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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
What is the equation for Ohm's Law?
F = delta P / R ``` F = Flow P = Pressure R = Resistance ```
26
What is the equation for Poiseuille's Law?
Q = (pi*deltaP*r^4)/8ln ``` Q = flowrate deltaP = change in pressure r = radius l = length n = viscosity ```
27
What is the relationship between radius and flowrate using Poiseuille's Law?
Q (directly proportional to) r^4 ``` Q = flowrate r = radius ```
28
Describe the phases of a cardiac action potential
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
29
Describe the two types of refractory periods
- Absolute: Membrane will not respond to any stimulus. | - Relative: Membrane will respond to stimulus greater than usual.
30
Describe excitation-contraction coupling
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.
31
What are muscle fibres made up of?
Myofibrils.
32
What are myofibrils made up of?
- 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
33
What is the difference between pulmonary and systemic circulation?
- Pulmonary goes to the lungs | - Systemic has just arrived from the lungs and goes to the rest of the body
34
Where are arterial baroreceptors located?
Carotid sinus and aortic arch.
35
What do arterial baroreceptors detect?
Changes in blood pressure.
36
What happens if arterial baroreceptors detect a high blood pressure?
- 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)
37
Are arterial baroreceptors responsible for short-term or long-term regulation?
Short-term
38
What happens if blood pressure is different for a few days?
Baroreceptors reset to new baseline value.
39
Where are central chemoreceptors found?
Medulla oblongata
40
What do central chemoreceptors detect?
Changes in pH, and so changes in paCO2
41
How do central chemoreceptors respond to an increase in PaCO2?
Vasoconstriction
42
Define local factors
Factors independent of nerves or hormones
43
Name 2 local factors causing vasoconstriction
- Endothelin-1 | - Internal blood pressure (controlled by myogenic mechanism)
44
Name 4 local factors causing vasodilation
- Hypoxia - Bradykinin - Adenosine - Nitric Oxide
45
Define neural factors
Factors relating to the NS
46
Name a neural factor causing vasoconstriction
Sympathetic nerves releasing noradrenaline
47
Name a neural factor causing vasodilation
Parasympathetic nerves releasing Nitric Oxdie
48
Name 3 hormonal factors causing vasoconstriction
- Adrenaline (when acting on alpha receptors) - Angiotensin 2 - ADH
49
Name 2 hormonal factors causing vasodilation
- Adrenaline (when acting on beta receptors) | - Atrial natriuretic peptide secreted by heart cells
50
What is hyperaemia?
An increase in blood flow to tissues
51
What is active hpyeraemia and what causes it?
- Inc metabolic activity at tissue organs leading to increased blood flow to area via arteriolar dilation
52
What is reactive hpyeraemia and what causes it?
- Increased blood flow to an area where arterial flow had been previously occluded
53
What enables hyperaemia to occur?
- Intrinsic autoregulation | - Myogenic mechanism
54
What is the P wave in an ECG?
Atrial depolarsation
55
What is the QRS complex in an ECG?
Ventricular depolarisation
56
What is the T wave in an ECG?
Ventricular repolarisation
57
What is the PR interval of an ECG? How long does it last?
From the start of P to Q. Time between onset of atrial depolarisation and ventricular depolarisation. Lasts 120 - 200 ms
58
How long does the QRS complex last?
120 ms
59
What is the ST segment of an ECG and how long does it last?
End of S to start of T. Time between ventricular depolarisation and ventricular repolarisation. Lasts 80 - 120 ms
60
What is the QT interval and what controls its length?
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
What is QTc, and what is considered a prolonged QTc?
QTc is corrected QT interval if the HR was 60bpm. QTc > 440 ms in men or QTc > 460 ms in women considered prolonged.
62
What is sinus rhythm and how is it shown on an ECG?
Indicates that electrical activity originates from the SAN. Shown on ECG by correctly orientated p wave.
63
What is a 'lead' in a 12-lead ECG?
An imaginary line between 2 electrodes
64
Where is lead 1 placed?
Right arm (-) to left arm (+)
65
Where is lead 2 placed?
