Physiology Flashcards
1
Q
d: autorhythmicity
A
Can beat rhythmically without external stimuli
2
Q
How is the heart controlled?
A
electronically controlled
3
Q
Where does heart excitation begin?
A
Sinoatrial node pacemaker cells
4
Q
where is the SA node, anatomically?
A
Upper RA close to superior Vena Cava
5
Q
What is normal heart rhythm called?
A
Sinus Rhythm
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
7
Q
d:Pacemaker potential
A
the slow depolarisation of membrane potential to a threshold
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
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
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
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
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
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
14
Q
Anatomically, where is the Atrioventricular node located?
A
at the base of the RA
15
Q
What is the only point of contact between the atria and ventricles?
A
AV node
16
Q
Why is the conduction delayed and where?
A
AV node
allows atrial systole (contraction) to precede ventricular systole
17
Q
f: bundle of His, purkinje fibres
A
allow rapid spread of action potential to the ventricles
18
Q
f: ventricular muscle
A
cell-to-cell conduction
19
Q
d: ventricular myocytes
A
specialised cardiac cells responsible for contraction
20
Q
d:artrial myocytes
A
specialised cardiac cells aka pacemaker cells
21
Q
What is the resting potential for myocytes at rest?
A
-90mV
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
23
Q
what is phase 1 of ventricular muscle action potential?
A
closure of Na+ channels and transient K+ efflux
24
Q
what is phase 2 of ventricular muscle action potential?
A
Mainly Ca2+ influx
25
what is phase 3 of ventricular muscle action potential?
Closure of Ca2+ channels and K+ efflux
26
what is phase 4 of ventricular muscle action potential?
Resting membrane potential
27
what is the plateau phase of ventricular muscle action potential? What is this unique to?
The membrane potential is maintained near the peak of action potential for few hundred milliseconds
contractile cardiac muscle cells
28
What causes the plateau phase?
is mainly due to INFLUX of Ca++ through L-type Ca++ channels
29
What is the falling phase (repolarisation) of action potentials in ventricular muscles caused by? What does it result in?
caused by inactivation of Ca++ channels and activation of K+ CHANNELS
K+ efflux
30
What changes the Heart Rate?
Autonomic nervous system
31
What increases HR?
sympathetic stimulation
32
What decreases the HR?
parasympathetic system
33
What nerve and what part of the ANS exerts a continuous influence on the SA node at rest?
Vagus nerve CN X
| parasympathetic
34
d: Vagal Tone
activity of vagus nerve
35
What nerve dominates under normal resting conditions?
Vagus nerve
36
f: Vagal tone
slows the intrinsic HR from 100bpm to produce normal resting heart rate of 70bpm
37
normal HR range?
60-100bpm
38
d: tachycardia
HR >100bpm
39
d:bradycardia
HR<60bpm
40
f:vagal stimulation
SLOWS HEART RATE and INCREASE AV NODAL DELAY
41
What ANS and type of receptors is responsible for SA and AV?
parasympathetic
| AcH muscarinic M2 receptors
42
What is used as a competitive inhibitor of acetylcholine to speed up the heart?
Atropine
43
What do cardiac sympathetic nerves supply?
SA node and AV node and Myocardium
44
f: sympathetic stimulation
increases HR and decreases AV nodal delay
| increases force of contraction
45
What is the neurotransmitter for sympathetic nerves in heart? What receptors do they act through?
noradrenaline
| β1 adrenoreceptors
46
What is the structure of cardiac muscle?
striated due to reg arrangement of contractile protein
| no neuromuscular joints
47
What are cardiac cells called?
myocytes
48
how are myocytes coupled?
electrically via gap junction
49
What are cardiac gap junctions?
protein channels which forms low resistance electrical communication pathways between neighbouring myocytes
50
f: cardiac gap junctions
ensure that each electrical excitation reaches all the cardiac myocyctes (All-or-none Law of the heart)
51
What provides mechanical adhesion between adjacent cardiac cells? What is their function?
desmosomes within intercalated discs provide adhesion
| ensure tension developed by one cell is transmitted to the next
52
What does each muscle fibre contain?
many myofibrils
53
what are the contractile units of muscle?
myofibrils
54
Describe the segments of the myofibrils
have alternating segments of thick and thin protein filaments
55
What are the thin filaments in myofibrils called? and why
Lighter contain ACTIN
56
What are the thick filaments in myofibrils called? and why
MYOCYIN (thick filaments) causes the darker appearance
57
What are actin and myocin arranged into within each myofibril?
