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Physiology Flashcards

1
Q

d: autorhythmicity

A

Can beat rhythmically without external stimuli

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2
Q

How is the heart controlled?

A

electronically controlled

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3
Q

Where does heart excitation begin?

A

Sinoatrial node pacemaker cells

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4
Q

where is the SA node, anatomically?

A

Upper RA close to superior Vena Cava

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5
Q

What is normal heart rhythm called?

A

Sinus Rhythm

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6
Q

How does Cardiac Excitement normally origninate?

A

Cells in SA node has no stable resting membrane potential
Instead they generate REGULAR SPONTANEOUS PACEMAKER POTENTIALS
Takes the membrane potential to a threshold
Every time threshold reached action potential generates
Results in generation of regular spontaneous action potentials in SA nodal cells

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7
Q

d:Pacemaker potential

A

the slow depolarisation of membrane potential to a threshold

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8
Q

What is the pacemaker potential due to?

A

o Permeability to K+ does not remain constant in pacemaker cells
• therefore Decrease in k+ efflux
• Na+ influx
• Transient Ca2+ influx

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9
Q

What happens once the threshold is reached in pacemaker cells?

A

The rising phase of action potential i.e. Depolarisation

The FALLING PHASE OF ACTION POTENTIAL i.e. REPOLARISATION

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10
Q

What is depolarisation caused by in the heart?

A

•Caused be activation of long-lasting L-type Ca2+ channels
•Results in Ca2+ influx
Fast Na+ Influx

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11
Q

What is repolarisation caused by in the heart?

A
  • Inactivation of L-type Ca2+ channels and
  • Activation of K+ CHANNELS
  • Resulting in K+ EFFLUX
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12
Q

What is the path of spread of Cardiac excitation in the heart?

A

Originates in SA node
Cell to Cell conduction in AV node
then to Bundle of His, branches and then purkinje fibers

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13
Q

Describe how SA and AV node conduct the impulse?

A

From SA node through both atria
From SA node to AV node within ventricles
ALL occurs due gap junctions
but there is also some internodal pathways

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14
Q

Anatomically, where is the Atrioventricular node located?

A

at the base of the RA

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15
Q

What is the only point of contact between the atria and ventricles?

A

AV node

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16
Q

Why is the conduction delayed and where?

A

AV node

allows atrial systole (contraction) to precede ventricular systole

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17
Q

f: bundle of His, purkinje fibres

A

allow rapid spread of action potential to the ventricles

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18
Q

f: ventricular muscle

A

cell-to-cell conduction

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19
Q

d: ventricular myocytes

A

specialised cardiac cells responsible for contraction

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20
Q

d:artrial myocytes

A

specialised cardiac cells aka pacemaker cells

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21
Q

What is the resting potential for myocytes at rest?

A

-90mV

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22
Q

what is phase 0 of ventricular muscle action potential?

A

RISING PHASE OF ACTION POTENTIAL (i.e. DEPOLARISATION) is caused by FAST Na+ INFLUX
This rapidly reverses the membrane potential to about +20 mV

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23
Q

what is phase 1 of ventricular muscle action potential?

A

closure of Na+ channels and transient K+ efflux

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24
Q

what is phase 2 of ventricular muscle action potential?

A

Mainly Ca2+ influx

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25
Q

what is phase 3 of ventricular muscle action potential?

A

Closure of Ca2+ channels and K+ efflux

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26
Q

what is phase 4 of ventricular muscle action potential?

A

Resting membrane potential

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27
Q

what is the plateau phase of ventricular muscle action potential? What is this unique to?

A

The membrane potential is maintained near the peak of action potential for few hundred milliseconds
contractile cardiac muscle cells

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28
Q

What causes the plateau phase?

A

is mainly due to INFLUX of Ca++ through L-type Ca++ channels

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29
Q

What is the falling phase (repolarisation) of action potentials in ventricular muscles caused by? What does it result in?

A

caused by inactivation of Ca++ channels and activation of K+ CHANNELS
K+ efflux

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30
Q

What changes the Heart Rate?

A

Autonomic nervous system

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31
Q

What increases HR?

A

sympathetic stimulation

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32
Q

What decreases the HR?

