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Phase 1 Med > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the stages of the cardiac cycle?

A

1 - Ventricular filling
2 - Ventricular systole
3 - Ventricular diastole

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2
Q

Describe the main events of the cardiac cycle

A

1 - Ventricular filling:
Blood flows passively into open AV valve
Atria contract to force last bit of blood out

2 - Ventricular systole
Ventricles contract so AV valve closes (isovolumetric contraction)
SL (aortic) valve opens, blood flows into aorta

3 - Ventricular diastole
LV stops contracting and SL (aortic) valve closes
AV valve opens and cylce repeats

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3
Q

Describe the pressure and volume changes in the cardiac cycle

A

1 - Ventricular filling:
Slight increase in atrial pressure due to systole
Increase in ventricular volume due to filling

2 - Ventricular systole
Increase in LV pressure due to systole
Decrease in LV volume as blood leaves (due to systole)
Increase in aortic pressure as blood enters it

3 - Ventricular diastole
Decrease in LV pressure and volume as LV stops contracting
Small increase in aortic pressure as blood flows back against close SL (aortic) valve = dicrotic notch

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4
Q

What is isovolumetric contraction?

A

When the ventricle initially contracts and all valves are closed, meaning pressure rises, but volume remains the same for a short period of time.

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5
Q

How long is one cardiac cycle? How much is occupied by systole and diastole?

A
  • Total = 0.8s
  • Systole = 0.3 s
  • Diastole = 0.5 s
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6
Q

What is Frank Starlin’s Law of the Heart?

A

The stroke volume increases as end-diastolic volume increases, when all other factors remain constant.

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7
Q

Define end diastolic volume

A

Volume of blood in the ventricles after ventricular filling

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8
Q

Define stroke volume

A

Volume of blood ejected from the ventricle

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9
Q

Define preload

A

A.K.A. end-diastolic volume. The initial stretching force on a muscle (i.e. the amount of blood in the ventricle after filling/before systole)

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10
Q

Define afterload

A

The pressure the heart must work against during ejection of blood from ventricles during systole

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11
Q

Define contractility

A

Strength of contraction independent of/at any given EDV during systole

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12
Q

Define elasticity

A

Myocardial ability to recover its normal shape after removal of systolic stress

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13
Q

Define compliance

A

How easily a chamber of the heart expands when filled with blood. i.e. C = delta V / delta P

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14
Q

Define resistance

A

The force which opposes blood flow (i.e. must be overcome to push blood through the circulatory system.)

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15
Q

Define mean arterial pressure (MAP)

A

Average pressure during one cardiac cycle

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16
Q

What effect does sympathetic stimulation have on force of contraction and how?

A

Increases force via accelerator nerve acting on ventricular muscle

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17
Q

What effect does sympathetic stimulation have on heart rate and how?

A

Increases heart rate via accelerator nerve acting on SAN

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18
Q

What effect does parasympathetic stimulation have on hear rate and how?

A

Decreases heart rate via vagus nerve acting on SAN

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19
Q

What is the equation for stroke volume?

A

SV = EDV - ESV

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20
Q

Define end systolic volume (ESV)

A

The amount of blood in ventricles at the end of systole, just before ventricular filling occurs

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21
Q

What is the equation for cardiac output?

A

CO = HR * SV

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22
Q

Define cardiac output

A

The volume of blood pumped by each ventricle per minute

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23
Q

What is the equation for mean arterial pressure (MAP)?

A

MAP = DP + 1/3 (SP - DP)

DP = diastolic pressure
SP = systolic pressure
[SP-DP=Pulse Pressure]

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24
Q

What is the equation for pulse pressure?

A

PP = SP - DP

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25
Q

What is the equation for Ohm’s Law?

A

F = delta P / R

F = Flow
P = Pressure
R = Resistance
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26
Q

What is the equation for Poiseuille’s Law?

A

Q = (pideltaPr^4)/8ln

Q = flowrate 
deltaP = change in pressure
r = radius
l = length
n = viscosity
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27
Q

What is the relationship between radius and flowrate using Poiseuille’s Law?

