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Cardiology 2023 1MB > Physiology Creator: Cameron McCloskey > Flashcards

Physiology Creator: Cameron McCloskey Flashcards

1
Q

True or False: Bachmann’s bundle is located in the left atrium.

A

True

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2
Q

The SA node fires at a rate of?

A

60-100pbm

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3
Q

Where does excitation originate in the heart?

A

SA node

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4
Q

What causes the rising phase of the action potential (depolarisation) in SA node cells?

A

Opening of Ca++ channels, resulting in Ca++ influx

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5
Q

On an EKG the P-wave represents what area of the heart?

A

Atrial contraction mid to late ventricular diastoly

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6
Q

What gives rise to pacemaker potential?

A

A

Decrease in K+ efflux

Slow Na+ influx

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7
Q

What causes the falling phase of the action potential (repolarisation) in SA node cells?

A

Opening of K+ channels, resulting in K+ efflux

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8
Q

Where is the SA node located

A

Upper right atrium (close to SVC entry)

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9
Q

Summarise the phases of the SA node action potential

A

A

Pacemaker potential: decreased K+ efflux, slow Na+ influx
Rising phase: Ca++ influx
Falling phase: K+ efflux

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10
Q

When the heart is controlled by the SA node, it is said to be in what type of rhythm?

A

Sinus rhythm

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11
Q

Which structure in the heart does NOT propagate action potentials?

A

The annulus fibrous

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12
Q

AV node cells are large and slow to conduct. True/False?

A

False

They are small and slow to conduct

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13
Q

which structure is propagation of the action potential the fastest in the heart?

A

c. The bundle of His

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14
Q

In which structure is propagation of the action potential the slowest in the heart?

A

b. The AV node

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15
Q

What is the pacemaker potential due to? 3charges

A
  1. Increase in funny current 2. Background current of potassium influx (Ib) 3. Transient Ca2+ influx
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16
Q

which structure in the heart is there a plateau in the cardiac action potential?

A

e. The ventricular myocardium

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17
Q

what is intercalated discs

A

is a combination of bundles of gap and desmosome junctions

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18
Q

Why is AV nodal delay present?

A

A

To allow time for atrial systole to precede ventricular systole

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19
Q

what is (1) Funny 𝑵+channels (𝑰𝒇)

A

These channels are open when the cell is at rest Allows more slow movement of Na+ to move into cell making inside of cell + + Allows less slow movement of K+ to move out of cell making inside of cell

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20
Q

How calcium in the cell is shunted back into the sarcoplasmic reticulum during repolarisation ?

A
  • Into SR: ATP dependent Ca++/H+ exchanger. Na+/ Ca++ exchanger via secondary active transport
  • Out of cell: ATP dependent Ca++/H+ exchanger. Na+/ Ca++ exchanger via secondary active transport
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21
Q

What happens when the pacemaker potential reaches threshold?

A

L-type calcium channels open allowing for calcium influx

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22
Q

What are the 2 main causes of the falling phase in a nodal action potential?

A
  1. Inactivation of L-type calcium channels - This reduces the inward flow of calcium ions, which contributes to depolarization, and starts to decline during the falling phase.
  2. Activation of outward potassium channels - This leads to an efflux of potassium ions out of the cell, resulting in repolarization of the membrane potential during the falling phase.

So, to summarize, the falling phase in a nodal action potential is due to both the inactivation of L-type calcium channels and the activation of outward potassium channels.

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23
Q

What permits the spread of excitation between myocardial cells?

A

Gap junctions

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24
Q

Where is the AV node located?

A

At the base of the right atrium just above the atrium/ventricular junction

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25
Q

What is the purpose of the AV node?

A

To allow conduction to spread to the ventricles from the atria

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26
Q

What attribute of the AV node allows for heart contraction coordination?

A

It has a low conduction velocity allowing there to be delay between atrial and ventricular contraction

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27
Q

What is the bundle of His?

A

This is a bundle of nerve fibres which carries the impulse from the AV node to the ventricles where the impulse passes upwards via Purkinje fibres in the ventricles

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28
Q

What is the resting potential of a myocardial cell?

A

-90mv

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29
Q

In a myocardial action potential, what is phase 0

A

Rapid depolarisation from -90mv to +20mv due to Na+ influx

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30
Q

Which type of channels are phosphorylated by stimulation of the SNS?

