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Semester 2: Cardiorespiratory Fitness > PBL Topic 2 Case 4 > Flashcards

PBL Topic 2 Case 4 Flashcards

1
Q

Describe the movement of ions through the sodium potassium pump

A
  • 3 sodium ions out

- 2 potassium ions in

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2
Q

What is the value of the resting potential?

A
  • -90 mV
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3
Q

What occurs during depolarisation?

A
  • Membrane becomes permeable to sodium ions
  • Large numbers of sodium ions diffuse into the axon
  • Reaches around +35mV
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4
Q

What occurs during repolarisation?

A
  • Sodium channels close
  • Membrane becomes permeable to potassium ions
  • Large numbers of potassium ions diffuse into the axon
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5
Q

Describe the structure of a voltage gated sodium channel

A
  • Activation (m) gate near outside of channel

- Inactivation (h) gate near inside of channel

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6
Q

Why is the conductance of potassium ions much greater than that of sodium ions?

A
  • Presence of leak channels
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7
Q

What are intercalated discs?

A
  • Cell membranes that separate cardiac cells from one another
  • That form gap junctions
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8
Q

Why do intercalated discs allow easy transfer of action potentials between cells?

A
  • Intercalated discs form gap junctions

- Allowing mostly free diffusion of ions

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9
Q

Why is cardiac muscle described as syncytium?

A
  • Cardiac cells are so interconnected

- That when one cells

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10
Q

What causes the plateau seen in a cardiac action potential

A
  • L-Type Calcium Channels

- Which are slower to open and remain open for longer

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11
Q

Which type of potassium channel is responsible for repolarisation in cardiac muscle?

A
  • Inward rectifier channels
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12
Q

What is the absolute refractory period and what is its duration?

A
  • Period in which cardiac impulse cannot re-excite an already excited area
  • 0.2 to 0.3 seconds in ventricles
  • 0.15 seconds in atria
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13
Q

What is the relative refractory period and what is its duration?

A
  • Period in which only large impulses can re-excite an already excited area
  • 0.05 seconds
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14
Q

What is a T tubule?

A
  • Modified voltage-sensitive calcium channel

- Known as the dihydropyridine receptor

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15
Q

What occurs when an action potential passes over a T tubule?

A
  • Calcium ions enter sarcoplasm
  • Which bind to ryanodine receptors on sarcoplasmic reticulum
  • Causing release of calcium into sarcoplasm
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16
Q

Explain how calcium ions exposure myosin binding sites

A
  • Calcium enters myofibrils
  • Calcium binds to troponin
  • Troponin moves away from tropomyosin
  • Exposing myosin binding site
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17
Q

Explain the process of power stroke

A
  • Cross bridge head of myosin binds to active site on actin
  • Head tilts forward and drags actin filament with it
  • Head breaks away and process is repeated at a distant site
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18
Q

How is sarcoplasmic calcium concentration restored (and hence muscle relaxation)?

A
  • Calcium-ATPase pumps
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19
Q

What is the cardiac cycle?

A
  • The events that occur from the beginning of one heartbeat to the beginning of the next
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20
Q

Where does the cardiac cycle begin?

A
  • Sinus node
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21
Q

What is the duration of the delay between the atria and ventricles and what is the purpose of this delay?

A
  • 0.1 seconds

- Allows atria to fully contract ahead of ventricular contraction

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22
Q

What is the difference between systole and diastole?

A
  • Systole refers to the period of contraction

- Diastole refers to the period of relaxation

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23
Q

What causes the P wave?

A
  • Atrial depolarisation
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24
Q

What is the duration between the P wave and QRS complex?

A
  • 0.16 seconds
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25
Q

What causes the QRS wave?

A
  • Ventral depolarisation
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26
Q

What causes the T wave?

A
  • Ventricular repolarisation
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27
Q

What percentage of blood flows directly into the atria?

A
  • 80 per cent
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28
Q

What causes the a wave?

A
  • Atrial contraction
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29
Q

What causes the c wave?

A
  • Ventricular contraction (causing backflow of blood)
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30
Q

What causes the v wave?

A
  • Ventricular relaxation (passive flow of blood into the atria)
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31
Q

What is meant by isometric contraction?

