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ESA2 Unknown > CVS > Flashcards

CVS Flashcards

0
Q

Muscular arteries

A

Same as elastic, but less elastic membranes, more SMC and unmyelinated nerve endings

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1
Q

Structure of elastic arteries

A

TI endothelial, sub endothelium of CT
TM fence started elastic membranes, SMC, collagen
TA fibroelastic CT and vaso vasorum

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2
Q

Structure of arterioles

A

D<0.1mm
1-3 SMC
External elastic lamina is abscent
TA is scant

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3
Q

Length of systole and diastole

A

280ms

700ms

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4
Q

Spread of excitation down septum

A

Endocardial to epicardial

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5
Q

Define ionotropy and chronotropy

A

Ionotropy is contract ability

Chronotropy is rate

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6
Q

Receptor that is responsible for vasoconstriction

A

Alpha 1

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7
Q

Autonomic nervous system that dominates heart at rest
Natural heart rate
If parasympathetic knocked out

A

Parasympathetic dominates
60bpm
100bpm

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8
Q

The autonomic changes involved in increasing heart rate

A

Decrease in parasympathetic

Then increase in sympathetic

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9
Q

Link resistance, flow and pressure drop in arterioles

A

Flow constant in all CVS so due to high R, high pressure drop

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10
Q

Pulse pressure and average pressure

A

Pulse: difference between systolic and diastolic
Average: diastolic + 1/3’systolic pressure

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11
Q

Name the vasodilator metabolites

A

H+, K+, Adenosine

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12
Q

Define pre load and after load

A

Pre load- end diastolic stretch of myocardium

After load- force necessary to expel blood into the arteries

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13
Q

How the body prevents pulmonary oedema in excercise

A

Heart rate already high so stroke vol kept low but CO is high

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14
Q

How haemorrhage effects venous pressure

A

Decreased blood vol, decreased CO and arterial pressure, recognised by barro receptors that increase HR and TPR which lowers VP and hence AP even further

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15
Q

What is special about SAN myocardium a membrane potential

A

Less negative so fast Na chan remain inactive, only slow Na chan open during repolarisation so you get timed depolarisation

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16
Q

Causes of Arrhythmias

A

Ectopic Pace Maker activity
After Depolarisation
Reentry loop

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17
Q

Class 1 anti arrythmic

A

V gated Na chan blockers eg lidocaine, this prevents after depolarisations

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18
Q

Class 2 anti arrythmic

A

Beta adrenoceptor antagonists eg propranolol and atenolol

Decreases ionotropy and chronotropy so reduced O2 demand from myocardium

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19
Q

Class 3 anti arrythmic

A

K+ chan blockers! lengthened absolute refractory period preventing another AP too soon,
Not generally used

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20
Q

Class4 anti arrythmic

A

Ca2+ chan blockers eg Verapamil
Decreases HR and AV node conduction
Decreases contractile force

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21
Q

What does adenosine do as an antiarrythmic?

A

Resets the heart as it hyper polarises the cell

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22
Q

How do ACE inhibitors work?

A

Prevent vasoconstrictor angiotensin 2 so decreases pre and after load
Also decreases aldosterone and therefor blood vol.

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23
Q

What is the action of an organic nitrate spray?

A

SMC release NO2 -> NO which is a vasodilator

Primarily acts as a venodilator, then on coronary arteries

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24
Q

The colours of the limb leads

A

Red RU
Yellow LU
green LL
Bike RL

25
Q

Placement of chest leads

A

1 is 4th intercostal space RHS of sternum
2nd is LHS of above
4th is 5th intercostal space mid clavicular line
6th is mid axillary

26
Q

How to work out ECG rate

A

300/no of squares

27
Q

What would a ventricular ectopic beat look like

A

Wider, taller and may be every 3rd or 4th

28
Q

ECG of atrial fibrillation

A

P wave abscent, instead irregular fibrillation waves between QRS complexes

29
Q

What does ventricular fibrillation look like on ECG

A

Uncoordinated contraction

30
Q

1st degree heart block

A

PR interval elongated from 200ms, conduction delay

31
Q

2nd degree T1 heart block

A

PR interval is erratic, gets longer till a QRS complex is dropped

32
Q

2nd degree T2 heart block

A

Excitation sometimes fails to pass AVN or bundle of His

33
Q

Compete 3rd degree heart block

A

No conduction at AVN, ventricles have ectopic pacemaker but beats are slower

34
Q

Bundle branch block

A

Lengthened QRS complex

35
Q

Blood flow of pulmonary cvs

A

Low r, short, wide vessels, low pressure

36
Q

How is blood diverted from alveoli not well oxygenated?

A

Hypoxia pulmonary vasoconstriction

37
Q

How does coronary endothelium produce a high basal flow?

A

Continuous production of NO

38
Q

3 cerebral circulation protection mechanisms

A

Myogenic auto regulation: increased bp causes vasoconstriction across trans mural wall
Metabolic Regulation: increased CO2 causes vasodilation
Regional activity: highly active has high release of adenosine

39
Q

Cushings reflex

A

Increased ICP decreases blood flow to vaso motor control regions and increases it’s sympathetic activity so increased arterial blood pressure

40
Q

Chest pain from heart problems location

A

Central retrosternal

41
Q

Signs of unstable angina

A

Ischemic chest pain at rest, depressed ST

42
Q

Treatment of angina

A

Acute - Nitrate spray,
Prevent - beta and Ca chan blockers and oral nitrates
Prevention of cardiac event: aspirin, statins, ACE inhibitors

43
Q

Cause of thrombosis from atheroma?

A

Exposure of thrombogenic necrotic core

44
Q

She do you get NSTEMI MI

A

Infarct is not full thickness

45
Q

Class 1 heart failure

A

None symptomatic but limitation of physical activity (LPA)

46
Q

Class 2 heart failure

A

Slight LPA leading to symptoms, none at rest

47
Q

Class 3 heart failure

A

Marked LPA and symptoms, none at rest

48
Q

Class 4 heart failure

A

Inability to do activity without symptoms and some symptoms at rest

49
Q

Congestive heart failure

A

Both sides of the heart failing

50
Q

Describe RAAS

A

Renin angiotensin aldosterone system, makes HF worse
Decreased bp causes renin release from kidneys
Angiotensin 1 converted to angiotensin 2, this is a vasoconstrictor and causes release of aldosterone increasing blood vol

51
Q

Action of cardiac glycosides

A

Increase CO and heart contractility by inhibiting Na/K pump so inhibits NCX so intra cellular Ca raises

52
Q

Define shock

A

Inadequate distributed tissue perfusion

53
Q

Cardiogenic shock

A

Inability to eject enough blood eg Arrhythmias

54
Q

Mechanical shock

A

Restriction of filling the heart eg cardiac tamponade

55
Q

Hypovolaemic shock

A

Loss of circulating fluid eg haemorrhage

56
Q

Normovolaemic shock -

A

Fall in TPR eg sepsis

57
Q

How to treat shock?

A

Fluids and adrenaline

58
Q

Pericardial sac in to out

A

Serous, parietal, fibrous

59
Q

Phrenic nerves

A

C3 C4 C5, motor and sensory to diaphragm, sensory to pericardium
Right phrenic nerve over RA
Left over left

60
Q

How is heart attached to sternum?

A

Sternopericardiac ligament

ESA2 Unknown (3 decks)

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