Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Easter revision 2018 > CVS > Flashcards

CVS Flashcards

1
Q

How does ANP work?

A

Released when the atrial myocytes are stretched, and it vasodilates afferent arteriole to kidney to increase kidney blood flow in order to decrease Na reabsorption and lower fluid level (i.e. it causes natriuresis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which two endocrine glands does angiotensin II act on?

A

Adrenal gland to release aldosterone (increases Na reabsorption) and hypothalamus to produce ADH (increase water reabsorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe murmurs for mitral stenosis and regurg

A

Mitral regurg is holosystolic murmur, mitral stenosis is diastolic rumble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe murmurs for AV stenosis and regurg

A

AV regurg is early decrescendo diastolic, AV stenosis is crescendo decrescendo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does aldosterone act?

A

On principle cells of collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name three stages of hypertension?

A

Stage 1 - 140/90, 2 - 160/100, 3- 180 or 110

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of secondary HTN?

A

Renal artery stenosis, CKD, Conn’s syndrome (aldosterone secreting adenoma) or Cushing’s syndrome (excess cortisol stimulates aldosterone Rs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Complications of HTN?

A

Retinopathy, stroke, MI, LV hypertrophy (from increased afterload), HF, kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How to calculate maBP?

A

actual formula is maBP = TPR x CO

but can work out with maBP = diastolic P + 1/3 pulse pressure e.g. 60 + 10 = 70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is shock? Give types

A

Shock is inadequate blood flow, so either due to reduced CO or reduced TPR.
Reduced CO: mechanical shock where it can’t fill, cardiogenic shock where it can’t pump, hypovolemic shock (haemorrhage, burns, D&V, hyponatremia)
Reduced TPR: toxic shock or anaphylactic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of mechanical shock?

A

Can’t fill e.g. cardiac tamponade due to fluid in pericardial space (treat with pericardiocentesis) or massive PE occluding large pulmonary artery so RV can’t empty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

At what % of fluid loss will you display signs of shock?

A

Less than 20% no shock, 20-30% some signs, 30-40% serious shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Signs of shock?

A

Tachycardic, low BP, sweaty, flushed, pale, weak pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is septic shock?

A

Persisting hypotension despite fluids following sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe what electrical events each part of an ECG is representing

A 
P wave - atrial depol
Q wave- IV septum depol
R wave - apex of ventricle depol 
S wave - base of ventricle depol 
T wave - repol of ventricles (double negative so appears +)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which leads show inferior heart problems?

A

aVF, II, III (RCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which leads show lateral heart problems?

A

aVL, I, V5,6 (LCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which leads show anterior heart problems?

A

v1,V2,V3,V4 (LAD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

On ECGs how much are the boxes worth?

A

5 large squares 1sec, one large square 200ms, one small square 40ms, 25 small squares are 1sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How to calculate HR from ECG?

A

300/no. of large squares = bpm

Or if irregular count how many in six secs (30 large boxes) and times by 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How long should a PR interval be?

A

3-5 small boxes (120-200ms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How long should a QRS interval be?

A

<3 small boxes (<120ms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How long should QT interval be?

A

11-12 small boxes (<0.45 in M, <0.47 in F)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the types of heart block (= problem with conduction between A and V)

A

1st degree - PR interval >5 small boxes
2nd degree - Mobitz Type 1 (Wenkebach phenomenon) is where PR gets longer and longer until one QRS isn’t transmitted
2nd degree - Mobitz Type 2 where PR normal then suddenly drops. High risk of progression to 3rd degree
3rd degree - complete heart block, atrial depol normal but NOT conducted to Vs so ventricular escape rhythm, wide QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the types of heart block (= problem with conduction between A and V)

A

1st degree - PR interval >5 small boxes
2nd degree - Mobitz Type 1 (Wenkebach phenomenon) is where PR gets longer and longer until one QRS isn’t transmitted
2nd degree - Mobitz Type 2 where PR normal then suddenly drops. High risk of progression to 3rd degree
3rd degree - complete heart block, atrial depol normal but NOT conducted to Vs so ventricular escape rhythm, wide QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is ventricular tachycardia?

A

Consecutive ventricular ectopics. High risk of VF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does VF result from?

