Physio Flashcards
1
Q
What is the order of electrical flow within the conducting system of the heart?
A
1) SA node
2) Internodal tracts
3) AV node
4) Main branch
5) L/R Bundle
6) Purkinje Fibre
2
Q
How frequently does the SA node usually depolarise?
A
~80 times/min
3
Q
True or false: Every part of the heart’s conducting system is capable of discharging electrical signals autonomously.
A
True
4
Q
When does the SA node NOT set the pace of the heart? What happens then?
A
When the SA node is compromised, slower components (eg. AV node) will take over and set the pace of the heart.
5
Q
How does the conducting system help the atria function as a priming pump?
A
There is a SA-AV delay (0.13s) in depolarisation, allowing time for the atrium to fully fill the ventricles before they pump.
6
Q
Describe the blood supply of the conductive system of the heart.
A
Right Coronary Artery supplies everything
Left Anterior Descending Artery supplies (i) Right bundle (ii) Left bundle
7
Q
Which part of the brain controls the regulation of heart rate via the autonomic nervous system?
A
Vasomotor centre
8
Q
What are 4 receptors/inputs that communicate information to the vasomotor center to regulate heart rate?
A
1) Afferent pain fibres (pain → ↑HR)
2) Chemoreceptors (↓pH/↑CO2 → ↑HR)
3) Respiratory centre (Inspiration → ↑HR)
4) Baroreceptors (↓BP → ↑HR)
5) H+ ions
9
Q
Describe how the ANS system can regulate heart rate.
A
Sympathetic:
NE → ß1 of SAN → ↑Na+/Ca+ influx → depolarise → ↑HR
Parasympathetic:
ACh → Muscarinic of SAN → ↑K+ influx → polarise → ↓HR
10
Q
Describe the heart rate can be regulated directly (w/o ANS).
A
1) Temperature (↑temp → ↑HR)
2) Thyroxin (thyroid hormone → ↑HR)
3) Catecholamines (stress hormone → ↑HR)
11
Q
How does sympathetic and parasympathetic activation affect the membrane potential and action potential?
A
Sympathetic: more +ve resting, shorter pre-potential
Parasympathetic: more -ve resting, longer pre-potential
12
Q
What are the 5 phases of ventricular muscle contraction?
A
0) Fast voltage-gated Na+ channel → Na+ influx → depolarisation
1) Outward-rectifying K+ channel → K+ efflux → slight repolarisation
2) Voltage-gated Ca2+ channel → Ca2+ influx → continued but slow repolarisation (depolarisation masked by K+ repolarising)
3) more outward-rectifying K+ channel → ↑K+ efflux → repolarisation back to resting potential
4) inward-rectifying K+ channel → maintain resting potential (~-85mV)
13
Q
Which part of the cardiac cycle corresponds to the P wave of an ECG?
A
Atrial depolarisation
14
Q
Which part of the cardiac cycle corresponds to the QRS complex of an ECG?
A
Ventricular depolarisation
15
Q
Which part of the cardiac cycle corresponds to the T wave of an ECG?
A
Ventricular repolarisation
16
Q
Which part of the ECG corresponds to AV nodal delay?
A
PR interval
17
Q
Which part of the ECG corresponds to electrical conduction in the ventricles?
A
QT interval
18
Q
Which part of the ECG corresponds to when the ventricles are isoelectric?
A
ST interval
19
Q
What does a tall QRS complex indicate in a px?
A
Hypertrophy
20
Q
What does a tall T wave indicate in a px?
A
Hyperkalaemia
21
Q
What does an elevated ST-segment indicate in a px?
A
Myocardial Infarction
22
Q
What does a depressed ST-segment indicate in a px?
A
Myocardial Ischaemia
23
Q
What does a RSR- indicate in a px?
A
Ventricular block
24
Q
What does a tall p wave indicate in a px?
A
Atrial hypertrophy
25
Which leads face the septal region of the heart?
V1, V2
Reciprocal: None
26
Which leads face the anterior region of the heart?
V3, V4
Reciprocal: None
27
Which leads face the lateral region of the heart?
I, aVL, V5, V6
Reciprocal: II, III, aVF
28
Which leads face the inferior region of the heart?
II, III, aVF
Reciprocal: I, aVL (Lateral)
29
Which leads face the posterior region of the heart?
