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Phase 1 > CVR: Cardiology > Flashcards

CVR: Cardiology Flashcards

1
Q

When do the coronary arteries fill with blood?

A

During diastole.

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2
Q

Where on the ECG does ventricular repolarisation occur?

A

In the T wave.

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3
Q

What is a normal PR interval?

A

120-300 ms (3-5 small squares on an ECG).

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4
Q

What is a normal QRS complex width?

A

less than 120ms (3 small squares on an ECG).

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5
Q

What is the QT interval a measurement of?

A

Measure of time from ventricular depolarisation to repolarisation.

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6
Q

What is the difference between normal QT intervals for men and women?

A

Women can be 20ms longer (350-460ms) than men (350-440ms).

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7
Q

What does a bipolar lead on a 12 lead ECG measure?

A

Measures potential difference (voltage) between two electrodes; one electrode designated positive, other negative.

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8
Q

Name the three bipolar leads on a 12 lead ECG.

A

Leads I, II, and III are all bipolar leads.

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9
Q

What does a unipolar lead measure on a 12 lead ECG?

A

Measures potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative) using data from other electrodes. Reference point on a 12 lead ECG is the middle of the heart.

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10
Q

Name the nine unipolar leads on a 12 lead ECG.

A

aVR, aVL, and aVF are all unipolar.
V1-V6 are also unipolar.

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11
Q

On a normal 12 lead ECG, lead I and II both have positive QRS complexes. What is left axis deviation?

A

When lead I is positive QRS, lead II is negative.
They are Leaving each other. Left axis deviation.

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12
Q

On a normal 12 lead ECG, lead I and II both have positive QRS complexes. What is right axis deviation?

A

Lead I has negative QRS, lead II positive.
They are Reaching toward each other. Right axis deviation.

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13
Q

Which coronary artery is represented by the inferior leads?

A

RCA (right coronary artery).

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14
Q

On a 12 lead ECG, the inferior leads represent the right coronary artery. Name the three inferior leads.

A

Lead II, III, aVF.

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15
Q

Which coronary artery is represented by the lateral leads?

A

Left circumflex.

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16
Q

On a 12 lead ECG, the lateral leads represent the left circumflex artery. Name the four lateral leads.

A

Lead I, aVL, V5 & V6

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17
Q

Which plane of the heart do the limb leads represent?

A

Coronal plane.

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18
Q

Which plane of the heart do the chest leads represent?

A

Transverse plane.

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19
Q

Which chest leads represent the septal part of the heart and which coronary artery does this relate to?

A

V1 & V2
LAD (Left Anterior Descending).

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20
Q

Which chest leads represent the anterior part of the heart and which coronary artery does this relate to?

A

V3 & V4
LAD (Left Anterior Descending).

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21
Q

ECG as a graph, what is the X axis and what is the Y axis?

A

X = time
Y = voltage

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22
Q

What are capacitance vessels?

A

Veins and venules; they hold the majority of blood in the body and can accommodate changes in blood volume.

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23
Q

What holds a larger percentage of blood volume, large systemic veins or systemic arteries?

A

Systemic veins; 20%
(systemic arteries = 10%)

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24
Q

What would happen to MAP if the aortic valve failed?

A

Diastolic pressure would be lost, therefore MAP would decrease.

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25
Q

Which vessels provide the principal site of resistance to vascular flow?

A

The arterioles.

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26
Q

What is the relationship between radius and flow in Total Arteriolar Resistance (TPR)?

A

When vascular smooth muscle contracts (vasoconstriction), radius decreases, which increases resistance, therefore decreasing flow.

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27
Q

What does the nernst equation calculate?

A

Resting membrane potential.

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28
Q

Name a channel/pump that is active in myocyte membrane during resting potential.

A

Na/K ATPase pump.

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29
Q

Why are Na/K ATPase pumps active during resting potential?

A

Using active transport, K+ is pumped into cell and Na+ is pumped out of cell, against their concentration gradient, creating a voltage.

