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Transition block 1 > Physiology - cardiology > Flashcards

Physiology - cardiology Flashcards

1
Q

Cardiac muscle is not striated (T/F)?

A

False - the striation is caused by regular arrangement of contractile protein

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2
Q

How does electrical excitation of cardiac muscle occur?

A

Cardiac muscle does not have neuromuscular junctions but the myocytes are electrically coupled by gap junctions. Gap junctions are protein channels which form low resistance electrical communication pathways between neighbouring myocytes

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3
Q

What separates cardiac myocytes?

A

Intercalated discs joined by gap junctions

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4
Q

What structure in the intercalated discs provides mechanical adhesion between adjacent cardiac cells?

A

Desmosomes - they ensure that the tension developed by one cell is transmitted to the next

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5
Q

Each muscle fibre contains many _____ which are the contractile units of muscle

A

Myofibrils

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6
Q

Myofibrils have alternating bands of thick and thin protein filaments, what are these called?

A 
Actin = thin filaments, causes the lighter appearance in myofibrils
Myosin = thick filaments, causes the darker appearance
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7
Q

What is the collective name for the arrangement of actin and myosin?

A

Sarcomere

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8
Q

How is muscle tension produced?

A

By sliding of actin filaments on myosin filaments - this force generation is ATP dependent

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9
Q

What ion is required to switch on cross bridge formation?

A

Calcium

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10
Q

Where is calcium released from and what is its release dependent on?

A

Released from the sarcoplasmic reticulum and is dependent on the presence of extra-cellular calcium

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11
Q

What happens to the AP after systole?

A

The AP has passed so Ca influx ceases and Ca is re-sequestered in the SR by Ca-ATPase, heart muscle relaxes

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12
Q

Why is the long refractory period so important to normal cardiac function?

A

Prevents generation of tetanic contraction

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13
Q

In which parts of the AP does the long refractory period occur?

A

During the plateau phase of ventricular action potential the Na channels are in the depolarised closed state i.e. not available for opening
During the descending phase of AP the K channels are open and the membrane cannot be depolarised

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14
Q

What is the stroke volume?

A

The volume of blood ejected by each ventricle per heart beat

SV = EDV - ESV

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15
Q

What is the EDV and what does it determine?

A

EDV = end diastolic volume

Determines the cardiac preload and is determined by the venous return to the heart

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16
Q

What is Starling’s law?

A

The more the right ventricle is filled with blood during diastole (EDV) the greater the volume of ejected blood will be during the resulting systolic contraction (SV) and thus the venous return to the LA from pulmonary veins increases (EDV) and therefore increases the SV into the aorta

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17
Q

What is afterload?

A

The resistance into which the heart is pumping

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18
Q

How does Frank-Starling mechanism correct increased afterload?

A

If afterload increases, at first the heart is unable to eject entire SV, which increases the EDV. Force of contraction then rises

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19
Q

What happens if afterload is persistently increased?

A

Eventually the ventricular muscle mass increases to overcome resistance e.g. untreated hypertension -> ventricular hypertrophy

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20
Q

What type of nerve fibres and neurotransmitters supply the ventricular muscle of the heart?

A

Sympathetic nerve fibres and noradrenaline (NA) is the neurotransmitter

21
Q

What does positive inotropic effect mean and how is it caused?

A

Stimulation of sympathetic nerves increases the force of contraction = positive inotropic effect

22
Q

What else (other than a positive inotropic effect) does sympathetic stimulation cause in the heart?

A

Positive chronotropic effect i.e. increases the heart rate

23
Q

What effect does sympathetic stimulation have on ventricular contraction in terms of the AP?

A

Force of contraction increases (activation of Ca channels - greater Ca influx)
Peak ventricular pressure rises - contractility of heart at a given EDV rises (Frank-Starling curve shifted to the left)
Rate of ventricular relaxation increases (increased rate of Ca pumping)
This reduces the duration of diastole

24
Q

What is the effect of parasympathetic stimulation of ventricular contraction?

A

Vagal stimulation has major influence on rate, not force, of contraction

25
Q

What effect do adrenaline and NA have on the heart?

A

Released from adrenal medullar and have an inotropic and chronotropic effect

26
Q

What is cardiac output?

