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Cardio > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the mechanism of action of the neurotransmitter acetylcholine on the heart?

A

The acetylcholine activates the M2 muscarinic cholinoreceptors, largely found in the nodal cells
The M2 receptor then couples with adenylyl cyclase through a Gi protein alpha subunit - inhibiting the adenylyl cyclase and reducing cAMP
It also couples to the specific potassium channels, the GIRKs (G protein coupled inward rectifiers) in the SA node through the Gi protein beta/ gamma subunit dimer - opening the channel

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2
Q

What is the resulting effect of parasympathetic action on heart rate?

A

a negative chronotropic effect because the frequency of nodal action potentials is decreased
they are decreased due to the GIRKs causing hyperpolarisation
The threshold for action potential generation being increased
And the pacemaker potential slope being decreased

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3
Q

What is the resulting effect of parasympathetic action on heart force?

A

it has a negative inotropic effect

contractility of the heart has been decreased as phase 2 is decreased and Ca2+ entry is also decreased

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4
Q

What is the resulting effect of parasympathetic action on electrical conduction in the heart?

A

decreased conduction in AV node (negative dromotropic effect) – due to decreased activity of voltage-dependent Ca2+ channels and hyperpolarization via opening of GIRK K+ channels

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5
Q

What is the mechanism of action of the neurotransmitter noradrenaline and the hormone adrenaline on the heart?

A

They activate B1 receptors in nodal cells and myocardial cells
The B1 receptor coupling with the adenylyl cyclase through the Gs protein alpha subunit stimulates it to increase the intracellular concentration of cyclic AMP [cAMP]I

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6
Q

What is the resulting effect of sympathetic action on heart rate?

A

a positive chronotropic effect, increases action potential frequency in the SA node
the action increases the slope of the pacemaker potential
the action reduces the threshold required for an action potential to be fired

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7
Q

What is the resulting effect of sympathetic action on heart force?

A

positive inotropic effect
increase in phase 2 of the cardiac action potential in atrial and ventricular myocytes and enhanced Ca2+ influx
sensitisation of contractile proteins to Ca2+

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8
Q

What is the resulting effect of sympathetic action on electrical conduction in the heart?

A 
increased conduction velocity in AV node (positive dromotropic response) 
increased automaticity (i.e. tendency for non-nodal regions to acquire spontaneous activity)
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9
Q

What are the other effects of sympathetic action on the heart?

A

positive lusitropic effect - decrease in the duration of systole
Increased activity of the Na+/K+ -ATPase (pump)
increase in cardiac muscle mass

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10
Q

How does Ivabradine reduce heart rate?

A

It is a selective channel blocker of HCN channels, it therefore reduces the funny current and so reduces the slope of pacemaker potential and therefore reduces the heart rate
This is beneficial in angina because it reduces the hearts O2 requirement and angina reduces the hearts O2 supply

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11
Q

What is the process of excitation contraction coupling in cardiac muscle?

A
  1. Ventricular action potential
  2. Opening of voltage-activated Ca2+ channels (mainly L-type) during phase 2 of action potential
  3. Ca2+ influx into cytoplasm
  4. Ca2+ release from the sarcoplasmic reticulum (Calcium-Induced Calcium Release – CICR). Caused by Ca2+ activating the ryanodine type 2 channel (RyR2)
  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 the sliding filament mechanism
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12
Q

What is the mechanism of relaxation in cardiac muscle following excitation contraction coupling?

A
  1. Repolarization in phase 3 to phase 4
  2. Voltage-activated L-type Ca2+ channels return to closed state
  3. Ca2+ influx ceases. Ca2+ efflux occurs by the Na+/Ca2+ exchanger 1 (NCX1)
  4. Ca2+ release from the sarcoplasmic reticulum ceases. Active removal of Ca2+ from the cytoplasm by Ca2+-ATPase now dominates
  5. Ca2+ dissociates from troponin C
  6. Cross bridges between actin and myosin break resulting in relaxation
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13
Q

How does activating B1 receptors increase cardiac contractility?

A
  1. activating the B1 receptors increases the cAMP
  2. cAMP increase acts on protein kinase A causing more Ca++ to be pumped into the sarcoplasmic reticulum, increasing the rate of relaxation
  3. the action of protein kinase A also causes the troponin to be more sensitive to the calcium and therefore there is greater contraction of the cardiac muscle
  4. the combination of all these factors on the cardiac muscle causes an increase in the cardiac contractility
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14
Q

What is the effect of adrenoreceptor agonists on the heart?

