Cardiac Disorders Flashcards

0
Q

Define stenosis.

A

STENOSIS = narrowed valve e.g. aortic stenosis produces murmur in rapid ejection phase

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1
Q

What causes the sound of a heart murmur?

A

Laminar flow usually produces no sound. Abnormal flow causes turbulent blood which produces sound.

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2
Q

Define incompetence.

A

INCOMPETENCE = valve not closing properly, causing backward flow of blood (REGURGITATION)

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3
Q

What are the acyanotic congenital heart defects?

A
Patent ductus arteriosus
Patent foramen ovale 
Atrial septal defects (left -> right shunt)
Ventricular septal defects (left -> right shunt)
Aortic stenosis 
Pulmonary stenosis 
Coarctation of aorta 
Mitral stenosis
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4
Q

What are the cyanotic congenital heart defects? What is required?

A

Tetralogy of Fallot
Tricuspid atresia
Transposition of great arteries
Hypoplastic left heart

Right -> left shunt AND distal obstruction required (pressure normally lower in the right than the left)

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5
Q

Describe patent ductus arteriosus.

A

Ductus arteriosus fails to close (fibrose?)

Deoxygenated blood from pulmonary trunk mixes with oxygenated blood in aorta

Left-sided heart failure (+pulmonary vascular disease -> Eisenmenger’s syndrome)

Treat by ligation

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6
Q

Describe patent foramen ovale.

A

Foramen ovale fails to close at birth

Usually clinical silent as the higher atrial pressure functionally closes the valve

BUT it can allow a venous embolism to reach the systemic circulation (paradoxical embolism)

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7
Q

Describe atrial septal defects.

A

Left —> right (blood from left returned to lungs instead of going to body)

e.g. ostium primum/secundum atrial defect (inadequate formation of/excessive resorption of), sinus venosus defect

Increased pulmonary blood flow —–> right ventricular overload ———> pulmonary hypertension ———-> right heart failure

Eisenmenger’s syndrome may result

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8
Q

Describe ventricular septal defects.

A

Left —-> right (blood from left returned to lungs instead of going to the body)

Most commonly in membranous portion of interventricular septum

Left ventricle volume overload ——–> pulmonary venous congestion ——–> pulmonary hypertension

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9
Q

Describe aortic stenosis.

A

Obstructed aortic valve ——> increased left ventricular pressure ——–> hypertrophy of left ventricle ———-> increased pulmonary artery pressure ——> increased cardiac output ——> heart failure

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10
Q

Describe pulmonary stenosis.

A

Can be valve, outflow, or branch

Increased RV pressure -> right ventricular hypertrophy -> right-sided heart failure

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11
Q

Describe coarctation of the aorta.

A

Narrowing of aortic lumen around ligamentum arteriosum —–> increased afterload of left ventricle —–> left ventricular hypertrophy —–> heart failure (shortly after birth)

Normal perfusion of head and upper limbs (supplied before narrowing) but poor perfusion to the rest of the body

Weak delayed femoral pulses and upper body hypertension

Common in Turner syndrome (XO)

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12
Q

Describe mitral stenosis.

A

Increased left atrial pressure —-> transudation of fluid into lung interstitium ——-> pulmonary hypertension ——–> increased jugular venous pressure ——–> ascites & liver congestion

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13
Q

Describe tetralogy of Fallot.

A

Outflow of interventricular septum too far anterior and cephalad ->
Ventricular septal defect + overriding aorta (receives blood from both ventricles) + pulmonary stenosis + right ventricular hypertrophy

Pulmonary stenosis —–> increased resistance in bloodflow to lungs —–> right ventricular hypertrophy (compensatory; also due to VSD reducing pressure in ventricle)

Right -> left shunt (deoxygenated blood bypasses lungs -> cyanosis)

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14
Q

Describe tricuspid atresia.

A

Lack of development of tricuspid valve

No inlet into right ventricle

Complete right -> left shunt required to return blood to right atrium
(e.g. atrial septal defect, patent foramen ovale) + shunt allowing blood flow into the lungs required (e.g. ventricular septal defect, patent ductus arteriosus)

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15
Q

Describe transposition of the great arteries.

A

Two unconnected, parallel circulations

Right ventricle connected to aorta, left ventricle connected to pulmonary trunk

Not compatible with life unless there is a shunt

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16
Q

Describe hypoplastic left heart.

A

Left ventricle and ascending aorta fail to develop

Patent ductus arteriosus + patent foramen ovale/atrial septal defect required

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17
Q

What is Eisenmengen’s syndrome?

