VT Bradycardias Answ

Questions in cardiology
4th & 6th course 2015/2016
Ventricular arrhythmias. Bradycardias.
1. What are the signs of ventricular extrasystoles (premature beats) [PVC=

premature ventricular complex] on ECG? * (0,5)
• Premature ventricular depolarization  Premature QRS
• Followed by a compensatory pause
• Wide QRS complex =>0.12s
• Monotropic and monomorphic: Arising from a single ectopic focus; each
PVC is identical (identical QRS morphology).
• Polytropic and polymorphic: Arising from two or more ectopic foci;
multiple QRS morphologies.
2. What does ventricular bigeminy mean? (0.5) What does ventricular trigeminy
mean? (0,5) (1 point)
• Bigeminy — every other beat is a PVC.
• Trigeminy — every third beat is a PVC.
3. Please explain what does „monomorphic” and “polymorphic” ventricular

extrasystoles mean? (1)
• Monomorphic: each QRS has the same morphology
• Polymorphic: multiple QRS morphologies
4. What are the possible clinical manifestations of ventricular extrasystoles? (1)

• May be asymptomatic
• Patients may complain of:
o Irregular beats
o Missed beat-pause-heart stopping for a moment-pulse deficit
o Strong beat-jumping heart
5. What is the definition of ventricular tachycardia? (Rate and minimal number

complexes)* (1)
• HR = or >100bpm, minimum 3PVCs
6. Which ECG signs are characteristic of ventricular tachycardia (at least 5 signs)?
(2)
• Scattered P waves (less frequent than QRS and not related to them AV
discordance)
• Captured beat: Narrow QRS among wide QRS (due to SV source)
• Fusion beat: QRS complex that is narrower or different from the wide
QRS complexes of VT (due to fusion of SV and ventricular source)
• Concordant QRS in V1-V6: Similar or identical configurations of QRS
(e.g., all negative or positive)
• QRS does not correspond LBBB or RBBB pattern (not entirely reliable
sign as some reentry VTs may resemble BBB)
• Wide QRS = or >0.12s
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• Brugada sign:distance from the beginning of QRS to S deepest point

>100ms
• Josephson’s sign: S wave descending part is curved
7. What does non-sustained and sustained ventricular tachycardia mean? (1)

• Non sustained: duration <30s
• Sustained: duration >30s
8. What is the differential diagnosis of wide-QRS complex tachycardias (name what

kind of tachycardias and in which cases may be with wide-complexes)? (2)
• SVT with Hiss bundle branch aberration
• SVT with Hiss bundle branch complete block
• SVT with accessory conduction pathway-WPW syndrome antidromic type
• Pacemaker related tachycardia
9. What does „monomorphic” and “polymorphic” ventricular tachycardia mean? (1)

• Monomorphic ventricular tachycardia has QRS with only one morphology
during the episode
• Polymorphic ventricular tachycardia has more morphologically distinct
QRS complex occurring during the same episode
10. What does pirouette-type tachycardia (“Torsades de pointes”) mean? What are the
ECG signs? (1)
• Is a form of polymorphic VT
• Characteristic beat by beat twisting around the baseline QRS changes
• Predisposed by prolonged QT (>0.42s at 60bpm)
• Usually paroxysmal
• May degenerate in VFib
• ECG signs:
o Irregular QRS that are wide and with changing amplitude
o QRS rotate about the baseline, deflecting downward and upward
o Usually no P waves
o Usually rate 150-200bpm
11. In which cases patients will have high risk of developing pirouette-type
tachycardia (“Torsades de pointes”)? Which parameter changes on ECG are
characteristic? (0,5)
• More common in women
• Predisposed by prolonged QT (>0.42s at 60bpm)
o Congenital proloneged QT syndrome
o QT prolonging medications + - hypokalemia or hypomagnesemia
or hypocalcemia
• ECG signs:
o Irregular QRS that are wide and with changing amplitude
o QRS rotate about the baseline, deflecting downward and upward
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o Usually no P waves
o Usually rate 150-200bpm
12. Which electrolyte metabolism disorders may lead to “Torsades de pointes”? (1)
• Hypokalemia
• Hypomagnesemia
• Hypocalcemia
13. What are possible clinical manifestations of ventricular tachycardia?* (2)

• Palpitations (ryhtmic)
• Dyspnoe, angina
• Presyncope: transitory dizziness, fatigue
• Syncope +- seizures, tongue biting, spontaneous urination or defecation
• Sudden cardiac death: unexpected circulatory arrest leading to death
within 1 hour from onset of symptoms
• Sudden cardiac arrest: unexpected circulatory arrest within 1 hour from
onset of symptoms; patient resuscitated with medical intervention
(defibrillation)
14. Why the ventricular tachycardia usually is more dangerous than supraventricular
tachycardia?* (0,5)
• Lack of rate limiting properties of AV node (abnormal impulses generated
in ventricle)
• Ventricles quiver uselessly  no effective blood pumping  decreased
cardiac output  decreased organs perfusion  risk of hypoxia/ischemia
and infarctions
• Drugs acting on AV node are ineffective in management
15. What kind of additional investigations can be performed to diagnose paroxysmal

ventricular tachycardia (in a patient without ventricular tachycardia on
examination)? (2)
• Holter
• Echo (for etiology)
• Blood biochemistry and electrolites (for etiology)
• Electrophysiologic studies:transesophageal (differential dx: SVT vs. VT),
intracardiac
• Implantable cardiac monitor REVEAL (if causes of symptoms unclear)
• Pharmacologic provocation tests
16. What is the first and primary method of treatment if the patient develops pulseless
ventricular tachycardia?* (1)
• CPR and immediate DC shock
17. What is the first and primary method of treatment if the patient develops
ventricular tachycardia with hemodynamic instability (acute left ventricular
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failure)?* (1)
• General anesthesia and DC shock (synchronized biphasic => 100J)
18. What is the first and primary method of treatment if patient develops ventricular
tachycardia without hemodynamic disorders (acute left ventricular failure)?* (1)
• Drug therapy iv:
A) Amiodaron (contraindicated in Torsades de pointes!)
▪ 300 mg i/v (or 5 mg/kg) bolus
▪ � repeated bolus 150 mg i/v
▪ � infusion + beta blocker
B) Lidocain i/v
▪ 1-1.5 mg/kg i/v bolus
▪ � repeated bolus 0.5-0.75 mg/kg (max. 3 mg/kg)
▪ � infusion 1-4 mg/min
19. Which drugs can be used to terminate paroxysm of ventricular tachycardia? (1)
Name the dose and type of usage! (1) (2 points)
• Amiodaron (contraindicated in Torsades de pointes!)
▪ 300 mg i/v (or 5 mg/kg) bolus
▪ � repeated bolus 150 mg i/v
▪ � infusion + beta blocker
• Lidocain i/v
▪ 1-1.5 mg/kg i/v bolus
▪ � repeated bolus 0.5-0.75 mg/kg (max. 3 mg/kg)
▪ � infusion 1-4 mg/min
• Second line agents:
o Magnesium i/v 1-2 g
o Procainamide 17 mg/kg slow infusion i/v
20. Which drugs can be used to stop the paroxysm of pirouette tachycardia
(“Torsades de pointes”)? (1)
• MgSO4 2 g IV over 1 to 2 min +- 2nd bolus in 5 to 10 min, and a
magnesium infusion of 3 to 20 mg/min.
• Lidocaine (shortens the QT interval) may be effective especially for drug-
induced torsades de pointes.
• Resistant cases: isoproterenol iv (try to increase HR to shorten QT)
21. Which medications are used in long-term ventricular tachycardia treatment

(prevention of new paroxysms)? (2)
• Amiodarone p.o. + B-Blocker
22. What are contemporary long-term treatment methods of ventricular tachycardia

(in order to avoid recurrent or primary paroxysm and prevent sudden death)? (2)
• ICD
• Treatment of the underlying disease and promoting factors:
revascularization, Tx of heart failure, avoidance of imbalance of
electrolites etc.
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23. What is bradycardia and what is severe bradycardia? (1)

• Bradycardia: HR<60bpm in adults
• Severe: HR so low to cause symptomatic hypoperfusion of organs
24. What are two main electrophysiological causes of bradycardia (the pathogenic
mechanisms)? (1)
• Depressed heart automaticity-disorders of SA node (Sick Sinus Syndrome)
• AV Conduction blocks
25. What are possible clinical manifestations of bradycardia?* (2)

• Dizziness
• Sudden transitory weakness
• Presynkope
• Syncope (with seizures)
• Morgagni-Adams-Stokes (MAS) syndrome /attacks
• Hypotension
• Compensatory resistant HT (if slow onset)
26. What is Morganji-Adams-Stokes attack? (1)

• Syncope-loss of consciousness +- anoxic seizures due to sharp decrease in
cardiac output and subsequent cerebral ischemia
27. Name four major manifestations of sick sinus node syndrome? (1)
• Sinus bradicardia (<40 bpm)
• Sinus arrest (pause, esp., >3s)
• Sinoatrial block (typically 2:1)
• Tachycardia-bradycardia syndrome
28. What degree of atrioventricular block may lead to unconsciousness? (1)

• Mobitz II second degree
• Complete AV block
29. What is vasovagal syncope (pathogenesis)? In which cases is it observed?

Describe the clinical manifestations! (2)
• Neurocardiogenic- Reflectory irritation of vagal nerve
o Reduced venous return (during manipulations, after prolonged
standing, in hypohydration,irritation of carotid sinus or
baroreceptors or A. Vertebralis)
o  strong left ventricular contraction
o  afferent signals from the left ventricle override the baroreceptor
responses, leading to an inappropriate decrease in sympathetic tone
and an increase in parasympathetic (vagal) tone. Paradoxically the
clinical picture is one of sudden hypotension reflecting diminished
sympathetic vasoconstrictor tone accompanied by vagally induced
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inappropriate bradycardia.
• Symptoms:
o Paradoxically sudden hypotension reflecting diminished
sympathetic vasoconstrictor tone
o Vagally induced inappropriate bradycardia.
30. What infectious diseases in Latvia can cause atrioventricular block? (1)
• Lyme disease
• Diphetria
• Aortic root abscess in infectious endocarditis
31. What medication overdose may cause severe bradycardia? (1)

• Digoxin
• B-blockers
• Ca Channel Blockers
• Amiodarone
• Clonidine
32. What is Frederick syndrome?

• Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative
disease caused by a defect in the gene encoding for the mitochondrial
protein frataxin.
• The cardiac involvement seen in FRDA is a consequence of mitochondrial
proliferation as well as the loss of contractile proteins and the subsequent
development of myocardial fibrosis.
• Manifestations include
o concentric or asymmetric hypertrophy (mostly)
o dilated cardiomyopathy (more rarely)
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o dilated cardiomyopathy and arrhythmia are associated with

mortality in patients with FRDA
33. Which methods can be used in bradycardia diagnostics (what kind of

investigations should be performed if there is a suspicion of transitory
bradycardia)? (2)
• Rest ECG
• Holter
• [Stress test?]
• Transesophageal electrophysiologic testing:
o Sinus node recovery time
o Venkebach’s point
• Tilt table test (for dg of vagal syncopes)
• REVEAL monitoring
34. Which methods can be used in sick sinus node syndrome diagnostics? (2)
• ECG
• Holter
• REVEAL
• Electrophysiological studies:
o SA node recovery time,
o SA conduction time
o SA and atrial tissue refractory periods
35. What is the first aid for a patient with vasovagal presyncope / syncope? (2)
• Remove promoting factor!
• Strong coughing
• Horizontal position; if possible – Trendelenburg’s position
• Fresh air, O2
• Saline rapidly 500 cc i/v (+/- colloids)
• Atropine i/v 0.5-1 mg (rarely up to 2-3 mg), if needed
• Usually trasitory and respond to therapy. In more severe cases add
dopamine as i/v infusion.
• Temporary pacing usually not necessary  if it is suspect other cause!
36. What is the first-line drug to treat severe acute bradycardia?* (1)
• Atropine 1mg iv (max 3mg)
37. What is the treatment algorithm in case of acute severe bradycardia?* (2)
• Acute bradycardia, unconscious
o CPR, O2
o Atropine 1 mg iv (max 3mg)
o Symopatomimetics iv infusion (dopamine, dobutamine, others…)
o Temoprary cardiac pacing: Transthoracic (short-term) =>
transvenous (up to ~1 week)
o Implantation of permanent pacemaker, if cause irreversible
• Acute bradycardia, haemodynamic instability
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o Management as above
o Transthoracic pacing if severe condition (rare; +analgesia or
sedation if patient is conscoius).
o First aid:
▪ horizontal posture, legs elevated (Trendelenburg’s position)
▪ strong coughing
38. Explain what does electrocardioversion (ECV) mean? What are the most common
indications for ECV? (1)
• Application of a selected amount of electric current by electrodes/paddles
to convert an abnormal cardiac ryhtm to sinus rhythm
• Most common indications:
o AFib
o Aflutter
o VT
39. Explain what does electrocardiostimulation (cardiac pacing) mean? What are the
most common indications for a pacemaker? (1)
• Device composed of a generator and one or more leads connecting the
generator to the heart and providing elelctrical impulses to stimulate
myocardial contraction
• Types of pacemakers:
o Implantable pulse generators with endocardial or myocardial
electrodes
o External, miniaturized, patient portable, battery-powered, pulse
generators with exteriorized electrodes for temporary transvenous
endocardial or transthoracic myocardial pacing
o Console battery or AC-powered cardioverters or monitors with
high-current external transcutaneous or low-current endocardial or
myocardial circuits for temporary pacing in asynchronous or
demand modes, with manual or triggered initiation of pacing
• Indications:
o Sick sinus syndrome
o Acquired AV block
o Chronic bifascicular block
o After acute phase of myocardial infarction
o Neurocardiogenic syncope and hypersensitive carotid sinus
syndrome
o Post cardiac transplantation
o Hypertrophic cardiomyopathy
o Pacing to detect and terminate tachycardia
o Cardiac resynchronization therapy in patients with severe systolic
heart failure
o Patients with congenital heart disease
40. What is the difference between electrocardiostimulation (pacemaker) and

electrocardioversion? (1)
4th & 6th course 2015/2016
• Cardioversion terminates arrhythmias such as, atrial fibrillation, atrial

flutter, atrioventricular nodal re-entrant tachycardia, atrioventricular re-
entrant tachycardia, or haemodynamically stable ventricular tachycardia,
by delivering a synchronised shock. By depolarising all excitable tissue of
the circuit and making the tissue refractory, the circuit is no longer able to
propagate or sustain re -entry. As a result, cardioversion terminates those
arrhythmias.
• Pacing: pacemaker performs two basic functions, pacing and sensing.
Pacing refers to depolarization of the atria or ventricles, resulting from an
impulse (typically 0.5 msec and 2 to 5 volts) delivered from the generator
down a lead to the heart. Sensing refers to detection by the generator of
intrinsic atrial or ventricular depolarization signals that are conducted up a
lead. Sensed events are used by the pacemaker logic to appropriately time
the pacing impulses.
41. What does ICD mean? Explain what it is and when it is used. (1)
• Implantable device able to perform defibrillation, cardioversion and
pacing of the heart
• Indications:
o Secondary prevention of sudden cardiac death (SCD) in patients
with prior sustained ventricular tachycardia (VT), ventricular
fibrillation (VF), or resuscitated SCD thought to be due to VT/VF
o Primary prevention of SCD in patients at increased risk of life-
threatening VT/VF
42. In which cases temporary pacemaker is used? (1) What kind of temporary
pacemakers do you know? (1) (2 points)
• Types:
o Temporary atrial
o Dual chamber pacing
o External cardiac defibrillator
o Transcutaneus
• Indications:
o Transient AV block
o Other arrhythmias complicating acute MI or cardiac surgery
o Rhythm maintenance in other situations of reversible bradycardia
(eg metabolic disturbances)
o Bridge to permanent pacing
43. What are possible electrode insertion sites of the temporary transvenous
pacemaker? Name three! (1)
• Internal jugular
• Subclavian
• Femoral vein
• External jugular
• Ante cubital-brachial
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44. What does permanent pacemaker implantation mean? How is it performed? (1)
• Device composed of a generator and one or more leads connecting the
generator to the heart and providing elelctrical impulses to stimulate
myocardial contraction, implanted permanently for long term rhythm
control.
• Steps:
o Cath lab, anesthesia (usually local)
o Transvenous access to the heart chambers, usually bysubclavian
vein, the cephalic vein (cut-down technique), or rarely the axillary
vein, the internal jugular vein or the femoral vein
o A small incision (3.8-5.1 cm) is made in the infraclavicular area
and a subcutaneous pocket is created, where the generator will be
implanted
o A guide wire is advanced and placed on the right atrium or the
vena caval area under fluoroscopy. A second guide wire can be
positioned, if necessary, via the same route either by a second
puncture or by a double-wire technique in which two guide wires
are inserted through the first sheath.
o A sheath and dilator are advanced, and when sheath is set in the
right place the guide wire and the dilator are retracted. Then the
lead is inserted into the sheath and advanced under fluoroscopy to
the appropriate heart chamber, where is attached to the
endocardium either passively with tines or actively via screw-in
leads.
o When leads are securely placed, then the sheath is removed.
o Specifics tests for sensing and pacing are held.
o Occasionally, PM can be implanted surgically via a thoracotomy,
and the generator is placed in the abdominal area
45. What is the characteristic of ECG finding in a patient with permanent ventricular
pacemaker? (1)
• Preserved AV synchronicity
• Ventricular rate increase with sinus node
• Lower prevalence of arryhtmia
• Ventricular pacing triggererd by a sensed sinus P wave/inhibited by a
sensed spontaneous QRS
• “Demand” pacing  pacing spike seen only if intrinsic HR below
threshold  capture
• Fusion beat union of native depolarisation and pacemaker impulse
• Capture beats  return of atrial control over ventricular conduction
following a period of AV dissociation
• Pseudofusion  pacemaker impulse occurs just after cardiac
depolarisation  ineffective  distant QRS morphology
46. What does DDD mode of pacemaker mean? (1)
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• Universal/fully automatic:
o Pace: atrium + ventricle
o Sense: atrium+ ventricle
o Response: inhibited/ triggered
47. What does VVI mode of pacemaker mean? (1)
• Synchronous:
o Pacing: ventricular
o Sensing: ventricular
o Response: inhibit to sensed
48. What does AAI mode of pacemaker mean? (1)
• Synchronous:
o Pacing: atria
o Sense: atria
o Response: inhibit to sensed P
49. Emergency algorithm in case of cardiac arrest, if the mechanism is VT/VF?* (2)
See picture for 49-51
50. Emergency algorithm in case of cardiac arrest, if the mechanism is asystole?* (2)
51. Emergency algorithm in case of cardiac arrest, if the mechanism is pulseless
electrical activity (electromechanical dissociation)?* (2)
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52. What are the most common causes of pulseless electrical activity
(electromechanical dissociation)? (1)
• Hypovolemia
• Hypoxia
• Acidosis
• Hyper/hypokalemia
• Hypoglycaemia
• Hypothermia
• Cardiac tamponade
• Tension pnrumothorax
• Thrombosis  MI, TE
• Tachycardia
• Traumas blood loss-hypovolemia
• Drugs-toxicity-overdose
53.
54. Patient, 68 years old male, complaining of frequent dizziness, had lost
consciousness three times, once in a lying position. Pulse was not counted. He is
hospitalized after another episode of unconsciousness. Objective findings: general
condition is severe, the patient is conscious, but not alert, reply to the questions
with difficulties. Skin pale, dry, cool. Heart rate rhythmic, 28 beats per minute,
murmurs are not auscultated. BP=80/40 mmHg. ECG finding: P waves with
frequency 70 times per minute and QRS complexes with frequency 28 times per
minute. Formulate primary clinical diagnosis! (1) Tactics of emergency
treatment? (1) What kind of tests should be performed? (1) What will be the
treatment strategy for this patient if the transitory causes are not found? (1)
(4 points)
55. Patient, 70 years old female, with permanent atrial fibrillation, regularly uses
metoprolol and digoxin. She is hospitalized after unconsciousness episodes.
Patient is conscious on admittance, but with delayed mental status. Heart rate
rhythmic, 32 beats per minute, murmurs are not auscultated. BP=85/60 mmHg.
What is the primary clinical diagnosis? (1) Tactics of emergency treatment? (1)
Tactics of investigations (1) and further treatment (1)? (4 points)
56. Patient, 35 years old, who had a weakness when the nurse took blood sample from
the vein for analysis. He has nausea. Objective findings: skin pale-gray, clammy,
patient sits sweaty, not alert. Heart rate rhythmic, 34 beats per minute, murmurs
are not auscultated. BP=70/40 mmHg. What is the primary clinical diagnosis? (1)
Tactics of emergency treatment? (2) (3 points)
57. Patient, 56 years old, who had Q-myocardial infarction in left ventricular anterior
wall three months ago. He was regularly taking aspirin, atorvastatin, perindopril
and bisoprolol. Patient is hospitalized with shortness of breath, which started two
hours before and gradually increased. No chest pain. At the time of admission the
general condition is severe – severe dyspnoe, the patient is reclining, tachypnoe
28 times per minute; on lung auscultation - vesicular breathing, and bilateral basal
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rales. BP=90/60 mmHg. Heart rate rhythmic, 180 times per minute, murmurs are
not auscultated. ECG finding: wide-QRS complex tachycardia 180x '(QRS 0.16 s,
V1-6 concordance). Formulate the primary clinical diagnosis! (1) Tactics of
emergency treatment? (1) What kind of tests should be performed? (1) What is
the long-term treatment strategy for this patient? (1) (4 points)
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Valvular heart disease.
1. Please name the types of echocardiography! (1) Describe the essence of them! (1) (2
points)
Main role of echocardiography: Size of the heart chambers, ventricle function, valvular function
and pericardium
Transthoracic (TTE)
• The most common type
• Non-invasive  the transducer is placed on the chest
Transesophageal (TEE)
• Clearer pictures of the upper chambers, the valves between the atria and ventricle
and to visualize the aorta better
• Invasive  transducer is attached to a thin tube that passes through the mouth and
down the throat to the esophagus
Intracardiac
• Passed through the femoral vein to the heart
• ICE largely replaced TEE for ..
Fetal
• Used to check the for congenital heart problems
• Usually done 18 – 22nd week of pregnancy
Stress echocardiography
• Exercise or medication induced (dobutamine)
• Echo performed before and after the exercise/medication injection
• Diagnose CHD, aortic stenosis, LV dysfunction
Contrast echocardiography
• Used for improving echocardiographic resolution and providing real time
assessment of intracardiac blood flow
• Uses agitated saline contrast provides contrast in the right hear and enables
detection of right to left shunts
2. Please name the indications of transthoracic echocardiography! (2)
TTE indications
• Assessment of LV function
• Diagnosis/quantification of severity of valve disease
• Identification of vegetation in endocarditis
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• Identification of structural heart diseases  cardiomyopathies, congenital

• Detection of pericardial effusions
• Intracardiac thrombus in systemic circulation
3. What are the advantages of transesophageal echocardiography compared to

transthoracic echocardiography? (1)
• Transthoracic sometimes produces poor images especially in obesity, thick chest

wall, obstructive airways disease
• Some structures difficult to visualize in TTE
o LA appendage
o Pulmonary veins
o Thoracic artery
o Interatrial septum
• TOE
o Positioned immediately behind the LA
o Produces high resolution images
o Investigating
▪ Prosthetic valve dysfunction  especially mitral
▪ Congenital abnormalities  ASD
▪ Aortic dissection
▪ Infective endocarditis  vegetations which are too small to be detected by
TTE
▪ Systemic embolism
4. Which parameters can be evaluated on transthoracic echocardiography? (2)
• Heart structure and function  valve stenosis

• LV wall thickness, ejection fraction
• Pericardial effusion
5. What is vena contracta? How is it measured? In what valvular pathology evaluation

is it used? (1)
Definition
• Point in a fluid stream where the diameter of the stream is the
least, and fluid velocity is at its maximum
• Area of the jet as it leaves the regurgitant orifice; it reflects thus
the regurgitant orifice area
• Used for AR and MR severity assessment
6. Explain facies mitralis! (1)
• Distinctive facial expression associated with mitral stenosis

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• Malar flush on the cheeks (due to vasodilation)  rosy cheeks

• Peripheral cyanosis  bluish tinge on the lips
• Low cardiac output  peripheral cyanosis often in lips, tip of nose and cheeks
7. Explain cor bovinum! (1)
• Dilation of both atriums and ventricles due to hypertrophy of the LV due to

volume overload
• Causes
o Tertiary syphilis  syphilitic aortitis
o Chronic aortic regurgitation
o Hypertension
o Ischemic heart disease
8. What parameters are used to evaluate grade

of aortic stenosis? (1)
• Echocardiography is the main method to

asses AS severity
o Peak velocity
o Mean pressure gradient
o Aortic valve area (AVA)
• The table is from the European Society
of Cardiology (ESC)
9. Define valvuloplasty! In which cases is it performed? Define balloon valvuloplasty!