A

a. L- type Ca++ channels

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31
Q

In a myocardial action potential, what is phase 4

A

Resting membrane potential is achieved (-90mv)

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32
Q

The PSNS can affect the contractility of the heart. a. True b. False

A

False

only nodes

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33
Q

During the relative refractory period APs can be
triggered.

A

True

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34
Q

The SNS has a positive chronotropic action. a. True/ false

A

True

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35
Q

In a myocardial action potential, what is phase 3

A

Closure of Ca2+ channel influx and K+ efflux begins

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36
Q

In a myocardial action potential, what is phase 2

A

L-type Ca2+ channel influx

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37
Q

In a myocardial action potential, what is phase 1

A

Closure of Na+ channels and transient K+ channels

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38
Q

What is the plateau phase and what causes it?

A

Maintained during phase 2 of a myocardial AP. Due to Ca2+ influx through L-type channels. Maintains peak AP

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39
Q

How does the sympathetic system affect heart rate?

A

Increases

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40
Q

How does the parasympathetic system affect heart rate?

A

Decreases

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41
Q

What is vagal tone?

A

Continuous influence of the vagus nerve on SA node lowering heart rate to normal levels

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42
Q

What is the normal range for heart rate?

A

60-100bpm

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43
Q

What is the term for low heart rate (<60bpm)?

A

Bradycardia

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44
Q

What is the term for high heart rate (>100bpm)?

A

Tachycardia

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45
Q

On which receptors does acetylcholine from the vagus nerve act?

A

Type 2 Muscarinic

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46
Q

What type of drug is atropine and what may it be used for?

A

Competitive acetylcholine inhibitor Treats bradycardia by speeding up heart rate

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47
Q

What three effects does sympathetic stimulation have on the heart?

A
  1. Increase HR 2. Decrease AV node delay 3. Increases contractile force
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48
Q

Noradrenaline from the sympathetic system acts on which receptors in the heart?

A

B1

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49
Q

What is a chronotropic effect?

A

Something which influences heart rate e.g. positive chronotropic increases HR

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50
Q

In an ECG what does the P wave represent?

A

Atrial depolarisation

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51
Q

In an ECG what does the QRS complex represent?

A

Ventricular depolarisation

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52
Q

In an ECG what does the T wave represent?

A

Ventricular repolarisation

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53
Q

In an ECG what does the PR interval represent

A

AV node delay

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54
Q

In an ECG what does the ST segment represent?

A

Ventricular systole

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55
Q

In an ECG what does the TP interval represent?

A

Diastole

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56
Q

How long does the cardiac cycle normally last?

A

lasts about 0.8 seconds or 800

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57
Q

What 5 events comprise the cardiac cycle?

A
  1. Passive Filling 2. Atrial Contraction 3. Isovolumetric ventricular Contraction 4. Ventricular Ejection 5. Isovolumetric ventricular Relaxation
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58
Q

Describe passive filling

A

Pressure in atria is slightly higher than ventricles allowing for passive filling of ventricles with blood

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59
Q

Passive filling accounts for what percentage of ventricular filling?

A

80%

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60
Q

Describe how atrial contraction contributes to ventricular filling

A

The final 20% of ventricular filling is achieved by atrial conraction

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61
Q

Describe isovolumetric ventricular contraction

A

Ventricular pressure rises past atrial pressure upon contraction cause AV valves to close. Semilunar valves remain close so pressure builds around a closed volume

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62
Q

Describe ventricular ejection

A

Ventricular pressure exceeds aortic/pulmonary valve pressure causing ejection of stroke volume

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63
Q

What is the end systolic volume?

A

This is the amount of blood left behind in the ventricles after contraction

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64
Q

How is stroke volume calculated?

A

SV = EDV - ESV

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65
Q

When do the semilunar valves close?

A

When ventricular pressure falls after contraction?

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66
Q

What causes the first hearts sound?

A

Closing of AV valves during isovolumetric ventricular contraction

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67
Q

What causes the second heart sound?

A

Closing of semilunar valves after ventricular ejection

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68
Q

What causes the dicrotic notch in the pressure curve?

A

Valve vibration

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69
Q

What does isovolumetric ventricular relaxation involve?

A

The closing of aortic and pulmonary valves

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70
Q

What causes the third heart sound (S3)?

A

Occurs after 2nd heart sound - due to acceleration and deceleration of blood into the ventricles - can signify cardiac disease

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71
Q

What causes the fourth heart sound (S4)?

