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CVS > Lecture 14 > Flashcards

Lecture 14 Flashcards

1
Q

What are some examples of arrhythmias/dysrythmias?

A
  • bradycardia
  • atrial flutter
  • atrial fibrillation
  • tachycardia (ventricular/supraventricular)
  • ventricular fibrillation (extreme- no contraction so CO is 0)
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2
Q

Causes of tachycardia:

A
  • ectopic pacemaker activity (damaged area of myocardium/latent pacemaker region activated due to ischaemia becomes depolarised and is spontaneously active-fast rate dominating over SAN)
  • afterdepolarisations (abnormal depolarisations following AP: triggering activity)
  • atrial flutter/fibrillation
  • re-entry loops
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3
Q

When could you develop sinus tachycardia?

A

Patient with overactive thyroid- enhances sympathetic nervous system

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4
Q

How do you develop sinus bradycardia?

A

-Fit and healthy person
-extrinsic factors (beta blockers)
-sick sinus syndrome (SAN not functioning normally, drives HR but at a slower rate)
(Sinus rhythm but going slowly)

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5
Q

What is a cause of bradycardia?

A

Conduction block

  • problems at AVN/bundle of his
  • slow conduction at AVN due to extrinsic factors (beta blockers/Calcium channel blockers)
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6
Q

When do delayed after depolarisation occur?

A

High intracellular calcium concentration (due to sodium/calcium exchanger)

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7
Q

What do delayed after depolarisations cause?

A

Trigger AP, before it should be triggered

-happening repeatedly= ventricular tachycardia (in ventricles)

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8
Q

What are early after depolarisations?

A

Occur in hypokalaemia-lengthens AP duration (QT interval) due to maybe the potassium channels reacting to low levels of potassium by reducing the permeability to potassium channels

  • occur as repolarisation is starting
  • lead to oscillations
  • ventricular tachycardia
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9
Q

What makes you more prone to arrhythmias?

A

People with a longer QT intervals are more prone to arrhythmias

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10
Q

How does a re-entrant mechanism cause arrythmia?

A

Normally (triangle shape)

  • spread of depolarisation meets a point where it diverges left and right
  • when these meet they cancel each other out

-may be block on one side but this doesn’t create a problem as one branch still works and can spread in the other direction

Problem
Area that conducts at a slower rate setting up a circuit- causing tachycardia as it doesn’t require input form the SAN

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11
Q

What causes atrial fibrillation and what is it?

A

Cause:
-damage to atria, stretching
-multiple re-entry circuits created
=often supraventricular tachycardia as more impulses are getting through AVN

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12
Q

What is AV nodal re-entry?

A

Fast and slow pathway in AVN can set up a circuit
-many more depolarisations come down the bundle of his
=supraventricular tachycardia

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13
Q

What is an accessory conduction pathway?

A

Accessory pathway between ventricles and atria
Can create a re-entry loop
=ventricular pre-excitation

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14
Q

What are the 4 classes of anti-arrhythmic drugs?

A
  • block voltage sensitive sodium channels
  • beta adrenoceptor antagonists
  • drugs that block potassium channels
  • drugs that block calcium channels
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15
Q

How do drugs that block voltage gated sodium channels work and give example?

A

Lidocaine (local anaesthetic)
-given to affect cardiovascular system intravenously
-dissociates rapidly, so next AP is normal (not much effect)
Block voltage gated Na+ channels much more in the depolarised state (when they are inactive/open)
-allows AP to occur

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16
Q

Where does lidocaine have best effect?

A

Damaged myocardium-depolarised

Block channels preventing spread of depolarisation from damaged areas

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17
Q

Why is lidocaine sometimes given to a patient following an MI?

A

If patient shows signs of ventricular tachycardia (damaged areas of myocardium could be damaged, depolarised and fire automatically)
-intravenously

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18
Q

How is lidocaine administered?

A

IV

-not prophylactically (treatment to prevent reoccurrence) as does not work

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19
Q

How do beta adrenoceptor antagonists work to prevent arrhythmia? Give an example of one

A

Propranolol/atenolol
-block sympathetic action (slow down pacemaker potential slope at AVN/SAN)

  • prevent supraventricular tachycardias (slow conduction at AVN, slowing ventricular rate in patients with AF)
  • used following an MI: sympathetic activity increases (pale and sweaty)-arrythmias may be due to increased sympathetic activity
  • reduces oxygen demand (beneficial following and MI)
20
Q

Can tachycardia affect the CO?

A

Tachycardia can reduce CO as ventricles don’t have time to fill

21
Q

How do drugs that block potassium channels work?

A

Prolong action potential
-lengthens the absolute refractory period so in theory would prevent another AP firing too soon

BUT BECAUSE THEY PROLONG THE AP THEY ARE NOW CLASSED AS PROARRYTHMIC

22
Q

Which drug is an exception to K+ blocking drugs?

A

Amiodarone

  • as well as blocking potassium channels, it blocks calcium channels/beta blocker
  • works due to other actions

Prevents ventricular arrhythmias post MI

23
Q

What drug is used to treat the Wolff-Parkinson-White syndrome (re-entry loop due to extra conduction pathway)?