In which cases is it performed? (2 points)
• A surgical procedure to open a narrow heart valve by using a thin catheter with a
balloon on the tip and then inflating the balloon which expands the opening of the valves
the separates the leaflets, the balloon is then deflated and removed
• Used in
o Repair of stenotic aortic valve
o Correction of an uncomplicated mitral valve
o Congenital pulmonary stenosis
10. What are the most common causes of aortic stenosis? (1)
• Middle-aged to elderly
o Senile calcification: Thickening of aortic valve structures by fibrosis and
calcification, degeneration of the aortic leaflets
o Rheumatic fever
• Congenital defects of the valve
o Bicuspid aortic valve (predispose to develop AS)
o Subvalvular or supravalvular stenosis (congenital membrane or fibrous ring just
beneath the aortic valve- uncommon)
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11. Explain bicuspid aortic valve! What pathologies can it lead to? (1)
• Inherited form of heart disease in which two of the leaflets fuse resulting in a two-
leaflet valve instead of tricuspid
• Complications
o Calcification  leading to AS or if leaflets don’t close properly AR
o Aortic lesions which are associated with aortic aneurysmal lesions
o Aortic narrowing  AS
o Coarctation of aorta has also been associated with bicuspid aortic valve
12. Describe the pathophysiologic changes in the case of aortic stenosis! What are
characteristic changes of left ventricle ? (1)
Increase of the LV load (LV outflow obstruction)  LV hypertrophy (concentric)  impaired

relaxation  diastolic dysfunction  overload  LV dilatation and systolic dysfunction (low
EF)  LV failure
13. Name 3 main symptoms of aortic stenosis! (1)
SAD:
• Syncope (exertional, nonexertional)
• Angina
• Dyspnea (heart failure)
14. Describe auscultative finding in patient with aortic stenosis!(1)
Auscultation on aortic valve or Erb’s point:

• Systolic (mesosystolic), harsh crescendo-decrescendo
• Late systolic ejection murmur
• Radiates to the right clavicle and both carotids (sin>dx)
• Soft S2
• S4 best heard at the apex
• Early systolic ejection click
• In elderly patients murmur is musical and better auscultated on ictus cordis
• Gallavardin’s phenomen – the highest frequency component irradiates most to the apex
and reminds the murmur of mitral regurgitation
15. What other pathology can cause murmur resembling aortic stenosis? (1)
• Hypertrophic cardiomyopathy
• Sub or supravalvular stenosis
• Bicuspid aortic valve
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16. What pulse is characteristic in patient with aortic stenosis? (1)
• Pulsus parvus et tardus (reduced in amplitude and delayed compared with LV

contraction, low pulse pressure, slowly increasing and decreasing)
• Systolic thrill that radiated to the left
17. What changes in ECG can be observed in patient with aortic stenosis? Why? (1)
• Left axis deviation due to left ventricle hypertrophy and overload
18. What echocardiographic finding indicate severe aortic stenosis? (1)
• Severe stenosis: aortic valve area  1.0 cm2
19. Name criteria for surgical therapy of aortic stenosis! (1)
• Symptomatic
• LV dysfunction
• Asymptomatic + worsening ECG + severe AS
20. Explain TAVI. When is it performed? (1)
• Transcatheter aortic valve implantation (old, damaged valve NOT removed)

• Minimally invasive surgical procedure where a balloon catheter equipped with a
replacement valve is inserted at transfemoral/transapical site then guided to aortic valve
 the balloon catheter inflates to expand the replacement valve into the aortic valve’s
space
• It is performed for symptomatic AS patients who are considered an intermediate
or high-risk patient for standard valve replacement surgery
21. Which cases balloon valvuloplasty is performed in aortic stenosis? (1)
• In very young patients

• Aortic rheumatic valve diseases
• As a "bridge" to surgery in hemodynamically unstable patients who are at high
risk for aortic valve replacement
• Use for palliation in patients with serious comorbid conditions that prevent
performance of aortic valve replacement
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22. What medical therapy can be used in case of heart failure due to aortic stenosis?
What medication and why should be avoided or used with maximal precaution? (1)
• Medical treatment is limited to symptomatic patients with AS who are not

candidates for surgery
• In patients with pulmonary congestion cautious use of digoxin, diuretics (loop),
ACEi might be attempted
• Beta-blockers might be used if the predominant symptoms is angina
“The patient with severe aortic stenosis is relatively "afterload fixed and preload
dependent" -- meaning cardiac output does not increase with after-load reduction. Thus
all afterload reducing agents (angiotensin-converting enzyme inhibitors, calcium
channel blockers blockers) are contraindicated. However, in patients with mild to
moderate aortic stenosis vasodilators such as hydralazine can increase cardiac output.
Nitrates and diuretics can be used to treat angina and congestion, but with great care,
as they may provoke a decrease in cardiac output.”
23. Please name the most common causes of aortic regurgitation (1) and separately
specify those that can cause acute aortic regurgitation (1)! (2 points)
Most common:
• Idiopathic degeneration of the aortic valve, root or ascending aorta
• Rheumatic fever
• Infective endocarditis (acute or chronic AR)
• Bicuspid or fenestrated aortic valve (2% of men and 1 % of women)
• Severe arterial hypertension (diastolic BP 110 mmHg)
Acute:
• Infective endocarditis
• Trauma
• Dissection of the ascending aorta
24. What are the pathophysiologic changes in the case of aortic regurgitation? (1)
• LV receives aortic blood regurgitated in diastole (in addition to blood from the
pulmonary veins and left atrium) → LV overload → LV eccentric hypertrophy,
dilatation, systolic dysfunction (EF is normal for a long time)
• Pulse pressure increases because of decreasing of diastolic pressure (sinus carotis
baroreflex and backflow)
25. Please describe the complaints of a patient with severe aortic regurgitation! (1)
• (Often asymptomatic )
4th & 6th course 2015/2016
• Progressive exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea

• Palpitations
• Angina
• Non-coronary chest pain
• Vertigo
26. Describe auscultative finding in patient with aortic regurgitation! (1)
• S3
• Protodiastolic murmur (pandiastolic in severe AR)
o Decrescendo, best heard when the patient is leaning forward with breath held at
end-expiration
o Heard near the axilla or mid left thorax
o Increases in volume in response to maneuvers that increase afterload (squatting,
handgrip)
• Aortic ejection murmur
• Ejection click after S1
• Austin-Flint murmur
o mimics the diastolic murmur of mitral stenosis (relative mitral stenosis)
o results from rapid regurgitant flow into the LV, causing mitral valve leaflet
vibration at the peak of atrial flow
o heard over ictus cordis
• Femoral artery auscultation
o Traube’s sign – sharp sound heard over the femoral pulse (pistol-shot sound)
o Duroziez’s murmur - femoral systolic bruit distal and a diastolic bruit proximal to
arterial compression
27. Please name objective signs (excluding heart auscultation) which correspond to
aortic regurgitation? (1)
• Pale skin
• Corrigan’s sign – pulsation of the carotid arteries
• Becker’s sign - pulsation of the retinal arteries
• Rosenbach’s sign - pulsation of the liver
• Gerhard’s sign – pulsation of the spleen
• de Musset, Musset’s sign - head bobbing
• Quincke’s sign – pulsation of the fingernail capillaries, best seen with slight pressure - or
uvula (Muller’s sign)
• “Homo pulsans”
28. Please describe the pulse in the case of aortic regurgitation! * (0.5)
• Pulsus celer et altus – large-volume pulse with rapid rise and fall
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29. Please describe the characteristics of arterial blood pressure in the case of severe
aortic regurgitation! (0.5)
• Decreased diastolic pressure

• Increased systolic pressure
• Increased pulse pressure
30. Describe echocardiographic finding in severe aortic regurgitation. (1)
• Color Doppler evaluation

• Regurgitant jet through the aortic valve
• Gradation I-IV
• LV dilation
• LV wall thickness
• EF
• Dilation of the ascending aorta
31. Name indications for surgical therapy in case of severe aortic regurgitation. (1)
• Symptomatic severe AR
• Asymptomatic chronic severe AR and left ventricular EF < 50%
• Severe AR when undergoing other cardiac surgery
• Asymptomatic severe AR with normal LVEF (≥50%) but with severe LV dilation
(LVESD >50mm)
32. What medical therapy can be used in case of heart failure due to aortic
regurgitation? (1)
Dobutamine
• Augment cardiac output
• Shorten diastole
Sodium nitroprusside
• Reduce afterload in hypertensive patients
Vasodilation therapy
• Reduces wall stress and thereby improves
LV ejection fraction
33. What are the most common causes of mitral

stenosis? (1)
4th & 6th course 2015/2016
• Rheumatic fever
• Less common – congenital MS
• Atrial myxoma
• SLE
• Malignant carcinoid syndrome with an atrial right-to-left shunt.
34. Please name the pathophysiologic changes in the case of mitral stenosis! (1)
• LA dilation (atriomegaly) → increase of pulmonary venous and capillary pressures →

may cause secondary pulmonary hypertension → right ventricular heart failure and
tricuspid and pulmonic regurgitation
• LV dysfunction – rare (~25%)
• Pulmonic complications:
o PATE (due to RV failure), lung infarction
o chronic bronchitis
o pneumonias - lung fibrosis
35. What are the clinical complaints of patient with mitral stenosis? (1)
• Typically, don’t appear until 15 to 49 years after an episode of rheumatic fever

• Symptoms of HF
o Exertional dyspnea
o Orthopnea
o Paroxysmal nocturnal dyspnea
o Fatigue
• Paroxysmal or chronic atrial fibrillation – exacerbates existing diastolic
dysfunction, precipitating pulmonary edema and acute dyspnea when ventricular rate is
poorly controlled
• AF also cause palpitations, in up to 15 % of un-anticoagulated patients causes
systemic embolism with symptoms of stroke or leg ischemia
• Hemoptysis
• Diminishing of symptoms, when LV failure develops and/or TR appears.
36. Describe auscultative finding in patient with mitral stenosis! (1)
• Loud S1 – caused by leaflets of a stenotic mitral valve closing abruptly (M1), best heard
at the apex
• Normally split S2 with an exaggerated P2 – due to pulmonary hypertension
• Early diastolic opening snap – as the leaflets billow into the left ventricle, which is
loudest close to left lower sternal border
• Low-pitched decrescendo-crescendo rumbling diastolic murmur – heard best with the
bell of the stethoscope at the apex (or over the palpable apex beat) at end-expiration when
the patient is in the left lateral decubitus position
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• Protodiastolic decrescendo
• Presystolic crescendo
• Graham-Steell’s murmur – soft decrescendo diastolic murmur heard best along the left
sternal border and caused by pulmonic regurgitation secondary to severe pulmonary
hypertension
37. What are most common complications of mitral stenosis? Name at least 3 ! (1)
• Atrial fibrillation  thromboembolic events

