Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LC Cardiology Week 1 > Pharmacology - drugs modifying cardiac rate and force > Flashcards

Pharmacology - drugs modifying cardiac rate and force Flashcards

1
Q

What does coupling through Gs protein activities eating ardently cyclase to increase (CAMP) cause?

A

Increased HR
Increased force
Increased conduction velocity in the AV node
Increased automaticity (more chance for spontaneous beats)
Increased activity of Na+/K+-ATPase pump (important for repolarisation)
Increase mass of cardiac muscle
Decreased duration of systole
Decreased cardiac efficiency (O2 consumption increasing disproportionately with increasing work)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a positive lusitropic effect?

A

decreased duration of systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does coupling through Gi protein, inhibiting adenylyl cyclase, decreasing (CAMP) and opening K+ channels (GIRK) cause?

A

Decreased HR
Descreaed contractility
Decreased conduction through AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What might parasympathetic stimulation cause?

A

Parasympathetic stimulation may cause arrhythmias to occur in the atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe vagal manoeuvres? What might they do?

A

Increase parasympathetic output and may be used in atrial tachycardia (atrial flutters, AF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What 2 vagal manoeuvres might you get?

A

Valsalva manoeuvre - activates aortic baroreceptors

Massage of bifurcation of carotid artery - stimulates carotid sinus baroreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The pacemaker potential is modulated by a depolarising funny current, what mediated this current?

A

Channels that are activated by:

Hyperpolarisation 
Cycle AMP (HCN channels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does hyperpolarisation following the action potential activate?

A

Hyperpolarization following the action potential activates cation selective HCN channels in the SA node facilitating a slow, phase 4, depolarization (the pacemaker potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does block of the HCN channels do?

A

Decreases the slope of the pacemaker potential and reduces the heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What drug is a selective blocker of HCN channels that is used to slow the heart rate?

A

Ivabradine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Ivabradine used in commonly?

A

Angina (a condition where coronary artery diseases reduces the blood supply to cardiac muscle - slower HR thus reduces O2 consumption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the steps in the excitation contraction coupling in cardiac muscle? (In phase 2)

(cross bridge formation of cardiac cells)

A
  1. Ventricular AP
  2. Opening of voltage gated Ca2+ channels (mainly L type) during phase 2 of AP
  3. Ca2+ influx into the cytoplasm
  4. Ca2+ induced release from the SR (CICR)
  5. Ca2+ binds to troponin C and shifts tropomyosin out of the actin cleft
  6. Cross bridge formation between actin and myosin resulting in contraction via sliding filament mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the steps in Excitation Contraction Coupling in Cardiac Muscle Relaxation?

(cross bridge relaxation of cardiac cells)

A
  1. Repolarization in phase 3 to phase 4
  2. Voltage-activated L-type Ca2+ channels close
  3. Ca2+ influx ceases. Ca2+ efflux occurs by the Na+/Ca2+ exchanger 1 (NCX1) a plasma membrane ATPase (not illustrated) is less important
  4. Ca2+ release from the sarcoplasmic reticulum ceases. Active sequestration via Ca2+-ATPase (SERCA) of Ca2+ from the cytoplasm now dominates
  5. Ca2+ dissociates from troponin C
  6. Cross bridges between actin and myosin break resulting in relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name some beta adrenoceptor agonists?

A

Adrenaline, dobutamine noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some of the pharmacodynamic effects of beta adrenoceptor agonists?

A

Increased force, rate and cardiac output, and O2 consumption
Decreased cardiac efficiency ( O2 consumption increased more than cardiac work)

They can also cause disturbances in cardiac rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical uses of Adrenaline?

A

Alpha and beta agonist

Given in cardiac arrest and anaphylactic shock

17
Q

Describe how adrenaline works on beta 1, 2 and alpha 1 receptors?

A 
B1 = positive inotropic and chronotropic actions 
B2 = dilation of coronary arteries 
A1 = redistribution of blood flow to the heart (constricts blood vessels in the skin, mucosa and abdomen)
18
Q

Describe dobutamine?

A

Selective for B adrenoceptors
Used in acute HF
Can cause less tachycardia than others B1 adrenoceptors

19
Q

Describe beta adrenoceptor antagonists?

A

Can get non selective or selective

20
Q

Describe non selective blockers?

A

Example propranolol
Cause little effect at rest
During exercise or stress cause significant depression in force, rate and CO
Coronary vessel diameter marginally reduced.

21
Q

What are some clinical uses of Beta adrenoceptor antagonists?

A

Treat arrhythmias
- BB decreases excessive sympathetic drive and help restore normal sinus rhythm
- AF and SVT
- BB delay conduction through the AV node and help restore normal sinus rhythm
Treat angina
Treat HF (compensated + low dose0
Treat hypertension (no longer first line)

22
Q

What are some side effects of beta blockers as a class?

A

Bronchospasm (due to block of airway smooth muscle B2 adrenoceptors) - can be a problem in asthma
Aggravation of cardiac failure - okay in low dose compensated
Bradycardia
Hypoglycaemia
Fatigue
Cold extremities

23
Q

Describe the Effect of Non-Selective Muscarinic ACh Receptor Antagonists Upon The Heart

A

Increased HR in normal subjects at low doses

24
Q

Give an example of a non selective muscarinic ACh receptor antagonist?

A

Atropine

25
Q

Give the clinical uses of Atropine?

A

In sever bradycardia particularly following an MI

26
Q

What is an inotropic drug?

A

Inotropic agents, or inotropes, are medicines that change the force of your heart’s contractions.

27
Q

What do inotropic drugs like digoxin and dobutamine do?

A

Enhance contractility

28
Q

What do inotropes specifically cause on the Frank startling curve?

A

An upward and leftward shift so that SV increases at any given EDP

29
Q

How does digoxin increase contractility?

A

By blocking the sarcolemma ATPase

30
Q

Name a calcium-sensitiser?

A

Levosimendan

31
Q

What do calcium sensitisers do?

A

They bind to troponin C in cardiac muscle, sensitising the action of Ca2+
They also open K(ATP) channels in vascular smooth muscle causing vasodilation (reduces after load and cardiac work)

32
Q

What would levosimendan be used in?

A

acute decompensated heart failure (IV)

33
Q

Does cAMP increase or decrease the activation of HCN channels?

A

cAMP increases the activation of HCN channels

LC Cardiology Week 1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions