Brainscape's Knowledge GenomeTM

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


See full index

ESA 2 > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

1
Q

What factors affect diffusion

A

Concentration gradient, area available for exchange and diffusion resistance

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

What factors are included in ‘diffusion resistance?’

A

Nature of molecule, nature of barrier, diffusion path length.

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

What determines the area that’s available for exchange at capillaries?

A

Capillary density (how many capillaries there are per unit volume) highest in most metabolically active tissues

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

Which factor affecting exchange at capillaries is the most limiting?

A

Concentration gradient

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

Which organs have an absolute requirement for blood flow that doesn’t vary?

A

Brain of 0.75 l/minKidneys of 1.2 l/min

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

What is the minimum and maximum blood flow to heart, gut, muscle and skin?

A

Heart 0.3-1.2 l/minGut 1.4 - 2.4 l/minmuscle 1-16 l/minskin 0.2 - 2.5 l/min

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

What is the distribution of blood volume at rest?

A

11% in arteries and arterioles17% in lungs and heart67% in veins5% in capillaries

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

Describe the position of the heart

A

Sits in the pericardium which is within the middle mediastinum, between ribs 2-5

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

What’s the main nerve supply to the heart?

A

Phrenic nierve C3-C5 and vagus nerve

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

What are the main histological characteristics of large, elastic arteries?

A

fenestrated elastic membrane with smooth muscles cells and collagen in between. vasovasorum in adventitia

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

What are the main histological characteristics of muscular arteries?

A

Many layers of smooth muscle cells, connected by gap junctions. Slight vaso vasorum.

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

What are the main histological characteristics of arterioles

A

Few smooth muscle cels. Scant adventitia

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

What are the 3 types of capillaries and where are they found?

A

Continuous - in most locations eg muscles, nervous tissue, connective tissue, exocrine glands and lungs.Fenestrated - in parts of the gut, endocrine glands and renal glomerulusSinusoidal - in bone marrow, liver and spleen

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

What are the main histological features of venules?

A

Very thin layer of smooth muscle cells. Contain valves

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

What are the main histological features of veins?

A

Less elastic and muscle fibres than accompanying arteries but more connective tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are venae commitantes?

A

2 veins either side of a small artery, all wrapped in one sheath. Pulsing of artery promotes venous return

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

What is the most common congenital heart syndrome associated with Down Syndrome?

A

Atrioventricular septal defect

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

What do the different parts of the primitive heart tube develop into in an adult?

A

Truncus arteriosus - Roots of aorta and pulmonary trunk
Bulbus cordis - Right ventricle, Ventricular outflow
Ventricle - Left ventricle
Atrium - Auricles of atria
Sinus venosus - Right atrium

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

Where does the cardiogenic field form?

A

At cephalic end of splanchnic mesoderm

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

How do valves attach to the heart wall?

A

Attached to chordae tendinae which attach to papillary muscles which make up part of the heart wall near the valve

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

What muscle forms the rough surface of the ventricles?

A

Trabeculae carnae

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

What is pectinate muscle?

A

Forms rough walls of atria, more prevalent in right atrium which has greater input from primordial atrium

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

Where can you listen for the 2 atrioventricular valves?

A

Mitral (left AV) listen at 5th intercostal space, mid clavicular line
Tricuspid (right AV) listen at 4th intercostal space, left sternal edge

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

Where can you listen for the 2 semilunar valves?

A

Aortic valve listen at 2nd intercostal space, right sternal edge
Pulmonary valve, listen at 2nd intercostal space, left sternal edge

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

What control does the parasympathetic nervous system exert over the CVS?

A

Vagus nerve releases ACh which acts on M2 receptors in the AV node to reduce heart rate

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

What control does the sympathetic nervous system exert over the CVS?

A

Noradrenaline release at Beta1 receptors in AV and SA nodes and in myocardium to increase force and rate of contraction.
Circulating adrenaline also acts on Beta2 receptors to cause vasodilation although pharmacologically active noradrenaline causes vasoconstriction by acting on alpha1

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

What determines the flow through a vessel, with a given pressure gradient?