None
Reciprocal: I, II, III, IV (Anteroseptal)
30
Which coronary vessels could be affected/occluded in a px with ST-elevation in leads V1-4 and no reciprocal?
Left Anterior Descending
31
Which coronary vessels could be affected/occluded in a px with ST-elevation in leads I, aVL, V3-6 and reciprocal in II, III, aVF?
Left Circumflex Artery
32
Which coronary vessels could be affected/occluded in a px with ST-elevation in leads II, III, aVF and reciprocal in I, aVF?
Right Coronary Artery
33
Which coronary vessels could be affected/occluded in a px with no ST-elevations but inverted in V1-4?
Right Coronary Artery (posterior descending branch)
34
Where are the electrodes placed for a 12 lead ECG reading?
Limb leads:
LA: L wrist
RA: R wrist
LL: L ankle (medial side)
N: R ankle (medial side)
Chest leads:
V1: 4th ICS R of sternum
V2: 4th ICS L of sternum
V3: btwn V2&4
V4: 5th ICS Mid-clavicular
V5: 5th ICS Anterior axillary
V6: 5th ICS Mid-axillary
34
Which of the ECG electrodes are standard limb leads (bipolar)?
I, II, III
34
Which of the ECG electrodes are augmented vector limb leads (unipolar)?
aVL, aVF, aVR
34
How do you determine if the mean QRS axis is normal?
I and aVF are +ve
or I +ve, aVF -ve but II +ve
35
What is the mean QRS axis deviation if I+, aVF-, II-?
Left axis deviation
36
What is the mean QRS axis deviation if I-, aVF-?
Extreme axis deviation
37
What is the mean QRS axis deviation if I-, aVF+?
Right axis deviation
38
Right ventricular hypertrophy would lead to ________ QRS axis deviation.
Right
39
Left ventricular hypertrophy would lead to ________ QRS axis deviation.
Left
40
Myocardial contraction occurs when calcium binds to ______.
Troponin C
41
Calcium enters myocardial cells through _____________.
Voltage-gated Ca2+ channels.
42
Calcium is removed from the myocardial cytoplasm by the _______________.
Na/Ca exchanger
43
Ventricular muscle relaxation is a (passive/active) process.
Active
44
What is the Frank Starling Mechanism?
The intrinsic ability of the heart to adjust pumping capacity to handle changing volumes presented to it.
↑VEDL → ↑SV (until it plateaus)
45
What is the definition of contractility?
The change in work performed by the heart, not brought about by a change in initial fiber length
46
Contractility of the heart is regulated by the _______________.
Sympathetic nervous system
47
What is the difference between contractility and starling's mechanism?
Stroke volume increase in both, but:
Starlings: ↑EDV → ↑SV
Contractility: same EDV but ↑SNS → ↑SV
48
How is contractility of the heart measured?
Ejection fraction= (SV/EDV) x 100%
49
What is the normal range of ejection fraction?
55-75%
50
In the cardiac cycle, filling occurs at (high/low) pressures whilst blood is ejected at (high/low) pressures.
Filling: low pressure
Ejection: high pressure
51
How does the heart alternate between phases of high and low ventricular pressures between systole and diastole?
Rapid ↑P: Isovolumetric contraction (Both AV and SL closed before aortic open)
Rapid ↓P: Isovolumetric relaxation (Both AV and SL closed before AV open)
52
When does the mitral valve open and close?
opens at end of isovolumetric relaxation when P ventricle
53
When do the AV valve open and close?
opens at end of isovolumetric contraction when P ventricle>P aorta (start of ejection phase of systole)
closes at end of ejection phase (end of systole)
54
What produces the S1 heart sound?
Closure of Mitral valve at start of isovolumetric contraction
55
What produces the S2 heart sound?
Closure of AV valves at end of ejection/systole
56
What produces the S3 heart sound?
After opening of MV by rapid ventricular filling
57
In what type of px is S3 heard?
S3 can be a normal finding in children, pregnant females and well-trained athletes
Abnormal in normal adults (don't usually have very compliant ventricles)
58
What produces the S4 heart sound?