A

Q (directly proportional to) r^4

Q = flowrate
r = radius
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28
Q

Describe the phases of a cardiac action potential

A

4 - Resting membrane potential -90mV sue to constant leakage of K+.
0 - Action potential from neighbouring cell/pacemaker cell, passing through a gap junction (type of intercalated disc) causes voltage-gates Na+ channels of cell membrane to open. Rapid influx of Na+ ions = depolarisation.
1 - Na+ channels close, K+ channels open. K+ leave the cell, returning membrane potential to 0mV.
2 - L-type Ca2+ channels open, creating a small and constant inward current of Ca2+ ions from T-tubules. Meanwhile K+ ions still move out, maintaining a constant membrane potential - plateau.
3 - Ca2+ channels close while K+ remain open and K+ ions move out of cell. This causes repolarisation

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29
Q

Describe the two types of refractory periods

A
  • Absolute: Membrane will not respond to any stimulus.

- Relative: Membrane will respond to stimulus greater than usual.

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30
Q

Describe excitation-contraction coupling

A

1) The Ca2+ from the T-tubules in the cardiac action potential causes a release of more Ca2+ ions from the sarcoplasmic reticulum, into the cytosol.
2) The cytosolic Ca2+ concentration increases. The extra Ca2+ binds to troponin C, causing troponin I to pull tropomyosin to expose the actin-myosin binding site on the myosin head.
3) Actin binds here, displacing ADP+Pi, which causes the power stroke. New ATP binds to myosin, displacing actin, and ATP –> ADP+Pi, with the energy returning the myosin head to resting position. Cycle repeats.

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31
Q

What are muscle fibres made up of?

A

Myofibrils.

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32
Q

What are myofibrils made up of?

A
  • Z-lines of actin at each side
  • M-line of myosin down the middle
  • A-band: The whole length of myosin (A band has All)
  • H-zone: Just myosin by itself
  • I-bands: Only the overlap of actin and myosin
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33
Q

What is the difference between pulmonary and systemic circulation?

A
  • Pulmonary goes to the lungs

- Systemic has just arrived from the lungs and goes to the rest of the body

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34
Q

Where are arterial baroreceptors located?

A

Carotid sinus and aortic arch.

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35
Q

What do arterial baroreceptors detect?

A

Changes in blood pressure.

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36
Q

What happens if arterial baroreceptors detect a high blood pressure?

A
  • CV centre in medulla stimulated.
  • Leads to increased parasympathetic outflow (and therefore decrease in sympathetic outflow).
  • This causes decreased heart rate and contractility.
  • Also causes vasodilation (i.e. inhibits vasoconstriction)
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37
Q

Are arterial baroreceptors responsible for short-term or long-term regulation?

A

Short-term

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38
Q

What happens if blood pressure is different for a few days?

A

Baroreceptors reset to new baseline value.

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39
Q

Where are central chemoreceptors found?

A

Medulla oblongata

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40
Q

What do central chemoreceptors detect?

A

Changes in pH, and so changes in paCO2

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41
Q

How do central chemoreceptors respond to an increase in PaCO2?

A

Vasoconstriction

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42
Q

Define local factors

A

Factors independent of nerves or hormones

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43
Q

Name 2 local factors causing vasoconstriction

A
  • Endothelin-1

- Internal blood pressure (controlled by myogenic mechanism)

44
Q

Name 4 local factors causing vasodilation

A
  • Hypoxia
  • Bradykinin
  • Adenosine
  • Nitric Oxide
45
Q

Define neural factors

A

Factors relating to the NS

46
Q

Name a neural factor causing vasoconstriction

A

Sympathetic nerves releasing noradrenaline

47
Q

Name a neural factor causing vasodilation

A

Parasympathetic nerves releasing Nitric Oxdie

48
Q

Name 3 hormonal factors causing vasoconstriction

A
  • Adrenaline (when acting on alpha receptors)
  • Angiotensin 2
  • ADH
49
Q

Name 2 hormonal factors causing vasodilation

A
  • Adrenaline (when acting on beta receptors)

- Atrial natriuretic peptide secreted by heart cells

50
Q

What is hyperaemia?

A

An increase in blood flow to tissues

51
Q

What is active hpyeraemia and what causes it?

A
  • Inc metabolic activity at tissue organs leading to increased blood flow to area via arteriolar dilation
52
Q

What is reactive hpyeraemia and what causes it?

A
  • Increased blood flow to an area where arterial flow had been previously occluded
53
Q

What enables hyperaemia to occur?

A
  • Intrinsic autoregulation

- Myogenic mechanism

54
Q

What is the P wave in an ECG?