A

Resistance which is determined by the nature of the fluid and the vessel

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

Define flow and velocity

A

Flow - Volume of fluid passing a given point per unit time

Velocity - rate of movement of fluid particles along a tube

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

At a given flow, how does velocity relate to diameter of a vessel?

A

At a given flow, velocity is inversely proportional to cross-sectional area

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

At a constant pressure, what determines flow?

A

Mean velocity, which depends on viscosity and radius.

Viscosity is inversely propotional to velocity

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

Define viscosity

A

The extent to which fluid layers resist sliding over each other

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

At a given pressure, how does velocity relate to diameter?

A

At a given pressure, velocity is proportional to cross sectional area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does poiseulle’s law state?

A

That pressure is equal to flow x resistance

Change in pressure = flow x 8 x viscosity x length/ PiR^4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is effective resistance calculated for vessels in series and vessels in parallel?

A

In series - add all different resistances together

In parallel - and all resistances together and divide by 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where do pressure drops occur in the circulation?

A

Large pressure drop between Arteries and arterioles (high resistance)
Small pressure drop over capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does TPR affect diastolic pressure?

A

A higher TPR means it’s harder for blood to leave arteries so diastolic pressure is higher

37
Q

What is the pulse pressure?

A

Difference between systolic and diastolic pressures - measure of how hard the heart pumps

38
Q

How is the average pressure calculated?

A

Diastolic pressure + (pulse pressure/3)

39
Q

What is reactive hyperaemia?

A

The massive increase in blood flow after circulation to an area is cut off momentarily. Vessels are dilated due to build of vasodilatory metabolites

40
Q

How does TPR affect central venous pressure?

A

Decreased TPR increases venous pressure

41
Q

What is stroke volume?

A

Difference between volumes at the end of systole and the end of diastole.
Increased filling leads to increased contraction so increased stroke volume

42
Q

What is contractility?

A

Intrinsic ability of cardiac muscle to contract and generate tension. Related to performance of the heart.

43
Q

What is force of contraction determined by?

A

End diastolic volume and contractility

44
Q

What is the response of the CVS to a long term increase in blood flow?

A

There’s increased venous pressure and cardiac output so arterial pressure increases.
The increased blood flow decreases concentration of metabolites so there’s vasoconstriction, increasing TPR and further increasing arterial pressure.
Eventually, arterioles develop more smooth muscle to maintain high TPR and there’s maintained high arterial pressure so there’s hypertension

45
Q

What’s the response of the CVS to standing up?

A

Blood pools in superficial veins of the legs so central venous pressure falls transiently and there’s a fall in cardiac output and arterial pressure.
Heart rate increases, as does TPR as response by sympathetic nervous system so arterial pressure increases again

46
Q

What’s the response of the CVS to haemorrhage?

A

Massive decrease in blood volume causes a fall in venous and arterial pressure. Body increases TPR but also increases heart rate so venous pressure is massively reduced.
There’s venoconstriction and autotransfusion to increase venous pressure

47
Q

How do cardiac glycosides work?

A

Block Na/K/ATPase which normally provides gradient for Na/Ca exchanger so Ca2+ accumulates in the cell and there’s positive inotropy of heart

48
Q

How do organic nitrates work?

A

Produce NO2- which forms NO which is a vasodilator by activating cGMP which decreases intracellular Ca2+

49
Q

What cardiac uses are there for beta blockers?

A

After MI to prevent ventricular arrhythmias and decrease workload of heart
In heart failure for their negative inotropic and chronotropic effect
Angina to decrease workload
Hypertension

50
Q

How are warfarin and heparin used differently?

A

Heparin is used more acutely and given intravenously or fractionated heparin can be given subcutaneously
Warfarin is used more in long term and is given orally

51
Q

How do warfarin and heparin exert their antithrombotic effects?