A

Occurs shortly before the first heart sound - due to rapid blood flow into less compliant ventricles (usually left) causing turbulence

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72
Q

Where are the S3 and S4 heart sounds best heard?

A

Apex

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73
Q

Where is the aortic area?

A

2nd intercostal space Right parasternal

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74
Q

Where is the pulmonary area (for the valve )?

A

2nd intercostal space Left parasternal

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75
Q

Where is the tricuspid area which rib intercostal space

A

4th intercostal space Left parasternal

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76
Q

Where is the mitral area?

A

5th intercostal space Left parasternal

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77
Q

For which two reasons does arterial pressure never fall to zero?

A
  1. Contraction of arterial and arterioles muscle 2. Retraction of elastic fibres
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78
Q

What is blood pressure?

A

Hydrostatic (outward) pressure exerted on vessels by blood flow

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79
Q

What is the upper limit of blood pressure before treatment?

A

140/90mmHg

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80
Q

What is the term used to describe blood flowing without turbulence?

A

Laminar blood flow

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81
Q

What are Korotkoff sounds?

A

There are 5 and they are heard when blood pressure is taken

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82
Q

At which Korotkoff sound is diastolic pressure measured and why?

A

5

At sound 5, the change is more easily heard as any sound heard changes to silence

Technically the fourth Korotkoff sound is where diastolic pressure occurs

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83
Q

What drives blood circulation?

A

The pressure gradient between aorta and right atrium

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84
Q

How is mean arterial blood pressure (MABP) calculated? (3)

A
  1. MABP = (2 x diastolic + systolic)/3
  2. MAP = 1/3 (systolic – diastolic) + diastolic
  3. MABP = CO x TPR
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85
Q

What is the pulse pressure?

A

This is the difference between systolic and diastolic pressure

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86
Q

What is the range for MABP?

A

70 - 105mmHg

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87
Q

What is the minimum requirement of MABP to perfuse organs?

A

60mmHg

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88
Q

What can happen is MABP is too high?

A

Damage to organs, vessels and extra strain is placed on the heart

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89
Q

What is TPR?

A

Total peripheral resistance

The sum of all the resistances in systemic and peripheral circulations

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90
Q

What are the main resistance vessels and what eveidence is there for this?

A

Arterioles

The blood pressure drops the most after entering these vessels

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91
Q

What effect does parasympathetic stimualtion have on the cardiovascular system?

A
  1. Decreases heart rate
  2. Decreases cardiac output
  3. Decreases MABP
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92
Q

What effects does sympathetic stimulation have on the cardiovascular system?

A
  1. Increase heart rate
  2. Increase contractile strength
  3. Increase cardiac output (increased stroke volume)
  4. Increase MABP
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93
Q

What are baroreceptors?

A

Pressure receptors

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94
Q

Where is the control centre located for baroreceptors?

A

The medulla

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95
Q

What are the effectors for the baroreceptors?

A

The heart and blood vessles

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96
Q

Where are the two groups of baroreceptors located?

A
  1. Aortic arch
  2. Carotid sinus (bifurcation)
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97
Q

Which cranial nerves allow signals to be sent from baroreceptors to the brain?

A

9 and 10

(IX and X)

(Glossopharyngeal and Vagus)

98
Q

How do blood vessles “react” to increased carotid sinus afferent nerve fibre firing?

A

Vasodilate

99
Q

How do blood vessles “react” to cardiac vagal nerve efferent nerve fibres?

A

Vasodilation

100
Q

Explain the process baroreceptors go through when a person stands up quickly after lying down

A
  1. Venous return decreased due to a drop in blood pressure
  2. Firing rate of baroreceptors decreases
  3. Vagal tone of the heart decreases as the sympathetic system increases heart arte and stroke volume to attempt a blood pressure increase
  4. Sympathetic constrictor tone increases TPR which increases venous return and stroke volume correcting the low MABP and increasing it
101
Q

What happens to the baroreceptor response when blood pressure is maintained over a long period of time?

A

The baroreceptor response is designed tor respond to acute changes.

The response sets a new baseline value to an acute change, if this change is mainatined it will become the new “normal”

102
Q

How is MABP controlled long term?

A

Blood volume

103
Q

Total body fluid is made up of which two components?

A
  1. Extracellualr volume
  2. Intracellular volume
104
Q

What two components make up extracellular fluid volume?