During atrial systole, late in ventricular diastole
Produced by contraction of the atria pushing blood into a stiff or hypertrophic ventricle
59
In what type of px is S4 heard?
px with LVH (usually secondary to diastolic heart failure or active ischemia)
60
Which wave of an ECG/heart sound corresponds to the start of ventricular systole/isovolumetric contraction?
R wave, S1
61
Which wave of an ECG/heart sounds corresponds to the start of ventricular diastole?
End of T wave, S2
62
Which vein is observed for Jugular Venous Pulse?
Internal jugular vein
63
Why is the internal jugular vein used for examination of a px jugular venous pulse?
Internal jugular vein (IJV) connects to the right atrium without any intervening valves, resulting in a continuous column of blood. The presence of this continuous column of blood means that changes in right atrial pressure are reflected in the IJV (e.g. raised right atrial pressure results in distension of the IJV).
64
How can a jugular venous pulse be accentuated?
Use Hepatojugular reflex
65
When is JVP raised?
When RA pressure>0-5mmHg
eg. tricuspid/pulmonary stenosis/regurg, ASD, RHF
66
When does ventricular systole occur in a ECG?
Between R wave and end of T wave
67
What are the 5 components of the jugular venous pulsation?
A wave: atrial contraction
C wave: carotid transmission
X descent: ↓P following A
V wave: passive filling of atria from I/SVC
Y descent: ↓P during atrial + ventricular diastole
68
What causes the apex beat to be palpable?
The tapping of the LV against the chest wall during contraction
69
Where is the apex beat located normally?
5th ICS, mid clavicular line
70
True or false. The apex beat is caused by ventricular systole, pushing the apex of the heart against the chest wall.
False. The apex beat is the point farthest outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt.
71
When does splitting of S2 occur?
During inspiration when pulmonary valves close later than aortic valve (RV handles more blood during inspiration)
72
Which heart defect is associated with a ejection systolic mumur, heard on the 2nd R ICS, and L sternal edge?
Aortic stenosis
Can cause carotid bruit (radiation of murmur to R carotid artery)
73
Which heart defect is associated with a pansystolic mumur, heard over the apex?
Mitral regurgitation
74
Which heart defect is associated with a mid-diastolic mumur, heard over the apex?
Mitral stenosis
75
Which heart defect is associated with a early diastolic mumur, heard over the left sternal edge, 4th ICS?
Aortic regurgitation
76
What type of left ventricular hypertrophy is caused by aortic regurgitation?
Eccentric
77
How is BP affected by aortic regurg?
↑Systolic, ↓ Diastolic pressure
78
What type of left ventricular hypertrophy is caused by aortic stenosis?
Concentric
79
Why is most of the blood volume in the venous system?
High compliance of veins
80
What are the 2 ways to calculate cardiac output?
SV x HR
or
Arterial pressure / Total Peripheral resistance
81
What is the main site of resistance in the circulatory system?
Arterioles
82
What is the main factor in determining the resistance in arterioles?
Much smaller radius than arteries
83
Ohm's law governs _______ in circulation by relating flow, pressure and resistance.
Rate of blood flow
84
Poiseuille Hagen formula governs _________, particularly in arterioles.
Resistance
85
When total peripheral resistance ↑, pressure in circulation (↑/↓) for any rate of flow.
TPR↑ → P↑
86
What is tissue perfusion?
Rate of blood flow into capillary network
87
What are 5 factors affecting tissue perfusion?
Blood flow in arteries: (Systemic factors)
1) Arterial BP
2) Cardiac output
Arteriolar vasomotor tone: (Local factors)
1) Local factors (↓flow → ↑metabolic products → ↑ local NO → arteriolar vasodilation)
2) Autoregulation (reflex vasoconstriction to ↑BP)
3) Circulating hormones (Epinephrine, Norepinephrine, ADH)
4) SNS
88
How is tissue perfusion clinically assessed?
Capillary refill time
## Footnote
The performing examiner applies manual pressure to the ventral surface of the distal phalanx of fingers or toes until the nailbed is blanched. This pressure is maintained for ten seconds and then released. The amount of time, in seconds, that transpires before reperfusion occurs and normal color returns to the digit is the CRT.
89
What are 4 starling's forces at the capillary determining capillary exchange?