A

Heparin inhibits thrombin production and warfarin inhibits vitamin k which is needed for clotting factor synthesis

52
Q

What makes the pulmonary circulation low resistance?

A

Short wide vessels
Lots of capillaries in parallel
Relatively little smooth muscle in capillaries

53
Q

How do diameter of vessels in lungs differ due to gravity?

A

When upright (orthostasis) there’s an increase in hydrostatic pressure in lower lung vessels so vessels are distended and vesels towards the apex collapse in diastole due to low pressure

54
Q

How does pulmonary circulation react to exercise?

A

There’s an increased cardiac output so increase in pulmonary arterial pressure so apical vessels open and there’s increased oxygen uptake throughout lungs

55
Q

How is cerebral circulations adapted to meet high oxygen demand?

A

Anastamoses between basilar and internal carotid arteries to form the Circle of Willis so if one route is blocked, brain will still get blood supply
brainstem regulates blood flow to other parts of the body to ensure its own needs are met
Myogenic autoregulation maintains blood supply in hypotension
Metabolic factors control blood flow through constriction and dilation
There’s also a high capillar density and high basal flow rate

56
Q

What is involved in cerebral myogenic autoregulation?

A

If blood pressure increases there’s vasoconstriction and if blood pressure decreases there’s vasodilation. This means blood flow is well maintained within limits of roughly 180-60mmg but outside of these limits, blood flow quickly changes

57
Q

How does cerebral circulation react to CO2?

A

Very sensitive. As it’s a metabolite, hypercapnia causes vasodilation and hypocapnia causes vasoconstriction so in ventilation there’s vasoconstriction, dizziness and fainting

58
Q

What is cushing’s reflex?

A

Maintains cerebral blood flow in increased intracranial pressure by increased sympathetic activity to increase arterial blood pressure

59
Q

How is coronary circulation adapted to meet its demand for oxygen?

A

High capillary density
Continuous production of NO by coronary endothelium which is a vasodilator
Blood flow increases to meet demand through vasodilation

60
Q

Why can there be angina flare ups in the cold?

A

Cold temperatures causes sympathetic induced coronary vasoconstriction

61
Q

How is skeletal muscle circulation adapted to meet demand?

A

Resistance vessels are richly innervated by sympathetic fibres so are very responsive
Different muscle types have different capillary densities depending on needs eg postural muscles have high capillary density
High vascular tone which allows high degree of vasodilatation so blood flow can rapidly increase when needed
At rest, only abot 50% of capillaries are being used at any one time so there can be increased recruitment of remaining capillaries if needed

62
Q

How do arteriovenous anastamoses help regulate body temperature?

A

Found in apical skin so if there’s an increase in core body temperature, there’s decreased sympathetic output and passive vasodilation of AVAs and a low resistance shunt to venous plexus closer to surface so blood flows closer to the skin and there’s heat dissipation.
Opposite happens if core body temperature falls

63
Q

How does non apical skin react to cool temperatures?

A

Increased sympathetic output so noradrenaline acts on venules and arterioles to cause vasoconstriction

64
Q

What are some signs and symptoms of left side heart failure?

A 
Fatigue
Breathlessness on exertion or lying flat
Tachycardia
Dyspnoea on walking on the flat
Displaced apex beat indicating cardiomegaly
Gallop rhythm
Basal pulmonary crackles
Mitral regurgitation
65
Q

What are some causes of right side heart failure?

A 
Secondary to left side heart failure
Chronic lung disease
Pulmonary embolism
Pulmonary hypertension
Left to right shunt
Pulmonary/tricuspid valve disease
Isolated right ventricular cardiomyopathy
66
Q

What drugs can be given to treat heart failure?

A 
Beta blockers
diuretics
ACE inhibitors
Calcium channel blockers
organic nitrates
cardiac glycosides
67
Q

What are some signs of right side heart failure?

A 
Peripheral oedema
Fatigue
Dyspnoea
Anorexia
Nausea
Raised JVP
Ascites
Pleural effusion
Hepatic enlargement
68
Q

What are some causes of left side heart failure?