A

parasympathetic system

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33
Q

What nerve and what part of the ANS exerts a continuous influence on the SA node at rest?

A

Vagus nerve CN X

parasympathetic

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34
Q

d: Vagal Tone

A

activity of vagus nerve

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35
Q

What nerve dominates under normal resting conditions?

A

Vagus nerve

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36
Q

f: Vagal tone

A

slows the intrinsic HR from 100bpm to produce normal resting heart rate of 70bpm

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37
Q

normal HR range?

A

60-100bpm

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38
Q

d: tachycardia

A

HR >100bpm

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39
Q

d:bradycardia

A

HR<60bpm

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40
Q

f:vagal stimulation

A

SLOWS HEART RATE and INCREASE AV NODAL DELAY

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41
Q

What ANS and type of receptors is responsible for SA and AV?

A

parasympathetic

AcH muscarinic M2 receptors

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42
Q

What is used as a competitive inhibitor of acetylcholine to speed up the heart?

A

Atropine

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43
Q

What do cardiac sympathetic nerves supply?

A

SA node and AV node and Myocardium

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44
Q

f: sympathetic stimulation

A

increases HR and decreases AV nodal delay

increases force of contraction

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45
Q

What is the neurotransmitter for sympathetic nerves in heart? What receptors do they act through?

A

noradrenaline

β1 adrenoreceptors

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46
Q

What is the structure of cardiac muscle?

A

striated due to reg arrangement of contractile protein

no neuromuscular joints

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47
Q

What are cardiac cells called?

A

myocytes

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48
Q

how are myocytes coupled?

A

electrically via gap junction

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49
Q

What are cardiac gap junctions?

A

protein channels which forms low resistance electrical communication pathways between neighbouring myocytes

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50
Q

f: cardiac gap junctions

A

ensure that each electrical excitation reaches all the cardiac myocyctes (All-or-none Law of the heart)

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51
Q

What provides mechanical adhesion between adjacent cardiac cells? What is their function?

A

desmosomes within intercalated discs provide adhesion

ensure tension developed by one cell is transmitted to the next

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52
Q

What does each muscle fibre contain?

A

many myofibrils

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53
Q

what are the contractile units of muscle?

A

myofibrils

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54
Q

Describe the segments of the myofibrils

A

have alternating segments of thick and thin protein filaments

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55
Q

What are the thin filaments in myofibrils called? and why

A

Lighter contain ACTIN

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56
Q

What are the thick filaments in myofibrils called? and why

A

MYOCYIN (thick filaments) causes the darker appearance

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57
Q

What are actin and myocin arranged into within each myofibril?

A

SARCOMERES

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58
Q

How is muscle tension produced in the heart?

A

produced by the sliding of actin filaments on myocin filaments

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59
Q

How does force generation occur in the heart?

A

produced by the sliding of actin filaments on myocin filaments

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60
Q

What does force generation depend on?

A

ATP-dependent interaction between thick (myosin) and thin (actin) filaments

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61
Q

What is required for both contraction and relaxation?

A

ATP

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62
Q

What is required to switch on cross bridge formation?

A

Ca2+

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63
Q

F: Ca2+ ions

A

Not possible for cross bridge to form if there’s no conformational change, this is what the Calcium ions do

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64
Q

When the muscle fibre is relaxed what happens with regards to the cross bridge?

A

no cross-bridge binding because the cross-bridge binding site on actin is physically covered by the troponin-tropomyosin complex

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65
Q

What pulls the thin filament inward during contractions?

A

• Binding of actin and myosin cross bridge triggers power stroke that pulls thin filament inward during contraction

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66
Q

When the muscle fibre is excited what happens in terms of the cross-bridge?

A

Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site; cross-bridge binding occurs

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67
Q

How does cardiac muscle contract?

A

influx of Ca2+

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68
Q

What need to be released so cardiac muscle can relax?

A

Ca2+

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69
Q

Why is a long refractory period required in normal cardiac function?

A

Ventricular muscle action triggers contraction

long refractory period prevents generation of tetanic contraction ie the cardiac muscle stays contracted for longer

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70
Q

Why is it important that the heart doesn’t contract tetanicily?

A

key for blood expulsion to the body from the heart chambers

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71
Q

d:refractory period

A

is a period following an action potential in which it is not possible to produce another action potential

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72
Q

what gives rise to the Stroke Volume (SV)?

