CVS 9.1 - Drugs and the Cardiovascular System Flashcards Preview

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Flashcards in CVS 9.1 - Drugs and the Cardiovascular System Deck (63):

What is arrhythmia? What can cause arrhythmia?

- Abnormal heart rate or rhythm

- Atrial flutter
- Atrial fibrillation
- Ventricular fibrillation
- Tachycardia ([supra]ventricular)
- Bradycardia


What can cause arrhythmias?

- Ectopic pacemaker activity

- After depolarisations

- Re-entry loops


How can ectopic pacemaker activity cause arrhythmias?

- Damaged myocardium becomes depolarised

- Causes hidden pacemaker areas due to ischaemia that over power SAN

- Activates spontaneously

- Slower depolarisation so prolonged QRS complex


What does an early ectopic pacemaker activity cause?

Increased myocyte excitability


What does a late ectopic pacemaker activity cause?

Conduction failure


What is an after depolarisation?

- Premature depolarisations after an action potential due to triggered activity


What is triggered activity?

- Impulse initiation in cardiac fibres dependent on after depolarisation

- Another action potential is caused if threshold is reached leading to arrhythmia


What can after depolarisations cause?

- Really long action potentials/ increased QT interval

- Increases intracellular calcium concentration

- Increases force of contraction


How are re-entry loops caused?

- Conduction is blocked at a damaged area

- Unidirectional block = incomplete conduction damage


How can re-entry loops cause arrhythmias?

- Excitation spreads in wrong direction through damaged area

- Causes a circuit looping back on itself

- Re-excites tissue in a circle

- Causes a circle of contractions = tachycardia


What can multiple re-entry loops result in?

- Lots of small entry loops in atria

- Multiple foci

- Mitral stenosis = increased difficulty to fill


What are the four groups of anti-arrhythmic drugs?

- Block vgNa+ channels

- Beta-adrenoceptor antagonists

- K+ channel blockers

- Ca2+ channel blockers


What are some risk factors for arrhythmia?

- Age (more common in older age)

- Heart disease/attack

- Leaky/narrow valves

- High blood pressure

- Diabetes

- Sleep apnoea (heart doesn't get enough O2 = stress)

- Over-under active thyroid


How does bradycardia affect systemic circulation?

- Decreases cardiac output

- Decreases arterial pressure


How does tachycardia affect systemic circulation?

- Decreased stroke volume

- Decreased cardiac output

- Decrease preload when contraction rate is high


How does atrial fibrillation affect systemic circulation?

- Decreases stroke volume and cardiac output during exercise

- Increased risk of thrombus formation


How does ventricular fibrillation affect systemic circulation?

Cardiac output is 0


How are drugs blocking Na+ channels e.g. local anaesthetics, used to treat arrhythmias?

- Block vg Na+ channels when open/inactivated (use-dependent)

- Depolarisation needs to happen first

- Rapid dissociation means that the next normal action potential can happen


Why do Na+ channel blockers only affect damaged areas rather than normal tissue?

- Damaged areas are depolarised

- Na+ channels are open during depolarisation

- Blocked by drugs as they are use dependent

- Ensures there is no automatic firing


When would be an appropriate time for local anaesthetics to be used to treat arrhythmias?

- Ventricular tachycardia before/after myocardial infarction

- Administered intravenously


How are beta adrenoreceptor antagonists used to treat arrhythmias?

- Block sympathetic action

- Block beta1 adrenoreceptor in the SAN

- Decreases pacemaker potential

- Negative chronotropy and inotropy


What are the overall effects of beta adrenoreceptor antagonists?

- Decrease work load

- Decrease blood volume

- Decrease O2 demand therefore decreasing myocardial ischaemia

- Negative chronotropy and inotropy


What are the effects on the heart in a beta adrenoreceptor antagonist acts on the AVN? When would this be an appropriate treatment?

- Slows AVN conduction

- During atrial fibrillation to prevent supraventricular tachycardia


Why can't propanolol be given to asthmatics?

- Non-selective for beta1 and beta2 adrenoreceptors

- Causes bronchoconstriction as well as decreasing HR and FOC


Why is atenolol a more appropriate treatment for asthmatics?

- Cardioselective for beta1

- Doesn't cause bronchoconstriction


What is meant by a therapeutic use?

The use of a drug where the effects are beneficial


What is the action of K+ channel blockers in treating arrhythmias?

- Theoretically prolongs action potential therefore prolonging absolute refractory period

- Prevents another action potential from being generated too soon


What is the problem with using K+ channel blockers?

- Actually promotes arrhythmias

- More likely to happen during long action potentials

- Due to after depolarisations

- Causes another action potential if threshold is reached


Which K+ channel blocker can actually be used to treat arrhythmias and why?

- Amiodarone

- Blocks other channels too which balances out effects


When would amiodarone be used?

Treatment of Wolff-Parkinson-White syndrome


What is Wolff-Parkinson-White syndrome?

- There is an extra electrical pathway between atria and ventricles

- Causes heart to beat really fast for periods of time (supraventricular tachycardia)


What is the action of Ca2+ channel blockers in treating arrhythmias when given intravenously?