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30
Q

When do voltage gated sodium channels open in myocyte cell membranes, and what happens?

A

Depolarisation, once certain action potential reached.
Large number of Na+ ions enter cell down their concentration gradient, causing charge inside the cell to increase rapidly.

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31
Q

What happens in the small dip at the end of depolarisation in the cardiac action potential graph?

A

Transient outward potassium channel triggered to open by depolarisation, small number of K+ ions allowed to leave cell causing a small repolarisation (the dip).

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32
Q

Why does the cardiac action potential graph plateau after depolarisation, instead of rapid repolarisation?

A

Slow calcium channels maintain the depolarisation by allowing slow influx of Ca+ ions into the cell.

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33
Q

When do delayed rectifier channels open during the cardiac action potential cycle?

A

During repolarisation to make charge inside the cell more negative again, cause large quantity of potassium to leave the cell by passive diffusion.

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34
Q

How does the action potential spread along a muscle fibre and through the myocardium syncytium (in three steps)?

A
  1. Local depolarisation activates nearby Na+ channels, Na+ ions rush into cell.
  2. This causes adjacent Na+ channels to open.
  3. At gap junctions, Na+ ions allowed to travel directly across from one cell cytoplasm to next.
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35
Q

During phase 2 of cardiac action potential, slow calcium channels allow calcium to diffuse into the cell. How does intracellular calcium concentration become further amplified during this phase?

A

When intracellular calcium levels reach a certain threshold, RyR calcium receptors trigger SR (sarcoplasmic reticulum) to release its stored calcium.

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36
Q

How does calcium cause contraction in the troponin-tropomyosin-actin complex (4 steps)?

A
  1. Calcium binds to troponin.
  2. Troponin moves tropomyosin to reveal myosin binding sites.
  3. Myosin head can then cross-link with actin.
  4. Myosin head pivots causing muscle contraction.
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37
Q

How does Sino-Atrial Node (SAN) myocytes differ in action potential from normal myocytes?

A

SAN myocyte has gradual increase towards depolarisation constantly, once reaches certain threshold triggers full depolarisation.
While normal myocytes do this too, SAN myocytes trend towards depolarisation more rapidly.

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38
Q

What is the funny current?

A

Mixed sodium/potassium inward channel in SAN myocytes that is always open, causes the more rapid trend towards depolarisation.

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39
Q

How is heart rate increased/decreased in relation to calcium channels in the SAN?

A

Through actions on either number or permeability of calcium ion channels.

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40
Q

Why does ageing affect heart rate?

A

Number of calcium channels decreases with age, causing slower depolarisation in SAN.

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41
Q

Why is the QRS complex higher voltage than P wave?

A

The ventricles have more muscle mass than the atria.

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42
Q

What is a chronotrope?

A

Something which increases the heart rate.

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43
Q

What is an inotrope?

A

Something which increases the force of contraction.

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44
Q

Does parasympathetic stimulation increase or decrease HR, force of contraction, and CO?

A

Decreases all three.

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45
Q

Which hormones control the sympathetic stimulation of the heart?

A

Adrenaline and noradrenaline.

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46
Q

What hormone controls parasympathetic stimulation of the heart?

A

Acetylcholine.

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47
Q

How does the His-Purkinje system allow rapid conduction of electrical impulse?

A

High permeability at gap junctions and very large fibres.

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48
Q

How does the Atrioventricular Node (AVN) delay the electrical impulse?

A

AVN has fewer gap junctions.

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49
Q

What happens to fast (voltage-gated) Na+ channels during the absolute refractory period (during plateau phase) in the cardiac cycle?

A

Closed and inactivatable, so depolarisation cannot occur too early, allowing heart time to refill.

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50
Q

The relative refractory period occurs during repolarisation. What are the Na+ and K+ channels doing in the relative refractory period?

A

Some Na+ channels are still inactivated, others have returned to a closed resting state.
K+ channels are still open.

51
Q

What affect does sympathetic stimulation have on the heart?