A
  1. Plasma volume
  2. Interstitial fluid volume
105
Q

What happens in order to balance a fall in plasma volume?

A

Compensatory mechanisms shift fluid from the interstitial fluid volume

106
Q

Blood volume and MABP are controlled by mechanisms regarding ____________ _____ ______

A

Extracellular Fluid Volume

(ECFV)

107
Q

Which two main factors affect ECFV?

A
  1. Water excess or deficit
  2. Na+ excess or deficit
108
Q

Which three systems are involves in regulating ECFV?

A
  1. Renin Angiotensin Aldosterone system
  2. Atrial Naturiuretic Peptide
  3. Antidiuretic Hormone (Vasopressin)
109
Q

How does the RAAS regulate MABP?

A

By regulating TPR and plasma volume

110
Q

Where is renin produced and what is its function?

A

Kidneys (juxtaglomerular apparatus)

Stimulates formation of angiotensin I in the blood from angiotensinogen (from liver)

111
Q

What happens to angiotensin I?

A

It is converted to angiotensin II by angiotensin converting enzyme (ACE, produced in pulmonary vascualr endothelium)

112
Q

What does angiotensin II stimulate?

A
  1. Release of aldosterone from adrenal cortex
  2. Causes systemic vasoconstriction increasing TPR
  3. Stimulates thirst and ADH release (contributes to increasing plasma volume)
113
Q

What does aldosterone do?

A

Acts on kidneys to increase sodium and water retention to increase plasma volume and hence MABP

114
Q

What can stimulate renin release form the juxtaglomerular apparatus in the kidneys?

A
  1. Renal artery hypotension
  2. Stimulation of renal sympathetic nerves
  3. Decreased [Na+] in renal tubuar fluid (sensed my macra densa)
115
Q

What are the macra densa?

A

Can detect [Na+] in renal tubular fluid

Specialised renal tubules composed of extraglomerular mesangial and granular cells (which release renin)

116
Q

What is atrial natriuretic peptide (ANP) and when is it released?

A

Atrial myocytes synthesise a 28-amino acid peptide (ANP)

Released in response to atrial distension (stretch) in hypervolaemic states

117
Q

What does ANP do?

A

Causes release of water and Na+ in urine.

The system reduces MABP and causes vasodilatation and reduced renin release.

This is a counter regulatory mechanism for RAAS

118
Q

What is ADH?

A

Anti-diuretic hormone (vasopressin)

A peptide hormone

119
Q

Where is ADH produced?

A

Precursor formed in hypothalamus and stored in posterior pituitary

120
Q

What will stimulate ADH secretion?

A

Reduced ECFV or increased extracellular fluid osmolarity

121
Q

What monitors plasma osmolarity?

A

Osmoreceptors

122
Q

How does ADH function?

A

Acts on kidney tubules to increase water reabsorption allowing for increased blood volume and MABP.

It will stimulate vasoconstriction to increase TPR and MABP

123
Q

What is shock?

A

An abnormality of the circulating system resulting in inadequate tissue perfusion

124
Q

What is the pathway for shock?

A
  1. Inadequate tissue perfusion
  2. Inadequate tissue oxygenation
  3. Anaerobic metabolism
  4. Waste product build up
  5. Cellular failure and death
125
Q

Which two factors are essential for there to be adequate tissue perfusion?

A

Adequate cardiac output and blood pressure

126
Q

Which three factors can affect the stroke volume?

A
  1. Preload
  2. Myocardial contractility
  3. Afterload
127
Q

What is the preload?

A

The preload is the amount of blood in the ventricles before systole - it is the EDV

128
Q

What is afterload?

A

This is the amount of blood left in the ventrciles after systole - provides resistance for contracting heart muscle during the next contraction

129
Q

Why does hypovolaemic shock occur?

A

Loss in blood volume

130
Q

Why does hypovolaemic shock lead to inadequate tissue perfusion?

A
  1. Loss in blood volume
  2. Venous return/EDV reduced
  3. Stroke/cardiac volume reduced
  4. Blood pressure lowered
  5. Inadequate tissue perfusion
131
Q

In response to hypovolaemic shock, which way does the Frank-Starling curve shift and why?

A

To the right

Decreased EDV (sub-optimal fibre length) hence stroke volume is reduced

132
Q

What is cardiogenic shock?