SARCOMERES
58
How is muscle tension produced in the heart?
produced by the sliding of actin filaments on myocin filaments
59
How does force generation occur in the heart?
produced by the sliding of actin filaments on myocin filaments
60
What does force generation depend on?
ATP-dependent interaction between thick (myosin) and thin (actin) filaments
61
What is required for both contraction and relaxation?
ATP
62
What is required to switch on cross bridge formation?
Ca2+
63
F: Ca2+ ions
Not possible for cross bridge to form if there’s no conformational change, this is what the Calcium ions do
64
When the muscle fibre is relaxed what happens with regards to the cross bridge?
no cross-bridge binding because the cross-bridge binding site on actin is physically covered by the troponin-tropomyosin complex
65
What pulls the thin filament inward during contractions?
• Binding of actin and myosin cross bridge triggers power stroke that pulls thin filament inward during contraction
66
When the muscle fibre is excited what happens in terms of the cross-bridge?
Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site; cross-bridge binding occurs
67
How does cardiac muscle contract?
influx of Ca2+
68
What need to be released so cardiac muscle can relax?
Ca2+
69
Why is a long refractory period required in normal cardiac function?
Ventricular muscle action triggers contraction
| long refractory period prevents generation of tetanic contraction ie the cardiac muscle stays contracted for longer
70
Why is it important that the heart doesn't contract tetanicily?
key for blood expulsion to the body from the heart chambers
71
d:refractory period
is a period following an action potential in which it is not possible to produce another action potential
72
what gives rise to the Stroke Volume (SV)?
Contraction of ventricular muscle
73
d: Stroke Volume
the volume of blood ejected by each ventricle per heart beat
74
What gives rise to a larger SV?
o The more the ventricle is filled with blood, the more the heart is stretched and results in bigger stroke volume
75
What is the equation for SV?
SV = End Diastolic Volume (EDV) – End Systolic Volume (ESV)
76
SV is regulated by intrinsic/extrinsic mechanisms?
both
77
Where is the intrinsic control?
the heart muscle itself
78
What provides the extrinsic control?
nervous and hormonal control
79
What are changes in SV brought about by in intrinsic control?
brought about by changes in the Diastolic stretch/length of Myocardial Fibres
80
What is the diastolic length/stretch determined by?
End diastolic Volume (edv)
81
d: end diastolic Volume (EDV)
the volume of blood within each ventricle at the end of diastole
82
What determines the Cardiac Preload?
EDV
83
d: cardiac preload
how much the heart is loaded with blood before it contracts
84
What determines the EDV?
the VENOUS RETURN to the heart
85
d: Frank-Starling Law of the heart
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
86
What increase the affinity of troponin for Ca2+?
stretch
87
How is optimal length in cardiac muscle achieved?
via stretching it
88
due to starling's law, what happens if venous return to RA increases?
EDV of RV increases, Starling's law leads to increased SV into pulmonary artery
89
due to starling's law, what happens if venous return to LA increases from pulmonary vein?
EDV of left ventricle increases
| Starling’s Law leads to increased SV into aorta
90
d: afterload
is the pressure the heart must work against to eject blood during systole (ventricular contraction)
91
Due to Staling's Law, what happens to EDV if afterload increases? What happens to the force of the contraction?
at first, heart unable to eject full SV, so EDV increases
| Force of contraction rises by Frank-Starling mechanism
92
What happens if the afterload continues to exist?
(e.g. untreated hypertension), eventually the ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance
93
What part of the cardiac cycle is the systole?