• Pulmonary hypertension and edema
• Congestive heart failure
• Enlarged LA (rare)  esophageal compression, recurrent laryngeal nerve palsy
38. What echocardiographic parameters are used to evaluate indications for surgical or
percuteneous intervention in case of mitral stenosis? (2)
• Diagnostic  extent of restriction

o Signification stenosis if valve orifice < 1.0 cm2
• RV hypertrophy
• LA enlargement
• Valve morphology
39. Explain percutaneous mitral

commisurotomy! How and in
what cases is it performed? (2)
4th & 6th course 2015/2016
40. Please name the most common causes of mitral regurgitation (1) and separately
specify those that can cause acute mitral regurgitation (1)! (2 points)
Acute:
• Endocarditis
• Rupture/dysfunction of papillary muscles (ischemia or myocardial infarction
• Mitral valve prolapse
Organic:
• Myxomatous degeneration
• Ischemic papillary muscle dysfunction (ischemia or myocardial infarction)
• Rheumatic fever
• Horda’s rupture
• Calcification of the mitral annulus (mainly in elderly women)
• Mitral valve prolapse
• Colagenoses
• Congenital endocardial cushion defect with a cleft anterior leaflet
Relative (most common!): LV enlargement of any cause
41. What is the difference between primary and secondary mitral regurgitation? Name
examples for both! (1)
Primary
• Usually caused by an anatomic defect of one or more structures comprising the mitral
valve apparatus – the annulus, leaflets, chordae tendineae and papillary muscles
• Genetic or idiopathic cause, also known as degenerative
• Myxomatous degeneration (90%)
• Rheumatic, infective endocarditis
Secondary
• Also known as functional MR
• Results from LV dysfunction and dilation, which
causes otherwise normal valve components to fail
and result in MR
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• Coronary artery disease , dilated cardiomyopathy and left-sided heart failure
42. Describe myxomatous degeneration ! What is the etiology ? (1)
• Connective tissue disorder characterized by thickening and elongation of the

mitral leaflets and chordae and by dilatation of the mitral annulus
o Pathologic increase in the deposition of glycosaminoglycans in tissue
o Can be caused by Marfan syndrome, Ehlers-Danlos syndrome
• The elongation and stretching of the leaflets and chordeae tendinae prevents the
valves of fully coming together when the valves close  leaflets prolapse into LA
• Most common cause of mitral valve prolapse
43. What is mitral valve prolapse and corresponding auscultative finding? (1)
• Caused by structural defect of the mitral valve that results in mitral leaflets
bulging into the left atrium during systole
• Most commonly caused by myxomatous degeneration
• Complications include mitral regurgitation, endocarditis, valve rupture and
possibly thromboembolism
• On auscultation
o Mitral valve prolapse click: high-frequency mid-systolic click followed by a late
systolic murmur which may radiate to axilla
o If severe MR, S3 may be heard
44. Describe auscultative finding in patient with mitral regurgitation! (1)
• Holosystolic murmur best heard at the apex when patient is in lying position
o Radiates to the left axilla
o Decreases in intensity with standing or Valsalva maneuver
o May be confused with TR murmur (TR is augmented during inspiration)
• S1 may be soft or absent (if valve leaflets are rigid, eg, in combined MS and MR due to
rheumatic fever)
• S2 widely split unless severe pulmonary hypertension has developed
• S3 loud at the apex in proportion to the degree of MR (reflects a greatly dilated LV)
• S4 characteristic of recent ruptured chordae (when LV has not enough time to dilate).
45. Describe pathophysiologic changes in the case of mitral regurgitation! (1)
• Regurgitant jet from LV to the left atrium

o → LA enlargement
o → congestion in LA and lungs
o → right ventricle failure
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• Compensatory LV enlargement and hypertrophy, which initially compensate for

regurgitant flow (preserving forward stroke volume) → eventually decompensates
(reducing forward stroke volume)
• Complications of chronic MR: atrial fibrillation and thromboembolism, infective
endocarditis
46. Describe symptoms characteristic to mitral insufficiency! (1)
• Asymptomatic for a long time, signs develop only when MR becomes moderate to
severe
• First symptoms
o Palpitations, atrial fibrillation
o Exertional dyspnea (HF symptom)
o Orthopnea – severe MR
o Right ventricle failure signs (severe MR)
47. What kind of ECG changes can be observed in the case of mitral regurgitation? (1)
• Atrial fibrillation
• Left cardiac hypertrophy and P mitrale
• Later, signs of right heart strain with P pulmonale
48. Describe echocardiographic finding in case of mitral regurgitation! (1)
• Doppler Echo – regurgitant jet to LA

• Gradation – I-IV
• Dilation of LA
• Possible cause – calcification, vegetations, papillary muscle rupture
49. Name the most common etiology of tricuspidal regurgitation! (1)
Functional/secondary
• RV dilatation due to chronic left HF
• Right ventricular infarction
• Pulmonary hypertension
Primary
• Rheumatic heart disease
• Endocarditis
• Congenital
o ASD
o Ebstein’s congenital anomaly
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50. What physical signs point to tricuspidal regurgitation? (1)
• Asymptomatic or vague weakness and fatigue

• Elevated JVP
• Pansystolic murmur  lower sternal edge on inspiration
• Pulsatile hepatomegaly
• Jaundice
• Ascites
51. What are mechanical prosthesis and bioprosthesis? Name advantages and
disadvantages. Name principles of choosing prosthesis type in cardiac surgery! (2)
Mechanical
• Made on non-biological material
(pyrolytic carbon, polymeric silicone substance,
titanium)
• Preferred in young patients who have a
life expectancy >10-15 years
• Disadvantage: Require long-tern
anticoagulant therapy eg. warfarin
Bioprosthesis
• Made from animals, most commonly
porcine
o Some risks associated with this xenograft
such as the human body’s tendency to
reject foreign material
• The more common type utilizes biological tissue to make leaflets that are sewn
into metal frame
o From the pericardial sac of cows or horses  extremely durable physical property
• No need for the patient to take anticoagulants
• Disadvantage: don’t last more than 10-15 years  used in elderly who can’t take
long-term anticoagulant therapy
Prosthetic heart valve
Mechanical prosthetic valve Biological prosthetic valve

Pros • Valve has a long lifespan • Anticoagulation only necessary
for 3 months post operation
Cons • Life-long anticoagulation • Short lifespan due
necessary (warfarin, aspirin) to sclerotic degeneration
• May need to be
replaced every ten years
Indications
• Younger patients • Older patients
4th & 6th course 2015/2016
Prosthetic heart valve
Mechanical prosthetic valve Biological prosthetic valve
• Previously anticoagulated patients (e.g.,

• Patients with a high risk of
with pre-existing atrial fibrillation) bleeding
• Women with a desire to have
children
52. What anticoagulation therapy is indicated after implantation of mechanic

prosthesis? Is any monitoring needed, if yes, specify! What are target parameters of
anticoagulation therapy? (1)
• Anticoagulants used are vitamin K antagonists (VKA, generally for long-term)

and heparin (mainly unfractionated or low molecular weight heparin; generally for short-
term bridging therapy)
• INR goal for mechanical AORTIC valves 2.5 (2.0 – 3.0)
• INR goal for mechanical MITRAL valves 3.0 (2.5 – 3.5)
53. In which case will you think about prosthetic valve dysfunction (patient’s
complaints, physical examination)? (1) Which investigations should be performed to
prove it? (1) (2 points)
• Mechanical valve thrombosis signs may include muffled mechanical heart sounds,
a new murmur, dyspnea, heart failure and cardiogenic shock
• Thrombosis of right-sided valves causes right-sided heart failure, characterized by
swelling of the legs, abdomen or both, without pulmonary congestion
• Diagnosis to differentiate also from pannus formation
o TTE
o TEE
o If inadequate TTE/TEE then cardiac CT
54. In which cases patients with valvular heart disease should undergo cardiac
cathetherization? (1)
• Done in case there are discrepant clinical and echo findings

• Clinical findings not consistent with Doppler  further hemodynamic assessment
• Coronary angiography before aortic valve replacement in patients at risk for CAD
• Assessment of severity of AS in symptomatic patients when
o Aortic valve replacement is planned
o Non-invasive tests are inconclusive
o Discrepancy exists in the clinical findings regarding the severity of AS or the need
of surgery
• With infusion of dobutamine it can be useful for evaluation of patients with low-
flow AS and LV dysfunction
4th & 6th course 2015/2016
4th and 6th course 2015/2016
Supraventricular tachycardias.
1. How can you differentiate atrial fibrillation from extrasystoles (premature

beats) only by anamnestic data (patients complaints)? (1)
AF = Irregular pulse, dyspnea, orthopnea, lower limb oedema, fatigue, angor,

acute limb ischemia
Premature beats = skipped beat felt by the patient
2. How will the pulse differ (palpatory) in case of atrial fibrillation and sinus
rhythm?* (1)
Irregular pulse in case of AF

Presence of pulse deficit in case of AF
3. How is it possible to differentiate sinus rhythm and atrial fibrillation on

auscultation?* (1)
AF = irregular rhythm, pulse deficit present

Sinus rhythm = regular rhythm
4. How atrial fibrillation can be differentiated from extrasystoles (premature

beats) by pulse palpation?* (1)
Premature beats = Occasionally irregular pulse

AF = Irregularly irregular pulse
5. What are the patient’s complains in case of atrial fibrillation paroxysm? (1)
Heart palpitations, shortness of breath, chest pain, weakness, dizziness
6. Describe ECG signs of a supraventricular premature beat! * (0,5)
P wave absent or abnormal

Narrow QRS complex similar as preivous QRS complexes
Altered PR intervals in the premature beat
Compensatory pause felt by the patient
7. Explain „re-entry”! Which arrhythmias are based on this mechanism?
Reentry is continuous circulating electricity in which an impulse reenters and

repetitively excites a region of the heart such as AF (micro-reentry) or AFlutter
(macro-re-entrant) or AV node re-entry
8. Is it possible to differentiate supraventricular extrasystole and ventricular

extrasystol by electrocardiography and clinical data? How (explain from the
clinical and ECG point of view)? (1)
Yes
30
VPBs = wide QRS, altered PR intervals, if looks like LBBB  Comes from right
ventricule
If looks like RBBB  Comes from left ventricule
Symptoms = skipped beatm lightheadedness, dizziness
SVPBs = narrow QRS of same morphology, altered PR intervals, P wave absent

or abnormal
Followed by compensatory pause
Asymptomatic
9. What is the difference between paroxysmal and persistent atrial fibrillation?

