Clinical Physiology Flashcards
1
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Sinus tachycardia
2
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Sinus bradycardia
3
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Wandering atrial pacemaker
4
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Respiratory sinus arrhythmia
5
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Sick-sinus syndrome
6
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Premature contraction (PC) and
related terms
7
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Atrial premature contractions
8
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9
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10
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Atrial reentry tachycardia
11
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Multifocal atrial tachycardia
12
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Atrial flutter
13
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Atrial flutter with alternating 2:1
and 4:1 block
14
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Atrial fibrillation
15
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Atrial fibrillation
16
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Accelerated junctional rhythm
and junctional tachycardia
17
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Junctional escape beat
18
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Junctional escape rhythm
19
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Idioventricular escape beat and
idioventricular escape rhythm
20
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Ventricular premature contractions
21
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22
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23
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24
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Ventricular premature beats with a
bigeminal pattern
25
Idioventricular acceleration
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27
28
29
Ventricular tachycardia
30
Ventricular flutter
31
Ventricular fibrillation
32
First degree AV block
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Second degree AV block – Mobitz I
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Second degree AV block – Mobitz II
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Second degree AV block – 2:1 AV block
36
Third degree AV block
37
Left anterior hemiblock (LAH)
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Left posterior hemiblock (LPH)
39
Left bundle branch block (LBBB)
40
Right bundle branch block (RBBB)
41
Right atrial hypertrophy
(P-pulmonale)
42
Left atrial hypertrophy
(P-mitrale)
43
Left ventricular hypertrophy
44
Right ventricular (right heart)
hypertrophy
45
TYPICAL T WAVE ALTERATIONS
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TYPICAL ST ALTERATIONS
47
Q WAVE
48
THE DYNAMICS OF MYOCARDIAL INFARCTION (STEMI)
Phases
49
LOCALIZATION OF THE MYOCARDIAL INFARCTION
- Anterior
- Antero-lateral
- Extensive anterior
- High lateral
- Inferior
- Posterior
- Extensive inferior
- Right ventricular
ANTERIOR (ANTEROSEPTAL): V1-V4
ANTEROLATERAL: I, aVL, V5-V6
EXTENSIVE ANTERIOR: I, aVL, V1-V6
HIGH LATERAL: I, aVL
INFERIOR: II, III, aVF
POSTERIOR: VD1-VD3 (V1-V2: mirror im.)
EXTENSIVE INFERIOR: II, III, aVF, VD1-VD3
RIGHT VENTRICULAR: V1, V3R, V4R
(regularly combines with an inferior
myocardial infarction)
50
A NON-Q MYOCARDIAL INFARCTION
51
Indications for exercise stress test ECG
- It is advisable to be performed if the suspicion of coronary artery disease is raised and there are no contraindications to the test.
- After a myocardial infarction (>10 days) to detect residual ischemia if no reperfusion treatment was applied.
- Monitoring after a revascularization therapy (PTCA, CABG)
- To assess exercise capacity in heart failure.
- Searching for exercise-induced arrhythmias and chronotropic
incompetence (SSS) or to determine refractoriness of the accessory
pathway in WPW syndrome.
- To assess exercise tolerance and perioperative risk before high-risk
surgery (lungs, great vessels).
52
Contraindications for
exercise stress test ECG
- Acute stage of AMI (first few days)
- Unstable angina
- Severe aortic stenosis and hypertrophic cardiomyopathy
- Current high blood pressure (RRsystolic >160 mmHg)
- Hypokalaemia;
- Severe or unstable heart failure (NYHA class III-IV);
- Severe disturbances of impulse formation and conduction, ventricular
arrhythmias;
- Acute pericarditis, myocarditis, febrile illness, anemia;
- Left ventricular thrombus, acute thromboembolism.