A

Atrial depolarsation

55
Q

What is the QRS complex in an ECG?

A

Ventricular depolarisation

56
Q

What is the T wave in an ECG?

A

Ventricular repolarisation

57
Q

What is the PR interval of an ECG? How long does it last?

A

From the start of P to Q. Time between onset of atrial depolarisation and ventricular depolarisation. Lasts 120 - 200 ms

58
Q

How long does the QRS complex last?

A

120 ms

59
Q

What is the ST segment of an ECG and how long does it last?

A

End of S to start of T. Time between ventricular depolarisation and ventricular repolarisation. Lasts 80 - 120 ms

60
Q

What is the QT interval and what controls its length?

A

Start of Q wave to end of T wave. Time for depolarisation and then repolarisation. The faster the HR, the shorter the QT interval.

61
Q

What is QTc, and what is considered a prolonged QTc?

A

QTc is corrected QT interval if the HR was 60bpm. QTc > 440 ms in men or QTc > 460 ms in women considered prolonged.

62
Q

What is sinus rhythm and how is it shown on an ECG?

A

Indicates that electrical activity originates from the SAN. Shown on ECG by correctly orientated p wave.

63
Q

What is a ‘lead’ in a 12-lead ECG?

A

An imaginary line between 2 electrodes

64
Q

Where is lead 1 placed?

A

Right arm (-) to left arm (+)

65
Q

Where is lead 2 placed?

A

Right arm (-) to left leg (+)

66
Q

Where is lead 3 placed?

A

Left arm (-) to left leg (+)

67
Q

Where is aVR lead placed?

A

Right arm (+) to left arm and left leg (-) [i.e. midpoint of lead 3]

68
Q

Where is aVL lead placed?

A

Left arm (+) to right arm and left leg (-) [i.e. midpoint of lead 2]

69
Q

Where is aVF lead placed?

A

Left leg (+) to right arm and left arm (-) [i.e. midpoint of lead 1]

70
Q

Where are unipolar chest leads 1 and 2 (V1, V2) placed?

A

4th intercostal space. 1 to right of sternum, 2 to left of sternum.

71
Q

Where are unipolar chest leads 3 to 6 (V3 - V6) placed?

A

5th intercostal space. 3 left of sternum, 4 centre of clavicle, 5 next to 4, 6 under left arm (i.e. going across chest)

72
Q

Outline the conduction pathway in the heart

A
  • Generation of action potential in SAN (top of right atria) which creates wave of contraction in atria
  • AP travels from cell to cell via gap junctions (type of intercalated disc)
  • Conducted from SAN to AVN vis internodal pathways
  • Some also goes down Bachmann’s bundle at this point
  • Propagation through the AVN is relatively slow, allowing atrial contraction to finish before ventricular contraction begins
  • AP travels from AVN to bundle of His, which then branches into left and right bundle branches in the interventricular septum
  • These lead to the apex of the heart where each one travels up ventricle walls to cause conduction from the bottom upwards, along purkinje fibres.
73
Q

What causes the first heart sound?

A

Closing of the mitral/(bicuspid) and tricuspid valves (AV valves)

74
Q

What causes the second heart sound?

A

Closing of aortic and pulmonary valves (semilunar valves)

75
Q

What is blood?

A

Cells and cell fragments suspended in plasma

76
Q

What percentage of blood is plasma and haematocrit?

A

55% plasma 45% hametocrit

77
Q

What is haematocrit?

A

% of blood volume that is RBCs (erethrocytes)

78
Q

What is the name for production of red blood cells and where does it occur?

A

Erythropoiesis, occurs in red bone marrow.

79
Q

Describe the structure of red blood cells

A
  • Biconcave disc shape
  • No nucleus or organelles (so only live 120 days)
  • Production controlled by erythropoietin
  • Contain Hb (2 alpha and 2 beta chains, Fe2+ etc)
80
Q

List 3 substances needed for RBC production

A
  • Iron
  • B12
  • Folate (folic acid)
81
Q

Where are white blood cells (leukocytes) produced?

A

Bone marrow

82
Q

What is the production of white blood cells (leukocytes) controlled by?

A

Granulocyte-colony stimulating factor (G-CSF)

83
Q

List the 5 types of white blood cells

A

Neutrophils, monocytes, lymphocytes, basophils, eosinophils

84
Q

Describe the role of neutrophils

A

Phagocytose bacteria, contain defensins to destroy bacteria.