A

Contraction of ventricular muscle

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73
Q

d: Stroke Volume

A

the volume of blood ejected by each ventricle per heart beat

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74
Q

What gives rise to a larger SV?

A

o The more the ventricle is filled with blood, the more the heart is stretched and results in bigger stroke volume

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75
Q

What is the equation for SV?

A

SV = End Diastolic Volume (EDV) – End Systolic Volume (ESV)

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76
Q

SV is regulated by intrinsic/extrinsic mechanisms?

A

both

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77
Q

Where is the intrinsic control?

A

the heart muscle itself

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78
Q

What provides the extrinsic control?

A

nervous and hormonal control

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79
Q

What are changes in SV brought about by in intrinsic control?

A

brought about by changes in the Diastolic stretch/length of Myocardial Fibres

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80
Q

What is the diastolic length/stretch determined by?

A

End diastolic Volume (edv)

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81
Q

d: end diastolic Volume (EDV)

A

the volume of blood within each ventricle at the end of diastole

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82
Q

What determines the Cardiac Preload?

A

EDV

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83
Q

d: cardiac preload

A

how much the heart is loaded with blood before it contracts

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84
Q

What determines the EDV?

A

the VENOUS RETURN to the heart

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85
Q

d: Frank-Starling Law of the heart

A

that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant

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86
Q

What increase the affinity of troponin for Ca2+?

A

stretch

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87
Q

How is optimal length in cardiac muscle achieved?

A

via stretching it

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88
Q

due to starling’s law, what happens if venous return to RA increases?

A

EDV of RV increases, Starling’s law leads to increased SV into pulmonary artery

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89
Q

due to starling’s law, what happens if venous return to LA increases from pulmonary vein?

A

EDV of left ventricle increases

Starling’s Law leads to increased SV into aorta

90
Q

d: afterload

A

is the pressure the heart must work against to eject blood during systole (ventricular contraction)

91
Q

Due to Staling’s Law, what happens to EDV if afterload increases? What happens to the force of the contraction?

A

at first, heart unable to eject full SV, so EDV increases

Force of contraction rises by Frank-Starling mechanism

92
Q

What happens if the afterload continues to exist?

A

(e.g. untreated hypertension), eventually the ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance

93
Q

What part of the cardiac cycle is the systole?

A

Ventricular contraction

94
Q

What part of the cardiac cycle is the diastole?

A

during which the heart refills with blood after the emptying done during systole

95
Q

What is the ventricular muscle supplied by in terms of muscle fibres? What is the neurotransmitter?

A

sympathetic

Noradrenaline

96
Q

d: inotropic effect

A

Stimulation of sympathetic nerves INCREASES the FORCE of contraction (positive effect)

97
Q

d: chronotropic effect

A

Stimulation of sympathetic nerves to the heart also causes a positive chronotropic effect (i.e. increase the heart rate)

98
Q

Describe the effect of Sympathetic Stimulation on ventricular Contraction

A

Force of contraction increases (activation of Ca++ channels - greater Ca++ influx)
The effect is cAMP mediated
The peak ventricular pressure rises
Rate of pressure change (dP/dt) during systole increases
This reduces the duration of systole
Rate of ventricular relaxation increases (increased rate of Ca++ pumping)
This reduces the duration of diastole

99
Q

As peak ventricular pressure rises, what happens to the contractility of the heart? And Frank-Starling Curve?

A

contractility of heart at a given EDV rises

•Frank-Starling Curve is shifted to the left

100
Q

What happens to the Frank-Starling curve in heart failure? What is this effect?

A

shifts to the right

negative inotropic effect

101
Q

What is the effect of Parasympathetic nerves on ventricular contraction?

A

Vagal stimulation has major influence on rate, not force, of contraction

102
Q

What has greater effect on heart parasympathetic or sympathetic nerves, why?

A

Sympathetic

Very little innervation of ventricles by vagus in heart

103
Q

What hormones have an inotropic and chronotropic effect, where are they released from?

A

Adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effect

104
Q

d: Cardiac Output (CO)

A

volume of blood pumped by each ventricle per minute

105
Q

eqn: CO

A

CO = SV x HR

106
Q

What is the resting CO in a healthy adult?