A
  • Period required for ventricles to build up sufficient pressure to open semi-lunar valves?
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32
Q

What is the duration of isometric contraction and at what pressure do the semi-lunar valves open?

A
  • 0.02 to 0.03 seconds

- Above 80 mm Hg

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33
Q

What is meant by the term rapid ejection?

A
  • First 1/3 of ventricular contraction

- Emptying 70 per cent of ventricular volume

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34
Q

What is meant by isometric relaxation and what is the duration of this process?

A
  • Period in which ventricles continue to relax even though the ventricular volume does not change
  • 0.03 - 0.06 seconds
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35
Q

What is the value of end-diastolic volume?

A
  • 110 - 120 ml
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36
Q

What is the value of the stroke volume ouptut?

A
  • 70 ml
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37
Q

What is the value of the end-systolic volume?

A
  • 50 ml
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38
Q

What is the ejection fraction?

A
  • The fraction of end diastolic volume that is rejected

- Usually 60 per cent

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39
Q

Where is the tricuspid valve located?

A
  • Between the right atrium and ventricle
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40
Q

Where is the mitral valve located?

A
  • Between the left atrium and ventricle
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41
Q

Why is closure of the AV-valves described as passive?

A
  • Backward pressure gradient forces them to close
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42
Q

What do the papillary muscles attach to?

A
  • The vanes of the atrioventricular valves

- By the chordae tendinae

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43
Q

How do the papillary muscles prevent the budding of the valves toward the atria during ventricular contraction?

A
  • Pull vanes of valves inward toward ventricles
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44
Q

Where is the aortic valve located?

A
  • Between left ventricle and aorta
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45
Q

Where is the pulmonary valve located?

A
  • Between right ventricle and pulmonary trunk
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46
Q

Identify four ways in which semilunar valves to A-V valves

A
  • Snap to closed position
  • Velocity of blood ejection is far greater
  • Subjected to greater abrasion
  • Not supported by chordae tendinae
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47
Q

What is meant by preload?

A
  • Degree of tension on the muscle when it begins to contract
  • Corresponds with end diastolic pressure
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48
Q

What is meant by afterload

A
  • Degree of tension of the muscle against which the muscle exerts its contractile forces
  • Corresponds with systolic pressure
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49
Q

What is the Frank-Starling mechanism?

A
  • The greater the heart muscle is stretched during filling (end-diastolic volume) the greater the force of contraction
  • The greater quantity of blood pumped into the aorta
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50
Q

Identify two effects of sympathetic innervation on cardiac output

A
  • Increases the heart rate

- Increases the force of contraction

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51
Q

Which regions of the heart are innervated by sympathetic stimulation?

A
  • The entire heart
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52
Q

Explain how sympathetic stimulation causes these changes

A
  • Noradrenaline binds to beta-adrenergic receptors
  • G proteins activate Adenylate Cyclase
  • Which converts ATP to cAMP
  • Which acts as a second messenger activate protein kinases
  • Protein kinases phosphorylate L-type calcium channels
  • Which causes influx of calcium ions for muscle contraction
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53
Q

How does sympathetic stimulation enhance myocyte relaxation and what is the significance of this?

A
  • Phosphorylation of Troponin I
  • Which inhibits myocyte interaction
  • Myocyte is ready for next interaction more quickly
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54
Q

What is the role of phospholambin?

A
  • Regulates return of calcium ions to sarcoplasmic reticulum
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55
Q

Which regions of the heart are innervated by the parasympathetic stimulation?

A
  • Atria
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56
Q

Explain how parasympathetic stimulation causes these changes

A
  • Acetylcholine binds to muscarinic receptors
  • Negative coupling to adenylate cyclase so inhibit L-type calcium channels
  • Open potassium channels and therefore have a hyper-polarising effect
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57
Q

Identify two effects of sympathetic innervation on cardiac output

A
  • Decrease heart rate

- Slightly decrease force of heart contraction

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58
Q

What is the resting potential of the sinus node and why is this value different to that of a ventricular muscle? What is the importance of this?