A

Volume of blood pumped by each ventricle per minute

CO = SV x HR

27
Q

What is atrial fibrillation?

A

Disorganised electrical activity of the atria resulting in an irregular heartbeat

28
Q

What is the underlying mechanism of AF?

A

Ectopic foci in muscle sleeves in the ostia of the pulmonary veins

29
Q

How is AF terminated?

A 
Pharmacologic cardioversion (30% effective) with anti-arrhythmic drugs e.g. flecainide, sotalol, amiodarone
Electrical cardioversion (90% effective) by direct current (DCCV)
Spontaneous reversion to sinus rhythm
30
Q

What are the different types of AF?

A

Paroxysmal - lasting less than 48 hours, often recurrent
Persistent - lasting >48 hours and can still be cardioverted to NSR, unlikely to spontaneously resolve to NSR
Permanent - inability of drugs or other methods to restore NSR

31
Q

What are some diseases associated with AF?

A

Hypertension, congestive HF, sick sinus syndrome, coronary heart disease, obesity, alcohol abuse, congenital heart disease, COPD, pneumonia

32
Q

What is lone (idiopathic) AF?

A

Absence of any heart disease and no evidence of ventricular dysfunction
Diagnosis of exclusion

33
Q

What are some of the symptoms of AF?

A

Palpitations, dizziness, syncope, chest pain, dyspnoea, sweatiness, fatigue

34
Q

What are the features of AF on ECG?

A

Atrial rate >300bpm
Rhythm is irregularly irregular
Absent P waves
Presence of f waves

35
Q

What can happen in patients with WPWS and AF?

A

AF in patients with pre-excitation (WPWS) can result in VF and sudden cardiac death

36
Q

How is AF managed?

A

Rhythm control or rate control

Anti-coagulation for both approaches if high risk of thromboembolism

37
Q

What are some examples of rate controlling drugs used in AF?

A

Digoxin, beta-blockers, verapamil and diltiazem

38
Q

What are some methods of rhythm control used in AF?

A

Pharmacological cardioversion - anti-arrhythmic drugs e.g. amiodarone
Direct current cardioversion (DCCV)
Maintenance of NSR - anti-arrhythmic drugs, catheter ablation, surgery

39
Q

What ion channel do class I anti-arrhythmic drugs block and what is their main use?

A

Na channels - act on phase 0 of the AP e.g. lignocaine, quinidine, flecainide
Rhythm control

40
Q

What ion channel do class II anti-arrhythmic drugs block and what is their main use?

A

Beta receptors - act on phase 4 of the AP e.g. propanolol

Rate control

41
Q

What ion channel do class III anti-arrhythmic drugs block and what is their main use?

A

K channels - act on phase 3 of the AP e.g. amiodarone, sotalol, dronedarone
Rhythm control

42
Q

What ion channel do class IV anti-arrhythmic drugs block and what is their main use?

A

Ca channels - act on phase 2 of the AP e.g. verapamil

Rate control

43
Q

When is anti-coagulation recommended in patients with AF?

A

Thyrooxicosis, HOCM, valvular AF (warfarin only) or >2 risk factors; age>75, hypertension, HF, previous stroke/thromboembolism, DM

44
Q

What is the risk scoring system used in AF?

A 
CHA2DS2VASc 
Congestive HF
Hypertension
Age>75
Diabetes mellitus
Stroke
Vascular disease
Age 65-74
Sex (female)
45
Q

Why is radiofrequency ablation used in AF?

A

To maintain sinus rhythm by ablating AF focus (usually in pulmonary veins)
For rate control - ablation of the AVN to stop fast conduction to the ventricles

46
Q

Why is left atrial catheter ablation used in AF?

A

Isolate triggers in the pulmonary veins by pulmonary in LA vein isolation

47
Q

What is atrial flutter?

A

Rapid and regular form of atrical tachycardia

Usually paroxysmal

48
Q

What are the features of atrial flutter on ECG?

A

Atrial rate >300bpm, ventricular rate usually 150bpm
Saw tooth wave
Regular rhythm

49
Q

How is atrial flutter treated?

A

Radiofrequency ablation
Pharmacological therapy - slow the ventricular rate, restore sinus rhythm and maintain SR
Cardioversion
Warfarin for prevention of thromboemboli

Transition block 1 (11 decks)

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