A

5L

107
Q

What will allow the regulation of CO?

A

regulated SV and HR

108
Q

when do heart valves produce a sound?

A

when they shut

109
Q

What triggers the recurring Cardiac cycle of atrial and ventricular contractions and relaxations?

A

orderly depolarisation/repolarisation sequence

110
Q

d: diastole

A

the heart ventricles are relaxed and fill with blood

111
Q

d: Systole

A

: the heart ventricles contract and pump blood into the
•aorta (LV)
•pulmonary artery (RV)

112
Q

At a HR of 75bpm what is the periods for ventricular diastole and ventricular systole?

A
  1. 5s dia

0. 3s sys

113
Q

Name the 5 events of the cardiac cycle

A 
Passive Filling
Atrial Contraction
Isovolumetric ventricular contraction
Ventricular Ejection
Isovolumetric ventricular relaxation
114
Q

What happens in passive filling?

A

pressure in atria and ventricles close to zero
AV valves open so venous return flows into the ventricles
Ventricles become ~ 80% full by passive filling

115
Q

What happens during passive filling in the Right side of the heart?

A

o Similar events happen in the right side of the heart, but the pressures (right ventricular and pulmonary artery) are much lower

116
Q

What is the aortic pressure when aortic valve is closed?

A

80mmHg

117
Q

What happens during Atrial Contraction?

A

o The P-wave in the ECG signals atrial depolarisation
o The atria contracts between the P-wave and the QRS
o Atrial contraction complete the END DIASTOLIC VOLUME

118
Q

What is the EDV in a normal resting adult?

A

130ml

119
Q

What happens during isovolumetric ventricular circulation?

A

o Ventricular contraction starts after the QRS (signals ventricular depolarisation) in the ECG
o Ventricular pressure rises
o When the ventricular pressure exceeds atrial pressure the AV VALVES SHUT
o The tension rises around a closed volume “Isovolumetric Contraction”

120
Q

What produces the first heart sound?

A

caused by closure of mitral and tricuspid valves. It sounds like a “lub”

121
Q

What happens once aortic valve is shut?

A

aortic valve is still shut, so no blood can enter or leave the ventricle

122
Q

Describe what happens during Ventricular Ejection

A

o The ventricular pressure rises very steeply
o When the ventricular pressure exceeds aorta/pulmonary artery pressure
o Aortic/pulmonary valve open - Remember this is a silent event
o Stroke Volume (SV) is ejected by each ventricle, leaving behind the End Systolic Volume (ESV)
o SV = EDV – ESV
= 135 – 65 = 70 ml
o Aortic pressure rises
o The T-wave in the ECG signals ventricular repolarisation
o The ventricles relax and the ventricular pressure start to fall
o When the ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut

123
Q

What produces the second heart sound?

A

is caused by closure of aortic and pulmonary valves. It sounds like a “dub”

124
Q

What produces a dicrotic notch in aortic pressure curve?

A

valve vibration

125
Q

What happens during Isovolumetric ventricular relaxation?

A

o Closure of aortic/and pulmonary valves signals the start of the isovolumetric ventricular relaxation
o Ventricle is again a closed box, as the AV valve is shut
o The tension falls around a closed volume “Isovolumetric Relaxation”
o When the ventricular pressure falls below atrial pressure, AV valves open (Remember this is a silent event), and the heart starts a new cycle

126
Q

What does the first heart sound signal?

A

the beginning of SYSTOLE

127
Q

What does the second sound signal?

A

the end of systole and the beginning of DIASTOLE

128
Q

How does arterial pressure not fall to zero during diastole?

A

o As when the blood gets ejected during systolic, stretches and then when relaxes muscle recoils maintaining pressure

129
Q

What does the JVP reflect?

A

Right atrial Pressure

130
Q

d: Blood Pressure

A

the outwards (hydrostatic) pressure exerted by the blood on the BV walls

131
Q

d: systemic systolic BP

A

 the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts

132
Q

d: systemic diastolic BP

A

 is the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes

133
Q

d: hypertension

A

 Clinic blood pressure of 140/90 mmHg or higher and day time average of 135/85 mmHg or higher

134
Q

What is the normal value for Pulse pressure?

