGMP-dependent protein kinase to activate myosin LC phosphatase - dephosphorylates myosin light chain prevening actin-mysoin cross bridge formation

*results: vascular smooth muscle cells relax

*active form of enzyme is in light blue

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14
Q

what are symptholytics? how are they used to treat angina?

A

drugs that inhibit the post ganglionic functioning of the SNS

  • examples used to treat angina = propranolol and metroprolol
  • they are B blockers that decrease the rate and orce of contraction of the heart - this decreases myocardial oxygen requirement
  • use is however contraindicted in patents with asthma and bradycardia
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15
Q

how is angina pectoris managed clinically?

A
  • lifestyle changes - reduction of atherosclerotic risk factors (smoking, hypertension, high cholesterol)
  • sublingual nitrates often prescribed for individuals suffering acute attacks (chest pain due to physical exertion)
  • maintenace monotherapy for hypertensive pateints might include Ca2+ channel blocker
  • maintenance therapy for normotensive patients involved long acting nitrates

*if monotherapy fails, Ca2+ channel blockers cna be combined with B blockers and some patients ma require nitrates added as well

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16
Q

what are arrhythmias

A
  • electrical alterations that cause abnormalities in the rhythm of the heart
  • can be the result of altered initiation of the sinoatrial node - which would affect the rate of contrction
17
Q

what are bradyarrhythmias and tachyarrhythmias

A
  • bradyarrhythmias = abnormal conduction that can occur via heart block (slow down)
  • tachyarrhythmias = abnormal re-entry conduction (speed up)
18
Q

how are arrhythmias classified?

A
  • based on the chamber of th heart they affect and are therefore categorized as atrial or ventricular

-

19
Q

what is normal heart rate? what what rate does atrial flutter occur?

A
  • normal heart rate is 60-80 beats/min
  • atrial flutters occur when regions of atria beat asynchroously between 200-350 beats/min
20
Q

what is the most common type of arrhythmia?

A

artial fibrilation (a-fib)

-occurs when heart rate is increased (300-500 beats/min(, irregular and disorganized

21
Q

relationship between atrial arrhythmias and ventricular arrhythmias

A

Atrial arrhythmias do not always result in ventricular arrhythmias - may not affect cardiac output

  • can lead to more serious and lethal rhythm disturbances or even stroke
22
Q

what are ventricular arrhythmias often the result of?

A

can be result of premature ventricular contrations - if they are occasional there is no need for treatment

  • can also be result of ventricular tachycardia which deos require treatment
23
Q

when is ventricular fibrilation?

A
  • irregular and rapid contraction of ventricles which means tht the ehart cannot pump blood properly
  • if not treated immediately result will be fatal
24
Q

what do defibrillators do?

A
  • used in emergencies stop fibrilation by temporarily stopping all electrical acitivty in heart to allow the SA and AV nodes to restore normal rhythm
25
Q

describe normal cardiac rhythm

A
  • cardiac rhythm refers to the rhythm of the beating heart - it is influenced by electrical activity in heart that arises at teh SA node, spreads through atria, discharges the atrioventricular node and propgates through purkinje cells
  • cadiac muscle cells contract by process called excitation contraction coupling
26
Q

how are resting membrane potential and action potential maintained

A
  • maintained by dsitribution of ions on either side of the muscle cell membrane
  • ions involve Na+, Ca+2 and K+
  • at rest - Na conc insdie cell is low and maintained by Na+/K+ ATPase.

depolarization opens ion specific channels and activates an action potential

27
Q

summarize the phases of action potential of a cardiac muscle fiber

A
  1. depolarization proceeds rapidly due to Na+ influx through rapidly opening Na+ channels
  2. plateau phase due to Ca+2 influx through more slowly opening Ca+2 channels
  3. repolarization due to closure of Ca+2 channels, K+ efflux through K+ channels
28
Q

summarize how cardiac cells contract

A

* via excitation-contraction coupling

  1. action potential increases Ca+2 (ion channels + release from sarcoplasmic reticulum)
  2. increasing Ca+2 binds troponin C and uncovers myosin binding site on actin
  3. actin and myosin cross-linkages form which results in contraction
29
Q

how does cardiac relaxation occur

A

Ca2+ is released frmo troponin and is pumped back into sarcoplasmic reticulum and out of the cell

  • actin and myosin are no longer cross linked
30
Q

what do anti-arrhythics do

A
  • aims to normalize cardiac rhythm by altering ion flow across the plasma membrane though ion channel blockers
  • anti-arrhythmics have a narrow therapeutic indec and can also cause arrhythmias

*phyician needs to evaluate risks and benefits of anti-arrhythmic therapy

31
Q

what are the 4 classes of anti-arrhythmic agents

A

Class I: sodium ion channel blockers

Class II: includes B vlockers

Class III: rpolongs action potentials or blocks K+ channels

Class IV: are Ca2+ channel blockers

32
Q

describe class I anti arrhythmic agents

A
  • ion channel blockers
  • capable of blocking ion channels like sodium
  • Sodium channel blockers reduce the recovery of Na+ channels and decrease conduction and excitation in the heart
  • ex: quinidine - oral anti-arrhymic that is efective at treating all types of arrhythmia but rarely used bc of side effects
  • lidocaine also used as an IV antiarrhymic to treat ventricular tachycardia and fibrilation
33
Q

what is quinidine

A

class I ion channel blocker

  • oral anti arrhythmic effective for all types of arrhythmia - but rarely used due to side effects
34
Q

what is lidocaine

A

class I ion channel blocker

  • used as an IV anti-arrhythmic for treating ventricular tachycardia and fibrilation
35
Q

describe class II anti-arrhythmics

A
  • beta blockers
  • ex: propranolol and metroprolol
  • inhibit SNS effects and slow down HR
  • drugs of choice for atrial arrhythmias

*good chocie for arrhythmias triggeredby inc sympathetic activity

36
Q

describe class III anti-arrhythmics

A

K+ channel blockers

  • inc duration of action potential and inc refractery period
    ex: amiodarone (not selective for K+ channels - also affects B receptors and Na+ and Ca2+ channels)
  • prolong the action potential which also prolongs the refractory period
  • Class III most commonly used anti-arrhythmics for atrial fibrillation and ventricular tachycardia
37
Q

what is amiodarone

A

class III anti-arrhythmic - K+ channel blocker

  • not selective for K+ channel also affects beta receptors and Na+ and Ca+2 channels
  • used for artial fibrilation and ventricular tachycardia
38
Q

describe class IV Anti-arrhythmics

A

Ca2+ channel blockers

  • ex: verapamil - Ca+2 channel blocker that decreases cardiac contractility and induces vasodilation
  • used for supraventircular tachycaria which can affect the AV node and purkinje fibers
39
Q

what is verapamil?

A

Class IV anti-arrhythmic

  • Ca+2 channel blocker
  • decreases cardiac contractility and induces vasodilation
  • used for supraventircular tachycaria which can affect the AV node and purkinje fibers

BIOM 3090 (22 decks)

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