A

Increases HR and contractility (positive inotropic and chronotropic effect)

52
Q

ECG paper is made of small 1mm squares and big 5mm squares. How many small squares is 1 second on an ECG?

A

25 x small squares (or 5 x big squares!)
(speed = 25mm/sec)

53
Q

How many squares represent 1mV on an ECG?

A

2 big squares (10x small 1mm squares).

54
Q

How would you calculate the rate on an ECG?

A

Number of QRS segments x6

(1 ECG = 10 seconds)

55
Q

What does a positive deflection mean on an ECG?

A

Net current flow is towards the lead.

56
Q

What part of the ECG represents the SAN firing and atria depolarising?

A

P wave.

57
Q

What is happening during the PR interval?

A

Delay of signal passing through AV node.

58
Q

How does the respiratory pump aid venous return during inspiration?

A

Diaphragm increases intra-abominal pressure, increasing pressure in abdominal veins. Decreases pressure in thorax, decreasing pressure in right atrium and intrathoracic veins.
This pressure difference increases venous return to the heart.

59
Q

What is the equation for cardiac output?

A

CO = HR x SV

(cardiac output = heart rate x stroke volume)

60
Q

What is cardiac output?

A

How many litres of blood the heart pumps in one minute.

61
Q

What is stroke volume?

A

The volume of blood pumped from the left ventricle per contraction.

62
Q

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

A

MAP = diastolic + 1/3 pulse pressure.

63
Q

How is pulse pressure calculated?

A

Pulse pressure = systolic - diastolic.

64
Q

In physics, Ohm’s law states voltage = current/flow x resistance (V=IR).
How does this relate to the equation for blood pressure?

A

BP = CO x TPR
V = I x R

65
Q

Poiseuille’s Law states flow = difference in pressure upstream-downstream / resistance to flow (Q=P1-P2/R).
What is important to remember about the calculation of resistance to flow in this equation, in relation to the radius of blood vessels?

A

Radius is to the power of 4, so is very influential.

Resistance to flow is inversely proportional to the radius; as radius is larger (vessels dilate), resistance decreases, which increases flow.

66
Q

In the Frank-Starling Mechanism, stroke volume increases as end-diastolic volume (EDV) increases, due to the length-tension relationship of muscle.
But what happens to stroke volume if EDV is too low or too high?

A

Stroke volume decreases.

EDV too low (e.g. hypovolaemia): sarcomeres aren’t stretched enough to contract forcefully.

EDV too high (e.g. heart failure): sarcomeres are overstretched and can’t contract efficiently.

67
Q

Arteries and arterioles maintain constant pressure by myogenic autoregulation. Explain how this occurs.

A

When vascular smooth muscle is under increased pressure it is stretched (vasodilation).
When pressure is lower, it responds by constricting (vasoconstriction).

68
Q

Nitric Oxide (NO) is produced in vascular endothelium; it is a type of Endothelium Derived Relaxing Factor (EDRF).
What effect does NO have on vascular endothelium?

A

Vasodilation.

69
Q

Endothelin is a peptide produced in vascular endothelium.
What effect does endothelin have on vascular smooth muscle?

A

Vasoconstriction.

70
Q

Name three inhibitors of endothelin production.

A

NO (Nitric Oxide).
Prostacyclin.
ANP (Atrial Natriuretic Peptide).

71
Q

Prostacyclin is produced in vascular endothelium.
What affect does prostacyclin have on blood vessels?

A

Vasodilation.

72
Q

Does adrenaline cause vasoconstriction or vasodilation?

A

Vasoconstriction in the skin, but causes vasodilation in vital organs to increase flow to these important areas.

73
Q

Where are the primary (high-pressure arterial) baroreceptors?

A

In the carotid sinus and aortic arch.

74
Q

Where are the secondary (low-pressure cardiovascular) baroreceptors?

A

Veins, atria, and pulmonary vessels.

75
Q

What nerve sends afferent signals from the carotid baroreceptors?

A

Glossopharyngeal (cranial nerve IX).