A

Occurs when the heart cannot pump enough blood around the body due to decreased cardiac contractility

133
Q

How does cardiogenic shock lead to inadequate tissue perfusion?

A
  1. Decreased contractility
  2. Decreased stroke volume
  3. Decreased cardiac output
  4. Reduced blood pressure
  5. Inadequate tissue perfusion
134
Q

How does cardiogenic shock affect the Frank-Starling curve?

A

Shifts very far to the right - more than heart failure alone

135
Q

What is obstructive shock?

A

Due to increased intrathoracic pressure which decreases venous return

(e.g. pneumothorax)

136
Q

Why does tissue perfusion become inaqequate in obstructive shock?

A
  1. Decreased venous return and EDV
  2. Decreased stroke volume
  3. Decreased cardiac output
  4. Reduced blood pressure
  5. Decreased tissue perfusion
137
Q

What does neurogenic shock involve?

A

Loss of sympathetic tone causing massive vasodilatation

138
Q

Why does neurogenic shock lead to a lack in tissue perfusion?

A
  1. Massive vasodilatation
  2. Reduced venous return and EDV
  3. Reduced stroke volume
  4. Reduced cardiac output and blood pressure
  5. Inadequate tissue perfusion
139
Q

What is vasoactive shock?

A

The release of vasoactive mediators causing massive vasodilatation and increased capillary permeability

140
Q

Why is capillary permeability a relevant factor to vasoactive shock?

A

This can lead to a decreased blood volume and cause hypovolaemic shock

141
Q

How does vasoactive shock lead to inadequate tissue perfusion?

A
  1. Massive vasodilatation
  2. Decreased venous return and EDV
  3. Decreased stroke volume and cardiac output
  4. Lowered blood pressure
  5. Inadequate tissue perfusion
142
Q

How should shock be treated?

A
  1. ABCDE approach
  2. High flow oxygen - makes most of tissue perfusion that does occur
  3. Increase blood volume
  4. Use of positive inotropes e.g. adrenaline for anaphylaxis
  5. In septic shock, vasopressors can be used to cause mass vasoconstriction and increase MABP
143
Q

What are the two main causes of hypovolaemic shock?

A
  1. Haemorrhage (trauma, surgery etc.)
  2. Vomiting, diarrhoea, excessive sweating (decreases ECFV)
144
Q

How is haemorrhagic shock characterised?

A

Tachycardia - baroreceptor reflex

Small volume pulse - cardiac output is lowered

145
Q

What is the myogenic (Bayliss) effect?

A

This involves the control of vessel dilatation/constriction to ensure blood flow remains constant when there is fluctuating blood pressure

It prevents damage to areas such as the brain

146
Q

What are the first vessels to arise from the aorta?

A

Right and left carotid arteries

147
Q

Where does coronary venous blood primarily drain?

A

Coronary sinus

148
Q

In the coronary circulation, what are the two main areas for occulusion?

A
  1. Left carotid
  2. Left anterior descending
149
Q

The coronary circulations have many special adaptions. List 4

A
  1. High capillary density
  2. High basal flow
  3. High oxygen extraction (75% vs normal 25%)
  4. Intrinsic and extrinsic control mechanisms for blood flow
150
Q

Decribe 3 intrinsic mechanisms that confer special adaptions to the coronary circulation

A
  1. Decreased PO2 causes vasodilatation
  2. Metabolic hyperaemia (increased blood flow) ensure blood flow meets demand
  3. Adenosine (from ATP) is a potent vasodilator
151
Q

Noradrenaline acts on which type of receptors in coronary arterioles?

A

Alpha 1

152
Q

The vasoconstricting effect of the sympathetic system is avoided by opposing factors that promote vasodilatation, what are these factors?

A
  1. Increased CO (due to increased HR/SV)
  2. Increased adenosine due to cardiac work
  3. Decreased PO2 due to increased work
  4. Increased metabolites (K, PCO2, H) due to increased metabolism
  5. Increased circulating adrenaline
153
Q

Why does the majority of blood flow in the coronary arteries occur during diastole?

A

The arteries are compressed during systole

154
Q

The brain is supplied by which two artery types?

A
  1. Carotid arteries
  2. Vertebral arteries
155
Q

A stoke can be caused by a _______ but also __________.

A

Thrombosis

Haemorrhage

156
Q

Special adaptions of the cerebral circulation include?