A

Amiodarone

24
Q

How do drugs that block calcium channels prevent arrythmias? Give examples

A

Verapamil/diltiazem (non-dihydropyridine-act more on heart)
(dihydropyridine-act on vasculature so not effective in preventing arrythmias)

Verapamil: block L-type calcium channels, decreasing slope (lengthening) of AP at SAN, decreasing AVN conduction and decreasing HR(Ca+ channels cause depolarisation)
-decreases force of contraction (negative inotropy)

25
Q

Give some examples of dihydropyridine Ca+ blocking drugs:

A

Amlodipine
Nifedipine
Nicardipine

26
Q

What is the function of adenosine?

A

Anti-arrhythmic drug (administered via IV/made in body)
-acts on A1 receptors at AV nodes
-very short half life: stops heart and lets things start
Enhances potassium conductance at AVN: hyperpolarises cells

Terminates supraventricular tachycardias

27
Q

What are ACE inhibitors? Give example

A

Inhibit angiotensin converting enzyme
E.g. perindopril
TREATMENT OF HYPERTENSION AND HEART FAILURE
-in heart failure, body feels as if not enough blood being pumped around body
-responds by retaining more fluid
-ACEi prevents fluid retention and vasodilates the vessels
=reducing afterload and preload of heart

28
Q

What is the function of angiotensin 2?

A
  • vasoconstriction
  • increase blood volume due to simulation of Na absorption
  • secretion of aldosterone high stimulate Na reabsorption
29
Q

What is the side effect of ACE inhibitors?

A

Dry cough

-causes excess bradykinin

30
Q

What do patients who can’t tolerate ACE inhibitors use?

A

Act on an angiotensin 2 receptor: AT-1 receptor
E.g. Losartan
= same effect as ACE inhibitors as the angiotensin 2 made can’t act not eh AT-1 receptor

31
Q

What class of drugs is used to treat patients with heart failure and hypertension?

A

Diuretics (act on kidneys to increase amount of fluid lost in kidneys- reduce amount of Na+ being taken up again)

-reduces pulmonary and peripheral oedema

32
Q

Give an example of a diuretic:

A

Furosemide

Acts on loop of henle (loop diuretics)

33
Q

How do dihydropyridine calcium blockers work?

A

Prevent calcium entering smooth muscle cells of the vasculature

  • reduce contraction
  • decreasing peripheral resistance
  • decrease arterial BP
  • reduce workload of the heart by reducing afterload
34
Q

In what conditions are calcium channel blockers effective?

A
  • hypertension
  • angina
  • coronary artery spasms
  • SVT’s by reducing conduction at AVN
35
Q

What are positive inotropes?

A

Things that increase contractility of the heart and therefore CO

36
Q

Give some examples of positive inotropes:

A

Cardiac glycosides: digoxin

B-adrenergic agonists: dobutamine

37
Q

What are cardiac glycosides used for?

A

Treat heart failure
-improves symptoms but not the long term outcome

Blocks Na+/K+ ATPase, causing a build up of Na in the cell
Na/Ca exchanger moves Na into cell, via sodium gradient, but if sodium concentration of cell increases, the activity of the Na/Ca exchanger doesn’t work as well
=increase in calcium concentration in the cell= more calcium in sarcoplasmic reticulum
=increased force of contraction

38
Q

How do cardiac glycosides affect the heart rate?

A

Act on medullary centre in brain to increase vagal activity (parasympathetic) to heart
-slow down HR by slowing AV conduction

=may be used in atrial fibrillation as an anti-arrythmic agent

39
Q

How does dobutamine increase force of contraction of the heart?

A

Selective B1 adrenoceptor agonist
-stimulate them at AVN/SAN/ventricular myocytes

=used in cardiogenic shock

40
Q

What is the issue with cardiac glycosides?

A

They make the heart work faster which is not good in the long run
‘Don’t flog a dying horse’
-better to reduce workload of the heart by giving ACE inhibitors/diuretics/beta blockers

41
Q

Why does angina occur?

A

Oxygen supply to the heart is compromised

-limited duration and doesn’t cause death to cardiac myocytes, only ischaemia

42
Q

How do organic nitrates treat angina?

A

Release nitric oxide (NO), this is also release endogenously from endothelial cells, helping to keep vessels open

  • given by GTN spray under tongue (quick and short acting)
  • isosorbide dinitrate

=POWERFUL VASODILATOR ON VEINS

43
Q

Which vessels does NO act on preferentially?

A

Veins
-as there is less endogenous NO released in veins
-lowering preload to heart, reducing workload of heart, lowering oxygen demand of the heart
-can act on coronary collateral arteries to improve oxygen delivery to ischaemic myocardium
(Very little effect on arterioles)

44
Q

How does NO cause vasodilation?

A

Increases levels of protein kinase G, decreasing calcium concentration in vascular smooth muscle cells
=relaxation

45
Q

What are the main aims for treating angina?

A
  • reduce workload of the heart

- improve blood supply to heart

46
Q

What conditions carry an increased risk of thrombus formation?

A
  • atrial fibrillation: risk of stroke
  • acute MI: risk of thrombus formation
  • mechanical prosthetic heart valves (patient put on anticoagulation as it predisposes you to getting clots)
47
Q

What are anti-thrombotic drugs?

A

Anticoagulants (prevent coagulation cascade to prevent thromboembolisms )
E.g. heparin (IV- inhibits thrombin)
E.g. warfarin (orally- antagonises action of vit K)
E.g. dabigatran (oral thrombin inhibitor)

Anti-platelets

  • aspirin
  • clopidogrel
  • MI: in arteriole side: clots are platelet rich

CVS (16 decks)

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