(1)
Paroxysmal AF = terminates within 7 days of onset either following treatment or

spontaneously
Persistent AF = Continuous AF for > 7 days and no self termination
10. What is the difference between persistent and permanent atrial fibrillation? (1)
Persistent = ECV or drugs can be used to reduced the AF

Permanent = If ECV or drugs failed (at least 2 times) or hasn’t been planned due
to patient condition
11. What is considered tachy-, normo-, bradysistolic atrial fibrillation? (1)
Tachy-, normo-, bradysystolic

(>100, 60-100, <60)
12. Name 5 most common supraventricular tachycardias! * (1)
Sinus tachycardia
Atrial fibrillation
Atrial flutter
WPW syndrome
AV nodal re-entry tachycardia
13. What are clinical and ECG signs of atrial fibrillation? (1)
No P waves
Irregular RR intervals
“f waves”
For at least 30s
Irregular HR: 120-180bpm
Better seen in II, III, aVF
14. What are clinical and ECG signs of atrial flutter? (1)
Regularity of RR intervals
“sawtooth” waveform “F waves”
Atrial rate = 300bpm
Conduction ratio  2:1
31
15. What is the tipical ventricular (and pulse) rate in patient with atrial flutter with
2:1 conduction ratio? (1)
150bpm
16. What are clinical and ECG signs of sinus tachycardia?
Sinus P waves
Similar PQ intervals
P waves positives
Rate about 130-140bpm
17. What is Frederick’s syndrome? (1)
Complet III degree AV block with atrial flutter / atrial fibrillation
18. Which endocrine disease is the most frequent cause of atrial fibrillation? (1)
Hyperthyroidism
19. What is pulse deficiency? (1)
The pulse deficit (difference between heart beats and pulsations at the periphery)
is determined by simultaneous palpation at the radial artery and auscultation at the
PMI, near the heart apex. It may be present in case of premature beats or atrial
fibrillation.
20. What additional examinations (laboratory and instrumental) are required if

paroxysmal atrial fibrillation is suspected? (2)
Rest ECG
T3, T4, TSH, ionogram (K+) +++
Renal function and renal clearance (for NOAC use)
24h Holter monitoring
Transthoracic Echo-Doppler
CBC, INR, Hemostasis (PT, aPTT)
21. What are the tipical clinical signs of AV re-entry tachycardia? (2)
Palpitations, dizziness, chest pain, dyspnea, syncopes

Urinary urgency
22. What age is typical for manifestation of AV re-entry tachycardia and WPW
syndrome tachycardia paroxysms? (0.5)
AVNRT = 32 +/- 18 years

WPW = 23 +/- 14 years
23. What age is typical for manifestation of atrial fibrillation and atrial flutter
paroxysms? (0.5)
32
>80 yo
24. What is WPW syndrome? Explain pathogenesis, clinical and ECG signs! (2)
Individuals with WPW have an accessory pathway that communicates between

the atria and the ventricles, in addition to the AV node. This accessory pathway
does not share the rate-slowing properties of the AV node, and may conduct
electrical activity at a significantly higher rate than the AV node. For instance, if
an individual had an atrial rate of 300 beats per minute, the accessory bundle may
conduct all the electrical impulses from the atria to the ventricles, causing the
ventricles to contract at 300 beats per minute. Extremely rapid heart rates such as
this may result in hemodynamic instability or cardiogenic shock. In some cases,
the combination of an accessory pathway and abnormal heart rhythms can trigger
ventricular fibrillation, a leading cause of sudden cardiac death.
Symptoms:
Palpitations, dizziness, chest pain, dyspnea, syncopes
Urinary urgency
ECG:
Shorter PR interval
Wide QRS complex
A delta wave, which is a slurred upstroke in the QRS complex
Discordant T, ST segment changes in V1-V4
25. What are typical ECG findings in case of WPW syndrome in a patient with
sinus rhythm? (1)
Shorter PR interval
Wide QRS complex
A delta wave, which is a slurred upstroke in the QRS complex
Discordant T, ST segment changes in V1-V4
26. Why is atrial fibrillation dangerous for a patient with WPW syndrome? (1)
Can lead to Ventricular fibrillation, a leading cause of sudden cardiac death
27. What is tachycardia-bradycardia syndrome? Explain mechanism and clinical

signs! (1)
Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome (caused by

a functional defect of the sinus node, the primary pacemaker of the heart) in which
slow and fast arrhythmias alternate
Symptoms:
Palpitations
Dyspnea
Angina pectoris
+ symptoms of bradycardia (Adams-Stokes attacks, dizziness)
33
28. What is holter monitoring? How is it performed? (0.5)
Ambulatory ECG device for cardiac monitoring for at least 24 to 48 hours (often
for two weeks at a time)
Its extended recording period is sometimes useful for observing occasional
cardiac arrhythmias which would be difficult to identify in a shorter period
The Holter monitor records electrical signals from the heart via a series of
electrodes attached to the chest. Electrodes are placed over bones to minimize
artifacts from muscular activity. The number and position of electrodes varies by
model, but most Holter monitors employ between three and eight. These
electrodes are connected to a small piece of equipment that is attached to the
patient's belt or hung around the neck, keeping a log of the heart's electrical
activity throughout the recording period.
29. Describe vagal meneuvers! (1.5) Which tachycardias can be discontinued with
these maneuvers? (1.5) (3 points)
Stimulation of carotid sinus triggers baroreceptor reflex and increases vagal tone,
affecting SA and AV nodes
SVTs can be discontinued by Vagal maneuver

The 2015 American College of Cardiology/American Heart Association/Heart
Rhythm Society guidelines recommend vagal maneuvers for acute treatment of
supraventricular tachycardia of unknown mechanism, for treatment of
atrioventricular reentrant tachycardia, and for treatment of atrioventricular nodal
reentrant tachycardia
30. Which drugs are contraindicated for patient with WPW syndrome (especially
during atrial fibrillation)? (2)
AV nodal blocking agents (Adenosise, verapamil, beta-blockers, digoxin,

amiodarone)
31. Which drugs can be used to bradicardize tachysystolic atrial fibrillation in a

patient with WPW? (2)
Procainamide, amiodarone
32. Which drugs can be used to stop AV re-entry tachycardia? (2)
34
i/v adenosine (5-6mg, don’t dilute rapidly)
i/v propranolol, metoprolol, esmolol (beta-blockers)
i/v verapamil diltiazem (CCB)
Digoxin (not in WPW)
Amiodarone, flecainide, ibutilid
33. Which drugs can be used to stop WPW re-entry tachycardia? (2)
Procainamide, sotalol, amiodarone (DRUGS OF CHOICE)

Adenosine, diltiazem, verapamil, other calcium channel blockers, and beta
blockers can also be used
34. Which non-pharmacological methods can be used to stop atrial flutter? (2)
Catheter ablation
Electric cardioversion
Transoesophageal over pacing
35. Which supraventricular tachycardias can be stopped with i/v β receptor

blocker (metoprolol) (2) ?
Sinus tachycardia, AFib, Atrial flutter, Narrow complex SV re-entry tachycardia
36. Which supraventricular tachycardias can be stopped with i/v digoxin? (2)
AFib, Atrial flutter, AVNRT, orthodromic AVRT
37. Which supraventricular tachycardias can be stopped with i/v adenosine? (2)
PSVT (AVNRT, orthodromic AVRT)
38. Which supraventricular tachycardias can be stopped with i/v verapamil? (2)
Sinus tachycardia, AFib, Atrial Flutter, AVNRT, orthodromic AVRT
39. Which supraventricular tachycardias can be stopped with i/v amiodarone? (2)
Broad complex SV re-entry tachycardia

WPW syndrome and AFib, Atrial Flutter
Orthodromic/Antidromic AVRT
40. What drugs bradycardize tachysystolic atrial fibrillation (name four examples
from different groups)? (2)
Metoprolol, Verapamil, Digoxin (if HF)

Other: esmolol, diltiazem, propanolol
41. What drugs can be used to stop atrial fibrillation paroxysm (at least three
examples)? (2)
Propafenone, amiodarone, flecainide
35
42. During what period of time from onset of atrial fibrillation paroxysm the sinus
rhythm can be restored without extra anticoagulation and specific
investigations? (1)
<48h after the onset
43. What methods can be used to restore sinus rhythm in a patient with atrial
fibrillation? (1)
ECV, chemical cardioversion

RFCA, Maze procedure
44. In what cases emergent cardioversion has to be performed in a patient with

atrial fibrillation? (1)
If AF >48h and unstable hemodynamics
45. What are the most frequent amiodarone side effects? (1)
Hypothyroidism, hyperthyroidism, photosensitivity, pulmonary fibrosis,

dyspepsy, polineuropathy, vision disorders, Torsades de pointes, bradycardia
46. What are the contraindications for amiodarone use? (1)
Second/Third degree atrioventricular heart block

Very rapid heartbeat - torsades de pointes
Bradycardia
Prolonged QT interval
Together with procainamide
Abnormal functioning of the sinus node of the heart
47. What does „rhythm control” and „frequency control” mean in patient with
persistent and paroxysmal atrial fibrillation? (1)
Reduction Slow rate

Young patients Age > 75
Ischemic cardiopathy Anti-arrhythmic contraindications
Symptomatic Metral stenosis
If AF > 2 ans
Failure of ECV or drug Cardioversion for 2
times
48. Which drugs are used for atrial fibrillation paroxysm prophylaxis
(prevention)? (2)
Class Ia: Hydroquinidine

Class Ic: Flecainide + beta-blockers
Classe III: Sotalol
Amiodarone (2nd intention)
36
49. Name non-pharmacologic method for long-term (not acute) treatment of
supraventricular tachycardias (to prevent the reccurrence of arrhythmia)! (1)
RFCA
50. Name a method that cures WPW syndrome! (1)
RFCA
51. What nonpharmacological method can reduce frequency of atrial fibrillation

paroxysms? (1)
RFCA, Maze procedure
52. Which drugs can effictively reduce risk of systemic cardioembolism in

patients with atrial fibrilation? Name at least 3 drug groups with at least 1
example from each. (2)
Vitamin K antagonist: Warfarin

Direct inhibitor of thrombin: dabigatran
Inhibitor of factor Xa: Apixaban
53. What is CHA2DS2-VASc ? (1) From what CHA2DS2-VASc level patient has
to start long term prevention of cardioembolism? (2)
37
Risk factors for emboli
54. Name example of vitamin K antagonists ! * (0.5)
Warfarin, fluindione
55. Name direct peroral anticoagulants! * (1)
Dabigatran
38
Rivaroxaban, Apixaban
56. Name peroral direct trombin inhibitor! * (1)
Dabigatran
57. Name peroral factor Xa inhibitor! * (1)
Apixaban, edoxaban, rivaroxaban
58. What factors in diet have to be taken to consideration if a patient uses

warfarin? Why? (1)
One nutrient that can lessen warfarin's effectiveness is vitamin K. It's important to
be consistent in how much vitamin K you get daily. The adequate intake level of
vitamin K for adult men is 120 micrograms (mcg). For adult women, it's 90 mcg.
Avoid: kale, spinach
59. Which parameter has to be controled regularly using warfarin?* (0.5) What is
the optimal range of this parameter if indication for usage is atrial fibrillation?
(0.5) (1 point)
INR = 2.0-3.0
60. What are the possible warfarin overdose complications?* (0.5) What
parameter will indicate warfarin overdose?* (0.5) (1 point)
Bleeding, skin necrosis, Purple toe syndrome, teratogenicity, osteoporosis

Monitor INR
61. Name warfarin antidotes! (1)
Vitamin K1 (phytonadione)
62. What non-specyfic antidote can be used to effectively inactivate peroral

anticoagulants (both K vitamin antagonists and direct POAC)? (1)
Activated Prothrombin Complex Concentrate

Fresh frozen plasma
63. Can antiagregants be used for long term prevention of cardioembolism? Please
explain! (1)
According to European guidelines and because antiplatelet agents are much less
effective in preventing cardioembolic stroke, it is now more prudent to
anticoagulate patients in whom cardioembolic stroke is strongly suspected.
64. Name two treatment strategies (from tromembolism prevention point of view)
for patient with prolonged atrial fibrillation paroxysm (> 48 h) in order to
restore the sinus rhythm! (2)
39
Case tasks
65. Patient, male, 56 y.o., with atrial fibrillation paroxysm for the first time, which
lasts 12 hours. Objective findings: BP 120/80 mmHg; non-rhythmic heart
action; average – 110x’. No evidence of another pathology. Formulate
complete primary clinical diagnosis! (0.5) What kind of examinations should
be performed? (1) What is sinus rhythm restoring tactics if there are no
contrindications to restore it? (1.5) (3 points)
Dg: Tachysystolic new-onset atrial fibrillation
Rest ECG
Holter monitoring
TT Echocardiography
T3, T4, TSH
Renal, hepatic function, FBC, INR
AF <48h and is not terminating by itself

 Start with pharmacological cardioconversion and antithrombotic therapy
according to risk
In this case, terminated by itself after 12h and no risk of cardioemboli