A

30-50mmHg

135
Q

d: Pulse Pressure

A

difference between systolic and diastolic BP

136
Q

What is the normal BF in arteries and can you hear it with stethescope?

A

laminar and no

137
Q

If cuff pressure exceeding the systolic BP is applied to the artery what would happen and be heard?

A

flow in that artery would be blocked

no sound heard

138
Q

If external BP is kept between systolic and diastolic pressure, what happens and is heard?

A

flow becomes turbulent when BP exceeds cuff pressure

such turbulent flow is audible through a stethoscope

139
Q

Why is no sound heard in stethoscope?

A

Cuff pressure>120mmHg and exceeds BP throughout the cardiac cycle
No blood flow through vessel
No sound heard as no flow

140
Q

Why are sounds heard and what are they called during sphygmomanometery?

A

when cuff pressure between 120-80mmHg
BF through vessel becomes turbulent when pressure released
sounds heard
Korotkoff sounds

141
Q

What Korotkoff sounds are heard?

A

peak systolic pressure

intermittent sounds

142
Q

Why are intermittent sounds heard when taking BP?

A

due to turbulent spurts of flow cyclically exceed cuff pressure

143
Q

If cuff pressure is below 80mmHg through cardiac cycle, what happens and is heard?

A

BF laminarly again, last sound heard at diastolic pressure, muffled and muted
no sound heard after and laminar flow is smooth

144
Q

Why is diastolic BP recorded at the 5th Korotkoff sound?

A

more reproduceable

145
Q

What drives the blood around systemic circulation?

A

a pressure gradient between RA and Aorta

146
Q

Why is main driving force for Blood MAP?

A

RA pressure close to 0

Pressure gradient = MAP- central venous (RA) Pressure CVP

147
Q

d: MAP

A

the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart

148
Q

How is the MAP calculated?

A

[ (2 X diastolic) + systolic]

divided by 3

149
Q

What is the normal MAP?

A

70 - 105 mm Hg

150
Q

what is the min MAP required and why?

A

60mmHg to perfuse coronary arteries, brain and kidneys

151
Q

Why cant MAP be too high?

A

cause strain on the heart

152
Q

What is the relationship between MAP and CO and SVR?? (Systemic Vascular Resistance)

A

MAP= CO X SVR

153
Q

D: systemic Vascular resistance

A

 is the sum of resistance of all vasculature in the systemic circulation
Arterioles are the Major Resistance Vessels

154
Q

How is BP controlled short term?

A

Baroreceptor Reflex

155
Q

What are the major resistance vessels in the heart?

A

arterioles

156
Q

Where do the Barorecptors signal to?

A

the medulla

157
Q

where are baroreceptors located?

A

carotid sinus + Aortic Arch

158
Q

How do Baroreceptors correct postural hypotension?

A

rapidly corrects transient fall in MAP, HR increases, SV increases, SVR increases.

159
Q

What prevents baroreceptors from correctly targeting chronic hypertension?

A

Baroreceptors only respond to acute changes in BP (they reset- so only fire again when there is an acute change in MAP

160
Q

What else apart from baroreceptors can BV and MAP be controlled by?

A

extracellular fluid volume

161
Q

how much of the total body fluid is made up by extracellular fluid?

A

1/3

162
Q

What is the ECF made up from?

A

plasma volume
interstitial fluid volume
(IVF)

163
Q

What happens if plasma volume falls?

A

if plasma falls compensatory mechanism shift fluid from IFV to plasma compartment) basically the extra cellular fluid volume is made up off the plasma in the blood and the interstitial fluid covering the lungs etc. If blood plasma falls, intracellular fluid is released from the cells into the plasma to make up this.

164
Q

Name the 2 main factors that affect extracellular fluid volume

A

water XS or deficit

Na+ XS or deficit

165
Q

d: hormones

A

are effectors that regulate EFV by regulating water and salt balance in our bodies

166
Q

Name the hormones that control ECF

A 
	The Renin-Angiotensin- Aldosterone System - RAAS
Natriuretic Peptides – NPs
Antidiuretic Hormone (Arginine Vasopressin) – ADH
167
Q

f: RAAS and how it works

A

Angiotensin II stimulates release of aldosterone from the adrenal cortex + causes systemic vasoconstriction (increases TPR). Aldosterone acts on kidneys to increase sodium and water retention

168
Q

f: ANP and how it works

A

Atrial Natriuretic Peptide, released in response to atrial distension (hypervolaemic state), causes excretion of salt water (probably less ADH) in the kidneys decreasing blood volume and blood pressure (vasodilator), Decreases renin release (counteracts RAAS)

169
Q

what is BNP and what does it do?

