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Life Support Systems (LSS) > Cardiovascular System 1 > Flashcards

Cardiovascular System 1 Flashcards

1
Q

Describe the structure of the wall of the heart, from medial to lateral.

A

Endocardium: one-cell thick interface between heart and blood.
Myocardium: thick layer of cardiac muscle cells.
Visceral pericardium: the epicardium; a layer of serous tissue between the myocardium and pericardial space.
Parietal pericardium: a layer of serous tissue.
Fibrous pericardium: connective tissue to protect the heart and hold its position.

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2
Q

What are the ‘nicknames’ for the different vessel types?

A

Arteries = conduit vessels
Arterioles = resistance vessels.
Capillaries = exchange vessels.
Veins and venules = capacitance vessels.

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3
Q

Give the 5 layers of a blood vessel, from medial to lateral.

A 
Tunica intima
Internal elastic lamina
Tunica media
External elastic lamina
Tunica externa (also known as the tunica adventitia)
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4
Q

What is the coronary sinus?

A

A large vessel which collects blood from all the coronary veins and delivers it to the right atrium.

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5
Q

After contraction of cardiac muscle, how are calcium ions removed from the cell?

A

They are either pumped back into the sarcoplasmic reticulum by Ca2+ ATPase, or into the T-tubule by Na+/Ca2+ exchangers, in which case sodium ions are brought into the cell.

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6
Q

What makes cardiac muscle more resistant to stretch and less compliant than skeletal muscle?

A

The properties of its ECM and cytoskeleton.

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7
Q

What are the in vivo correlates of preload?

A

As blood fills the heart in diastole, it stretches the resting ventricular walls. This stretch determines the preload on the ventricles before ejection.

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8
Q

What determines the preload in the heart and how can it be measured?

A

Preload is dependent on venous return to the heart. Measures include end-diastolic volume, end-diastolic pressure and right atrial pressure.

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9
Q

What is the in vivo afterload of the heart?

A

Afterload is the load against which the left ventricle ejects blood after opening of the aortic valve (pressure in the aorta). Any increase decreases the amount of isotonic shortening and decreases the velocity of shortening.

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10
Q

What is the Frank-Starling relationship?

A

Increased diastolic fibre length increases ventricular contraction. (As filling of the heart increases, force of contraction also increases).

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11
Q

What is the main consequence of the Frank-Starling relationship?

A

The ventricles pump a greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return.

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12
Q

What mechanisms underlie the Frank-Starling relationship?

A

Changes in the number of myofilament cross bridges which interact.
Changes in Ca2+ sensitivity of myofilaments. At longer sarcomere lengths, affinity of troponin for Ca2+ increased due to conformational change in : less Ca2+ for same force.

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13
Q

Define stroke work.

A

Work done by the heart to eject blood under pressure into aorta and pulmonary artery.
It is the volume of blood ejected during each stroke (SV) time the pressure at which it’s ejected (P).

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14
Q

What is the law of LaPlace?

A

When the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius.
Tension = pressure x radius.

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15
Q

How is the law of LaPlace applied to the heart?

A

The radius of the walls of the left ventricle is less than the radius of the walls of the right ventricle, allowing the left ventricle to produce more pressure when under similar stress.

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16
Q

What is the difference between the end diastolic and end systolic volumes?

A

End diastolic volume (EDV) = volume of blood in ventricles just before they contract.
End systolic volume (ESV) = volume of blood remaining after ventricles have contracted.

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17
Q

What is the equation for EJECTION FRACTION?

A

(Stroke volume/ End diastolic volume) * 100

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18
Q

Compare the flow of blood through the left and right heart.

A

Same VOLUME of blood ejected from both right and left ventricles. Pressure changes identical. Pressures much lower in right heart and pulmonary circulation than left heart.

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19
Q

Define contractility.

A

Contractile capability (strength of contraction) of the heart. Can be measured by ejection fraction. Increased by sympathetic stimulation.

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20
Q

What is the equation for blood pressure?