A
  • -55 to - 60 mV
  • Leaky channels for sodium and calcium
  • Which is responsible for self-excitation
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59
Q

Identify the regions of atrial tissue where conduction is rapid

A
  • Anterior interatrial band

- Anterior, middle and posterior internodal pathways

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60
Q

The transmission has a delay of:

[A] after its origin in the sinus node

[B] in the A-V node

[C] in the penetrating tissue

For a total delay of [0.16’ before the signal reaches the ventricles

A
  • [A] = 0.03
  • [B] = 0.09
  • [C] = 0.04
  • [D] = 0.16
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61
Q

What causes the delay in the A-V node?

A
  • Diminished number of gap junctions
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62
Q

Identify 2 reasons why Purkinje fibres transmit action potentials at high velocity

A
  • High level of permeability of the gap junctions

- Few myofibrils so little contraction

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63
Q

How long is the delay between the bundle branches in the ventricular septum to the terminations of the Purkinje fibres?

A
  • 0.03 seconds
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64
Q

How long is the delay between the endocardial and epicardial surfaces of the ventricles?

A
  • 0.03 seconds
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65
Q

What is cardiac output and what is the average value?

A
  • Volume of blood pumped into aorta per minute

- 5 L/ min

66
Q

Identify four factors that determine cardiac ouput

A
  • Metabolism
  • Exercise
  • Age
  • Size
67
Q

In which direction does an increase in intrapleural pressure shift the cardiac output curve? Why does this occur?

A
  • To the right
  • External cardiac pressure = Intrapleural pressure
  • An increase in intrapleural pressure increases cardiac output
68
Q

What is cardiac tamponade?

A
  • Accumulation of fluid in pericardiac cavity
69
Q

Opening of the thoracic cage increases the intrapleural pressure to 0 mm Hg, determine:

  • The direction in which the cardiac output curve will shift
  • How many mm Hg the cardiac output will shift in that direction
A

External cardiac pressure = Intrapleural pressure

Normal cardiac output pressure / intrapleural = -4 mm Hg

0 - -4 = +4 mm Hg

  • To the right due to an increase (positive) pressure
70
Q

Identify the three principal factors that determine venous return

A
  • Right atrial pressure
  • Systemic filling pressure
  • Resistance to blood flow
71
Q

Describe how mean systemic filling pressure occurs

A
  • Backward force of rising right atrial pressure decreases venous blood flow to heart
  • Pumping by heart approaches zero because of decreased venous return
  • Arterial and venous pressures come to equilibrium at 7 mm Hg (Psf)
72
Q

Describe how mean circulatory filling pressure occurs.

A
  • Right atrial pressure falls
  • This sucks the walls of the veins together
  • Pressure everywhere in the circulation becomes equal
73
Q

In the healthy human:

  • Venous return = [A] L/min
  • Mean systemic filling pressure = [B] mm Hg
  • Right atrial pressure = [C] mm Hg
  • Resistance to venous return = [D] mm Hg
A
  • [A] = 5
  • [B] = 7
  • [C] = 0
  • [D] = 1.4
74
Q

Identify the three main causes of heart failure

A
  • Ischaemic Heart Disease
  • Dilated Cardiomyopathy
  • Hypertension
75
Q

For each of the following causes of heart failure, identify a condition associated with it:

[A] Reduced Ventricular Contractility

[B] Ventricular outflow obstruction

[C] Ventricular inflow obstruction

[D] Arrhythmia

A
  • [A] = Myocardial Infarction
  • [B] = Hypertension
  • [C] = Mitral / Tricuspid Stenosis
  • [D] Atrial Fibrillation
76
Q

With regards to the body’s compensatory mechanisms to heart failure:

How does the body deal with a reduced ejection fraction?

A
  • Tachycardia

- Increase in venous pressure

77
Q

Outline the compensatory mechanisms involved in heart failure and how they are caused

A
  • Impaired ventricular function leads to a fall in cardiac output
  • This activates renin-angiotensin-aldosterone system
  • Which leads to vasoconstriction, salt and water retention and sympathetic nervous activation
  • All of which increase blood pressure and cardiac output
78
Q

What is the pathological outcome of increased salt and water retention? How is this compensated for?

A
  • Pulmonary Oedema

- Natriuretic Peptides

79
Q

What is the pathological outcome of increased sympathetic activation? How is this compensated for?

A
  • Cardiac Myocyte Apoptosis

- Down-regulation of B-receptors

80
Q

What is the typical right-sided heart failure?