A

Is very similar to ANP and is released by the brain in response to ventricular stretch receptors

170
Q

f: ADH (vasopressin) what it does and how it works?

A

Peptide hormone derived from a pre-hormone precursor synthesised by the hypothalamus and stored in the posterior pituitary of the brain (hypothalamus). Secretion stimulated by reduced EFV or increased extracellular fluid osmolarity (more fluid moving into the lung tissue).
Increases reabsorption of water in the kidney tubules, this would increase extracellular and plasma volume and hence increase CO and BP. Also acts on blood vessels to vasoconstrict.

171
Q

d: shock

A

abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

172
Q

d: hypovolemic shock

A

loss of BV

173
Q

d: cardiogenic shock

A

sustained hypotension caused by decreased cardiac contractility

174
Q

d: obstructive shock

A

obstruct the SVC and ability for heart to contract

175
Q

Give an eg of obstructive shock and what it does

A

Tension Pneumothorax

increased thoracic pressure decreases venous return

176
Q

d: neurogenic shock

A

loss of sympathetic tone> massive venous and arterial vasodilation>decreased venous return and SVR

177
Q

d: vasoactive shock

A

release of vasoactive mediators cause massive venous and arterial dilation
usually from a massive dump of NO

178
Q

Treatment of Shock generally

A

ABCDE
High flow O2
Volume replacement eg blood transfusion

179
Q

specific treatment of cardiac shock?

A

inotropes-increase force of contraction

180
Q

specific treatment of tension pneumothorax?

A

immediate chest drain

181
Q

specific treatment for anaphylactic shock?

A

adrenaline and antihistamines

182
Q

specific treatment for septic shock?

A

vasopressors eg dobutamine

183
Q

Causes of hypovolaemic shock

A

Haemorrhage (trauma, surgery etc) cause decrease in blood volume.
Vomiting, diarrhoea, excessive sweating cause decrease in ECFV

184
Q

Why is it > 30% of BV lost a problem?

A

compensatory mechanisms can maintain BP until then

185
Q

describe process of hypovolaemic shock

A 
Loss of blood Volume
Decreased BV
Decreased Venous return
Decreased EDV
Decreased SV
Decreased CO and Decreased BP
Inadequate tissue Perfusion
186
Q

describe the process of cardiogenic shock

A
  1. Decreased Cardiac Contractility
  2. Decreased SV
  3. Decreased CO + BP
  4. Inadequate Tissue Perfusion
187
Q

describe process of tension pneumothorax

A
  1. Increased intrathoracic pressure
  2. Decreased Venous return
  3. Decreased end diastolic Volume
  4. Decreased SV
  5. Decreased CO and BP
  6. Inadequate Tissue Perfusion
188
Q

describe the process of distributive shock neurogenic

A
  1. Loss of sympathetic tone to BV and Heart
  2. Massive Venous and arterial Vasodilation
  3. Effects HR
  4. Decreased Venous return and decreased SVR (total peripheral resistance TPR)
  5. Decreased HR, unlike other types of shock
  6. Decreased CO and BP
  7. Inadequate tissue perfusion
189
Q

describe process of distributive shock vasoactive

A
  1. Release of Vasoactive mediators
  2. Massive Venous and Arterial Vasodilation
    o Also increased capillary permeability
  3. Decreased venous return and SVR
  4. Decreased CO and BP
  5. Inadequate tissue Perfusion
190
Q

what is syncope in common terms?