A 
Mainly ischaemic heart disease
Hypertension
Dilated cardimyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Valvular heart disease
Arrhythmia
Pericardial disease
69
Q

How do you calculate heart rate from an ECG?

A

If regular 300/number of big squares between QRS complexes

If irregular - number of qrs complexes in 30 big squares, x 10

70
Q

What counts as a pathological Q wave?

A

More than 2 small squares deep

71
Q

On average, how long is the QRS complex?

A

Roughly 3 small squares

72
Q

How long should the PR interval on an ECG be?

A

3-5 small squares

73
Q

What is classed as a prolonged QT interval?

A

More than 2.5 big squares

74
Q

What is the ECG sign for right axis deviation?

A

Increased peak in lead 3 instead of lead 2 with lead 1 pointing downwards

75
Q

What are the different types of second degree heart block?

A

Mobitz type 2 - occasional dropped beat with waves being otherwise normal
Wenckebach phenomenon - progressive lengthening of PR interval until a beat is missed
2:1 / 3:1 - alternate conducted and non conducted beats. 2/3 p waves to every QRS complex

76
Q

What is the ECG sign for atrial flutter and atrial firillation?

A

Atrial flutter there is no flat baseline between P waves

Atrial fibrillation there are no p waves and QRS complexes occur at irregular intervals

77
Q

What is the progression of ECG changes in a STEMI?

A

ST elevevation
Pathological Q waves (both of these disappear in time)
Inverted T wave (permanent)

78
Q

What area of the heart is the most vulnerable to ischaemia?

A

Subendocardial area as myocardium is perfused from outside in and is closest to left ventricle which is under the most strain

79
Q

How do you differentiate between an NSTEMI and unstable angina?

A

By using biochemical markers such as troponin and creatine kinase MB. If these are present, it’s a NSTEMI

80
Q

What history indicated acute coronary syndrome?

A

Recurrent chest pain on minimal exertion or at rest.

Episodes last longer than 15 minutes

81
Q

How do atheromas cause angina?

A

Atheromas can either be stable, with a small necrotic core, or vulnerable with a fibrous cap. This fibrous cap can erode or fissure so blood is exposed to its thrombogenic necrotic center. Platelets from within the core emerge and react with fibrin to form a fibrin thrombus which traps RBCs to cause an occlusion

82
Q

How is angina treated?

A

If necessary, can carry out reperfusion through percutaneaous coronary intervention where a catheter’s inserted through groin and a stent is inflated or by coronary bypass graft.
Pharmacologically, can use beta blockers, ACE inhibitors, nitrates, calcium channel blockers, aspirin, statins

83
Q

What vessels can be used for a coronary bypass graft?

A

Internal thoracic artery
Saphenous vein
Radial artery

84
Q

How are STEMIs treated?

A

Reperfusion by PCI or fibrinolytic therapy
Revascularisation
ACEi
Antiplatelet drugs eg aspirin
Antiischaemia drugs eg nitrates/ beta blockers
Statins

85
Q

How are NSTEMIs treated?

A 
Pain control
Antithrombolytic therapy eg aspirin/heparin 
Statins
ACEi
Reperfusion
86
Q

What ECG leads will show abnormal readings if there’s an MI at the distal Left Anterior Descending coronary artery?

A

V3 and V4

87
Q

When does troponin peak as a biochemical marker for MI?

A

Peaks around 18 hours after event.

Levels begin to rise 3-4 hours after and slowly decline until 10-14 days after event

88
Q

What types of shock occur due a decrease in TPR?

A

Toxic shock

Anaphylactic shock

89
Q

What leads to development of mechanical shock?

A

Two different mechanisms
Eg in cardiac tamponade, there’s reduced filling of ventricles so cardiac output falls
or eg in massive pulmonary embolism, right ventricle can’t empty due to massive increase in pressure of pulmonary arteries so there’s reduced filling of left heart and cardiac output is reduced.

ESA 2 (4 decks)

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