A

Chronic Left -> right shunt initially

Severe pulmonary vascular obstruction -> vascular remodelling (due to the lungs activating) occurs until shunt reverses

Right -> left shunt (thereby becomes cyanotic)

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18
Q

Define arrhythmia. What conditions encompass arrhythmia?

A

ARRHYTHMIA = abnormality of heart rate or rhythm

  • bradycardia (HR no atrial contraction)
  • tachycardia (HR>100bpm; ventricular or supraventricular)
  • ventricular fibrillation (uncoordinated ventricular depolarisation -> no ventricular contraction)
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19
Q

What are some of the causes of arrhythmias?

A
  • ectopic pacemaker activity
  • afterdepolarisations
  • re-entry loops
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20
Q

Describe ectopic pacemaker activity.

A

Damaged area of myocardium becomes depolarised and spontaneously active

Ischaemia activates latent pacemaker region which dominates SAN

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21
Q

Describe afterdepolarisations.

A

Abnormal depolarisation following the AP

Early: more likely if AP is prolonged (longer QT)

Delayed: more likely if [Ca2+]i is high

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22
Q

Describe re-entry loops.

A

Accessory conduction pathways:
Connects ventricular myocardium rather than the Purkinjie fibres

  • conducts faster than the AVN (P-R interval is shortened)
  • slow spread through ventricles + concurrent AVN conduction = wide QRS complex with “slurred” initial upstroke (delta wave)

Unidirectional block:
Complete block = no arrhythmia
Incomplete block = excitation takes long route and spreads the wrong way through the damaged area - circus of excitation produced

note: several small re-entry loops in the atria (due to damage e.g. mitral valve stenosis) causes AF

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23
Q

What is Wolff-Parkinson-White syndrome?

A

Accessory conduction pathway causing supraventricular/ventricular tachycardia

  • conducts faster than the AVN (P-R interval is shortened)
  • slow spread through ventricles + concurrent AVN conduction = wide QRS complex with “slurred” initial upstroke (delta wave)

Common cause of sudden death in adults

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24
Q

Outline how arrhythmias can be treated.

A
  • block voltage-dependent Na+ channels
  • beta-adrenoceptor antagonists
  • block K+ channels
  • block Ca2+ channels
  • adenosine
25
Q

Name a drug that blocks voltage-dependent Na+ channels. How does this treat arrhythmia?

A

Lidocaine

Only blocks voltage-gated Na+ channels in open or inactive state (not when closed or repolarised)

Dissociates in time for the next AP.

Use-dependent block: blocks when depolarisation begins

note: lidocaine used following MI if there are signs of VT to prevent damaged areas of myocardium from firing automatically

26
Q

Name a drug that is a beta-adrenoceptor antagonist (beta blocker). How do these treat arrhythmias?

A

Propanolol, atenolol

Block beta-1-adrenoceptors in heart to block sympathetic action & decrease the slope of the pacemaker potential (reduce HR)

Arrhythmias can be caused by increased sympathetic activity.

Used after MI (MIs also increase sympathetic activity) to reduce ischaemia by lowering HR & negative inotropy

Also slow AVN conduction (prevent supraventricular tachycardia)

27
Q

Name a drug that blocks K+ channels. How do these help prevent arrhythmias?

A

Amiodarone (treats Wolff-Parkinson-White syndrome)

Prolong the AP, in theory preventing another AP from occurring too soon

BUT in reality these drugs can be pro-arrhythmic (as will all anti-arrhythmic drugs) so are not generally used

28
Q

Name a drug that blocks Ca2+ channels. How do these treat arrhythmias?

A

Verapamil

  • decrease slope of pacemaker AP
  • decrease AVN conduction
  • negative inotropy
  • coronary & peripheral vasodilatation

note: DHP Ca2+ channel blockers are not effective in preventing arrhythmias but do act on vascular smooth muscle

29
Q

How does adenosine treat arrhythmia?

A

Acts on adenosine-1 receptors at AVN

Enhances K+ conductance —> hyperpolarises cell —> reduces c.AMP

Temporarily stops heart so that correct rhythm can be re-established

note: produced endogenously

30
Q

What is heart failure? How can it be treated?

A

HEART FAILURE = chronic failure of the heart to provide sufficient output to meet the body’s requirements

  • reduced force of contraction
  • reduced cardiac output
  • reduced tissue perfusion —> peripheral & pulmonary oedema

Treat by increasing force of contraction (to increase cardiac output) OR by reducing the workload of the heart.