1) Capillary pressure (hydrostatic by blood)
2) Colloid osmotic pressure (inward pull by proteins eg. albumin)
3) Interstitial fluid pressure (-ve, maintained by lymphatics)
4) Interstitial colloid pressure (+ve from proteins)
90
What is the net starling's force at the capillary (inward/outward) and how is it removed?
Net outward ~0.3mmHg
Excess extravasated fluid (3L/day) removed by lymphatic system
91
How does heart failure cause edema?
↑Venous pressure → ↑outward capillary pressure → ↑ fluid extravasation
92
How does Nephrotic syndrome cause edema?
Plasma protein (eg. albumin) loss → ↓oncotic pressure → ↑ fluid extravasation
93
How does filariasis cause edema?
Obstruct lymphatic flow → extravasated fluid not cleared, accumulates locally
94
How does acute inflammation cause edema?
↑ Capillary permeability → ↑ fluid extravasation
95
What is the definition of cardiac output?
Volume of blood pumped by left ventricle into the aorta per min
96
What are 3 cardiac factors affecting cardiac output?
1) Preload (volume)
2) Heart (contractility, HR)
3) Afterload (TPR)
97
What are 2 definitions of heart failure?
1) Failure of heart to pump at sufficient rate to meet metabolic requirements of tissues
2) Only able to meet metabolic Dd at elevated filling pressures (after compensation)
98
How does Hemorrhage affect CO?
↓ Preload and afterload → ↓CO
↑contractility and HR (compensatory)
99
How does MI or bradycardia affect CO?
↓ contractility and HR respectively → ↓CO
100
How does hypertension affect CO?
↑Afterload → ↓CO
101
What are the typical presentation for px with acute heart failure that manifest as a result of acute compensation?
↑SNS, ↓PNS:
↑HR
↑Sweating
↑contractility (heart palpitations)
pallor
102
What are the typical presentation for px with chronic heart failure that manifest as a result of chronic compensation?
RAAS activation:
Oliguria
Oedema
SOB (orthopnea, NPD)
Low BP
Fatigue
Raised JVP
103
How is RAAS activated in heart failure?
↓BP → detected by macula densa → JG secrete renin
Renin → AT1 → AT2 → ↑BP
AT2 → Aldosterone → Salt and water retention → ↑BP
104
Why is activation of RAAS maladaptive?
Chronically elevated levels of AT2
→ remodels heart (inflammation, fibrosis, hypertrophy) → ↓effective as a pump
→ decreases NO (impt vasodilator) → ↑TPR → ↑workload/afterload
105
What is the criteria for HFrEF?
EF<40%
106
What is the criteria for HFpEF?
EF>50%
107
What is the criteria for borderline HFpEF/HFmrEF?
40%
108
How do you differentiate left and right heart failure?
RHF: Backpressure on systemic venous circulation
1) Raised JVP
2) Hepatosplenomegaly
3) Peripheral Oedema
LHF: Back pressure on pulmonary circulation
1) Engorged pulmonary veins
2) SOB (exertional dyspnea, Orthopneam NPD)
3) Raised JVP
4) Coarse crepitations in lungs
5) 3rd heart sound
109
What are 6 Ix for a px with suspected HF?
1) CXR (venous distention, pulmonary edema)
2) ECG (STEMI)
3) BNP
4) EF
5) Troponin 1
6) Echo (E/A ratio)
## Footnote
E/A >2 → Restrictive filling
E/A <1 → LV diastolic dysfunction
110
What counteracts the effects of AT2?
AT1-7 produced by ACE 2 enzyme
111
Why is the endothelial layer of the coronary arteries most vulnerable to ischaemia?
1) Coronary arteries branch into myocardium ( impact when flow ↓)
2) Coronary vessels in myocardium are compressed in systole
3) Tension > in myocardium
112
A full thickness infraction results in a STEMI/NSTEMI?
STEMI
113
An NSTEMI is caused by what degree of myocardial infarction?
Non-full thickness (between endo/myocardium)
114
What is the normal coronary blood pressure/flow?
60-160mmhg
115
How is coronary blood flow kept relatively constant between mean arterial pressures of 60 to 140 mmHg?
Autoregulation by:
1) NO → vasodilation
- produced by endothelium under shear stress and local metabolites
- ↓Ca release by myocardium → inhibit vasoconstrictor endothelin-1
- inhibiting the release of norepinephrine from sympathetic nerve terminals
2) Myogenic response
- “stretch-sensitive” receptors/channels on myocytes
- ↑P → depolarisation and Ca release → vasoconstriction.