Ventricular contraction
94
What part of the cardiac cycle is the diastole?
during which the heart refills with blood after the emptying done during systole
95
What is the ventricular muscle supplied by in terms of muscle fibres? What is the neurotransmitter?
sympathetic
| Noradrenaline
96
d: inotropic effect
Stimulation of sympathetic nerves INCREASES the FORCE of contraction (positive effect)
97
d: chronotropic effect
Stimulation of sympathetic nerves to the heart also causes a positive chronotropic effect (i.e. increase the heart rate)
98
Describe the effect of Sympathetic Stimulation on ventricular Contraction
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
As peak ventricular pressure rises, what happens to the contractility of the heart? And Frank-Starling Curve?
contractility of heart at a given EDV rises
| •Frank-Starling Curve is shifted to the left
100
What happens to the Frank-Starling curve in heart failure? What is this effect?
shifts to the right
| negative inotropic effect
101
What is the effect of Parasympathetic nerves on ventricular contraction?
Vagal stimulation has major influence on rate, not force, of contraction
102
What has greater effect on heart parasympathetic or sympathetic nerves, why?
Sympathetic
| Very little innervation of ventricles by vagus in heart
103
What hormones have an inotropic and chronotropic effect, where are they released from?
Adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effect
104
d: Cardiac Output (CO)
volume of blood pumped by each ventricle per minute
105
eqn: CO
CO = SV x HR
106
What is the resting CO in a healthy adult?
5L
107
What will allow the regulation of CO?
regulated SV and HR
108
when do heart valves produce a sound?
when they shut
109
What triggers the recurring Cardiac cycle of atrial and ventricular contractions and relaxations?
orderly depolarisation/repolarisation sequence
110
d: diastole
the heart ventricles are relaxed and fill with blood
111
d: Systole
: the heart ventricles contract and pump blood into the
•aorta (LV)
•pulmonary artery (RV)
112
At a HR of 75bpm what is the periods for ventricular diastole and ventricular systole?
0. 5s dia
| 0. 3s sys
113
Name the 5 events of the cardiac cycle
```
Passive Filling
Atrial Contraction
Isovolumetric ventricular contraction
Ventricular Ejection
Isovolumetric ventricular relaxation
```
114
What happens in passive filling?
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
What happens during passive filling in the Right side of the heart?
o Similar events happen in the right side of the heart, but the pressures (right ventricular and pulmonary artery) are much lower
116
What is the aortic pressure when aortic valve is closed?
80mmHg
117
What happens during Atrial Contraction?
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
What is the EDV in a normal resting adult?
130ml
119
What happens during isovolumetric ventricular circulation?
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
What produces the first heart sound?
caused by closure of mitral and tricuspid valves. It sounds like a “lub”
121
What happens once aortic valve is shut?
aortic valve is still shut, so no blood can enter or leave the ventricle
122
Describe what happens during Ventricular Ejection
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
What produces the second heart sound?
is caused by closure of aortic and pulmonary valves. It sounds like a “dub”
124
What produces a dicrotic notch in aortic pressure curve?
valve vibration
125
What happens during Isovolumetric ventricular relaxation?
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
What does the first heart sound signal?
the beginning of SYSTOLE
127
What does the second sound signal?
the end of systole and the beginning of DIASTOLE
128
How does arterial pressure not fall to zero during diastole?
o As when the blood gets ejected during systolic, stretches and then when relaxes muscle recoils maintaining pressure
129
What does the JVP reflect?
Right atrial Pressure
130
d: Blood Pressure
the outwards (hydrostatic) pressure exerted by the blood on the BV walls
131
d: systemic systolic BP
the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts
132
d: systemic diastolic BP
is the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes
133
d: hypertension
Clinic blood pressure of 140/90 mmHg or higher and day time average of 135/85 mmHg or higher
134
What is the normal value for Pulse pressure?