A

Blood pressure (MAP) = cardiac output (CO) * resistance (TPR)

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21
Q

What relationship is highlighted by Poiseuille’s equation?

A

R is inversely proportional to r^4. Hence, small changes in vascular tone produce large changes in flow: Halving the radius decreases the flow 16 times.

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22
Q

Describe laminar flow.

A

Velocity of fluid constant at any one point and flows in layers. Blood flows fastest closest to centre of lumen, due to smaller adhesive forces between fluid and surface.

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23
Q

Describe turbulent flow.

A

Blood flows erratically, forming EDDYS. Prone to pooling. Associated with pathophysiological changes to the endothelial lining of the blood vessels.

24
Q

How can blood pressure be measured?

A

Inflate cuff on upper arm and begin to deflate. Hold stethoscope on brachial artery. The point at which you can hear blood squirting through (cuff pressure doesn’t quite occlude artery) = systolic blood pressure. When laminar flow returns (sound disappears) = diastolic blood pressure.

25
Q

Give the equation for pulse pressure and relate it to mean arterial pressure.

A 
PP = SBP - DBP
MAP = DBP + 1/3 PP
26
Q

What is the Windkessel effect?

A

During ejection, blood enters the aorta faster than it leaves. The aorta expands and recoils to reduce pulse pressure and maintain a near constant flow.

27
Q

How is the law of LaPlace related to distension?

A

Tension = pressure x radius.
Transmural pressure causes tension.
If the radius of a vessel increases, to maintain the internal pressure, the inward force exerted by the wall must also increase. If the muscle fibres have weakened, the force needed can’t be produced.
A balloon-like distension will expand until it ruptures.

28
Q

Give the 7 stages of the cardiac cycle.

A

1) Atrial systole. P wave.
2) Isovolumetric Contraction. Interval between AV valves closing and semi-lunar valves opening. QRS complex. 1st heart sounds due to closure of AV valves.
3) Rapid Ejection. Begins with opening of pulmonary and aortic valves (pressure in ventricles exceeds the pressure in the 2 arteries).
4) Reduced Ejection. End of systole. Reduced pressure gradient. SL valves begin to close.
5) Isovolumetric Relaxation. All valves closed. Pressure in atria builds. 2nd heart sound due to closure of SL valves.
6) Rapid passive filling. AV valves open, blood flows into ventricles due to pressure gradient.
7) Reduced passive filling (diastasis). Ventricular volume fills more slowly. The ventricles fill considerably without the contraction of the atria.

29
Q

What does the resting membrane potential rely on?

A

The flow of K+ out of the cell.

30
Q

Why are cardiac action potential much longer (200-300ms) than nervous APs (2-3ms)?

A

Long, slow contractions required to produce an effective pump (allows filling).
Also, the long refractory period means it’s not possible to re-excite the muscle and hence cardiac muscle can’t be tetanised.

31
Q

What are the 4phases of a cardiac action potential?

A 
Phase 0 = upstroke.
Phase 1 = early repolarisation.
Phase 2 = plateau
Phase 3 = repolarisation
(Phase 4 = resting membrane potential).
32
Q

What happens in early repolarisation and plateau?

A

P(K+) increases leading to efflux of K+ ions. However, the L-type calcium ion channels begin are activated shortly after, so there is influx of Ca2+ (CICR) which balances the efflux of K+ until IK1 opens.

33
Q

Which channel proteins is responsible for full repolarisation of cardiac cells?

A

I(K1) - these are large K+ channels allowing great efflux.

34
Q

Describe the characteristic of an SA node action potential.

A

No resting membrane potential.
No I(K1)
Very little Na+ influx
Upstroke produced by Ca2+ influx (via L-type Ca2+ channels).
T-type Ca2+ channels are present, which activate at more negative potentials than L-types.

35
Q

What does SNS innervation do to the heart?

A 
Increases heart rate (positive chronotropy)
Increases contractility (positive inotropy)
36
Q

Where is the SAN located?

A

Just below the epicardial surface at the boundary between the right atrium and the superior vena cava.

37
Q

Describe electrical conduction through the heart.

