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3rd Year > Clinical Physiology > Flashcards

Clinical Physiology Flashcards

1
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Sinus tachycardia

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2
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Sinus bradycardia

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3
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Wandering atrial pacemaker

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4
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Respiratory sinus arrhythmia

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5
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Sick-sinus syndrome

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6
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Premature contraction (PC) and
related terms

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7
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Atrial premature contractions

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8
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9
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10
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Atrial reentry tachycardia

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11
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Multifocal atrial tachycardia

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12
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Atrial flutter

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13
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Atrial flutter with alternating 2:1
and 4:1 block

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14
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Atrial fibrillation

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15
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Atrial fibrillation

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16
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Accelerated junctional rhythm
and junctional tachycardia

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17
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Junctional escape beat

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18
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Junctional escape rhythm

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19
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Idioventricular escape beat and
idioventricular escape rhythm

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20
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Ventricular premature contractions

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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

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25
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Idioventricular acceleration

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26
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27
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28
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29
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Ventricular tachycardia

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30
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Ventricular flutter

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31
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Ventricular fibrillation

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32
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First degree AV block

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33
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Second degree AV block – Mobitz I

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34
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Second degree AV block – Mobitz II

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35
Q
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Second degree AV block – 2:1 AV block

36
Q
A

Third degree AV block

37
Q

Left anterior hemiblock (LAH)

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38
Q

Left posterior hemiblock (LPH)

A
39
Q

Left bundle branch block (LBBB)

A
40
Q

Right bundle branch block (RBBB)

A
41
Q

Right atrial hypertrophy
(P-pulmonale)

A
42
Q

Left atrial hypertrophy
(P-mitrale)

A
43
Q

Left ventricular hypertrophy

A
44
Q

Right ventricular (right heart)
hypertrophy

A
45
Q

TYPICAL T WAVE ALTERATIONS

A
46
Q

TYPICAL ST ALTERATIONS

A
47
Q

Q WAVE

A
48
Q

THE DYNAMICS OF MYOCARDIAL INFARCTION (STEMI)

Phases

A
49
Q

LOCALIZATION OF THE MYOCARDIAL INFARCTION

  • Anterior
  • Antero-lateral
  • Extensive anterior
  • High lateral
  • Inferior
  • Posterior
  • Extensive inferior
  • Right ventricular
A

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
Q

A NON-Q MYOCARDIAL INFARCTION

A
51
Q

Indications for exercise stress test ECG

A
  • 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
Q

Contraindications for
exercise stress test ECG

A
  • 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
Q

(MET) Unit of body O2
consumption

A
54
Q

Limits of cardiac O2 uptake
during exercise testing

A
  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
Q

Protocols of exercise testing

A

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
Q

Physiologic ECG alterations
during exercise testing

A
  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
Q

Pathologic ECG alterations during
exercise testing

A

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
Q
A
59
Q

Define AAI, VVI, DDD, VDD

A
60
Q
A

AAI pacemaker

61
Q
A

VVI pacemaker

62
Q
A

DDD pacemaker

63
Q
A

VDD pacemaker

64
Q

Testing the pacemaker function

A
  • 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
Q

Normal pacemaker function with seemingly
abnormal ECG signs

A

Pseudofusion
Fusion
Hysteresis

66
Q

Real PM disorders

A

I. Ineffective stimulation
exit block
missing pacemaker spike
alterations in pacing frequency

II. Disorders of impulse sensing
undersensing
oversensing

67
Q

General characteristics of reentry
arrhythmias

A
  • 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
Q

Clinical forms of reentry arrhythmias

A
  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
Q
A

Torsade de pointes

70
Q

Hypokalaemia

A
71
Q

Hyperkalaemia

A
72
Q

Hypocalcaemia

A
73
Q

Hypercalcaemia

A
74
Q

Digitalis effect on ECG

A
75
Q

Clinical forms of heart failure

A
76
Q

Activation of the Frank-Starling mechanism and the
neurohumoral system in HFrEF

A
77
Q

The role of natriuretic peptides in heart failure

  • and as therapeutical targets
A

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
Q

Functions of vascular endothelium

A

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
Q

Angiotensin and Bradykinin

A
80
Q

Nitric oxide (NO)

A
81
Q

Agonists of NO production

A
82
Q

EDHF (endothelium derived hyperpolarizing factor)

A

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
Q

Interactions during health and disease

Endothelium

A
84
Q

Interactions during disease

Endothelium

A
85
Q
A

3rd Year (21 decks)

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