A
  1. Autoregulation - Bayliss effect
  2. Direct sympathetic stimulation has little effect
  3. The brain does not participate in baroreceptor reflexes
157
Q

Increased PCO2 in the brain causes what?

A

Cerebral vasodilatation

158
Q

Decreased cerebral PCO2 causes what?

A

Cerebral vasoconstriction

159
Q

Why does hyperventilation cause fainting?

A

PCO2 is reduced so cerebral vasoconstriction occurs

This limits blood flow to the brain

160
Q

The process by which (sympathetic) vasoconstrictor effects is termed what?

A

Functional symptholysis

161
Q

How is cerebral perfusion pressure calculated?

A

CPP = MABP - ICP

(ICP = intracranial pressure)

162
Q

How can intracranial pressur be increased?

A

Haemorrhage, tumour, and other factors introducing more material into the confined cranial space

163
Q

What forms the blood brain barrier?

A

The tight intercellular junctions formed between cerebral capillaries

164
Q

The blood brain barrier allows ______ _______ and ______ to cross but not ___________ substances

A

Carbon dioxide and oxygen

Hydrophilic subtances

165
Q

How does glucose pass the BBB?

A

Via specific carrier molecules

166
Q

How is the pulmonary circulation resistant to oedema?

A

Absorptive forces exceed filtrative forces

167
Q

How is skeletal blood flow increased during exercise when the sympathetic system induces vasoconstriction?

A
  • Local metabolic hyperaemia overcomes the sympathetic vasoconstrictor activity
  • Circulating adrenaline acts on B2 adrenergic receptors
  • Increased cardiac output contributes to increased muscular blood flow
168
Q

Describe the action of the skeletal muscle pump

A
  • Large veins lie between skeletal muscle
  • The contraction of skeletal muscle aids blood flow
  • Valves present backflow of blood
169
Q

What causes varicose veins?

A

The failure of venous valves leading to the pooling of blood in the lower limbs

170
Q

What are:

a) The major capacitance vessels
b) the major resistance vessels

A

a) Veins
b) Arterioles

171
Q

Which factors can affect the stroke volume?

A
  • Pre-load
  • Myocardial contractility
  • Afterload
172
Q

Total peripheral resistance is mostly controlled by what?

A

Vascualr smooth muscle in walls of arterioles

173
Q

Resistance to blood flow is directly proportional to what?

A
  1. Blood viscocity
  2. Blood vessel length
174
Q

Resistance to blood flow is inversely proportional to what?

A

The radius of blood vessels

175
Q

Vascualr smooth muscle is innervated by sympathetic nerve fibres. This utilises which neurotransmitter and which receptor?

A

Normadrenaline on alpha receptors

176
Q

What is vasomtor tone and what causes it?

A

The state of vascular smooth mucle always being contracted

This is due to tonic discharge of noradrenaline

177
Q

Where are two regions of the body where the parasympathetic system has influence over blood vessels?

A
  1. Penis
  2. Clitoris
178
Q

Adrenaline has what effect when it binds to beta 2 receptors?

A

Vasodilatation

(of skeletal muscle and cardiac arterioles)

179
Q

Angiotensin II can have what effect on arteries?

A

Vasoconstriction

180
Q

Intrinsic mechanisms of vascular smooth muscle include which two factors?

A
  1. Chemical factors
  2. Physical factors

These allow for matching between blood flow and metabolic need

181
Q

Intrinsic controls are able to _________ the extrinsic controls for vascular smooth muscle contraction

A

Override

182
Q

Give three examples of humoral agents which can cause vasodilatation

A
  1. Histamine
  2. Bradykinin
  3. Nitric oxide
183
Q

How is nitric oxide produced?

A

Produced by vascular endothelium from L-arginine by action of nitric oxide synthase

184
Q

When will nitric oxide be released?

A
  • It is always released by tonic discharge
  • Endothelial stress (e.g inside the heart endocardium layer)
  • Receptor activation
185
Q

How does nitric oxide exert its effect?

A

Diffuse into smooth muscle cells and activate cGMP - a secondary messenger

This allows for smooth muscle relaxation

186
Q

Give 4 examples of humoral agents which can stimulate contraction of smooth muscle?

A
  1. Serotonin
  2. Thromboxane A2
  3. Leukotrienes
  4. Endothelin
187
Q

Of the two, endothelial vasoconstrictors or vasodilators, which one contributes to vascular health and which does the opposite promoting thrombosis, inflammation and oxidation?