Right arm (-) to left leg (+)
66
Where is lead 3 placed?
Left arm (-) to left leg (+)
67
Where is aVR lead placed?
Right arm (+) to left arm and left leg (-) [i.e. midpoint of lead 3]
68
Where is aVL lead placed?
Left arm (+) to right arm and left leg (-) [i.e. midpoint of lead 2]
69
Where is aVF lead placed?
Left leg (+) to right arm and left arm (-) [i.e. midpoint of lead 1]
70
Where are unipolar chest leads 1 and 2 (V1, V2) placed?
4th intercostal space. 1 to right of sternum, 2 to left of sternum.
71
Where are unipolar chest leads 3 to 6 (V3 - V6) placed?
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
Outline the conduction pathway in the heart
- 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
What causes the first heart sound?
Closing of the mitral/(bicuspid) and tricuspid valves (AV valves)
74
What causes the second heart sound?
Closing of aortic and pulmonary valves (semilunar valves)
75
What is blood?
Cells and cell fragments suspended in plasma
76
What percentage of blood is plasma and haematocrit?
55% plasma 45% hametocrit
77
What is haematocrit?
% of blood volume that is RBCs (erethrocytes)
78
What is the name for production of red blood cells and where does it occur?
Erythropoiesis, occurs in red bone marrow.
79
Describe the structure of red blood cells
- 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
List 3 substances needed for RBC production
- Iron - B12 - Folate (folic acid)
81
Where are white blood cells (leukocytes) produced?
Bone marrow
82
What is the production of white blood cells (leukocytes) controlled by?
Granulocyte-colony stimulating factor (G-CSF)
83
List the 5 types of white blood cells
Neutrophils, monocytes, lymphocytes, basophils, eosinophils
84
Describe the role of neutrophils
Phagocytose bacteria, contain defensins to destroy bacteria.
85
Describe the role of monocytes
Circulate in blood and migrate to tissue/organs to become macrophages.
86
Describe the role of lymphocytes
B - Produced in bone marrow. Generate antibodies. | T - Produced in thymus. Aid B cells (helper cells)/ kill bacterial cells directly (cytotoxic killer cells)
87
Describe the role of basophils
Migrate to tissue and become mast cells. Secrete histamine and secrete surface protein IgE.
88
Describe the role of eosinophils
Role in inflammation/allergic response
89
Describe the structure and function of platelets
- Anucleate cells. - Circulate in inactive form. - Produced when megakaryocytes fragment.
90
What is platelet production controlled by?
Thrombopoietin
91
What is primary haemostasis and what is responsible for it?
- Stoppage of bleeding. | - Platelet plug is responsible.
92
Describe the formation of a platelet plug.
- 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
When and why does a coagulation cascade occur?
In secondary hameostasis when a platelet plug alone is not enough to stop bleeding.
94
Describe a coagulation cascade.
- 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
Why are there multiple steps in a coagulation cascade? Give 2 reasons.
- Allows for biological amplification. | - Allows for regulation, not an all-or-nothing response (i.e. a graduated response.)
96
What is the main protein in plasma and what does it do?
Albumin regulates oncotic pressure.
97
What are the main 2 types of groupings used in blood?
ABO and Rhesus systems
98
What type of antigens are on red blood cells?
Carbohydrates
99
In group A blood, what antigen is on RBCs and what antibody is in the plasma?
- A | - Anti-B
100
In group B blood, what antigen is on RBCs and what antibody is in the plasma?
- B | - Anti-A
101
In group AB blood, what antigen is on RBCs and what antibody is in the plasma?
- A and B | - None
102
In group O blood, what antigen is on RBCs and what antibody is in the plasma?
- None | - Anti-A and anti-B
103
How can you type blood?
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
In Rhesus typing, which antigen is dominant?
D is dominant. So DD or Dd = +ve and dd = -ve
105
Describe haemolytic disease of the newborn
- 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
What are the platelet receptors for vWF/fibrinogen?
GPiib/iiia receptors
107
Describe a pacemaker cell action potential
- 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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