The Cardiac Conduction System Flashcards

1
Q

How are varicose veins classified?

A
  • Primary: the majority are idiopathic, caused by an underlying primary valve defect
  • Secondary: only a minority have an underlying cause:
  • -Pelvic mass occluding venous return (pregnancy, fibroids, ovarian tumour, colorectal cancer, testicular tumour)
  • -Previous DVT
  • -Arteriovenous fistula
  • -Klippel-Trenaunay syndrome
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2
Q

What is Klippel-Trenaunay syndrome?

A

A venous abnormality giving rise to large varicose veins, port-wine stains and limb overgrowth.

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3
Q

What are the 2 venous drainage systems of the lower limb?

A
  • Superficial: drains the skin and subcutaneous tissues, formed by the long and short saphenous veins
  • Deep: lies within deep fascia and drains muscles
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4
Q

What is thrombophlebitis?

A

An inflammatory process that causes a blood clot to form and block one or more veins, usually in your legs.

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5
Q

What is saphena varix? What can a saphena varix be mistaken for?

A

Dilatation of the saphenofemoral junction.

It characteristically disappears on lying down and has a bluish tint.

Can be confused with femoral hernia due to positive cough impulse

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6
Q

What is peripheral vascular disease? What is it caused by?

A

PVD occurs when there is narrowing of the arteries. It’s almost always caused by atherosclerosis, but may occur secondary to thromboembolism or inflammation.

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7
Q

What is the major cause of death in people with PVD of the legs?

A

Coronary heart disease.

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8
Q

What are the clinical features for PVD?

A
  • Intermittent claudication
  • hair loss on your legs and feet
  • numbness or weakness in the legs
  • brittle, slow-growing toenails
  • ulcers (open sores) on your feet and legs, which do not heal
  • changing skin colour on your legs, such as turning pale or blue
  • shiny skin
  • in men, erectile dysfunction
  • the muscles in your legs shrinking (wasting)
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9
Q

What is Raynaud’s phenomenon?

A

Cold-induced spasm of the arterioles, most commonly of the hands but also the feet.

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10
Q

What are the 2 main types of Raynaud’s phenomenon?

A

Raynaud’s disease: benign condition. Isn’t the result of an underlying medical condition.

Raynaud’s syndrome: associated with underlying disease process. Symptoms often more severe.

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11
Q

What is thoracic outlet syndrome?

A

A group of disorders that occur when blood vessels or nerves in the space between your collarbone and your first rib (thoracic outlet) are compressed. This can cause pain in your shoulders and neck and numbness in your fingers.

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12
Q

What is a cervical rib?

A

An extra rib that is present above the first rib.

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13
Q

What is the most common cause of thoracic outlet syndrome?

A

Presence of a cervical rib.

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14
Q

What is Buerger’s disease? What is it also known as?

A

AKA Thromboangiitis obliterans

A recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet.

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15
Q

Who does Buerger’s disease almost always affect?

A

Young middle aged adults whom smoke heavily.

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16
Q

What is cellulitis?

A

Inflammation of subcutaneous connective tissue.

17
Q

Tricuspid valve controls blood flow between where?

A

Right atrium and right ventricle.

18
Q

How does stimulation of the vagus nerve effect the heart?

A

Parasympathetic effect, decreasing heart rate.

19
Q

What is the resting potention in the SA node?

A

-55mv

20
Q

What is the resting potential in a cardiac myocyte?

A

-90mV

21
Q

Explain the process of a cardiac action potential.

A

Phase 4: – Occurs at rest during diastole. Voltage is fairly constant (-90mV). – Maintained by ATP dependant Na+-K+ pumps.

  • Phase 0: – Action potential arrives at a neighbouring cell and triggers a rapid influx of Na+ (some Ca2+).
  • Phase 1: – Closure of the Na+ channels and brief opening of K+ (small notch as K ions flow out).
  • Phase 2: – ‘Plateau phase’ with some K+ ions flowing out and Ca ions flowing in.
  • Phase 3: – Ca2+ channels close and various K+ channels open leading to repolarisation.
22
Q

Basic ECG

A
23
Q

Why does the AV node delay the impulse from the SA node?

A

The AV node acts to delay the impulses by approximately 120ms, to ensure the atria have enough time to fully eject blood into the ventricles before ventricular systole.

24
Q

Purkinje fibres

A

The Purkinje fibres (sub-endocardial plexus of conduction cells) are a network of specialised cells. They are abundant with glycogen and have extensive gap junctions.

These cells are located in the subendocardial surface of the ventricular walls, and are able to rapidly transmit cardiac action potentials from the atrioventricular bundle to the myocardium of the ventricles.

This rapid conduction allows coordinated ventricular contraction (ventricular systole) and blood is moved from the right and left ventricles to the pulmonary artery and aorta respectively.

25
Q

What is the most common indication for a pacemaker?

A

The most common indication for a pacemaker is bradycardia.

Note:Pacemakers can also be used to treat some tachycardias, certain types of heart block and other rhythm abnormalities

26
Q

What are the sympathetic and parasympathetic neurotransmitters that control heart rate?

A

Sympathetic = noradrenaline

Parasympathetic = acteylcholine

27
Q

What innervates the SA node?

A

Vagus nerve

Reduces rate to 60-80bpm

28
Q

Pacemaker action potential

A
29
Q

How do sympathetic and parasympathetic activation alter heart rate?

A

Sympathetic activity releases noradrenaline increases slope of phase 4 and decreases time to reach threshold.

Parasympathetic activity releases acetylcholine decreases slope of phase 4 and therefore extends time to reach threshold.

30
Q

Refractory period.

A

• Time between Phase 0 & 3 when sodium channels are inactivated – no response to stimulus.

  • a change in this can lead to arrhythmias.
31
Q

Acetylcholine acts on what receptors to slow heart rate?

A

Muscarinic receptors.

32
Q

Parasympathetic activation affects the heart how?

A
  • Leads to:
  • Cardiac slowing (SA node),
  • Inhibition of AV conductance.
  • Reduction in adenylate cyclase activity and subsequent reduction in cAMP - reduces Ca2+ influx and shortens plateau.
  • Negative inotropic effect (reduced force of atrial contraction).
  • Negative chronotropic effect (reduced heart rate).
  • Negative dromotropic effect (reduced conduction velocity).
  • Negative lusitropic effect (reduced rate of relaxation).
33
Q

Drug-induced long QT syndrome is caused by what?

A
  • Direct blockage of hERG channels
  • Interference with hERG channel trafficking to the cell surface