- Block Ca2+ entry into the cell

- Decreases pacemaker potential at SAN

- Decreases AVN conduction

- Negative inotropy

- Vasodilation of some coronary and peripheral vessels


What is the significance of using dihydropyridines?

Only act on smooth muscle


Why are Ca2+ channel blockers given intravenously?

- Due to vasoconstrictive nature

- Could cause tissue necrosis


When would Ca2+ channel blockers be used as treatment?

- Anti-hypertensive

- Arrhythmias

- Heart failure

- Angina


What is the general action of negative inotropic drugs?

- Decrease heart rate

- Decrease force of contraction


What is the action of adenosine when given intravenously?

- Enhances K+ conductance at A1 receptors on AVN

- Hyperpolarisation of cell = further from threshold

- Restores sinus rhythm


What is heart failure?

Chronic failure of the heart to provide sufficient output to meet the requirements of the body


What are the effects of heart failure on the heart and circulation?

- Decreased force of contraction

- Decreased cardiac output

- Decreased perfusion

- Oedema (peripherally if RV fails)


Why does heart failure cause oedema?

- Causes venous congestion

- Increases hydrostatic pressure


What can be used to treat heart failure?

- Positive inotropes to increase cardiac output

- Beta adrenoreceptor AGONISTS (cardiogenic shock)

- Cardiac glycosides (only if there's a lot of oedema and want to increase CO)


What is the action of cardiac glycosides?

- Block Na+K+ATPase

- Increases [Na+]in

- Increases [Ca2+]in

- NCX is more inefficient

- Increases force of contraction/ positive inotropy


Why can cardiac glycosides be used during heart failure and atrial fibrillation?

- Increase in vagal activity

- Slows AVN conduction

- Decreases heart rate


What are the overall effects of drugs used to treat heart failure?

- Decrease work load of the heart

- Decrease afterload and therefore TPR

- Decrease preload (venous return)


What is the general action of ACE inhibitors?

Inhibit the angiotensin converting enzyme


What is the renin-angiotensin-aldosterone system?

Hormonal regulation of blood pressure and fluid balance. It is up-regulated during heart failure


What is the first step of the renin-angiotensin-aldosterone system?

- Liver releases angiotensin (hormone)

- Kidney releases renin (enzyme)

- Renin cleaves angiotensin to form angiotensin 1


What stimulates the release of renin?

- Decrease in Na+ delivery to distal tubules

- Renal artery hypotension

- Beta1 agonism by the SNS


What is the second step of the renin-angiotensin-aldosterone system?

- Vascular endothelium in the lungs releases ACE (converting enzyme)

- ACE + Angiotensin 1 = angiotensin 2 forms

- Causes heart to work harder


What is the effect of angiotensin 2 in the zona glomerulosa of the adrenal glands?

- Stimulates aldosterone secretion

- Increases Na+ absorption

- Increases fluid which increases blood pressure

- Decreases K+ absorption


What is the effect of angiotensin 2 in the kidneys?

- Vasoconstriction in arterioles

- AT1 receptors are coupled to G-alphaQ proteins

- Follows IP3 pathway

- Increases blood pressure due to increased resistance


What is the action of ACE inhibitors?

- Prevent angiotensin 2 from forming

- Vasodilates arterioles in kidneys

- Venous dilation = decreased afterload (↓ vasomotor tone and ↓ blood pressure) and ↓preload (↓ fluid retention = ↓blood volume)

- ↓blood volume by ↓Na+ absorption in zona glomerulosa = ↓ preload (antihypertensive treatment)


Which three groups of drugs decrease the work load of the heart?

- ACE inhibitors

- Beta adrenoreceptor antagonists

- Diuretics


What is angina?

- Severe chest pain that spreads due to an inadequate coronary blood supply that is caused by atheromatous arteries

- Is transient and has no cell death (just ischaemia)


How can angina be treated?

- ↓ work load

- Beta adrenoreceptor blockers
- Ca2+ channel antagonists (improves blood supply)
- Organic nitrates (improves blood supply a little)


What is the action of organic nitrates?

- React with smooth muscle

- Releases NO2-

- NO2- is reduced to NO (produced by endothelium anyway)

- Causes vasodilation


How does NO cause relaxation of cardiac smooth muscle?

- Activates guanylate cyclase = ↑cGMP = ↓[Ca2+]in = activates protein kinase G = ↑[Ca2+] in SR

- Activates K+ channels = hyperpolarises the cell

- Stimulates a protein kinase for activation of MLCP = myosin light chain is dephosphorylated


What is the result of vasodilation of veins when organic nitrates are pharmalogically administered?

- ↓ preload = ↓ filling = ↓ work load

- ↓ O2 demand


What can happen in the heart to increase the risk of thrombus formation?

- Atrial fibrillation

- Acute myocardial infarction

- Prosthetic heart valves


What is the action of anticoagulants and antiplatelets?

- Anticoagulations = thrombin/vitamin K inhibition

- Antiplatelets = ↓ platelets


What are the effects of hypertension on circulation?

- ↑ arterial blood pressure

- ↑ total peripheral resistance

- ↑ Na+ and water uptake


What is the equation for pressure?

Pressure = Flow x Resistance


What is the equation for blood pressure?

Blood pressure = Cardiac output x Total Peripheral Resistance

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