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ESA 2 > Cvs 5-9 > Flashcards

Cvs 5-9 Flashcards

0
Q

What is transmural pressure and what does it determine?

A

Pressure difference across vessel wall. Determines amount of stretch and recoil of a vessel wall.

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1
Q

Describe the relationship between velocity and surface area.

A

At a given flow, if surface area increases then velocity will decrease.

At a given pressure gradient then if surface area increases velocity will increase due to laminar flow - further from vessel walls then the faster the blood flow.

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2
Q

What is the relationship between resistance and radius

A

Resistance decreases with 4th power of radius

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3
Q

What are the advantages of having distensible walls?

A

Unlike non distensible (linear relationship between flow and pressure) distensible walls have a much higher flow at a set pressure. The recoil may also give them a capacitance so they can store pressure.
Note at low pressures there may be no flow as the walls collapse

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4
Q

How does blood flow match tissue O2 demand

A

Vasodilatator metabolites relax sm increasing bF.

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5
Q

What is reactive hyperaemia?

A

Blood supply is cut off it then returns with an enormous increase due to vasodilator metabolites

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6
Q

What is the connection between tpr and demand for O2

A

More demand for O2 more dilation so lower tpr

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7
Q

What does central venous pressure depend on

A

Pumping of heart.
Return of blood from body.
Gravity and muscle action

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8
Q

What is the role of baroreceptors?

A

Sense arterial pressure and increase sympathetic - HR and contractility
Via medulla

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9
Q

How can high venous pressure increase CO?

A

Starlings curve

Bainbridge reflex - sensed high pressure in ra leading to reduced parasympathetic activity

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10
Q

Describe eating a meal

A

Increased O2 demand at gut
Increased blood flow there
Decreased arterial pressure/ increase venous pressure
Increased Co

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11
Q

Decribe effect of HR increasing alone

A

Arterial rises, venous falls, SV decrease, CO the same

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12
Q

Describe the effects of instant exercise

A

Fall in Arterial and rise in venous
Risk of PO/ fainting from low BP/ overfilling of heart on starlings curve.
HR quickens instantly to avoid this.

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13
Q

Describe sequence of events standing up

A 
Blood pools in superficial veins of legs
CO falls, arterial pressure falls,
Baroreceptors increase TPR
Further reduces venous pressure
Solved with veins constricting.
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14
Q

Describe the sequence of events associated with haemorrhage.

A

Arterial pressure fall, venous pressure falls.
HR increases due to baroreceptors, SV falls die to starlings curve.
Fixed via constriction of veins and auto transfusion (volume increase)

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15
Q

Describe what a long term increase in BV can lead to.

A

Kidneys increase Bv
Increases VP, CO then AP
More flowing through tissues, but body only takes what it needs so constricts increasing TPR.
Increases AP further.

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16
Q

Describe the signal recorded by a probe near a myocardial cell during systole.

A

Positive signal (de) followed by a negative signal (re)

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17
Q

What causes the Q signal?

A

Depolarisation of ventricles away from probe.

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18
Q

How can signals be amplified in an ECG? What do all amplified signals e.g. I, II, III use?

A

Reverse negative electrode result/ use positive and add to another positive reading (vectors will be accounted for) so view point is in between.

When you reverse the negative electrode you then have the positive view from the other side of the heart.

They all use one posit I and one negative electrode.

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19
Q

Give positivism of all V leads

A

V1 4th intercostal space right side
V2 4th intercostal space left side
V3 in between V2 and V4
V4 5th intercostal space inline with clavicular midline
V5 5th intercostal space at beginning of axilla
V6 5th intercostal space directly beneath axilla.

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20
Q

Describe locations of avr avl, avf and N leads

A

Avr, right arm
Avl, left arm
Avf, left foot,
N right foot.

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21
Q

Describe the views of I, II and III and the electrodes they use

A

Lead I: LA-RA left side
Lead 2: LL - RA apex
Lead 3: LL - LA bottom

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22
Q

What does atrial fibrillation look like?