A

fainting

191
Q

d: syncope

A

Transient loss of consciousness due to cerebral hypoperfusion, characterized by rapid onset, short duration, and spontaneous complete recovery

192
Q

D: tloc

A

A state of real or apparent loss of consciousness with loss of awareness, characterized by amnesia for the period of unconsciousness, loss of motor control, loss of responsiveness, and a short duration

193
Q

Name some conditions TLOC can result from:

A 
Head Trauma
Suncope
Epileptic seizures
TLOC mimics
other causes
194
Q

Name the 3 categories Syncope can be classified into

A

reflex syncope
orthostatic Hypotension
Cardiac Syncope

195
Q

What happens in reflex syncope?

A

neural reflexes modify the HR(cardioinhibition)
and/or vascular tone (vasodepression) hence predisposing the fall in MAP (systemic hypotension) of sufficient severity to affect cerebral perfusion causing a transient period of cerebral hypoperfusion resulting in syncope or near syncope

196
Q

Describe the pathway for reflex syncope

A

When activated, the reflex causes cardioinhibition through vagal stimulation. This decreases heart rate (Bradycardia) and cardiac output (CO)

And/or vasodepression through depression of sympathetic activity to blood vessels. This decreases systemic vascular resistance (Vasodilatation), venous return, stroke volume and CO

The decrease in CO and SVR, decreases mean arterial blood pressure (MAP)

Resulting in cerebral hypoperfusion and syncope or near syncope

197
Q

Name the different types of reflex syncope

A

Vasovagal VVS
Situational
Carotid Sinus

198
Q

What is the most commonest type of reflex syncope?

A

vasovagal

199
Q

What is Faint triggered by?

A

emotional distress( pain, fear or blood phobia)

orthostatic stress

200
Q

symptoms of vasovagal syncope

A

pallor
sweating
nausea

201
Q

How can it be prevented?

A

horizontal gravity neutralisation position or leg crossing

202
Q

Why do certain manoeuvres help in preventing fainting?

A

increase venous return

203
Q

What is the main risk in VVS?

A

risk of injury

204
Q

How can Fainting be avoided?

A

education
reassurance
avoidance of triggers
hydration

205
Q

What is situational reflex syncope?

A

faint during or immediately after a specific trigger eg cough micturition swallowing etc

206
Q

How is situational reflex syncope treated?

A

treat the cause if poss
get patient to lie down
hydrated and avoid alcohol
cardiac permanent pacing may be needed to stop it

207
Q

What is carotid Sinus Reflex Syncope?

A

is triggered by mechanical manipulation of the neck, shaving, tight collar, etc.

208
Q

Who is carotid sinus reflex syncope most common in?

A

elderly males

209
Q

What is an associated condition with carotid sinus syncope?

A

carotid artery atherosclerosis

210
Q

When may CCS occur?

A

after head and neck surgery

radiation

211
Q

How can CSS be treated?

A

cardiac permaent pacing

212
Q

d: Postural Hypotension

A

Results from failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

213
Q

RF associated with Postural Hypotension

A 
Age related
Medications
Certain diseases
Reduced intravascular volume
Prolonged bed rest
214
Q

How is Postural Hypotension diagnosed?

A

A positive result is indicated by a drop, within 3 minutes of standing from lying position:
in systolic blood pressure of at least 20 mmHg (with or without symptoms) or
a drop in diastolic blood pressure of at least 10 mm Hg (with symptoms)

215
Q

Symptoms of Postural Hypotension

A

cerebral hypoperfusion such as: lightheadedness, dizziness, blurred vision, faintness and falls

216
Q

What is cardiac Syncope caused by?

A

a cardiac event resulting in a sudden drop in CO

217
Q

What can Cardiac Syncope be caused by?

A

Arrhythmias: resulting in severe bradycardia or tachycardia
Acute myocardial Infarction
Structural Cardiac Disease
eg aortic stenosis, hypertrophic cardiomyopathy
Other Cardio disease eg PE or aortic dissection

218
Q

What is the investigations required for a patient presenting with TLOC?

A

A careful history
Full physical examination, including
Orthostatic blood pressure (BP) measurement
12-lead ECG

219
Q

What type of syncope would be indicative of happening during excretion or when supine?

A

Cardiac Syncope

220
Q

If a patient had the presence of a structural cardiac abnormality or CHD, family history of sudden death at a young age
sudden onset palpitations immediacy followed by syncope, ECG suggestive of arrhythmic syncope, what type of syncope?

A

Cardiac

Cardio (28 decks)

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