Long-term:

  1. ACE inhibitors
  2. Beta-adrenoceptor agonists e.g. bisoprolol (beta-1 selective), carvedilol (mixed beta/alpha)
  3. Spironolactone

Short-term:

  1. Diuretics
  2. Cardiac glycosides (digoxin)

Prosthetic/mechanical valve replacement
Pacemakers

31
Q

Name a cardiac glycoside. How do these treat heart failure?

A

Digoxin

Block Na+/K+-ATPase —> increase [Na+]i —> decrease NCE activity —> increase [Ca2+]i —> increase Ca2+ stored in SR —> increase force of contraction

Short term:

  • positive inotropy
  • reduced AVN conduction (increased vagal activity)
  • reduced HR (increased vagal activity)
32
Q

Name a beta-adrenoceptor agonist. How do these treat heart failure?

A

Dobutamine

Short term increase in myocardial contractility.

Used to treat acute, reversible heart failure e.g. following heart surgery, cardiogenic shock

33
Q

Name an ACE inhibitor. How do these treat heart failure?

A

Ramipril

Inhibit angiotensin converting enzyme which converts angiotensin I to angiotensin II

Angiotensin II is a vasoconstrictor (increases peripheral resistance —> increases workload) and increases sodium and water reabsorption by the kidney (increased blood volume —> increased workload)

ACE inhibitors:

  • reduce vasomotor tone —> reduce HR —> reduce afterload
  • reduce blood volume —> reduce preload
34
Q

How can angina be treated?

A

Reduce workload of heart:

  • beta-blockers
  • Ca2+ channel antagonists (peripheral vasodilatation)
  • organic nitrates (vasodilatation)

Improving blood supply to the heart:

  • Ca2+ channel antagonists (peripheral vasodilation)
  • organic nitrates (vasodilatation)
35
Q

What do organic nitrates do?

A

React with thiols (-SH) in vascular smooth muscle to release NO2- which is reduced to NO (nitric oxide).

NO is a vasodilator.

Stimulates guanylate cyclase —> increased c.GMP —> reduced [Ca2+]i —> relaxation of vascular smooth muscle

Also dilates collateral arteries in the heart to improve O2 delivery to the ischaemic myocardium (BUT DOES NOT DILATE ARTERIOLES - THESE ARE ALWAYS FULLY DILATED)

36
Q

Name some classes and examples of antithrombic drugs. When should these be used?

A

Anticoagulants:

  • IV heparin (inhibits thrombin) (acute)
  • fractionated heparin (subcutaneous)
  • oral warfarin (Vit. K antagonist) (chronic)

Antiplatelets:
- aspirin

Use with conditions with increased risk of thrombus formation

e. g. AF (thrombi form in atria which can embolise to the systemic circulation)
e. g. MI (stasis of blood)
e. g. mechanical prosthetic heart valves

37
Q

What is hypertension? How is it treated?

A

HYPERTENSION = systolic 140mmHg<
- associated with increases in blood volume or increased peripheral resistance

Therapeutic targets:

  • reduce blood volume
  • reduce cardiac output
  • reduce peripheral resistance

Drugs:

  • diuretics (reduce Na+ & water retention by kidneys -> reduce blood volume)
  • ACE inhibitors (reduce Na+ & water retention by kidneys -> reduce blood volume AND vasodilatation -> reduce total peripheral resistance)
  • beta-blockers (reduce cardiac output)
  • alpha-1-adrenoceptor antagonists (vasodilatation -> reduce total peripheral resistance)
38
Q

Why would a sudden increase in parasympathetic activity to the heart be dangerous? Give some examples of when this might occur.

A

Decrease in heart rate, therefore decreased perfusion to cerebrum and heart (can result in cardiac arrest)

  • carotid sinus massage increases parasympathetic activity to the heart (increased discharge from carotid sinus) thereby reducing heart rate and stroke volume
  • mammalian diving reflex: cold water on face causes bradycardia and peripheral vasoconstriction due to activation of cranial nerve X (vagal nerve)
  • valsalva manoeuvre: forcible exhalation caused by coughing/straining traps blood in great veins due to increased intrathoracic pressure; when able to inhale again the intrathoracic pressure rapidly drops, the trapped blood rushes to the heart, causing tachycardia. Reflex bradycardia occurs to counter this
39
Q

Why do occlusions of coronary arteries cause more problems during exercise than at rest?

A

Shorter diastole during exercise, therefore coronary vessels fill less (even lower perfusion)

40
Q

Why does hyperventilation lead to syncope?

A

Hypercapnia causes vasoconstriction which reduces cerebral perfusion

41
Q

How should you treat someone who has fainted due to a temporary reduction in cerebral blood flow?

A

Lie them down

Effect of gravity on blood flow minimised, therefore maintains cerebral blood flow

42
Q

Describe pericarditis.