A

No P waves

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23
Q

Describe the 3 classes of heart block and their ECG appearance

A

1st, lengthened PR
2nd erratic relationship between P and R e.g. Lengthening time or skips QRS in regular pattern.
3rd degree, no relationship between P and R waves.

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24
Q

How can an ECG appear different in bundle branch block?

A

Lengthened QRS and changes it’s shape.

25
Q

What is ST depression indicative of and why?

A

Myocardial ischemia (often along with angina) due to depolarisation occurring after QRS as damage effects current flow.

26
Q

What is ST elevation indicative of and why? What else would indicate this? Which of these things will remain me why?

A

MI as dying tissues produce injury currents.

Pathological q waves (deep and wide) and inverted T waves.

Q waves due to altered flow due to fibrous repair.

27
Q

State the normal blood pressures in the pulmonary artery, vein and capillaries

A 
Artery = 12-15
Capillaries= 9-12
Vein = 5
28
Q

What is ventilation and perfusion and how does ventilation affect perfusion in the lungs.

A

Ventilation - amount of O2 to area
Perfusion - amount of blood to area.
If ventilation decreases to an area of lung e.g. Emphysema. Hypoxia occurs, triggering vasoconstriction and decreasing perfusion to that part of lung (therefore increasing to another part). Ventilation perfusion ratio is kept around 0.8 which is optimal.

29
Q

Explain starlings forces and explain how this can lead to pulmonary oedema.

A

Forces= hydrostatic out and oncotic in.
So normally fluid out at arterial but back in at venous end.
If venous pressure increases e.g. Mitral valve stenosis/ left ventricular failure.

30
Q

Describe blood flow in the right and left coronary arteries

A

Left most during diastole. Right more uniform.

31
Q

Describe key features of coronary circulation

A

High capillary density

Constant NO production

32
Q

How is the brain supplied

A

Anastomoses between basilar and internal carotid arteries.

33
Q

How is the cerebral circulation auto regulated?

A

Hypocapnia- vasoconstriction
Hypercapnia- vasoconstriction
In haemorrhage, inter cranial pressure increases, impairs BF to vasomotor control regions which increases sympathetic activity, increasing BP and perfusion to brain. - cusings reflex.
Blood brain barrier stop metabolites affecting VM tone.

34
Q

Name some vasodilatators

A

K+ H+ inorganic phosphates, adrenaline, adenosine.

35
Q

How does skeletal muscle blood flow control arterial pressure

A

Baroreceptors control their blood flow through sympathetic innervation.

36
Q

What are AvAs (arteriovenous anastomoses)?

A

Found only in apical system. A low resistance shunt from arterial to venous system. Affects blood flow and temp loss by smpathetic innervation from the brain not local metabolites.
Note- also Vasodilatator in non apical skin when hot.

37
Q

Give differential diagnoses from chest pain/ IHD

A

Gastroesphageal reflux (GERD)
Lung and pleura disorders e,g. Pneumonia
Cholesystitis

38
Q

When do you get angina? How is it different from unstable?

A

Plaque occluded more than 70% of lumen.

Unstable - Pain at rest, increasing

39
Q

Treatment of angina

A

Sublingual nitrate spray- acute
B blockers, ca channel blockers, oral nitrates - prevent episodes (dilation)
Asprin, statins and ace inhibitors - prevent cardiac events
Re vascularisation

40
Q

Difference between nstemi and stemi?

A

N - infarction is not full thickness of myocardium, st depression, t wave inversion or no changes

Both necrosis and troponin

41
Q

How might a previous MI be identified?

A

Pathological Q wave

42
Q

Describe changes to ECG after mi

A

Mins - hours st elevation
Hours-day1/2 st elevation, decreasing R, st inversion, Q wave begins
Day 1/2, same but st elevation begins to fall
Days after, same but st normalises
Weeks after only pathological q wave

43
Q

How is angina diagnosed?