30-50mmHg
135
d: Pulse Pressure
difference between systolic and diastolic BP
136
What is the normal BF in arteries and can you hear it with stethescope?
laminar and no
137
If cuff pressure exceeding the systolic BP is applied to the artery what would happen and be heard?
flow in that artery would be blocked
| no sound heard
138
If external BP is kept between systolic and diastolic pressure, what happens and is heard?
flow becomes turbulent when BP exceeds cuff pressure
| such turbulent flow is audible through a stethoscope
139
Why is no sound heard in stethoscope?
Cuff pressure>120mmHg and exceeds BP throughout the cardiac cycle
No blood flow through vessel
No sound heard as no flow
140
Why are sounds heard and what are they called during sphygmomanometery?
when cuff pressure between 120-80mmHg
BF through vessel becomes turbulent when pressure released
sounds heard
Korotkoff sounds
141
What Korotkoff sounds are heard?
peak systolic pressure
| intermittent sounds
142
Why are intermittent sounds heard when taking BP?
due to turbulent spurts of flow cyclically exceed cuff pressure
143
If cuff pressure is below 80mmHg through cardiac cycle, what happens and is heard?
BF laminarly again, last sound heard at diastolic pressure, muffled and muted
no sound heard after and laminar flow is smooth
144
Why is diastolic BP recorded at the 5th Korotkoff sound?
more reproduceable
145
What drives the blood around systemic circulation?
a pressure gradient between RA and Aorta
146
Why is main driving force for Blood MAP?
RA pressure close to 0
| Pressure gradient = MAP- central venous (RA) Pressure CVP
147
d: MAP
the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart
148
How is the MAP calculated?
[ (2 X diastolic) + systolic]
| divided by 3
149
What is the normal MAP?
70 - 105 mm Hg
150
what is the min MAP required and why?
60mmHg to perfuse coronary arteries, brain and kidneys
151
Why cant MAP be too high?
cause strain on the heart
152
What is the relationship between MAP and CO and SVR?? (Systemic Vascular Resistance)
MAP= CO X SVR
153
D: systemic Vascular resistance
is the sum of resistance of all vasculature in the systemic circulation
Arterioles are the Major Resistance Vessels
154
How is BP controlled short term?
Baroreceptor Reflex
155
What are the major resistance vessels in the heart?
arterioles
156
Where do the Barorecptors signal to?
the medulla
157
where are baroreceptors located?
carotid sinus + Aortic Arch
158
How do Baroreceptors correct postural hypotension?
rapidly corrects transient fall in MAP, HR increases, SV increases, SVR increases.
159
What prevents baroreceptors from correctly targeting chronic hypertension?
Baroreceptors only respond to acute changes in BP (they reset- so only fire again when there is an acute change in MAP
160
What else apart from baroreceptors can BV and MAP be controlled by?
extracellular fluid volume
161
how much of the total body fluid is made up by extracellular fluid?
1/3
162
What is the ECF made up from?
plasma volume
interstitial fluid volume
(IVF)
163
What happens if plasma volume falls?
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
Name the 2 main factors that affect extracellular fluid volume
water XS or deficit
| Na+ XS or deficit
165
d: hormones
are effectors that regulate EFV by regulating water and salt balance in our bodies
166
Name the hormones that control ECF
```
The Renin-Angiotensin- Aldosterone System - RAAS
Natriuretic Peptides – NPs
Antidiuretic Hormone (Arginine Vasopressin) – ADH
```
167
f: RAAS and how it works
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
f: ANP and how it works
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
what is BNP and what does it do?
Is very similar to ANP and is released by the brain in response to ventricular stretch receptors
170
f: ADH (vasopressin) what it does and how it works?