85
Q

Describe the role of monocytes

A

Circulate in blood and migrate to tissue/organs to become macrophages.

86
Q

Describe the role of lymphocytes

A

B - Produced in bone marrow. Generate antibodies.

T - Produced in thymus. Aid B cells (helper cells)/ kill bacterial cells directly (cytotoxic killer cells)

87
Q

Describe the role of basophils

A

Migrate to tissue and become mast cells. Secrete histamine and secrete surface protein IgE.

88
Q

Describe the role of eosinophils

A

Role in inflammation/allergic response

89
Q

Describe the structure and function of platelets

A
  • Anucleate cells.
  • Circulate in inactive form.
  • Produced when megakaryocytes fragment.
90
Q

What is platelet production controlled by?

A

Thrombopoietin

91
Q

What is primary haemostasis and what is responsible for it?

A
  • Stoppage of bleeding.

- Platelet plug is responsible.

92
Q

Describe the formation of a platelet plug.

A
  • Platelets circulate in inactive state then migrate to damaged blood vessels, which have exposed underlying collagen.
  • Platelets adhere to collagen via von Willebrand Factor, a plasma protein secreted by endothelial cells and platelets.
  • Positive feedback then occurs where new platelets adhere to old ones. This is platelet aggregation.
  • This is amplified by thromboxane A2 and mediated by fibrinogen (forms cross links between platelets).
93
Q

When and why does a coagulation cascade occur?

A

In secondary hameostasis when a platelet plug alone is not enough to stop bleeding.

94
Q

Describe a coagulation cascade.

A
  • Series of enzymes circulate in inactive state.
  • Sequentially activated in cascade sequence in response to vessel damage.
  • End goal: convert soluble fibrinogen into an insoluble fibrin polymer to generate a stable clot. (Prothrombin converted to thrombin does this)
95
Q

Why are there multiple steps in a coagulation cascade? Give 2 reasons.

A
  • Allows for biological amplification.

- Allows for regulation, not an all-or-nothing response (i.e. a graduated response.)

96
Q

What is the main protein in plasma and what does it do?

A

Albumin regulates oncotic pressure.

97
Q

What are the main 2 types of groupings used in blood?

A

ABO and Rhesus systems

98
Q

What type of antigens are on red blood cells?

A

Carbohydrates

99
Q

In group A blood, what antigen is on RBCs and what antibody is in the plasma?

A
  • A

- Anti-B

100
Q

In group B blood, what antigen is on RBCs and what antibody is in the plasma?

A
  • B

- Anti-A

101
Q

In group AB blood, what antigen is on RBCs and what antibody is in the plasma?

A
  • A and B

- None

102
Q

In group O blood, what antigen is on RBCs and what antibody is in the plasma?

A
  • None

- Anti-A and anti-B

103
Q

How can you type blood?

A

Mix blood with anti-A and anti-B separately.
If agglutination occurs in anti-A sample, must mean A antigens are present so is A group.
If no agglutination occurs, must have no antigens so is O.
If agglutination occurs in both, must have A and B antigens and be type AB.

104
Q

In Rhesus typing, which antigen is dominant?

A

D is dominant. So DD or Dd = +ve and dd = -ve

105
Q

Describe haemolytic disease of the newborn

A
  • Rh -ve mothers can carry babies who are Rh +ve (inherited paternally)
  • If mother is exposed to baby’s RBCs, she will produce IgG anti-D and undergo classic immune response.
  • Doesn’t effect first pregnancy (as antibodies take a while), but can effect subsequent ones.
  • Risk increases with each Rh +ve pregnancy as mother becomes more and more sensitised
106
Q

What are the platelet receptors for vWF/fibrinogen?

A

GPiib/iiia receptors

107
Q

Describe a pacemaker cell action potential

A
  • Different than myocardial cells as is slower:
  • F-type (funny) channels open, allowing slow influx of Na+ until membrane potential reaches around -50mV when T-type Ca2+ channels open.
  • Ca2+ ions move in, causing slow depolarisation until about -40mV when L-type Ca2+ channels open.
  • Repolarisation then occurs as the Ca2+ channels close and K+ channels open.
  • Cycle repeats

Phase 1 Med (20 decks)

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