A
  • Chronic Lung Disease (Cor Pulmonale)
81
Q

Outline the pathophysiology of right-sided heart failure

A
  • Reduction in right ventricular output for any given right atrial pressure
82
Q

Outline four signs of right-sided heart failure

A
  • Raised jugular venous pressure
  • Hepatomegaly
  • Ascites
  • Peripheral pitting oedema
83
Q

What is the typical cause of left sided heart failure?

A
  • Ischaemic Heart Disease
84
Q

Outline the pathophysiology of left-sided heart failure

A
  • An acute increase in left atrial pressure causes pulmonary oedema

OR

  • A gradual increase in left atrial pressure causes pulmonary vasoconstriction which protects against pulmonary oedema at the cost of increasing pulmonary hypertension
85
Q

Outline five signs of right-sided heart failure

A
  • Raised jugular venous pressure
  • Pulmonary Oedema
  • Cardiomegaly
  • Pleural Effusions
  • Pitting oedema
86
Q

Identify three general symptoms of heart failure

A
  • Dyspnoea
  • Orthopnoea (dyspnoea while lying down)
  • Fatigue
87
Q

Identify a clinical finding from a blood test in the diagnosis of heart failure?

A
  • Increased brain natriuretic peptide
88
Q

Identify three clinical findings from a CXR in the diagnosis of heart failure

A
  • Enlarged cardiac silhouette
  • Enlarged hilar vessels
  • Pulmonary Oedema
  • Septal Kerley B lines
89
Q

Identify a clinical finding from echocardiography in the diagnosis of heart failure?

A
  • Valvular disease e..g occult mitral stenosis
90
Q

Identify the four classes of hear failure according to the NYHA

A
  • Class 1: Normal exercise does not cause fatigue, dyspnoea or palpitations
  • Class 2: Normal physical exercise produces fatigue,, dyspnoea or palpitations
  • Class 3: Gentle physical activity produces marked symptoms of heart failure
  • Class 4: Symptoms of heart failure even at rest
91
Q

Outline four aspects of management of pulmonary oedema

A
  • Administer a loop diuretic e.g. furosemide
  • Administer nitrates e..g glyceryl trinitrate
  • Sit the patient up
  • Oxygen e.g. CPAP
92
Q

Why are patients with ischaemic heart disease induced heart failure advised not to take sildenafil?

A
  • Patients with ischaemic heart disease are prescribed nitrates as vasodilators
  • Sildenafil is an erectile dysfunction tablet and is an example of a phosphodiesterase type 5 inhibitor, which also lower blood pressure
  • Administration of both may lead to profound hypotension
93
Q

Identify three essential aspects of monitoring a patient with heart failure

A
  • Functional capacity e.g. exercise tolerance
  • Fluid states e.g. body weight.
  • Cardiac rhythm e.g. ECG
94
Q

Identify an example of a loop diuretic

A
  • Furosemide
95
Q

Identify the mechanism of action of loop diuretics

A
  • Combine with Cl- binding site in ascending limb

- Natriuresis

96
Q

Identify three unwanted effects of loop diuretics

A
  • Hypotension
  • Hypovolaemia
  • Hypokalaemia
97
Q

Identify an example of an ACE Inhibitor

A
  • Ramipril
98
Q

Identify the mechanism of action of action of ACE Inhibitors

A
  • Inhibiting Angiotensin Converting Enzyme
  • Blocks the formation of angiotensin II, a powerful vasoconstrictor
  • Blocks the formation of aldosterone, resulting in natriuresis
99
Q

Identify three unwanted effects of ACE Inhibitors

A
  • Hypotension
  • Hyperkaleamia
  • Renal Dysfunction
  • Cough
100
Q

Identify three contraindications to the use of ACE Inhibitors

A
  • Renal artery stenosis
  • Pregnancy
  • Previous angiodema
101
Q

Identify an example of an Angiotensin II Receptor Antagonists and outline when they are used

A
  • Valsartan
  • Second line therapy in patients intolerant to ACE Inhibitors
  • Since they do not affect bradykinin metabolism or produce cough
102
Q

Identify two examples of beta blockers and provide a brief description of each

A
  • Carvedilol, non selective b-receptor antagonist with additional a1-blocking activity
  • Nebivolol, a b1-receptor antagonist
103
Q