Prevention of relapse
 Propafenone 450mg/day, Flecainide 200mg/day + beta-blockers,
Amiodarone 450-600mg/50mL i/v
66. Patient, female, 62 y.o., with anamnestic data of atrial fibrillation and atrial
flutter paroxysms – average 2 times a year. Currently hospitalized with
rhythmic tachycardia paroxysm, which lasts 12 hours. Objective findings: BP
40
120/80 mmHg, rhythmic heart action, average value – 150x’. No evidence of
another pathology. Formulate complete primary clinical diagnosis! (1) What
is sinus rhythm restoring tactics if there are no contrindications to restore it?
(1) What kind of treatment should be prescribed for prevention of reccurrent
paroxysms? (1) (3 points)
Dg: 2:1 Paroxysmal recurrent atrial flutter
No antithrombotic therapy
Pharmacological cardioversion  Ibutilide i/v, dofetilide p/o
 ECV if it fails
Prevention: RFCA
67. Patient, male, 60 y.o., atrial fibrillation established by accident one week ago,
duration time of AF is not known. During the recent year patient has noticed
that during heavy load gets tired easily. Objective findings: non-rhythmic
heart action, average frequency 104 x’, heart sounds are hollow, murmurs are
not auscultated. Hepatomegaly is not palpated. Edema is not present.
Formulate complete primary clinical diagnosis? (1) What is the examination
(1) and treatment (1) plan? (3 points)
Dg: Tachysystolic atrial fibrillation
Rest ECG
Holter monitoring
TT echocardiography
T3, T4, TSH
Troponin, CK-MB, BNP
TEE  If no thrombus in LAA  ECV with simultaneous heparin/warfarin

Cancel warfarin after one month
68. Patient, female, 58 y.o., was admitted for the first time with atrial fibrillation
paroxysm, which lasts 3 days. Objective findings: BP 120/80 mmHg, heart
action non-rhythmic, average 110x’. No evidence of another pathology.
What kind of examinations should be performed? (1) What is (are) sinus
rhythm restoring tactics if there are no contrindications to restore it? (1)
Which medications should be prescribed? (1) (3 points)
Dg: First detected paroxysmal tachysystolic atrial fibrillation
Rest ECG
Holter monitoring
TT echocardiography
T3, T4, TSH
AF lasts > 48h
41
TEE  If no thrombus in LAA  ECV with simultaneous heparin/warfarin
Cancel warfarin after one month
Prevention of relapse
 Propafenone 450mg/day, Flecainide 200mg/day + beta-blockers,
Amiodarone 450-600mg/50mL i/v
69. Patient, female, 80 y.o., atrial fibrillation paroxysms for 10 years. During
recent year regulary takes 1 tab. amiodarone (cordarone) per day, nevertheless
paroxysms are frequent, at least one time per month, that is why she regulary
calls for ambulance, which stops the atrial fibrillation using novocainamide.
This time novocainamide isn’t effective. Objective findings: BP 130/80
mmHg, non-rhythmic heart action, average 88x’, audible loud systolic
murmur in all sites of cardiac auscultation, murmur irradiates to carotid
arteries and over whole thorax. Formulate complete primary clinical
diagnosis? (1) What is the examination and treatment tactics? (1) Make the
plan of pharmacotherapy! (1) (3 points)
Long-standing normosystolic atrial fibrillation with congestive heart failure

Severe aortic stenosis. Mitral regurgitation.
Rest ECG
Holter monitoring
TT echocardiography
T3, T4, TSH
RFCA
70. Patient, 22 y.o., male, was admitted with complaints of rhythmic palpitations,
which started suddenly 2 hours ago. From anamnesis: similair paroxysms
since childhood, usually stopoed spontaneously or after holding a deep breath.
This time paroxysm didn’t stop. Objective findings: BP 130/80 mmHg,
rhythmic heart action 180x’. ECG: narrow complex tachycardia 180x’, p
waves are not seen. Formulate complete primary clinical diagnosis! (1.5)
What is the treatment tactics in acute stage? (1) What is long-term treatment?
(1) (3 points)
Dg: AV nodal re-entry tachycardia (AVNRT)
Vagal manoeuvre + i/v adenosine (5-6mg)
Long-term treatment:
RFCA
42
71. Patient, male, 38 y.o., with known WPW syndrome. Complaints of non-
rhythmic palpitations appeared 6 hours ago. Weakness and shortness of breath
developed gradually, cold sweat appeared. In the moment of examination
patient is delayed, skin is chilly, moisty. BP 85/50 mmHg, non-rhythmic heart
action, average 220 x’. Pulse is weak, average 120 x’. Lungs – vesicular
breathing, 30 times per minute, bilateral basal crepitation. SpO2 84%.
Formulate complete primary clinical diagnosis! (1.5) What is the treatment
tactics in acute stage? (1.5) What is long-term treatment? (1) (4 points)
Dg: WPW syndrome with unstable tachysystolic atrial fibrillation
General anesthesia and urgent ECV
Long term treatment:

RFCA (1st intention) or Flecainide, propafenone
43
4th course 2015/2016
Heart failure.
1. Please name the classification of heart failure! (1)

New York Heart Association classification (Functional classification)  refer to
Image in Questions 5-8
Also:
2. Describe the pathophysiology of congestive heart failure! (1)
4
4
4
5
Below is EXTRA DETAILS:
4
6
4
7
3. What are the most common causes of left-sided heart failure? (1)
Blue boxes in Diagram below
4
8
4. What are the most common causes of right-sided heart failure? (1)
Blue boxes in diagram below
The most common cause of right-sided heart failure is left-sided

heart failure
4
9
5. Describe complaints of the patient with heart failure NYHA Class I ! (1)
6. Describe complaints of the patient with heart failure NYHA Class II ! (1)
7. Describe complaints of the patient with heart failure NYHA Class III ! (1)
8. Describe complaints of the patient with heart failure NYHA Class IV ! (1)
Questions 5-8:
9. What are the most common complaints of the patient with left-sided heart
failure?* (2) Green boxes in diagram below (especially red circles)
5
0
10. What are the most common complaints of the patient with right-sided heart
failure?* (2) Similar to left sided HF + depending on etiology
Check Green boxes in Question no.4 Diagram AND Question no.12
11. What are the physical signs of the patient with left-sided heart failure?* (2)
Green boxes in diagram below AND the following pic.:
5
1
12. What are the physical signs of the patient with right-sided heart failure?* (2)
Check Green boxes in Question no.4 Diagram AND the following pic.:
5
2
13. Which physical signs point to fluid retention (congestion)? * (2)

• Peripheral pitting edema
• Stretched or shiny skin
• Aching of affected body parts
• Stiff joints
• Rapid weight gain over a few days or weeks
• Unexplained weight fluctuations
• Headache, Nausea and Loss of appetite
• Increased JVP
• Hepatosplenomegaly and abdominal RUQ discomfort
• Ascites
• Decreased amount of urine
• Paroxysmal Nocturnal Dyspnoea
• Orthopnoea
• Higher pulse rate and blood pressure
14. What are the manifestations of central cyanosis? Which ventricle failure does
it show to? (1)
Often due to a circulatory or ventilatory problem that leads to poor blood
oxygenation in the lungs, resulting in cyanosis of the cheeks, palates, tongue,
mucosa. It develops when arterial oxygen saturation drops below 85% or 75%.
Usually is shows in Left ventricular heart failure.
15. What are the manifestations of peripheral cyanosis? Which ventricle failure
does it show to? (1)
The blue tint in lips, nose, tips of fingers and toes, due to an inadequate or
obstructed circulation. Cyanosed areas feel cool, and local heating abolishes
cyanosis.
Usually it shows in Right ventricular HF.
16. Please describe acrocyanosis! Which ventricle failure does it show to? (1)
Acrocyanosis is persistent blue or cyanotic discoloration of the extremities,
most commonly occurring in the hands, although it also occurs in the feet and
distal parts of face.
Same thing as peripheral cyanosis.
17. What are the clinical signs of edema which is caused by heart failure? (1)
Appear or increase in afternoon or in evening.
Symmetric
Ankles→legs→sacrum (esp. when patient confined to bed), perineum
(hydrocoele – scrotal oedema) and anterior abdominal wall.
18. Please name the localization of edema for a walking patient with heart
failure!* (0.5)
19. Please name the localization of edema for a recumbent patient with heart
failure!* (0.5)
5
3
In congestive heart failure patients there is increased hydro static

pressure of the systemic venous system and hence dependant oedema (
pedal oedema in a walking patient / sacral oedema in recumbent patients).
If Pulmonary venous pressure increases Pulmonary oedema results.
20. Please define ascites!* (0.5) What does hydrothorax mean?* (0.5) (1 point)
Ascites is the abnormal buildup of fluid in the abdomen.
Hydrothorax is a type of pleural effusion in which transudate accumulates in
the pleural cavity.
21. Please define anasarca! Describe the signs! (1)

Anasarca – total, massive oedema of the whole body. Usually transudation
into parietal cavities is seen as well:
• Hydrothorax – pleural cavity (dx>sin)
• Hydropericardum – pericardial cavity
• Ascites – peritoneal cavity
Mostly due to right sided HF.
The swelling occurs in the entire body and the skin tends to look stretched and
shiny. At times, the severe swelling makes it difficult for an individual to
move.
22. How can a patient follow the fluid balance at home (and notice retention in
time)? (1)
Symptoms (question no.13)
• Daily weights
• Fluid balance chart
23. Which laboratory tests should be performed in a patient with heart failure?
Why? (2)
• BNP or NT-proBNP (a specific test indicative of heart failure)
• FBC (Ddx, e.g. check for anemia, which can cause similar symptoms
to CHF as well as contribute to CHF)
• Blood biochemistry (Hyponatremia is common in heart failure.
Vasopressin levels are usually increased, along with renin, angiotensin
II, and catecholamines in order to compensate for reduced circulating
volume due to inadequate cardiac output. "hypervolemic
hyponatremia": low sodium concentration due to high body fluid
retention) also (liver function [Albumin], kidney function [Creatinine],
thyroid function, CRP for infection suspicion)
24. Please describe the additional investigations (excluding laboratory tests) for a
patient with heart failure! Why? (2)
• ECG (Sinus trachy or rhythm disorders [PVB, PSVB, Atrial
fib/flutter], Left or right ventricular hypertrophy/overload, signs of
atrial abnormalities [P mitrale, P pulmonale], signs of cause of HF [e.g.
MI])
5
4
• EchoKG (MI, Valvular heart disease, LV hypertrophy, Ejection

fraction, Enlargement of chambers, Intrapericardial fluid)
• 6 minute walking test (exercise test with ECG, stress EchoKG, MPS)
• Chest X-ray (Configuration of heart shape, cardiomegaly, Venous
congestion, Hydrothorax)
• CT, CMR
• Coronary angiography (Heart failure may be the result of coronary
artery disease)
• Heart catheterization
• Endomyocardial biopsy
• Blood pressure (Often hypotension and decreased pulse pressure in late
stages of HF; Hypertension contributes to progression of HF; Should
be taken into account with drug treatment)
25. What does term left ventricle ejection fraction mean?* How it is
determined?* What is normal ejection fraction? (2)*
• It’s the volumetric fraction of blood ejected from the left ventricle with
each contraction.
• LVEF is calculated by dividing the volume of blood pumped from the
left ventricle per beat (stroke volume, SV) by the volume of blood
collected in the left ventricle at the end of diastolic filling (end-
diastolic volume, EDV).
• Normal LVEF is 67% (± 4.6%) – [Normally ranges between 55% and
70%]
26. Name pathologies causing low left ventricle ejection fraction! (1)
• Dilated Cardiomyopathy [<40%]
• Aortic stenosis
• Mitral & Aortic regurgitation
• Severe hypertension
• Myocardial infarction
27. What does term left ventricle systolic dysfunction mean? * (1) Name
echocardiographic signs in a case of systolic dysfunction of the left ventricle*
(1)
• Left ventricle cannot contract properly, leading to decrease Ejection
Fraction.
• Systolic dysfunction is easily assessable by estimation of global
ejection fraction and regional wall motion. A reduced LVEF, if
present, establishes systolic dysfunction.
28. What does term left ventricle diastolic dysfunction mean? * (1) Name
echocardiographic signs in a case of diastolic dysfunction of the left
ventricle!* (1)
• Left ventricle can’t relax and fill properly even though ejection fraction
is preserved. Atrium contracts against stiff ventricle.
5
5
• Diastolic dysfunction can be diagnosed indirectly by means of a

normal or nearly normal LVEF and changes of the mitral filling pattern
(Mitral inflow indices) in the context of LV failure. For an exact
determination of diastolic dysfunction LV catheterization is required.
29. What pathologies can cause left ventricle diastolic dysfunction? (1)
• Cardiac tamponade
• Myocardial ischemia
• Restrictive cardiomyopathy
• Myocardial fibrosis
They all lead to decreased EDV and thus diastolic dysfunction.
30. Which signs on chest x-ray will indicate left-sided heart failure? (1)
• In the lungs LV failure will lead to dilatation of pulmonary vessels,
leakage of fluid into the interstitium and the pleural space and finally
into the alveoli resulting in pulmonary edema.
• Stage I – Redistribution: Normally, the pulmonary vessels supplying
the upper lung fields are smaller and fewer in number than those
supplying the lung bases.
First there is equalisation of blood flow and subsequently
redistribution of flow from the lower to the upper lobes.
• Stage II - Interstitial edema: Characterized by fluid leakage into the
interlobular and peribronchial interstitium as a result of the increased
pressure in the capillaries. It is seen as thickening of septal lines,
thickening of the bronchial walls (peribronchial cuffing) and as loss of
definition of these vessels (perihilar haze).
• Stage III - Alveolar edema: This stage is characterized fluid leakage in
the alveoli (alveolar edema) and to leakage into the pleural space
(pleural effusion).
• Also cardiomegaly;
31. Which signs on chest x-ray will indicate right-sided heart failure? (1)
• Increased VPW due to dilatation of the superior vena cava
• Dilatation of azygos vein
• Dilatation of the right atrium
• In many cases there will be both signs of RV and LV failure
32. What pathologies cause right ventricle systolic dysfunction? (1)