- ↓P → muscle relaxes, maintaining blood flow
116
Why does angina pectoris occur?
Metabolic Dd > Coronary supply
117
What are 3 factors that ↑ the workload of the left ventricle, possibly leading to angina?
1) ↑Arterial pressure & Stroke volume (eg. HTN)
2) ↑HR (eg. stress, exercise)
3) ↑ventricle radius (eg. eccentric hypertrophy)
118
What are 2 factors that ↓ coronary supply, possibly leading to angina?
1) Occlusion (eg. atherosclerosis)
2) Diastolic duration (eg. Afib, tachycardia)
3) Diastolic pressure (eg. aortic regurg)
119
Blood flow in the left coronary artery is higher during (diastole/systole).
Blood supply to the LV occurs predominantly during diastole. The tension in the ventricular walls during systole impedes blood flow in the coronary arteries.
120
The (left/right) ventricle is more susceptible to changes in diastolic time and pressure.
Left
Blood flow to the right ventricle is about equal in both phases of the cardiac cycle. The tension in the walls of the right ventricle during systole is lower compared to the left ventricle.
121
What are 2 forms of acute CAD?
1) MI
2) Unstable angina
122
What are the medical interventions for acute CAD (4)?
1) Ix
2) Percutaneous coronary interventions
3) CBAG
4) Drugs + lifestyle modifications
123
What are 3 forms of chronic CAD?
1) Stable angina (#1)
2) Vasospastic angina
3) Microvascular angina
124
What are the medical interventions for chronic CAD (3)?
Address Dd
125
What are the differences between stable angina and unstable angina?
Unstable angina typically have pain even at rest
Stable: fixed obstruction (degree relatively stable/time)
Unstable: Dynamic obstruction (clots may break down and reform, can ↑ size rapidly)
126
Why are cardiac reserved diminished in the aged?
1) ↓organ performance
2) Pre-existing compensatory mechanisms already used
127
What are 5 reasons why maximal CO is reduced in the elderly?
1) Heart is stiffer
a) ↓Ca reuptake to SER → slower relaxation
b) Interstitial fibrosis of myocardium (by AG2)
c) ↑ TPR by (i) progressive replacement of elastic by cross-linked collagen (ii) endothelial dysfunction by oxidative stress/inflammation (iii) artherosclerosis
2) ↓early diastolic filling → ↑late filling by atrial systole
3) ↓ diastolic time (↑AP duration → longer systole)
4) ↓SV (↓ filling)
5) < responsive to SNS stimulation
128
A stiffer aorta leads to (higher/lower) systolic and (higher/lower) diastolic pressures.
Higher systolic
Lower diastolic
(widened pulse pressure)
129
Why are the elderly more predisposed to having postural hypotension?
Degeneration of baroreceptor reflexes
130
What are 3 factors that lead to the degeneration of baroreceptor reflexes in the aged?
1) ↓responsiveness of baroreceptors to stretch
2) ↓ elasticity of aorta and carotid arteries
3) change in ANS
4) ↓ responsiveness of heart to ANS
131
Why is exercise capacity reduced in older adults?
1) Max HR↓
2) Heart is less responsive to SNS → max contractility ↓
132
Why are older adults more prone to develop systolic hypertension?
Aortic stiffness:
→ ↓ buffering capacity of the aorta during systole
→ ↑ pulse pressure wave velocity → reflected pulse pressure wave to return to the aorta more quickly and in phase with systole of the next cycle → ↑ systolic BP
133
Why is diastolic BP lower in older adults?
Stiff aorta (↓elasticity)
(Diastolic BP is dependent on the elastic recoil of the aorta)
134
Why are older adults more prone to develop HF with atrial fibrillation (AF)?
↓ early diastolic filling (stiffer ventricles)
→ more dependent on atrial “kick” (contraction) for ventricular filling
- Atrial “kick” is absent in AF, no coordinated contraction of the atrial muscle → ↓ ventricular filling more significantly in older adults compared to younger patients
135
What are 5 reasons why are older adults more prone to develop ischemic heart disease?