Identify the mechanism of action of beta blockers

A
  • Antagonise B-adrenergic receptors
  • Prevent binding of noradrenaline
  • Reducing heart rate and contractility
104
Q

Identify three adverse side effects of beta blockers

A
  • Bronchoconstriction
  • Bradycardia
  • Fatigue
  • Hypoglycaemia
105
Q

Identify an example of a cardiac glycoside

A
  • Digoxin
106
Q

Identify the mechanism of action of cardiac glycosides

A
  • Cardiac slowing + increased force of contraction
  • Inhibition of Na/K pump
  • Increased intracellular sodium, which slows extrusion of calcium
  • Therefore increased intracellular calcium for storage in sarcoplasmic reticulum
107
Q

Identify five conditions that can be detected using an ECG

A
  • Myocardial Ischaemia
  • Myocardial Infarction
  • Arrhythmia
  • Pericarditis
  • Chamber Hypertrophy
108
Q

What is the voltage and time of the P wave?

A
  • 0.1 - 0.3 mV

- Less than 0.12 seconds

109
Q

What is the voltage and time of the QRS complex?

A
  • 1 - 1.5 mV

- Less than 0.1 seconds

110
Q

What is the voltage of the T wave?

A
  • 0.25 - 0.35
111
Q

What is the time of the PR interval?

What can a long and short PR interval suggest?

A
  • 0.16 seconds
  • Long = AV nodal conduction
  • Short = Wolf-Parkinson-White syndrome
112
Q

What is the time of the QT interval?

A
  • 0.35 seconds
113
Q

Describe how the current flow occurs in relation to direction

A
  • Flows with negativity towards the base of the heart

- Flows with positivity towards the apex of the heart

114
Q

What does the term bipolar mean in relation to limb leads?

A
  • Two electrodes

- On different sides of the heart

115
Q

In lead 1, where are the electrodes placed?

What is the axis of lead 1?

A
  • Negative terminal connected to right arm
  • Positive terminal connected to left arm
  • 0 degrees
116
Q

In lead 2, where are the electrodes placed?

What is the axis of lead 2?

A
  • Negative terminal connected to right arm
  • Positive terminal connected to left leg
  • 60 degrees
117
Q

In lead 3, where are the electrodes placed?

What is the axis of lead 3?

A
  • Negative terminal connected to left arm
  • Positive terminal connected to left leg
  • 120 degrees
118
Q

Using Einthoven’s law, determine the electrical potential of lead 3 when:

Lead 1 = +0.5 mV

Lead 2 = -0.3 mV

A

(+0.5) - (-0.3) = +0.8 mV

119
Q

Where do V1 and V2 lie?

A
  • Over the right ventricle
120
Q

Where do V3 and V4 lie?

A
  • Over the interventricular septum
121
Q

Where do V5 and V6 lie?

A
  • Over the left ventricle
122
Q

Are the QRS recordings of V1 and V2 positive or negative? Why is this the case?

A
  • Negative

- These leads are nearer to the base of the heart

123
Q

Are the QRS recordings of V4,5 and 6 positive or negative? Why is this the case?

A
  • Positive

- These leads are nearer to the apex of the heart

124
Q

Describe the pattern of the R wave in the chest leads

A
  • Grows from V1 - V4
125
Q

Describe the pattern of the S wave in the chest leads

A
  • Grows from V1 to V3

- Disappear in V6

126
Q

In which leads should the P wave be upright?

A
  • 1, 2, V2-V6
127
Q

In which leads should the ST segment start isoelectric?

A
  • V3-V6
128
Q

In which leads should there be no Q wave?

A
  • 1, 2, V2-V6
129
Q

In which leads should the T wave be upright?

A
  • 1, 2, V2-V6
130
Q

What is the mean QRS vector?

A

+59 degrees

131
Q

In Augmented Unipolar limb leads, where is the aVR lead connected?

What is the axis in this lead?

A
  • Right arm

- Positive 210 degrees

132
Q

In Augmented Unipolar limb leads, where is the aVL lead connected?

A
  • Left arm

- Negative 30 degrees

133
Q

In Augmented Unipolar limb leads, where is the aVF lead connected?

A
  • Left leg

- Positive 90 degrees

134
Q

The normal QRS axis sits in between which angles?