76
Q

What nerve sends afferent signals from the aortic baroreceptors?

A

Vagus (cranial nerve X).

77
Q

What happens to baroreceptors when there is long-term change e.g. in hypertension?

A

They adapt/reset to a new baseline.

78
Q

Which part of the brain receives information from baroreceptors, chemoreceptors to monitor and control blood pressure?

A

The medulla oblongata.

79
Q

What are the short-term and long-term controls of BP?

A

Short-term: baroreceptors.
Long-term: blood volume (controlled by kidneys, RASS)

80
Q

How are myocytes linked together?

A

The cells physically slot together at intercalated discs, and are linked by desmosomes and gap junctions.

81
Q

How do desmosomes provide mechanical strength and strong adhesion between cells?

A

By intercellular links joining the intermediate filaments of cells together.

82
Q

What organ receives the largest proportion of cardiac output?

A

The liver.

83
Q

What visceral sensory information do the chemoreceptors of the aortic bodies detect?

A

Arterial O2 and CO2 levels.

84
Q

Renin is a proteolytic enzyme.
What is the principal site of renin production?

A

Juxtaglomerular cells in the kidneys.

85
Q

Anti-diuretic hormone (ADH) acts on the kidneys to promote water retention.

What is the site of synthesis of ADH (antidiuretic hormone)?

A

Synthesised in the hypothalamus.

However, it is then stored in the posterior pituitary gland!

86
Q

Renin is a proteolytic enzyme. What is the key action of renin in the renin-angiotensin-aldosterone system (RAAS)?

A

Renin converts angiotensinogen into angiotensin I.

87
Q

Aldosterone is a steroid hormone in the renin-angiotensin-aldosterone system (RAAS).
Where is aldosterone synthesised?

A

The adrenal cortex.

88
Q

In the renin-angiotensin-aldosterone system (RAAS), release of aldosterone is stimulation by angiotensin II. What affect does aldosterone have in the kidneys?

A

Increases water retention by increasing sodium reabsorption and potassium secretion.

89
Q

Sensible fluid loss is that which is easily measured e.g. urine output, vomit, fluid in surgical drains.

Give an example of insensible fluid loss.

A

Sweating, water lost from respiration, evaporation during abdominal surgery.

(Insensible fluid loss is loss that is not easily measured)

90
Q

What are Starling forces?

A

The hydrostatic and oncotic forces involved in the movement of fluid between plasma in capillaries and interstitial fluid.

91
Q

The left ventricle forms the apex of the heart. Where is the apex beat palpable?

A

Left 5th intercostal space, midclavicular line.

92
Q

How do inotropes increase contractility?

A

Increase Ca+ ingress and release from sarcoplasmic reticulum, therefore more Ca+ binds to TnC, increasing contractility of myofibrils.

93
Q

What is excitation-contraction coupling?

A

Process of converting an electrical stimulus (excitation) to a mechanical response (contraction).

94
Q

“When the heart is relaxing it isn’t resting!”
What does this mean?

A

When the heart is relaxed, it is still working hard, using ATP to pump Ca ions back into sarcoplasmic reticulum or out of the myocytes.

95
Q

Why is the T-tubule important in myocytes?

A

To allow calcium into the cell closer to the SR and myofibrils.

96
Q

The myocyte uses the sodium/calcium exchanger to remove calcium from the cytoplasm during relaxation. How does this work?

A

Uses electrochemical potential to allow 3x sodium ions into the cell in exchange for 1x calcium ion to leave.

(Sodium gradient is then maintained by Na+/K+ ATPase)

97
Q

The protein titin acts like a molecular spring in the myofibrils, providing elasticity. What different parts of the myofibril does it attach to?

A

Attaches myosin to actin at the Z discs.

98
Q

What is the function of Troponin I (TnI) in the troponin complex?

A

TnI inhibits any interaction between actin and myosin.

99
Q

What is the function of Troponin C (TnC) in the troponin complex?