1) ↑ Atherosclerotic plaques
2) ↓ Elasticity of coronary arteries (↓ compensatory dilation)
3) ↓ Diastolic pressures by aortic stiffness → ↓myocardial perfusion
4) ↑ Afterload due to aortic stiffness and peripheral resistance
5) ↑ Afterload → LVH → ↑Dd
136
What are 3 ways to calculate mean arterial pressure calculated?
1) CO x TPR
2) 2/3 diastolic + 1/3 systolic
3) Diastolic + 1/3 pulse pressure
137
What is systemic pressure?
Pressure in the arterial system during systole
138
What is diastolic pressure?
Pressure during diastole due to elastic recoil by the arteries (aortic, pulmonary, large)
139
When can the pulse be auscultated with a sphygmomanometer?
When diastolic
140
What is pulse pressure?
Difference between systolic and diastolic pressures
141
What is the normal pulse pressure?
40mmHg
142
When is blood pressure at its physiological lowest?
During sleep 2200-0400hrs (diurnal variation)
143
How is blood pressure generated?
Ventricular contraction
144
How is high blood pressure from ventricular contraction maintained?
1) Valves in heart ensure directional flow
2) Thick walls → low R in arteries
3) Arterioles at end of arteries → high R
145
What is postural hypotension?
Sitting to standing
→ ↓venous return (veins very compliant)
→ ↓SV (↓ preload)
→ ↓ MAP
146
Under what blood pressures do baroreceptors have the greatest sensitivity to pressure changes?
Around their normal operating pressure of 100mmHg
147
What happens to baroreceptors in px with chronic HTN?
Their response curve shifts right (↑ mean operating point and ↑ range of greatest sensitivity)
(↑ "normal" BP)
148
How is arterial blood pressure autonomically regulated in the short term?
↑SNS
- Arteriolar vasoconstriction → ↑peripheral resistance
- Venous vasoconstriction → ↑ venous return
- ↑ ventricular contractility→ ↑CO
↓PNS
- ↑HR → ↑CO
149
How is arterial blood pressure autonomically regulated in the longterm?
RAAS
150
How is ↓BP detected in the kidneys?
1) JG cells: sense tension (BP) in arterioles
2) Macula densa: sense transport of Cl- (cotransported with Na and thus water)
151
What is the main etiology of primary/essential hypertension?
No known cause
152
How does smoking predispose a px to HTN?
Dysregulation of vascular smooth muscle tone → ↑ R of arteries and arterioles
153
How does obesity predispose a person to HTN?
1) Angiotensinogen released from adipocytes
2) ↑ blood volume/preload
3) Increased blood viscosity (dysregulation of clotting)
154
How does hypertension lead to increased risk of heart failure?
↑BP → ↑ afterload → myocardial hypertrophies → ↑Dd → HF
155
How does hypertension lead to increased risk of atherosclerosis, thrombosis, aneurysms, etc.?
Damage to blood vessels
156
What are 6 lifestyle changes to manage HTN?
1) Maintain BMI of 18.5 to 22.9kg/m^2
2) Exercise (150min moderate exercise/week; 10k steps/day)
3) 7-8 hours of sleep/day
4) Healthy diet (5-6g of sodium/day; higher potassium; more fruits, veg, fish, poultry, nuts; less dairy, red meats, sweets)
5) Quit smoking
6) Reduce caffeine and alcohol
7) Reduce stress
157
What is the definition of hypertension?
When arterial BP above a level that increases risk for developing complications
158
What is the definition of circulatory shock?
When arterial pressure is insufficient to maintain perfusion
Systolic < 80mmHg
Mean BP < 60mmHg
159
What are 4 types of shock?
1) Hypovolemic (loss of vol.)
2) Cardiogenic (inadequate CO/pumping)
3) Obstructive (Obstruction to blood flow)
4) Distributive (distributive vasodilation)
160
What are 2 examples of hypovolemic shock?
1) Haemorrhage
2) Severe diarrhoea, vomitting
161
What are 3 causes of cardiogenic shock?
1) MI
2) Arrhythmias
3) Severe valvular defects
162
What are 3 examples of obstructive shock?
1) Pulmonary embolism
2) Tension pneumothorax
3) Pericardial tamponade
163
What are 3 examples of distributive shock?
1) Sepsis
2) Anaphylactic
3) Neurogenic
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