A

Vasodilators - vascular health

Vasoconstrictors - negative impact on vascular health

188
Q

Name a physical factor responsible for the intrinsic control of vascular smooth muscle contraction

A

Temperature

189
Q

How does increased atrial pressure impact stroke volume?

A

Increases stroke volume

EDV increases leaving to a lerger stoke volume

190
Q

Name factors which aid venous return

A
  • Skeletal muscle pump
  • Respiratory pump
  • Increased blood volume
  • Increased atrial pressure
  • Increased venomotor tone
191
Q

What happens to the Frank-Starling curve during exercise?

A

It shift to the left

Ventricular pressure, SV and EDV rise

192
Q

Heart failure causes the Frank-Starling curve to shift to the what?

A

Right

193
Q

The p wave in an ECG represents which phase of the cardiac cycle?

A

Rapid filling phase

194
Q

What is end systolic volume?

A

Amount of blood left in the LV after it contracts

195
Q

Atrial contraction is triggered by:

A

Atrial depolarisation by Sa nodde

196
Q

How much blood is present in the ventricles during passive filling

A

70-80%

197
Q

what is heart’s septum ?

A

wall separating the right and left sides of the heart

198
Q

Pulmonary circulation loop

Systemic loop

SVC

IVC

A

veins transport oxygenated blood to the heart and pulmonary arteries transport deoxygenated blood to the lung.

from the heart to the aorta to the rest of the body

  • big superior vena cava
    • big inferior vena cava
199
Q

120/ 80 mmHg

A
  • 120 systolic contract sound lub
  • 80 diastolic relaxes sound dub
200
Q

What are the two moments where a new action potential cannot be generated?

A

A

Plateau phase (Na channels in closed state)
and

—-repolarisation (K channels open, thus membrane cannot depolarise)

201
Q

general purpose of refractory period

A

Preventing tetanic contraction of the heart

202
Q

What is meant by end diastolic volume (EDV)?

A

A

Volume of blood remaining in each ventricle following diastole.

Its determined by Venous return

203
Q

Describe the Frank-Starling Law of the Heart

A

A

The greater the EDV (as a result of more venous return), the greater the stroke volume will be during systole

204
Q

What is meant by positive inotropic effect?

A

A

Force of contraction increases (due to sympathetic stimulation)

only in sympathetic

205
Q

Normal cardiac out put is equal to

A

5L/ beat

206
Q

Positive chronotropic agents

A

Factors which .Increase heart rate include

207
Q

What is the similatory and differences between isoproterenol and atropine

A

Both are chronotropic agents Isoproterenol is selective Beat 1 agonist Atropine M2 antagonist thus Both increase HR

208
Q

What is atrial bainbridge reflex

A

Increase increase positive chrontropic agent

209
Q

Factors effect preload , contractility and after load

A
210
Q

What’s the differences between elastic arteries and muscular arteries

A

4 features Character Diameter Structure Function. Aorta and renal artery

211
Q

What is is special about Arterioles

A

High resistance vessels

212
Q

What is the 4 specialties of vein that help them push blood against gravity

A

Veins made of thin tunica media large lumen 1. Valves of tunica interna 2. Muscular milking 3. Respiratory pump 4. Sympathetic tone

213
Q

What is varicose veins

A

Twist which cause enlargement of blood vessels due to back flow

214
Q

Which layer of blood vessels is under vasomotor tone

A

Tunic media

215
Q

What is the Stimulators vasoconstriction of tunic media

A

Angiotensin II Norepinephrine and epinephrine Vasopressin (ADH) Endothelin

216
Q

What is the stimulators vasodilator of tunic media

A

Nitricnoxide and Prostaglandin Arterial natriuretic peptide Increase cellular activity Decrease oxygen Increase CO2 Increase proton (H+ )

217
Q

What is the vasa vasorum (vessels on vessels )

A

Small system of blood vessel that nourish the tunica extern supply blood to tunica media and adventitia

218
Q

What do the EDV and ESV depend on

A

EDV is pre pumped volume in ventricle base on venous return and stretchy myocardium ESV post pumped volume in ventricle base on contractility and afterload Therefore the factors which effect STROKE VOLUME are 1. Preload , 2. contractility and 3. Afterload.

219
Q

Factors effect after load

A

Increase vascular resistance in systemic circulation Diastolic hypertension Thrombus

220
Q

Bruit can be heard with stethoscope when ?

A

There is narrow lumen due to either plaque / thrombus .

221
Q

Mumurs can be heard with stethoscope when

A

There is valve stiffing or the heart muscles

222
Q

Korotkoff sounds

A

Sounds heard when measuring blood pressure via ausculatory method

223
Q

How RAAS is stimulated in during hypotension

A
  1. Decrease sympathetic stimulation on JG cells of the glomerulus 2. Decrease plasma electrode level by macula densa cells in distal converting tube 3. Decrease blood pressure which detect by renal Baroreceptors.
224
Q

Angiotensin II action pathway

A
  1. Act on adrenal cortex increase secretion of aldosterone 2. Act of posterior pituitary glands increase secretion of ADH 3. Act on hypothalamic thirst centre increase WATER absorption 4. Act in the kidney causes Na , Cl amd H2O reabsorption
225
Q

What there factors stimulate ADH real see from the posterior pituitary glands

A
  1. Increase angiotensin II plasma concentration 2. Decrease in blood plasma low H2O 3. LWO Na concentration in the glomerular filtration
226
Q

In general kidney will retain 😋 Na when

A

when activated by aldosterone

227
Q

When we want to inhibit noradrenaline mediated effect of vascular constriction what type of drug is mostly used to block action of noradrenaline

A

Alpha blockers e.g phentolamine this because most alpha blockers are located in blood vessels and when activated will cause vasoconstriction

228
Q

A 40 year old lady was running for the bus. As a result of the additional sympathetic output to her heart, positive inotropy and chronotropy would be observed in her left ventricle. What changes would you expect to occur with respect to her left ventricle?

A

Increased sympathetic output increases both the force (inotropy) and rate (chronotropy) of contractions, which results in increased pressure when the heart contracts (systolic pressure), stroke volume (amount of blood ejected), stroke work (work done by ventricles to eject blood) and heart rate, as the heart is working much harder. As more blood is ejected from the heart, it is logical that both the end-systolic and diastolic volumes will decrease

229
Q

In aortic pressure tracings, an incisura or dicrotic notch is seen at the end of systole.

What is the cause of this dicrotic notch?

A

At the end of the systole, ejection of blood from the left ventricles has just ended, such that the pressures in aorta just exceed the pressure in the left ventricle. As a result, the aortic valves close, which causes a slight backflow of blood into left ventricles. There is hence a slight temporary decrease in the aortic pressure, which is what the incisura or dicrotic notch refers to

230
Q

Adeno(S)ine = (S)lowing down, At(R)opine = make the heart (R)apid

A
231
Q

Depolarisation during an action potential is primarily caused by which gate channel

A

Influx of sodium through voltage-gated ion channels
NOT
ligand-gated ion channels do not play a primary role in the depolarization phase of the action potential. Ligand-gated ion channels open in response to the binding of specific molecules or ligands to the receptor sites on the channel protein, but they are not directly involved in generating the action potential.

232
Q

The “funny” current is activated by [blank] rather than depolarisation.

A

A

Hyperpolarisation

233
Q

How to measure the P-R interval

A

from the beginning of the P wave to the beginning of QRS complex

234
Q

ST segment is where

A

Ventricule systoly coccur

235
Q

the sympathetic stimulation cause what to the slop of pacemaker potential

A

It increases it Make it sharper

236
Q

in cornonry artery surgery

A

internal mammary artery can be used as graft

237
Q

If a patient had aggressive CPR what should be avoided

A

throumbolysis

238
Q

during passive filling the artries and ventricules is close to zero

A

True

239
Q

difference between first degree heart block and sinus bradycardai

A

First-degree heart block is a delay in the transmission of electrical impulses from the atria to the ventricles, which results in a prolonged PR interval on an ECG. Sinus bradycardia is a slower than normal heart rate due to a decrease in the firing rate of the sinoatrial node, with a normal rhythm and PR interval on an ECG.

240
Q

The additional heart sound heard on examination in this patient occurs in late diastole, just before the first heart sound.

A

S4

241
Q

Evaluation of sections of the myocardium demonstrates evidence of apple green birefringence with polarised light. What is the most likely diagnosis?

A

Amyloidosis
https://youtu.be/j962b8ZdU8w

Cardiology 2023 1MB (28 decks)

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