• Right ventricular infarction
• RV cardiomyopathies
• Tricuspid regurgitation
• Pulmonic valve disease
• Left heart failure
• Parenchymal lung disease (RDS, COPD, Bronchiectasis, Interstitial
ling diseases)
5
6
• Pulmonary vasculature disease (Acute pulmonary embolism, primary

pulmonary hypertension, sclerodemia, Lupus, RA, HIV)
33. What does term hypokinesia mean? (!) What pathologies can cause
hypokinesia? (1) (2 points)
Hypokinesia means reduced movement or contraction of a segment of the
heart muscle.
34. What does term akinesia mean? (!) What pathologies can cause akinesia? (1)
(2 points)
Akinesia means lack of movement or contraction of a region of the heart
muscle.
35. Can normal echocardiographic finding rule out diagnosis of CHD? (1) What
echocardiographic finding can be expected in patient with anamnesis of
myocardial infarction? (1) (2 points)
• No. Echocardiography is not routinely performed for diagnosis of MI
but may be helpful when a patient presents with one or more symptoms
or signs of MI and the diagnosis is uncertain.
• Diagnosis of an acute MI is typically based upon the history,
electrocardiogram (ECG), and serum troponins.
• Severe ischemia produces regional wall motion abnormalities
(RWMAs) that can be visualized echocardiographically within seconds
of coronary artery occlusion.
• These changes occur prior to the onset of ECG changes or the
development of symptoms.
• Since ischemic RWMAs develop prior to symptoms, chest pain in the
absence of RWMAs should not be due to active myocardial ischemia.
However, the converse is not true; the presence of RWMAs does not
establish the diagnosis of ischemia. There are a number of other causes
of RWMAs, including a prior infarction, focal myocarditis, prior
surgery, left bundle branch block, ventricular preexcitation via an
accessory pathway, and cardiomyopathy.
• Thus, echocardiography for an acute coronary syndrome (MI or
unstable angina) has a high sensitivity but a relatively lower
specificity.
• Dyskinesia/Hypokinesia can be seen in patient with anamnesis of
myocardial infarction  Reduced ejection fraction
• Echocardiography can detect and evaluate a number of complications
after MI:
1. Mechanical complications: ischemic mitral regurgitation;
cardiorrhexis mitral regurgitation (due to papillary muscle
rupture, ventricular septal defect [VSD], or ventricular rupture);
5
7
Septal perforation (VSD); Papillary muscle rupture; Papillary

muscle displacement;
2. Left wall rupture
3. Tricuspid regurgitation
4. LV thrombus
36. What is cardiac output? What does it characterize? In what units it is

expressed? (1)
• The volume of blood being pumped by the heart per unit time.
• Cardiac output is the product of the number of heart beats per minute
(bpm), and the stroke volume (SV), which is the volume of blood
pumped from the ventricle per beat [CO = HR × SV].
• Values for cardiac output are usually denoted as L/min.
• Diseases of the cardiovascular system are often associated with
changes in Q, particularly the pandemic diseases hypertension and
heart failure. Increased Q can be associated with cardiovascular
disease that can occur during infection and sepsis. Decreased Q can be
associated with cardiomyopathy and heart failure.
37. What is cardiac index? What does it characterize? In what units it is
expressed? (1)
• Cardiac index (CI) is a haemodynamic parameter that relates the
cardiac output (CO) from left ventricle in one minute to body surface
area (BSA).
• Thus relating heart performance to the size of the individual.
• The unit of measurement is litres per minute per square metre
(L/min/m2).
• If the CI falls acutely below 2.2 L/min/m2, the patient may be in
cardiogenic shock.
38. What is Swan-Ganz catheter? What is it used for? What parameters does it
detect? (1)
• AKA Pulmonary artery catheterization (PAC), or right heart
catheterization, is the insertion of a catheter into a pulmonary artery.
• Its purpose is diagnostic; it is used to detect heart failure or sepsis,
monitor therapy, and evaluate the effects of drugs.
• The pulmonary artery catheter allows direct, simultaneous
measurement of pressures in the right atrium, right ventricle,
pulmonary artery, and the filling pressure ("wedge" pressure) of the
left atrium.
39. What kind of lifestyle modifications will you advise for a patient with severe
heart failure (class III) and fluid retention? (2)
• Diet:
o Restrain salt (<5g/day) – substitute with “Pansalt” which has
low sodium. Pay attention to foods with salt “hidden salt”.
o In patient with congestion: Fluid restriction (<1.5L/day from all
sources)
o If etiology of HF is Toxic alcohol-induced cardiomyopathy,
stop alcohol.
5
8
o Eat healthy food

• Weight:
o Check weight regularly to detect fluid retention (once daily to
twice weekly)
o Eliminate obesity
• Activities:
o Regular physical activity (not causing symptoms)
o Avoid contests and extreme exercises (isometric exertion X)
o Special rehab programs
o Aim to: Increase non-oedematous weight, avoid myocardial
non-training, and prevent venous thrombosis
• Smoking: It’s time to stop lol (Quit it)
40. What are the main principles the patient should observe in order to reduce
fluid retention? (1)
Notice Symptoms (question no.13)
• Daily weights (Retention likely if weight increase >2kg / 3 days)
• Fluid balance chart
Do the following to reduce fluid retention:
• Restrain salts (<5g / day)
• Restrict fluids (<1.5L / day)
• Recognize hidden salts
• Regular physical activity  aim to increase non-oedematous weight.
• Don’t smoke
• No isometric exertion
41. Please name the classes of drugs used in the pharmacotherapy of the heart
failure (name the groups and examples)! (2)
• ACE inhibitors (or ARBS): Enalapril, Ramipril, Perindopril (or
Losartane, Valsartane, Candesartane)
• Beta blockers: Carvedilol, Metoprolol succinate CR, Metoprolol
Tartrate, Bisoprolol, Nebivolol
• Aldosterone antagonists (MRA – Mineralocorticoid receptor
antagonist)
• Ivabradine
• Omega-3
• Diuretics
• Nitrates
• Digoxin
42. Which drugs prolong the life of a patient with heart failure and systolic
dysfunction of the left ventricle? Name the groups and examples! (2)
• ACE inhibitors (or ARBS): Enalapril, Ramipril, Perindopril (or
Losartane, Valsartane, Candesartane)
5
9
• Aldosterone antagonists (MRA – Mineralocorticoid receptor

antagonist)
• Ivabradine
• Omega-3
43. Please name at least 2 drugs of ACEI group (preferably with doses) you will
prescribe for a patient with heart failure (* - at least one)! (1)
• Enalapril: Initial dose 2.5 mg x1 (x2); Target dose 10 mg x2
• Ramipril: Initial dose 1.25-2.5 mg x1; Target dose 2.5-5mg x2
44. Please name the contraindications for the use of ACEI! (1)
• Absolute contraindications:
o Angioneurotic edema due to any ACEI
o Pregnancy
o Known hypersensitivity to the given ACEI
o Bilateral or unilateral renal artery stenosis
• Cautions
45. What are the most common side-effects of ACEI? (1)

• Hypotension, cough, hyperkalemia, headache, dizziness, fatigue,
nausea, and kidney impairment.
46. Which diuretics will you choose for heart failure treatment (please name the
group, name of medication and dosage)? (* - at least one) (1)
• MRAs: Spironolactone 25mg x1 (12.5-50 mg x1)
• Loop diuretics:
o Bumetanide (Initial 0.5-1.0 mg; Max 5-10 mg)
o Furosemide (Initial 20-40 mg; Max 250-500 mg)
o Torsemide (Initial 5-10 mg; Max 100-200 mg)
• Thiazide diuretics include:
o Hydrochlorothiazide (Initial 25 mg; Max 50–75 mg)
o Metolazone (Initial 2.5 mg; Max 10 mg)
o Indapamide (Initial 2.5 mg; Max 2.5 mg)
• Potassium-sparing diuretics include:
o Amiloride (Initial w/ ACEI 2.5 mg, w/o ACEI 5 mg; Max w/
ACEI 20 mg, w/o ACEI 40 mg)
o Triamterene (Initial w/ ACEI 25 mg, w/o ACEI 50 mg; Max w/
ACEI 100 mg, w/o ACEI 200 mg)
o Spironolactone (Initial w/ ACEI 25 mg, w/o ACEI 50 mg; Max
w/ ACEI 50 mg, w/o ACEI 100-200 mg)
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0
47. Please name at least two loop diuretics (advisable with dosage and form of
use)! (* - at least one) (1)
• Loop diuretics:
o Bumetanide (Initial 0.5-1.0 mg; Max 5-10 mg) Tablet p/o
o Furosemide (Initial 20-40 mg; Max 250-500 mg) Tablet p/o
o Torsemide (Initial 5-10 mg; Max 100-200 mg) Tablet p/o
48. What are the side-effects of loop diuretics? (1)

• Hyponatremia, hypokalemia, hypomagnesemia, dehydration,
hyperuricemia, gout, dizziness, postural hypotension, syncope.
49. Which signs are showing to diuretics efficacy in patient treatment with heart
failure and fluid retention? (1)
• Improving of dyspnea and edema.
50. Please name potassium-sparing diuretics (with dosage)! (1)
• Amiloride (Initial w/ ACEI 2.5 mg, w/o ACEI 5 mg; Max w/ ACEI 20
mg, w/o ACEI 40 mg)
• Triamterene (Initial w/ ACEI 25 mg, w/o ACEI 50 mg; Max w/ ACEI
100 mg, w/o ACEI 200 mg)
• Spironolactone (Initial w/ ACEI 25 mg, w/o ACEI 50 mg; Max w/
ACEI 50 mg, w/o ACEI 100-200 mg)
51. Please name the aldosterone antagonists (preferably specify dosage and form
of use)! (1)
• Spironolactone: 25 mg x1 (12.5-50 mg x1) Tablet p/o
• Eplerenone: 25 mg x1 (50 mg x1) Tablet p/o
52. What are the most common side effects of aldosterone antagonists? (1)
• Gynecomastia (10% males!)
• Hyperkalaemia and/or increased creatinine levels.
53. Please name beta blockers which can be used in heart failure treatment! (1)
54. What are the principles of beta blockers administration for a patient with heart
failure (dosage specificity)? (1)
Tablet p/o
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1
55. Please name contraindications for use of beta blockers in a patient with heart
failure? (1)
• Symptomatic bradycardia,
• AV block,
• Decompensated heart failure,
• Asthma.
56. Please name long-acting nitrates!* (1) What is the role of them in heart failure
treatment? (1) (2 points)
• Isosorbide mononitrate
• Isosorbide dinitrate
They effectively reduce dyspnoea and orthopnoea due to LVD
57. Which drugs effectively decrease shortness of breath in patients with left-sided
heart failure?(1)
• Long acting (ISDN, ISMN) and short acting (NG) Nitrates
58. Please name examples of digitalis!* (1)