A
  • Negative 30 to Positive 90 degrees
135
Q

The QRS axis with left axis deviation sits in between which angles?

A
  • Negative 30 to Negative 90 degrees
136
Q

The QRS axis with right axis deviation sits in between which angles?

A
  • Positive 90 to Positive 180 degrees
137
Q

Identify three normal causes of left axis deviation

A
  • After deep expiration
  • When a person lies down
  • In stocky, fat people
138
Q

Identify three normal causes of right axis deviation

A
  • After a deep inhalation
  • When a person stands up
  • In tall, lanky people
139
Q

Identify two pathological causes of left axis deviation

A
  • Aortic valvular stenosis

- Aortic valvular regurgitation

140
Q

Identify two pathological causes of right axis deviation

A
  • Congenital pulmonary valvular stenosis

- Tetralogy of Fallot

141
Q

With regards to atrial fibrillation:

  • What does the ECG show?
  • How is the pulse described?
A
  • Normal but irregular QRS complexes
  • No P wave
  • Irregularly Irregular Pulse
142
Q

With regards to ventricular fibrillation:

  • What does the ECG show?
  • What is the clinical significance of this condition?
A
  • Shapeless, rapid oscillations

- It is fatal

143
Q

How does one determine heart rate of a regular rhythm from an ECG?

A
  • Rule of 300

- Large Squares / 300

144
Q

How does one determine heart rate of an irregular rhythm from an ECG?

A
  • 10 Second Rule

- Number of QRS complexes x 6

145
Q

What is the typical cause of Rheumatic Fever?

A
  • Pharyngeal Infection

- By Group A streptococci

146
Q

In which countries is Rheumatic Fever more common and why is this the case?

A
  • Developing countries

- Poorer hygiene and antibiotics

147
Q

Explain the pathophysiology of Rheumatic Fever

A
  • Group A Streptococci antigens cross react with cardiac myosin and sarcolemmal membrane protein
  • Inflammation of endocardium, myocardium and pericardium and joints of the skin
148
Q

What are Aschoff nodules?

A
  • Multinucleate giant cells surrounded by macrophages and T lymphocytes
  • Pathognomonic symptom of Rheumatic Fever
149
Q

Identify four clinical features of Rheumatic Fever

A
  • Fever
  • Anorexia
  • Lethargy
  • Joint Pain
150
Q

How is Rheumatic Fever diagnosed?

A
  • Revised Jones Criteria

- More than 2 major manifestations e.g. carditis, polyarthritis

151
Q

What is the mainstay treatment of Rheumatic Fever?

What drugs can treat the arthritis of Rheumatic Fever?

A
  • Oral phenoxymethylpenicillin 500 mg four times daily

- NSAIDs

152
Q

In longstanding left atrial regurgitation, why is there little increase in left atrial pressure?

A
  • Hypertrophy of left atrium

- To accommodate the left atrial dilation

153
Q

What is the significance of acute mitral regurgitation?

A
  • There is no hypertrophy
  • So atrial pressure increases
  • Resulting in pulmonary oedema
154
Q

Identify three symptoms of mitral regurgitation and briefly explain their cause

A
  • Palpitation (increased stroke volume)
  • Dyspnoea (pulmonary hypertension)
  • Fatigue and lethargy (decreased cardiac output)
155
Q

In the later stages of mitral regurgitation, the symptoms of which condition occur ?

A
  • Right sided heart failure
156
Q

Identify three signs of mitral regurgitation

A
  • Soft first heart sound
  • Prominent third heart sound
  • Mid-systolic click
  • Laterally displaced diffuse apex beat
  • Pansystolic murmur
157
Q

With mitral regurgitation, what would an ECG show?

A
  • Left ventricular / atrial hypertrophy
158
Q

With mitral regurgitation, what would a CXR show?

A
  • Enlarged left ventricle / atrium

- Pulmonary oedema / congestion

159
Q

With mitral regurgitation, what would echocardiography show?

A
  • Dilated left ventricle / atrium
160
Q

Identify the treatment of mitral regurgitation

A
  • Mitral valve repair / replacement
  • ACE Inhibitors
  • Diuretics
  • Anticoagulants

Semester 2: Cardiorespiratory Fitness (18 decks)

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