A

SAN –> internodal fibres –> AVN (delay and insulation from superior ventricular myocardium) –> Bundle of His –> Ventricular fibres.

38
Q

Which pressure determines the amount of blood flowing back to the heart?

A

Central venous pressure (mean pressure in the right atrium).

39
Q

Which neurotransmitters are used in the ANS?

A

PNS = ACh

SNS: pre-ganglionic = ACh. Post-ganglionic = NA.

40
Q

Which blood vessels are NOT innervated by SNS fibres?

Which are innervated by PNS nerves?

A

Capillaries, precapillary sphincters, some metarterioles

NO PNS innervation of vasculature.

41
Q

How are blood vessels made to contract and dilate?

A

Blood vessels receive SNS post-ganglionic innervation which always has some level of tonic activity, which can be increased or decreased.

42
Q

Give extrinsic and intrinsic factors which increase stroke volume.

A

Intrinsic: Increased venous return stretches atrial myocytes: by Starling’s law, this leads to an increase in stroke volume.
Extrinsic: Increased SNS efferents to heart. Increased plasma adrenaline.

43
Q

Where are baroreceptors located? How do they function?

A

Carotid sinus (via glossopharyngeal nerve) and aortic arch (via Vagus nerve). They change their firing rate in response to changes in pressure. Most sensitive at 90-100mmHg.

44
Q

Give 5 examples of circulating (non-endothelium derived) hormones which have effects on vascular tone.

A

Angiotensin II: vasoconstrictor
Vasopressin: binds to V1 receptors on smooth muscle to cause vasoconstriction.
Noradrenaline/adrenaline: secreted from adrenal gland, causing vasoconstriction.

Atrial natriuretic peptide (ANP): secreted from atria in response to stretch, resulting in vasodilation.
Kinins: stimulate NO synthesis by binding to endothelial cells, resulting in vasodilation.

45
Q

Give 4 examples of local (endothelium derived) hormones which have effects on vascular tone.

A

Nitric oxide - potent vasodilator. Produced from arginine.
Prostacylin - cardioprotective vasodilator.
Thromboxane A2 (TXA2). Vasoconstrictor.
Endothelins: Produced in nuclei of endothelial cells, vasoconstrictor.

46
Q

Define vascular tone.

A

The degree of constriction of a blood vessel compared to its maximally dilated state.

47
Q

What are autoregulation and active hyperaemia?

A

Autoregulation is where blood flow to a tissue is changed due to physical factors, such stretch.
Active hyperaemia is where it is chemically driven, such as by metabolites and oxygen usage.

48
Q

How do substances cross continuous capillaries?

A

They have water filled gap junctions. Small, water soluble substances diffuse through these. Lipid soluble substances diffuse through the cells.

49
Q

What are the 3 types of capillary?

A

Continuous, fenestrated and discontinuous. The blood brain barrier uses continuous capillaries with tight junctions.

50
Q

How is tissue fluid formed and drained?

A

Outward hydrostatic force. Inward oncotic force. Ultrafiltration more effective than reabsorption, so net loss of fluid, drained by the lymphatic system.

51
Q

Give examples of agonists of endothelin-1

A

Adrenaline, vasopressin (ADH), angiotensin II, IL-1

52
Q

Give examples of antagonists of endothelin-1

A

NO, PGI2 (Prostacylin), ANP, heparin.

53
Q

Explain the metabolic and myogenic theories of autoregulation.

A

Myogenic: VSMC contracts in response to stretch (important in skin and kidneys)
Metabolic: as blood flow decreases, metabolites accumulate (vasodilators) and the vessels dilate; subsequent increased flow ‘washes’ the vasodilators away.

54
Q

What causes the dichrotic notch?

A

Rebound pressure against aortic valve as distended aortic wall relaxes.

55
Q

How does NA binding to B1 receptors on VSMCs cause contraction?

A

Results in cAMP production, pKa production which augments the L-type Ca2+ channels, resulting in a larger Ca2+ influx.

Life Support Systems (LSS) (6 decks)

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