A

Multiple ectopic foci in ventricles, uncoordinated coordinate, ventricles quiver, no CO, shockable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is endothelial muscle more vulnerable to ischaemia than epithelial?

A

Because coronary arteries are on epithelial surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are STEMIs and NSTEMIs occlusions of?

A

STEMI is major coronary artery, NSTEMI is minor coronary artery or partial occlusion of major

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe ECG STEMI progression

A

ST elevation, T wave inversion, pathological Q waves persist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a pathological Q wave?

A

Post STEMI indicating myocardial death- more than one small square wide and more than 25% depth of QRS. Seen in leads V1-V3 and are more negative because fat LV wall no longer goes away from the electrode because its dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Does hypokalemia or hyperkalemia result in excitability?

A

In hypokalemia the inside of the cell is now more positive compared to the outside of the cell so the resting membrane potential is higher so in hypokalemia there is MORE excitability

33
Q

What are acute coronary syndromes?

A

STEMI, NSTEMI or unstable angina

34
Q

What can ischaemic heart disease cause?

A

stable angina, unstable angina, NSTEMI, STEMI

35
Q

Causes of HF?

A

IHD is primary cause. Also HTN or dilated cardiomyopathies

36
Q

What should ejection fraction be?

A

> 50-55 to 75%

37
Q

Differences between systolic and diastolic dysfunction as causes of HF?

A

Systolic dysfunction - pumping problem e.g. MI leading to reduced inotropy. Causes eccentric hypertrophy (chambers bigger and walls bit thicker)
Diastolic dysfunction - filling/relaxing problem due to decreased compliance from thick walls e.g. chronic HTN. Causes concentric hypertrophy (walls thicker but chambers same size)

38
Q

Drugs used for HF?

A

ACEi - inhibit RAAS to decrease preload
Beta-blockers - inhibit SNS activation to slow pacemaker
Diuretics - e.g. thiazide to reduce preload
Digoxin- blocks Na/KATPase which leads to rise in intracellular Ca which increases inotropy via the Na/Ca exchanger

39
Q

Name the four classes of antiarrhythmics

A 
I- Na (Flecainide), phase 0 
II- Beta blockers (Bisoprolol) prevent NA binding, phase 4
III- K (Amiodarone), phase 3
IV- Ca (Verapamil), phase 2
Flec a Biscuit Aloe Vera
40
Q

What makes an early and a late after-depolarisation more likely, respectively?

A

Early after-depol more likely if AP prolonged

Late after-depol more likely if Ca is high

41
Q

What causes atrial flutter and what does it look like on ECG?

A

An atrial re-entry loop, saw-tooth

42
Q

What causes AF and what does it look like on ECG?

A

Multiple atrial re-entry loops, no P waves and variable ventricular rate

43
Q

Name 4 types of re-entry loops

A

Atrial flutter, AF, accessory pathway in WPW between A and V, AVNRT (AVN has one slow one fast pathway)

44
Q

Causes of bradycardia

A

Conduction block e.g. 1st/2nd/3rd degree, or sick sinus syndrome (any SAN conduction problem)

45
Q

Venous thromboses are ____ rich and arterial thromboses are _____ rich

A

Venous are fibrin rich, arterial are platelet rich

46
Q

Name 3 presentations in peripheral arterial disease?

A

In chronic PAD: intermittent claudication and critical limb ischaemia. In acute PAD: acute limb ischaemia

47
Q

Name complications of peripheral venous disease?

A

Haemorrhage, varicose eczema, thrombophlebitis (inflam from venous thrombosis and haemosiderin staining), venous ulceration, lipodermatosclerosis

48
Q

Which murmurs can be heard better on inspiration?

A

RILE - R sided inspiration L sided expiration

49
Q

What is Buerger’s test?

A

Raise foot upwards and its pale (peripheral arterial supply can’t overcome gravity), hang over bed and become pink (reactive hyperaemia)

50
Q

How long do you have to fix acute limb ischaemia?

A

6 hours

51
Q

Is there generally oedema in HTN?

A

No, because it’s caused by increased TPR so AP has increased but VP has decreased

52
Q

How can chronic lung disease lead to RHF?

A

If not well perfused pulmonary vessels will vasoconstrict which increases pressure and afterload for RV

53
Q

Defects in teratology of fallot?

A

VSD, pulmonary stenosis, RVH, overriding aorta

54
Q

What receptor does ACh act on to decrease chronotropy?