A

Infection of visceral pericardium -> exudate -> friction rub of layers against each other (causing inspiration pain) -> Dressler’s syndrome (fever, pleuritic pain, pericardial effusion)

43
Q

How does hypertrophy lead to death?

A

Arrhythmias -> ventricular tachycardia/VF -> cardiac arrest

44
Q

Why do you give adrenaline to someone who is in cardiac arrest?

A

Stimulates alpha-1 receptors on vascular smooth muscle -> vasoconstriction -> increased peripheral resistance & HR -> increased coronary perfusion

Stimulates beta-1 receptors in heart -> positive inotropy -> increased cardiac output

45
Q

What is high output heart failure? Give an example

A

Normal cardiac output but increased demand for oxygen makes the heart unable to supply the demand

e.g. AV malformation

46
Q

What are the key symptoms of heart failure?

A

BREATHLESSNESS (dyspnoea)

  • exertional
  • orthopnoea (breathlessness preventing patient from lying down)
  • paroxysmal nocturnal dyspnoea (wakes up due to breathlessness)
\+ cardiomegaly 
\+ 3rd & 4th heart sounds 
\+ elevated JVP
\+ tachycardia 
\+ hypotension 
\+ lung crepitations 
\+ ascites 
\+ peripheral oedema 
\+ hepatomegaly (tender)
47
Q

What are some of the causes of heart failure?

A

Main:

  • IHD
  • cardiomyopathy
  • hypertension
  • valvular disease
  • congenital heart disease
  • alcohol/drugs
  • arrhythmias
  • infection
48
Q

What is the normal ejection fraction of the heart?

A

~ 50%

49
Q

What are the changes to the heart that occur with heart failure?

A
Loss of muscle 
Uncoordinated/abnormal muscle contraction (slippage of fibre orientation)
Increase in collagen 
Myocyte hypertrophy 
Myocytolysis 
DIASTOLIC = hypertrophy 
SYSTOLIC = dilation
50
Q

How can you distinguish a heart that has failed and a heart that has infarcted?

A

Infarction = asymmetric dilation (thins around fibrosis)

Heart failure = symmetric dilation

51
Q

What are the sympathetic changes that occur during heart failure?

A

Short term: (increases cardiac output)

  • increase in contractility
  • arterial and venous vasoconstriction
  • tachycardia

Long term:

  • down-regulation of beta-adrenoceptors
  • noradrenaline acts on alpha-receptors to stimulate necrosis, myocyte apoptosis, and cardiac hypertrophy (and also up-regulates renin-aldosterone-angiotensin system)
  • reduction in heart rate variability
52
Q

Outline the renin-angiotensin-aldosterone system.

A

Angiotensinogen —> Angiotensin I —> Angiotensin II & Angiotensin III

Angiotensin II acts on receptors:

1: vasoconstriction + activates aldosterone —> fluid & salt retention
2: increase in NO

Bradykinin acts on receptors to increase NO

53
Q

What do natriuretic peptides do?

A

Atrial stretch —> natriuretic peptides released —> vasodilatation & increased urinary sodium secretion

note: ADH also released in HF —> increased fluid retention, tachycardia, reduction in systemic resistance

54
Q

What does endothelin do?

A

Secreted by vascular endothelial cells

Autocrine system & renal vasoconstrictor —> activates renin-angiotensin-aldosterone system

Levels correlates with severity of heart failure

55
Q

What are the chemicals involved in heart failure?

A

Natriuretic peptides
ADH
Endothelin
Prostaglandins (stimulates by NA & RAAS —> vasodilation of renal arteries)
Nitric oxide (reduced in heart failure due to blunted NO synthase)
Bradykinin (promotes vasodilation & natriuresis & stimulates production of prostaglandins)
Tumour necrosis factor (depresses myocardial function)

56
Q

What are the skeletal muscle changes in heart failure?

A

Reduced bloodflow
Reduced muscle mass (cachexia) (limbs & respiratory)
Fatigue
Exercise intolerance

57
Q

What are the differences between left and right sided heart failure?

A

RIGHT=
Caused by chronic lung disease/left-sided heart failure
Causes peripheral oedema

LEFT=
Causes pulmonary oedema

58
Q

What is cor pulmonale?

A

Right heart failure secondary to pulmonary hypertension (lung disease)

59
Q

What are the reversible causes of cardiac arrest?

A

4Hs and 4Ts

Hypoxia
Hypovolaemia
Hypothermia
Hyperkalaemia

Tension pneumothorax (—> compresses heart —> hypoxia)
Tamponade (—> compresses heart —> hypoxia)
Toxins
Thrombosis