A

From history- looking at risk factors, LV dysfunction or evidence of atheroma elsewhere e.g. Peripheral vascular disease.
ECG is normal.
Stress test. Patient linked up to ECG on treadmill. Gradually increase difficulty until st depression/ other changes or pain or the patient reaches calculated maximum heart rate or other problems e.g. Low BP, arrhythmias.

44
Q

What is acute coronary syndrome

A

Stemi- occluded by thrombus, large scale myocardial necrosis, ST elevation, troponin.
Nstemi- same but partial occlusion and some necrosis and no st elevation (t wave inversion or st depression).
Unstable angina - same as nstemi but no necrosis or troponin.

45
Q

Give area of infarction, abnormal view leads and artery occluded

A 
Inferior - II, III avF. RCA
Anteroseptal - V1,2- LAD proximal
Antero apical - V3,4 II- LAD distal
Antero lateral v5,6 I aVL - circumflex
Extensive anterior - I aVL V2-6 proximal LCA
True posterior - tall r wave in V1, RCA
46
Q

Chemical markers after an MI

A

Troponin I and T - peak at 18-36 hours. Rises 3-4 hours. Declines for 10-14 days.
Creatine kinase peaks at 24 hours, rises at 3-8 and returns 2-3 days.

47
Q

Treatment of MI?

A

Prevent thrombosis - heparin, warfarin and aspirin
Restore perfusion - statin, organic nitrates, B blockers, ACE inhibitors, Ca channel blockers, O2
Pain control
In severe cases angioplasty - early precutaneous coronary intervention PCI- angiogram to detect blockage, catheter with balloon (possibly stent) inserted and balloon used to open artery. Stent is often left.
Also coronary bypass grafting (CBPG) e.g. Internal mammary artery, radial artery, small saphenous vein and grapht into heart.

48
Q

Signs and symptoms of acute pericarditis.

A

Causes:
Malignancy, Infection, kidney failure, autoimmune.

Cardiac tamponade, chest pain worsens with inspiration due to pleural inflammation. Worsened by lying down and better sitting up. May radiate to back.
Pericardial rub can be heard
Fever as inflammation possible.

49
Q

Define heart failure

A

The heart cannot maintain an adequate circulation to meet the needs of the body despite an adequate filling pressure

50
Q

Describe some causes of heart failure

A 
Congenital
IHD
Hypertension
Arrhythmia 
Dilated cardiomyopathy
51
Q

How does CVP vs Co because affected by heart failure

A

Starlings curve droops basically.

52
Q

Describe the classes of heart failure

A

I- no symptoms
II- symptoms with exercise
III symptoms with less than normal exercise
IV symptoms at rest or any physical activity

53
Q

What is congestive heart failure and why does it occur

A

Both sides of heart are failing.
Left side starts failing (normally not right unless chronic lung disease) increases pulmonary pressure, increase in right ventricular pressure –> heart failure

54
Q

Signs and symptoms of left sided heart failure

A 
Fatigue/ breathlessness 
Tachycardia 
3rd 4th galloping sounds
Murmur of mitral regurg
Peripheral oedema?
Basal pulmonary crackles
Cardiomegaly
55
Q

Signs and symptoms of right heart failure

A

Nausea, fatigue, anorexia
Ascities and liver enlargement
Oedema
Raised JVP

56
Q

Describe the renin- angiotensin- aldosterone system RAAS in heart failure

A

Increased sympathetic
Renin release from kidneys
Angiotensin to I then II via ACE
Angiotensin II vasoconstrictor and releases aldosterone.
Retention of salt and water so increase in BP.

57
Q

What counters RAAS

A

Natriuretic hormones

58
Q

ADH release in heart failure?

A

Increased

59
Q

What is endothelin and what is its effect on RAAS?

A

Secreted by vascular endothelial cells. More in HF and it increases RAAS

60
Q

Describe diastolic dysfunction

A

Hypertrophy due to hypertension, diabetes or obesity.

Affects filing.

ESA 2 (9 decks)

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