A

M2

55
Q

RMP of cardiac myocytes?

A

-90mV

56
Q

How does adrenaline act on heart, lungs, and blood vessels?

A

On B1 for increasing heart inotropy and chronotropy, a1 for vasoconstriction, b2 for bronchodilation

57
Q

Name the two pericardial sinuses

A

Transverse- between aorta and PA anteriorly and SVC posteriorly
Oblique- on posterior of heart between RPV RPV and LPV LPV

58
Q

Tell me about laminar blood flow

A

Has a parabolic profile, all layers of blood are the same from the wall

59
Q

Name the two limbs of the MAP graph?

A

Anacrotic limb (systole) and dicrotic limb (diastole)

60
Q

Name causes of narrow and wide pulse pressure?

A

Narrow- aortic stenosis, cardiac tamponade

Wide- mitral regurg

61
Q

Name the functional stages in a heart beat

A

Atrial contraction, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, reduced filling

62
Q

Causes of aortic stenosis and regurg?

A

AS- senile calcification, congenital bicuspid, chronic rheumatic fever
AR- rheumatic fever, aortic root dilation

63
Q

What are isovolumetric relaxation and contraction?

A

Isovol contraction - all valves closed, short time where pressure increases but no volume change in preparation to eject
Isovol relaxation - all valves closed, short time before filling where pressure reduces but no volume change

64
Q

Which aortic arch becomes the actual aortic arch and which one disappears?

A

IV becomes aortic arch, V disappears

65
Q

Name components that make fetal heart

A

Aortic roots, truncus arteriosis, bulbus cordis, primitive ventricle, primitive atrium, sinus venosusq

66
Q

What part of the ventricle does the bulbus cordis make?

A

The smooth RV & LV (the trabeculated muscly bit is from the primitive ventricle)

67
Q

Describe formation of the foramen ovale

A

Septum primum forms, leaving a hole at its inferior just above the endocardial cushion. Septum secondum forms to its right, and ostium primum closes but ostium secondum forms (a hole higher up in the septum primum).

68
Q

Tell me about spiral septum formation

A

So the truncus arteriosus that forms the aorta and the PT must be divided by a septum to make those two vessels.. The upper part of the truncus grows towards the right and the lower grows towards the left to twist the aorta/PT by 180 between its top and bottom. The septum forms due to migration of neural crest cells. Its the truncus arteriosis and the cordus (part of bulbus cordis) that make these vessels.

69
Q

What is overriding aorta?

A

Defect in ToF where aorta is over the VSD rather than over the LV so it straddles the ventricles and gets blood from both

70
Q

What tissue type forms the heart?

A

Mesoderm, which becomes primary and secondary heart fields.

71
Q

What do primary and secondary heart fields become?

A

Primary heart fields - everything but the RV and outflow tracts i.e. LA, RA, LV
Secondary heart fields- RV and outflow tracts

72
Q

What do you need to survive tricuspid atresia?

A

Another defect e.g. ASD, VSD

73
Q

What do you need to survive transposition of the great arteries?

A

A shunt working e.g. ductus arteriosus

74
Q

What inhibits platelet activation and vasodilates?

A

NO

75
Q

Differences between SAN and myocyte APs?

A

SAN is between -60 and +10, has a long slow depolarisation due to HCN funny currents. No RMP, just spontaneously depolarises.
Myocytes are -90 to +30 and have a RMP determined by K+.

76
Q

Describe role of calcium in excitation-contraction coupling in the heart and in skeletal muscles.

A

Heart- depol opens Ca channels in T tubules, triggers Ca release from SR, Ca binds to troponin C which moves tropomyosin to reveal actin binding site.
Skeletal muscle- voltage gated Ca channels open, Ca binds to calmodulin, Ca:Calmodulin (CCM) binds to MLCK, this complex phosphorylates myosin so it can bind to actin

77
Q

Which receptors for ANS act on the heart?

A

B1 (GPCR as) for sympathetic, M2 (GPCR ai) for parasympathetic

78
Q

In terms of ANS, the heart is ____ dominated and vessels are ____ dominated

A

Heart parasympathetic, blood vessels sympathetic

79
Q

Cause of unstable angina?

A

Coronary plaque rupture

Easter revision 2018 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions