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Year 1 - Cardiovascular (DP) > Cardiovascular Principles > Flashcards

Cardiovascular Principles Flashcards

0
Q

How do we treat a cardiac tamponade?

A

Pericardiocentesis

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1
Q

Pericardial cavity fills with blood?

A

Haemopericardium/Cardiac tamponade

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2
Q

What are the branches of the arch of aorta (from right to left)?

A

Brachiocephalic trunk
Left common carotid
Left subclavian a.

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3
Q

From right to left, what order do the great vessels appear when look at the anterior surface of the heart?

A

SVC
Aorta
Pulmonary trunk

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4
Q

What is the coronary sinus?

A

Venous conduit

Drains cardiac veins to RA

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5
Q

Do the coronary arteries arrive just above or just below the aortic valve?

A

Just above

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6
Q

Which artery supplies the RV?

A

Right marginal artery

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7
Q

Which artery supplies the posterior interventricular septum?

A

Posterior descending artery (r. coronary artery branch)

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8
Q

What artery supplies the posterolateral LV?

A

Circumflex artery (l. coronary branch)

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9
Q

What does the left anterior descending artery supply?

A

Anterolateral myocardium
Apex
Interventricular septum

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10
Q

What causes the first heart sound?

A

Tricuspid and mitral valve shutting

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11
Q

What causes the second heart sound?

A

Aortic and pulmonary valves shutting

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12
Q

When sympathetic nerves leave the spinal cord, what can they do?

A

Go into ganglion at that level
Travel in sympathetic chain
Pass through without synapsing then synapse at prevertebral ganglia
Pass to adrenal medulla

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13
Q

What does autonomic innervation of the heart do?

A

Increase heart rate

Increase contractility

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14
Q

What does parasympathetic innervation of the heart do?

A

Decrease heart rate

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15
Q

What afferent nerves are present in the arch of aorta?

A

Baroreceptor reflex afferents in vagus nerve

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16
Q

Where are visceral afferent nerves located in the heart?

A 
Inner aortic arch
PT
Around SA node
Outflow tracts of RV and LV
Papillary muscles
SVC and IVC
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17
Q

Where do somatic sensory action potentials travel to?

A

Postcentral gurus
Of the parietal lobe
In the cerebral cortex

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18
Q

Where are somatic motor sensations relayed back from?

A

Precentral gurus

Of the frontal lobe

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19
Q

What is phase 4/Funny current of the pacemaker potential?

A

Slow sodium ion influx

Decreased potassium ion efflux

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20
Q

What occurs in rapid depolarisation and what phase is this in the pacemaker AP?

A

Rapid calcium ion influx

Phase 0

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21
Q

What happens during repolarisation and what phase is this?

A

Increased potassium ion efflux

Phase 3

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22
Q

Describe the spread of excitation in the heart

A

From SA node to AV node
From SA node through both atria
From AV node through bundle of His
From bundle of His through Purkinje fibres

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23
Q

What type of cell junctions allow easy conduction in the heart?

A

Gap junctions

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24
Q

What three junctions form an intercalated disc as seen in heart muscle?

A

Gap junctions
Desmosomes
Fascia adherens

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25
Q

Where is the SA node located?

A

Near entrance of SVC into RA

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26
Q

Where is the AV node located?

A

At base of RA near junction to RV

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27
Q

What are each of the phases in the ventricular muscle action potential?

A 
Phase 0 - Rapid Na influx
Phase 1 - Slow potassium efflux
Phase 2 - Plateau due to Calcium influx
Phase 3 - Rapid potassium efflux
Phase 4 - Resting membrane potential (-90mV)
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28
Q

Why is the intrinsic heart rate slowed from ~100bpm to ~70bpm?

A

Continuous vagal tone influences SA node at rest

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29
Q

What is defined as sinus bradycardia?

A

<60bpm

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30
Q

What is defined as sinus tachycardia?

A

> 100bpm

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31
Q

What effects does the vagus nerve have on the heart?

A

Decreased SA node firing

Increased AV nodal delay

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32
Q

How does atropine work?

A

Inhibits ACh to increase HR

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33
Q

What effect does the vagal tone have on the pacemaker potential slope?

A

It is decreased

So it takes longer to reach threshold - Negative chronotropic can effect

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34
Q

What noradrenergic receptors play the biggest role in the heart?

A

Beta1

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35
Q

What effect does NA have on the heart pacemaker potential?

A

Increases slope

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36
Q

What is the role of desmosomes?

A

Provide mechanical adhesions

Ensure tension is transmitted cell to cell

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37
Q

What two filaments are Myofibrils made from?

A

Myosin (thick and dark)

Actin (thin and lighter)

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38
Q

How are the filaments in myofibrils arranged?

A

Into sarcoma reds

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39
Q

What is the A band?

A

Length of myosin

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40
Q

What is the I band?

A

Section containing only actin

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41
Q

What is the H zone?

A

Area of myosin only (ie no actin overlap)

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42
Q

How is a single sarcomere defined?

A

Segment between two Z lines

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43
Q

Briefly describe the process of a power stroke

A

In the presence of calcium ions, myosin cross bridge binds to actin
ATP on myosin is hydrolysed, bending the cross bridge
Actin pulled along
In presence of ATP, it binds to myosin
Myosin detaches and realigns

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44
Q

What occurs in the absence of further ATP during the power stroke?

A

Rigor mortis

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45
Q

Why are calcium ions required for initiation of the power stroke?

A

Pulls away the troponin-tropomyosin complex to allow myosin-actin binding

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46
Q

During systole, where do the calcium ions come from?

A

Calcium ions influx into cell
Calcium induced calcium release (CICR) from sarcoplasmic reticulum
(Contraction)

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47
Q

What happens to the calcium ions in the cell during diastole?

A

Calcium influx ceases
Calcium ions re-sequestered into SR by Calcium-ATPase
(Relaxation)

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48
Q

What is the refractory period?

A

Period of time after an AP when another cannot be generated

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49
Q

What is the equation for the stroke volume?

A

SV = EDV - ESV

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50
Q

What intrinsic factors determine the end diastolic volume and hence stroke volume?

A

Venous return

Preload

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51
Q

What is the preload of the heart?

A

The end diastolic pressure that stretches the ventricles ie the greatest length of the sarcomeres

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52
Q

What is the afterload of the heart?

A

The resistance into which it pumps

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53
Q

How does sympathetic stimulation increase the force of contraction?

A

Activated calcium channels

Greater calcium influx

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54
Q

How does sympathetic stimulation increase the HR?

A

Increased peak ventricular pressure - increased rate of change - decreased duration of systole

Increased rate of ventricular relaxation due to increased calcium efflux - decreased duration of diastole

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55
Q

At 75bpm, what is the approximate length of

  1. Diastole
  2. Systole
A
  1. 0.5s

2. 0.3s

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56
Q

What are the five events in 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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57
Q

How full do the ventricles become during passive filling (%)?

A

80%

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58
Q

What is the approximate EDV?

59
Q

What is the approximate ESV?

60
Q

Why does arterial pressure not fall to zero during diastole?

A

Aortic walls recoil
Maintains pressure
Forces blood forward

61
Q

When is blood flow audible?

A

When diastolic BP < external pressure < systolic BP

62
Q

What Korotkoff sounds do we use for BP measurements?

A 
1st sound - systolic
5th sound (silence) - diastolic
63
Q

What is the equation for mean arterial pressure (using DBP and SBP)?

A

MAP = ([Diastolic BP x 2] + Systolic BP)/3

64
Q

What MAP is needed to perfume the major organs?

65
Q

When BP falls, do cardiac sympathetic efferents or cardiac vagal efferents Fire more?

A

Sympathetic

66
Q

Where are baroreceptors located in the heart?

A 
Aortic arch (via CN x)
Carotid sinus (via CN ix)
67
Q

What events occur in postural hypotension?

A 
Decreased venous return
Transient decrease in MAP
Decreased baroreceptor firing
Decreased vagal tone/increased SNS tone
Increased HR and SV and TPR (vasoconstriction)
Increased venous return
68
Q

What happens to the baroreceptor response in sustained hypertension?

A

Firing decreases
They ‘reset’
Only fire of BP rises even hire
Control of MAP now relies solely on blood volume control

69
Q

What does renin do, when is it released, and where from?

A

Stimulates angiotensin i formation from liver angiotensinogen
Hypovolaemia/Hypotension
Kidney (juxtaglomerular apparatus)

70
Q

What does angiotensin ii do?

A

Stimulates aldosterone release
Vasoconstriction
Increases thirst
Increases ADH release

71
Q

What does aldosterone do?

A

Causes vasoconstriction
ADH release
Increased sodium and water retention
Increased BP

72
Q

How is RAAS regulated?

A

Renal artery hypotension
SNS stimulation
Decreased [Na+] in renal tubular fluid

73
Q

When is atrial natriuretic peptide released and what does it do?

A

In hypervolaemic states due to atrial stretching
Causes excretion of sodium ions and water
Decreases BP
Vasodilator
Decreases renin release

74
Q

Where is the majority of the body’s blood at any given time?

75
Q

What receptors does NA act on in vascular smooth muscle?

76
Q

What effect does adrenaline have on vascular smooth muscle presenting the following receptors?

  1. Alpha
  2. Beta
A
  1. Vasoconstriction

2. Vasodilation

77
Q

Where are alpha-receptors predominant?

A

Skin
Gut
Kidney arterioles

78
Q

Where are beta receptors predominant?

A

Cardiac muscle

Skeletal muscle

79
Q

What metabolic changes cause VSM relaxation?

A 
Decreased local PaO2
Increased local PaCO2
Increased local pH
Increased extracellular potassium
Increased ECF osmolariry
Adenosine release (ATP)
80
Q

What other chemicals cause vasodilation?

A

Histamine
Prostaglandins
Bradykinin
Nitric oxide

81
Q

What factors increase venous return?

A

Increased venomotor tone
Increased blood volume
Increased skeletal muscle pump
Increased respiratory pump

82
Q

What is the respiratory pump?

A

During inspiration

  • Intrathoracic pressure falls
  • Intra-abdominal pressure rises
  • Pressure difference between abdominal IVC and thoracic IVC pushes blood towards RA
83
Q

What is venomotor tone controlled by?

A

SNS -> Stimulation -> Constriction

84
Q

What is the skeletal muscle pump?

A

Large veins lie between muscles

Muscle contraction forces blood towards heart

85
Q

What is cardiogenic shock?

A

Decreased contractility resulting in hypotension

86
Q

How do we treat shock?

A
  • ABCDE
  • High flow oxygen
  • Volume replacement (14G cannulae in each antecubital fossa - 500ml 0.9% NaCl quickly)
  • Inotropes (Cardiogenic shock)
  • Adrenaline (Anaphylactic shock)
  • Vasopressors (Septic shock)
87
Q

What is the P wave and how long should it last?

A

Atrial depolarisation

0.08-0.10s (2-2.5 small squares)

88
Q

What is the QRS complex and how long should it last?

A

Ventricular depolarisation

89
Q

What is the T wave?

A

Ventricular repolarisation

90
Q

Why can we not see an atrial repolarisation wave?

A

It is masked by the QRS complex

91
Q

What does the PR interval represent and how long should it last?

A

AV nodal delay (atrial systole)

0.12-0.20s (3-5 small squares)

92
Q

What does the ST segment represent?

A

Ventricular systole

93
Q

What does the TP interval represent?

94
Q

Which leads are the septal leads?

95
Q

Which leads are the anterior leads?

A

V3 (Anteroseptal)

V4 (Anterolateral)

96
Q

Which leads are the lateral leads?

97
Q

Which leads are the inferior leads?

98
Q

How can we calculate the HR from an ECG?

A

300/Number of large squares between each R-R Interval

99
Q

How do we calculate the HR from an ECG in a person with an irregular heartbeat?

A

Count the number of peaks in 30 large squares (6 seconds) and multiply by ten

100
Q

What do NA and adrenaline activate and couple with in the heart?

A

Beta1 adrenoceptors

Gs (activates adenylyl cyclase and cGMP production)

101
Q

What does acetylcholine activate and couple with?

A 
M2 muscarinic 
Gi coupling (inhibits adenylyl cyclase and cAMP production)
102
Q

What is the name of the channels allowing the influx of sodium know as the funny current?

A

Hyperpolarisation-activated Cyclic Nucleotide gated channels (HCN)

103
Q

What does Ivabradine do?

A 
Blocks HCN
Slows HR (in angina reduces Oxygen consumption)
104
Q

What effect does the SNS have on the heart?

A

Increased contractility
Decreased AV nodal delay
Increased automacity

105
Q

Where are the sites of Protein Kinase A action and the effects?

A

L-type Calcium channels - greater influx
Ryanadine receptors - greater CICR
SERCA 2a - phospholamban dissociates allowing quicker removal of calcium at end of HB
Troponin - decreased affinity for calcium therefore increasing relaxation

106
Q

When are beta-blockers used?

A

Cardiac arrhythmias
Hypertension
Angina
CCF

107
Q

What are the side effects of Beta-Blockers?

A 
Bronchospasm
Aggravation of CCF
Bradycardia
Hypocalcaemia
Fatigue
Cold extremities
108
Q

What is an example of a non-selective muscarinic ACh antagonist?

109
Q

What drugs are used as anti-hypertensives?

A 
Thiazides
Calcium antagonists
Alpha blockers
ACe inhibitors
ARBs
110
Q

What drugs are used in angina?

A

Beta-blockers
Calcium antagonists
Nitrates
Nicorandil

111
Q

What three classes of anti-thrombotic drugs exist?

A

Antiplatelet
Anticoagulants
Fibrinolytics

112
Q

What are the side effects of diuretics?

A

Hypokaelamia
Hyperglycaemia
Gout
Impotence

113
Q

What are the two types of calcium channel antagonists and examples of each?

A 
Rate limiting
- Verapamil
- Diltiazem
Non-rate limiting
- Amlodipine
114
Q

When are alpha blockers used?

A

Hypertension
Prostatic hypertrophy
Eg is Doxazosin

115
Q

What are some side effects of ACE inhibitors?

A 
Cough
Renal dysfunction
Angioedema
Hyperkalaemia
Headache
Hypotension
116
Q

What are side effects of organic nitrates?

A

Morning headache
Hypotension
Tolerance

117
Q

When are anticoagulant drugs used?

A

DVT
PE
NSTEMI
AF

118
Q

What are some examples of fibrinolytic drugs?

A

Streptokinase

tPA

119
Q

What are the side effects of digoxin?

A 
Nausea
Vomiting
Yellow blurred vision
Bradycardia
Heart block
Ventricular arrhythmias
120
Q

What does Nicorandil do?

A

Opens ATP-mediated potassium channels in VSM

121
Q

Which has a stronger diuretic effect, thiazides or loop diuretics?

122
Q

What is an example of a potassium-sparing diuretic?

A

Triamterene

123
Q

What are the four major lipoproteins?

A

HDL
LDL
VLDL
Chylomicrons

124
Q

What apoproteins do the lipoproteins contain?

A

HDL - apoA1 and apoA2
LDL - apoB100
VLDL - apoB100
Chylomicrons - apoB48

125
Q

What do apoB containing lipoproteins do?

A

Deliver triglycerides to

  • Muscle (for ATP production)
  • Adipocytes (for storage)
126
Q

Where are chylomicrons formed and what is there function?

A

Intestine

Transport dietary fats

127
Q

Where are VLDLs formed and what is their function?

A

Liver

Transport synthesised fats

128
Q

What happens to chylomicrons and VLDLs after they have transported the fats?

A

Bind to lipoprotein lipase (LPL) via apoCII (from HDL)
Triglyceride core hydrolysed - they are now cholesterol rich
ApoCII exchanged for apoE - remnants
Metabolised by hepatic lipase
50% of apoB100 become LDLs

129
Q

Why is LDL bad?

A

It is oxidised in artery intima
Attracts macrophages - take in OXLDL - foam cells - fatty streak
Inflammation - collagen deposition
Atheromatous plaque forms

130
Q

Why is HDL good?

A

Brings cholesterol to the liver for elimination

131
Q

How do statins work?

A

Inhibit HMG-CoA reductase

Prevents cholesterol formation

132
Q

What are the side effects of statins?

A

Myositis

Rhabdomyolysis

133
Q

What does ezetimibe do?

A

Inhibits NPC1L1 transport protein - decreased cholesterol absorption

134
Q

What are the three layers of blood vessels (inner to outer)?

A

Tunica intima
Tunica media
Tunica adventitia

135
Q

Where does the outer half of the walls of elastic aeries get nutrients from?

A

Vasa vasorum

136
Q

What are the three types of capillary?

A

Continuous
Fenestrated
Sinusoidal/Discontinuous

137
Q

How are heart valves anchored?

A

Via chordae tendinae to papillary muscles

138
Q

Histologically, does the SA node appear darker or lighter than surrounding cells?

A

Lighter (less organelles present)

139
Q

How does digoxin work?

A

Blocks Na/K ATPase (binds to alpha subunit)
This increases intracellular [Na]
This increases [Ca]i
Increased Ca storage in sarcoplasmic reticulum
Increased CICR therefore increased contractility

140
Q

What is the levosimendan?

A

Makes TnC more sensitive to Ca

Used in acute decompensated heart failure

141
Q

What does active Myosin Light Chain Kinase do?

A

It converts myosin LC to myosin LC P

This results in contraction

142
Q

What is the role of active Myosin LC phosphatase?

A

Converts myosin LC P to myosin LC

This causes relaxation

143
Q

What is required for the activation of MLCK?

A

Calcium ions

144
Q

What is required for the activation of Myosin-LC Phosphatase?

145
Q

What does NO (and hence organic nitrates) do to VSM tone?

A

Activates guanylate cyclase
GTP -> cGMP
Activates protein kinase G
Relaxation

146
Q

What is isosorbide mononitrate do?

A

It is a prophylactic organic nitrate (longer half life)

Year 1 - Cardiovascular (DP) (6 decks)

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