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
d: shock
abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation
172
d: hypovolemic shock
loss of BV
173
d: cardiogenic shock
sustained hypotension caused by decreased cardiac contractility
174
d: obstructive shock
obstruct the SVC and ability for heart to contract
175
Give an eg of obstructive shock and what it does
Tension Pneumothorax
| increased thoracic pressure decreases venous return
176
d: neurogenic shock
loss of sympathetic tone> massive venous and arterial vasodilation>decreased venous return and SVR
177
d: vasoactive shock
release of vasoactive mediators cause massive venous and arterial dilation
usually from a massive dump of NO
178
Treatment of Shock generally
ABCDE
High flow O2
Volume replacement eg blood transfusion
179
specific treatment of cardiac shock?
inotropes-increase force of contraction
180
specific treatment of tension pneumothorax?
immediate chest drain
181
specific treatment for anaphylactic shock?
adrenaline and antihistamines
182
specific treatment for septic shock?
vasopressors eg dobutamine
183
Causes of hypovolaemic shock
Haemorrhage (trauma, surgery etc) cause decrease in blood volume.
Vomiting, diarrhoea, excessive sweating cause decrease in ECFV
184
Why is it > 30% of BV lost a problem?
compensatory mechanisms can maintain BP until then
185
describe process of hypovolaemic shock
```
Loss of blood Volume
Decreased BV
Decreased Venous return
Decreased EDV
Decreased SV
Decreased CO and Decreased BP
Inadequate tissue Perfusion
```
186
describe the process of cardiogenic shock
1. Decreased Cardiac Contractility
2. Decreased SV
3. Decreased CO + BP
4. Inadequate Tissue Perfusion
187
describe process of tension pneumothorax
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
describe the process of distributive shock neurogenic
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
describe process of distributive shock vasoactive
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
what is syncope in common terms?
fainting
191
d: syncope
Transient loss of consciousness due to cerebral hypoperfusion, characterized by rapid onset, short duration, and spontaneous complete recovery
192
D: tloc
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
Name some conditions TLOC can result from:
```
Head Trauma
Suncope
Epileptic seizures
TLOC mimics
other causes
```
194
Name the 3 categories Syncope can be classified into
reflex syncope
orthostatic Hypotension
Cardiac Syncope
195
What happens in reflex syncope?
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
Describe the pathway for reflex syncope
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
Name the different types of reflex syncope
Vasovagal VVS
Situational
Carotid Sinus
198
What is the most commonest type of reflex syncope?
vasovagal
199
What is Faint triggered by?
emotional distress( pain, fear or blood phobia)
orthostatic stress
200
symptoms of vasovagal syncope
pallor
sweating
nausea
201
How can it be prevented?
horizontal gravity neutralisation position or leg crossing
202
Why do certain manoeuvres help in preventing fainting?
increase venous return
203
What is the main risk in VVS?
risk of injury
204
How can Fainting be avoided?
education
reassurance
avoidance of triggers
hydration
205
What is situational reflex syncope?
faint during or immediately after a specific trigger eg cough micturition swallowing etc
206
How is situational reflex syncope treated?
treat the cause if poss
get patient to lie down
hydrated and avoid alcohol
cardiac permanent pacing may be needed to stop it
207
What is carotid Sinus Reflex Syncope?
is triggered by mechanical manipulation of the neck, shaving, tight collar, etc.
208
Who is carotid sinus reflex syncope most common in?
elderly males
209
What is an associated condition with carotid sinus syncope?
carotid artery atherosclerosis
210
When may CCS occur?
after head and neck surgery
| radiation
211
How can CSS be treated?
cardiac permaent pacing
212
d: Postural Hypotension
Results from failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position
213
RF associated with Postural Hypotension
```
Age related
Medications
Certain diseases
Reduced intravascular volume
Prolonged bed rest
```
214
How is Postural Hypotension diagnosed?
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
Symptoms of Postural Hypotension
cerebral hypoperfusion such as: lightheadedness, dizziness, blurred vision, faintness and falls
216
What is cardiac Syncope caused by?
a cardiac event resulting in a sudden drop in CO
217
What can Cardiac Syncope be caused by?
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
What is the investigations required for a patient presenting with TLOC?
A careful history
Full physical examination, including
Orthostatic blood pressure (BP) measurement
12-lead ECG
219
What type of syncope would be indicative of happening during excretion or when supine?
Cardiac Syncope
220
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?
Cardiac