A

TnC binds to calcium, moves TnI and TnT (hence tropomyosin) away from actin, exposes actin binding site to myosin heads.

100
Q

What is the function of Troponin T (TnT) in the troponin complex?

A

TnT binds to tropomyosin to anchor the troponin complex and helps position the tropomyosin on actin, to also prevent myosin binding to actin.

101
Q

What is a sarcomere?

A

The functional unit of myofibril, the region between two Z-lines.

102
Q

What is isovolumic contraction?

A

Part of the cardiac cycle where the ventricle contracts without causing any change in the volume of blood in the ventricle.

103
Q

What pressure does the left ventricle need to reach to open the aortic valve?

A

Diastolic pressure.

104
Q

The ejection fraction is the percentage of blood ejected with each beat. What is the ejection fraction in females vs males?

A

Females = 65%
Males = 55%

105
Q

What do the 1st and 2nd heart sounds (“Lub dub”) correspond to?

A

1st = closing of mitral valve “lub” This is just after the start of isovolumic contraction.
2nd = closing of aortic valve “dub” This is also the start of isovolumic relaxation.

106
Q

What is the early phase of filling?

A

When pressure in the left atrium increases above pressure in the left ventricle, blood rushes into ventricle passively prior to any atrial contraction.

107
Q

In a young healthy adult, what percentage of blood from the left atrium moves into the ventricle during early phase of filling?

A

85%

108
Q

In young healthy adults/athletes/pregnancy, the early phase of filling can create a 3rd heart sound (gallop). When is the 3rd heart sound pathological and what does it suggest?

A

In adults over middle age, suggestive of congestive heart failure.

109
Q

When does diastasis occur in the cardiac cycle?

A

When pressure in left atrium and left ventricle becomes equalised due to early phase of filling equalising the pressure.

110
Q

When might you hear the 4th heart sound?

A

Galloping sound of blood being forced into stiff or hypertrophic left ventricle during atrial contraction.

111
Q

A patient with AF has developed a hypertrophic left ventricle. Would you hear a 4th heart sound?

A

No! Because they don’t have any atrial augmentation/contraction.

112
Q

Preload is also called end-diastolic pressure. What does this refer to?

A

The volume of blood present before left ventricular contraction has started.

113
Q

What is afterload?

A

The amount of pressure the heart needs to exert against systemic vascular resistance to pump blood out of the ventricle.

114
Q

How does titin relate to Starling’s law?

A

Titin in myofibril keeps the unit tight. If the heart is overfilled and go beyond the capacity and stretch/elasticity of the titin, the heart is unable to contract efficiently.

115
Q

What is elasticity of the heart?

A

The ability of the myocardium to recover its normal resting shape.

116
Q

How is ejection fraction calculated?

A

Stroke volume/end-diastolic volume.

117
Q

What do pressure-volume loop graphs demonstrate?

A

Changing relationship between pressure and volume in left ventricle during cardiac cycle.

118
Q

What are three stages of atherogenesis that can lead to thrombosis by plaque rupture/fissure?

A
  1. Fatty streak
  2. Fibrous plaque
  3. Athero-sclerotic plaque
119
Q

What two arteries does the left coronary artery divide into?

A

Left anterior descending (LAD) and circumflex.

120
Q

Why is the oxygen saturation in coronary venous blood very low compared to other veins?

A

Oxygen extraction by the heart muscle is very high.

121
Q

Which part of the ECG has a normal duration of 120-200ms (0.12-0.2 sec)?

A

PR interval.

122
Q

Which lead in a 12-lead ECG yields complexes that are normally inverted compared to the anterior and inferior leads?

A

Lead aVR

123
Q

The end diastolic volume (EDV) in the average healthy person’s left ventricle is 120mls.

If we assume normal ventricular function, what is a normal end systolic volume (ESV)?

A

50ml

124
Q

Cardiac arrythmias can complicate a myocardial infarction.

Which artery most frequently supplies the Atrioventricular Node (AVN)?

A

The right coronary artery.

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