A

increased heart rate, increased force, increased cardiac output and increased O2 consumption
decreased cardiac efficiency - the O2 consumption increases more in proportion to the extra work that is being done
can cause disturbance in cardiac rhythm

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15
Q

3 examples of B-adrenoreceptor agonists

A

Dobutamine, adrenaline and noradrenaline

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16
Q

Clinical uses of dobutamine

A

Given via IV for
acute, but potentially reversible, heart failure (e.g. following cardiac surgery, or cardiogenic, or septic, shock). For reasons unknown, causes less tachycardia than other β1 agonists

17
Q

clinical uses of adrenaline

A

Given IM, SC, IV or as IV infusion
IV used for cardiac arrest as part of the Advanced Life Support (ALS) treatment algorithm- positive inotropic and chronotropic actions (β1)
redistribution of blood flow to the heart by constricting blood flow to places like the skin and increasing dilation of coronary arteries (β2)
anaphylactic shock (IM, not IV unless cardiac arrest occurs), very important in immediate management

18
Q

What are the adverse effects of B-blockers?

A
  1. Bronchospasm - only really in severe asthmatics (less risk if selective agonists are used)
  2. Potentially will aggrevate heart failure
  3. Bradycardia
  4. Hypoglycaemia
  5. fatigue
  6. cold extremities
19
Q

What are B blockers clinical uses in relation to the heart and CVS?

A
  1. to treat disturbances of cardiac rhythm (arrhythmias) - excessive sympathetic drive can cause tachycardia and latent cardiac pacemakers (outside of nodal tissue) therefore B blockers prevent this
  2. treating AF or SVT - B blockers delay the impulse at the AV node preventing this helping to restore sinus rhythm
  3. treating angina - 1st line an alternative to Ca entry blockers
  4. treating compensated heart failure - the rule is start low and slow as for some people it can make their heart failure worse
  5. treating hypertension - not first line only with co-morbidities
20
Q

What is the effect of atropine on the heart and CVS?

A

Increase in HR in normal subjects (at all but low doses) – more pronounced effect in highly trained athletes (who have increased vagal tone)
No effect upon arterial BP (resistance vessels lack a parasympathetic innervation)
No effect upon the response to exercise

21
Q

What class of drug is atropine?

A

a muscarinic Ach receptor antagonist

22
Q

What are the clinical uses of atropine in relation to the heart?

A

Atropine is the 1st line management of severe or symptomatic bradycardia.
Used particularly after an MI where vagal tone is elevated.
In MI given IV (with caution) in incremental doses - must be a dose over 300mg because less than this decreases HR further. Monitoring is required.

Glycopyrronium is an alternative to atropine

In anticholinesterase poisoning atropine is used to reduce excessive parasympathetic activity, e.g. bradycardia

23
Q

What is heart failure?

A

When the heart’s cardiac output is too little to produce adequate tissue perfusion

24
Q

What is the effect of inotropic drugs?

A

they enhance contactility of the heart e.g. digoxin, dobutamine

25
Q

How does digoxin effect the heart?

A

Competitively inhibitits the Na+/K+ ATPase
If there is low plasma K+ this can cause hypokalaemia
It indirectly icreases vagal activity slowing the heart rate
It directly reduces the duration of action potentials in the heart myocytes

26
Q

Clinical uses of digoxin

A

Used as IV in acute heart failure and orally in chronic heart failure when other drugs aren’t working at optimal dose
In heart failure accompanied with atrial fibrillation

27
Q

What are the adverse effects of digoxin?

A

excessive depression of AV node conduction (heart block)
propensity to cause arrhythmias
nausea
vomiting
diarrhoea
disturbances of colour vision – effects Na K ATPase in the cones

28
Q

What class of drugs does Levosimendan belong to?

A

calcium sensitizers

29
Q

How does levosimendan help with heart failure?

A

binds to troponin C sensitizing it to the action of Ca++
Opens KATP channels in cvascular smooth muscle causing vasodilation
(IV) given for acute decompensated heart failure

30
Q

What class of drugs do amrinone and milrinone belong to?

A

Inodilators

31
Q

When are inodilators used clinically?

A

IV administration in acute heart failure

32
Q

What is the effect of inodilators on the heart?

A

Increase cAMP by inhibiting phosphodiesterase in the cardiac and smooth muscle
They increase the myocardial contractility if the heart and dcrease the peripheral resistance in heart failure
They should be used cautiously because they worsen survival – perhaps due to increased incidence of arrhythmias

Cardio (36 decks)

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