53
(MET) Unit of body O2
consumption
54
Limits of cardiac O2 uptake
during exercise testing
1. Coronary stenosis
2. Increased O2 demand
3. Tachycardia
4. Low systemic diastolic and high left ventricular
end-diastolic pressure
5. Compression of subendocardial and subepicardial vessels
6. Pathological intramural blood redistribution
55
Protocols of exercise testing
Mechanical:
- static exercise (e.g. handgrip)
- dynamic exercise (e.g. ergometer, treadmill)
Pharmacodynamic:
- dipyridamol
- dobutamin
Combined:
- dipyridamol and myocardium scintigraphy (SPECT)
- dobutamin – dipyridamol and echocardiography
56
Physiologic ECG alterations
during exercise testing
1. Increase in heart rate
2. Reduction of PQ distance
3. Increase of P wave amplitude
4. Right axis
5. Reduction in R and T wave amplitudes
6. Ascending ST depression
57
Pathologic ECG alterations during
exercise testing
Pathologic ST-T changes:
- junctional ST depression
- horizontal ST depression
- descending ST depression
- ST elevation (with or without Q waves)
ST-T changes and location of ischaemia
58
59
Define AAI, VVI, DDD, VDD
60
AAI pacemaker
61
VVI pacemaker
62
DDD pacemaker
63
VDD pacemaker
64
Testing the pacemaker function
- ECG registration (at least 3 channels)
- activation of the pacemaker stimulating frequency
(carotis massage, or magnet)
- detection of a low battery (with or without magnet)
battery low: reduced stimulating frequency
increased duration of PM pulse (special unit is needed)
- 24-hour Holter monitoring
- chest X-ray (testing the electrode position)
65
Normal pacemaker function with seemingly
abnormal ECG signs
Pseudofusion
Fusion
Hysteresis
66
Real PM disorders
I. Ineffective stimulation
exit block
missing pacemaker spike
alterations in pacing frequency
II. Disorders of impulse sensing
undersensing
oversensing
67
General characteristics of reentry
arrhythmias
- start and stop abruptly (paroxismally)
- mostly initiated by a premature beat
- regularity
- terminated by increasing the refractoriness of one
part of the reentry circle (e.g. vagal maneuvers)
68
Clinical forms of reentry arrhythmias
1. Sinus node reentry tachycardia
2. Atrial reentry tachycardia
3. Atrial flutter
4. Atrial fibrillation
5. AV node reentry tachycardia (AVNRT)
6. Atrioventricular reentry tachycardia (AVRT)
7. Bundle branch reentry
8. Most ventricular tachycardias (VT) (90%)
9. Ventricular fibrillation (VF)
69
Torsade de pointes
70
Hypokalaemia
71
Hyperkalaemia
72
Hypocalcaemia
73
Hypercalcaemia
74
Digitalis effect on ECG
75
Clinical forms of heart failure
76
Activation of the Frank-Starling mechanism and the
neurohumoral system in HFrEF
77
The role of natriuretic peptides in heart failure
- and as therapeutical targets
Natriuretic peptides
* ANP, BNP, NT-proBNP, CNP, dendroaspis, urodilatin
* released from cardiomyocytes in response to atrial and ventricular wall stretch
* Inhibition of the sympathetic nervous system and the RAAS
* Natriuretic and diuretic effects (kidney and distal tubules)
* Vasodilatory effects, smooth muscle relaxation (decreased PVR)
* Vascular system: antiproliferative, antifibrotic and antihypertrophic effects
* Myocardial effects: direct lusitropy (relaxation)
as therapeutical targets : ARNI
78
Functions of vascular endothelium
Release of vasodilator agents
Nitric oxide (EDRF)
Prostacyclin (PGI2)
Bradikynin
EDHF (endothelium derived hyperpolarizing factor)
Release of vasocontrictor agents
Endothelins
Protection of vascular smooth muscle
vasoconstrictory → to vasodilatory stimuli
(acetylcholine and serotonin)
Antiaggregatory effect
Acts via NO (nitric oxide) and PGI2
(thrombocyte
activation ↓)
Prevention of coagulation
Thromboresistant surface (heparan sulfate – antithrombin
cofactor)
Immune and barrier function
Supply of antigens to immunocompetent cells
Secretion of interleukin I, E-selectin (rolling)
Enzymatic activity
Angiotensin-converting enzyme
Carbonic anhydrase (large amounts in lung endothelium)
Growth signal to vascular smooth muscle
VEGF (vascular endothelial growth factor), angiopoietin
Heparin-like inhibitors of growth
79
Angiotensin and Bradykinin
80
Nitric oxide (NO)
81
Agonists of NO production
82
EDHF (endothelium derived hyperpolarizing factor)
Soluble secretion of EDHF during Ach/
bradykinin evoked SM hyperpolarization/ relaxation when NO and PGI2
productions blocked.
Chemical structure is uncertain: CYP450
product, K+, H2O2 …
Half-life of action ~70 sec EDHF:in vessels with smaller diameter(resistance vessels)
NO: in vessels with higher diameter
EDHF independent SM hyperpolarization
may occur because of myoendothelial gap
junctions.
(If junctions are blocked, Ach induced
hyperpolarization develops only in
endothelial cells. Ach → Ca2+↑ → IK,Ca open → hyperpol.)
83
Interactions during health and disease
Endothelium
84
Interactions during disease
Endothelium
85