• These are Cardiac glycosides (digitalis):
o Digoxine
o Digotoxine
59. Please name contraindications for use of digitalis! (1)
60. Which clinical signs are evidenced in a case of digitalis overdose? (1)
• Nausea/vomiting, diarrhea, gastrointestinal pain, and anorexia
• Blurry vision with a yellow tint and halos, disorientation, weakness
61. Please name methods of non-medical treatment of heart failure! (1)

• Lifestyle modifications
• Patient education (self monitoring of symptoms and daily weight
check)
• Invasive procedures:
o Treatment of underlying cause: Revascularization; valve
replacement; etc.
o CRT (Cardiac resynchronization therapy)
o ICD (Intracardiac defibrillator)
o CRT-D (Combination of both above mentioned methods)
o Mitral valvuloplasty (For secondary MR as well)
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o Cardiomyoplasty, batista surgery (LV partial ventriculectomy)

o IABP (Intraaortic balloon pump)
o Ultrafiltration
o LVAD (Left ventricular assist device)
o Heart transplantation
o Artificial heart
62. Please explain what does CRT mean? (1)

• Cardiac resynchronisation therapy (CRT) is the insertion of
electrodes in the left and right ventricles of the heart, as well as on
occasion the right atrium, to treat heart failure by coordinating the
function of the left and right ventricles.
EXTRA:
• CRT is indicated in patients suffering from a low ejection fraction
(typically <35%) indicating heart failure, where electrical activity has
been compromised, with prolonged QRS duration to >120 ms.
• The key indication for CRT is left bundle branch block (LBBB) of
the heart,
• Heart failure patients are generally considered if in class II or III heart
failure, with current guidelines indicating CRT is inappropriate for
class IV heart failure.
63. Please explain what does ICD mean? (1)

• An implantable cardioverter-defibrillator (ICD) or automated
implantable cardioverter defibrillator (AICD) is a device implantable
inside the body, able to perform cardioversion, defibrillation, and (in
modern versions) pacing of the heart.
EXTRA:
• The device is therefore capable of correcting most life-threatening
cardiac arrhythmias.
• Implantation of ICD is meant to prevent sudden cardiac death and is
indicated under various conditions.
64. Please explain what does CRT -D mean? (1)

• CRT + IDC = CRT-D
• CRT defibrillators (CRT-D) are CRT devices that also incorporate the
additional function of an implantable cardioverter-defibrillator (ICD),
to quickly terminate an abnormally fast, life-threatening heart rhythm.
65. Male, 60 years old, with fatigue, weakness and progressive shortness of breath
for last two weeks. Complaints exacerbate during physical exercise. Patient
denies chest pain. Leg edema is observed. History: two myocardial infarctions
(5 years ago and a year ago), permanent atrial fibrillation. Echo was performed
before admission, which showed moderate dilatation of left ventricle and left
atrium, diffuse hypokinesia of the left ventricle walls, akinesia in inferior wall,
EF (ejection fraction) 20-25%. Please formulate the primary clinical
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diagnosis! (1) Please write the plan of investigations (1.5) and treatment (1.5)!
(4 points)
• Diagnosis: Chronic Severe Heart failure (Class IV) with reduced
ejection fraction + (plus sign means Congestive)
• Investigations: FBC, Blood biochemistry, BNP, Coronary
angiography, EchoKG, ECG, 6 minute walking test,
• Treatment: Lifestyle, Patient education, drugs:
o Furosemide (Initial 20-40 mg; Max 250-500 mg) tablet p/o
o Enalapril: (Initial 2.5 mg x1 (x2); Target 10 mg x2) tablet p/o
o Carvedilol (Initial 3.125 mg x2 (x2); Target 25 (50) mg x2)
tablet p/o
o Spironolactone 25mg x1 (12.5-50 mg x1)
o Digoxin (0.25 – 0.375 mg/day)
o Aspirin 81-325 mg tablet p/o
o CRT
o LVAD
o Heart transplant
66. Male, 56 years old, complaining of progressive shortness of breath for last
three weeks. Patient notes sleeping difficulties due to shortness of breath,
sitting position relieves the symptoms. Ankle edema is observed. There is no
chest pain. History: arterial hypertension more than 15 years, TA=190/100
mmHg, patient denies smoking and alcohol use. No data of positive family
history. On physical examination: TA=160/100 mmHg; heart rate irregular,
average 150 beats/min, basal crepitation in lungs on auscultation, distended
(filled) jugular veins. Hepatomegaly (+1 cm). Please formulate primary
clinical diagnosis! (1) Please write the plan of investigations (1.5) and
treatment (1.5)! (4 points)
• Diagnosis: Acute decompensated Heart failure (Class IV) + with
pulmonary edema. HVD
• Investigations: FBC, Blood biochemistry, BNP, EchoKG, ECG, 6
minute walking test, Chest x-ray,
• Treatment: Lifestyle (confined to bed), drugs:
o Spironolactone 25mg x1 (12.5-50 mg x1)
o Digoxin (0.25 – 0.375 mg/day)
o Ultrafiltration
o CRT
o LVAD
o Heart transplant
67. Female, 74 years old, complains of progressive weakness and shortness of

breath during everyday physical activity for a year. It is difficult to ascend the
stairs (1st floor) and to walk 100 m. Patient denies shortness of breath at night.
Ankle edema is observed. Before a month patient have lost consciousness. No
history of myocardial infarctions or chest pain, no history of arterial
hypertension, usage of alcohol. Objective findings: TA=130/80 mmHg, heart
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rate rhythmic, 92 beats/min, loud systolic murmur is auscultated in all

auscultation points, louder in 2nd intercostal space on l. parasternalis dx and in
Erb’s point, irradiates to both carotid arteries. Crepitation on lung auscultation.
Distensed (filled) jugular veins. Hepatomegaly (+1 cm). Ankle edema. Please
formulate full primary clinical diagnosis! (1) Please write the plan of
investigations (1.5) and treatment (1.5)! (4 points)
• Diagnosis: Chronic Moderate Heart failure (Class II) + with Aortic
stenosis
• Investigations: FBC, Blood biochemistry, BNP, Chest X-ray, EchoKG,
ECG, 6 minute walking test,
• Treatment: Lifestyle, Patient education, drugs:
o Carvedilol (Initial 3.125 mg x2 (x2); Target 25 (50) mg x2)
tablet p/o
o CRT
o Valve replacement
o Heart transplant
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Basics in ECG.
1. What colors are the four extremity ECG electrodes (0.5) and what is their localization
(0.5)? (1 point)
• Red – right hand

• Yellow- left hand
• Green – right leg
• Black – left leg
2. Name the 12 standard ECG leads!* (1)
• Six limb leads I, II, III, aVR, aVL, aVF and six chest leads V1 – V6
3. Name the possible additional ECG leads and specify pathologies they can reveal! (1)
• V7, V8, V9 used for diagnosis of true posterior myocardial infarction

• V3R and (mainly) V4R for diagnosis of right ventricular MI
4. How many seconds is one large and one small square if the ECG is recorded at a speed
25 mm/s?* (1)
• One large is 0.2 seconds and one small is 0.04 seconds
5. How many seconds is one large and one small square if the ECG is recorded at a speed
50 mm/s? (1)
• One large is 0.1 seconds and one small is 0.02 seconds
6. Describe heart rate calculation in patient with sinus rhythm! (2)
• HR= 60/ PP interval
7. Describe heart rate calculation in patient with atrial fibrillation! (2)
• HR= 60/ mean RR (6-8 RR intervals)
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8. What are the signs of sinus rhythm on ECG?* (1)

• Presence of P waves, all P waves are equal in the same lead and correspond to normal
sinus rhythm configuration
• Regular and equal PP intervals
• Equal PR intervals
9. What does P wave reflect on ECG?* (1)
• Atrial depolarization
10. What does PQ interval reflect on ECG?* (1)
• AV conduction
11. What does QRS complex reflect on ECG?* (1)
• Ventricular depolarization
12. What does ST segment and T wave reflect on ECG? (1)
• Ventricular repolarization
13. Name the criteria of pathological Q wave! (1) What does it indicate? (1) (2 points)
• Q wider than 0.03 seconds

• Q deeper than ¼ of R wave in the same lead
• Any Q wave in V1- V3
• It indicates a previous myocardial infarction, it occurs within hours of acute MI
14. Which leads are called the inferior leads? (1)
• II, III, aVF
15. Which leads are called the left (lateral) leads? (1)
• I, aVL, V5, V6
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16. Which leads are called the right leads? (1)
• V1, V2
17. Explain P pulmonale! [numeric criteria are not obligatory] When is it observed on ECG?
(1)
• High > 2.5 mm, right atrial enlargement.

• Typically high in II, III, aVF
18. Explain P mitrale ! [numeric criteria are not obligatory] When is it observed on ECG?
(1)
• Wide > 0.12 s with two humps, left atrial enlargement
19. What is the normal length of PQ interval? (1)
• 0.12 – 0.20 seconds
20. Explain WPW syndrome and describe its ECG signs! (2)
• Wolff-Parkinson-White syndrome (orhtodromic variant)

• Reentrant circuit enters ventriculi through AV node and returns back to atria through the
accessory pathway
• Short PR < 0.12 s
21. What does shortened PR interval (<0.12 s) indicate? (1)
• Fast AV conduction, typically due to accessory pathway (WPW)
22. What does constant PR interval prolongation indicate (> 0.20 s)?* (1)
• It indicates AV block
• >0.22 s in bradycardia
23. Name the ECG signs of first degree atrioventricular heart block! (2)
• PR interval equally prolonged and fixed

• RR intervals regular
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24. Name the possible types of second degree atrioventricular heart block? (2)
• Mobitz I
• Mobitz II
• 2:1
• Advanced
25. Name Mobitz I ECG signs! (2)
• Gradual prolongation of PR until one QRS complex drops out and P wave is followed by
another P wave
• Irregular RR intervals
26. Name Mobitz II ECG signs! (2)
• PR does not change

• Sudden disappearance of QRS, P followed by another P
• Irregular RR intervals
27. Name ECG signs of 2:1 atrioventricular block! (2)
• Every second P is followed by QRS complex, there are 2 P waves for each QRS and PR
duration is the same
• Regular RR
28. Explain complete AV block mean, name the ECG signs! Which degree AV block is it?
(2)
• 3rd degree AV block

• None of the impulses are conducted from atria to ventricles
• No relationship between P waves and QRS complexes
• Regular RR intervals
29. What pathologies can be determined by changes of QRS complex? (2)
• Electrical axis
• Ventricular hypertrophies
• Hiss bundle blocks
• Infarction
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30. What changes in QRS complex indicate ventricular hypertrophy? (1)
• R and S amplitude
31. What changes in QRS complex indicate disturbed conduction in His bundle – Purkinje
fibers system? (1)
• R and S duration, wide QRS
32. Name the ECG signs of left ventricle hypertrophy! (2)
• High R in left leads (I, aVL, V5, V6) and deep S in right leads (V1, V2)
• Initial: R in V6 becomes equal or higher than R in V5 and V4, S deeper in V1
• Definite: R in V5/V6  26 mm or V6 + S V1  35 mm
33. Name the ECG signs of right ventricle hypertrophy! (2)
• Initial: Increased R in V1 and presence of S in V5 and V6

• Definite: R>S in V1
34. What does horizontal or downslopping ST-segment depression indicate most commonly?
(2) When else (in which cases) it can be observed? (1)
• Subendocardial ischemia
• Angina attack
• During ischemia provoked by exercise test
• ACS without ST elevation (unstable angina or AMI)
35. What does ST-segment elevation indicate most commonly?* (2) When else (in which
cases) it can be observed? (1)
• Transmural ischemia, typically acute stage of MI

• Acute pericarditis
• Can be normal in some individuals in V1-V2 up to 1-2 mm
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36. What does downslopping ST-segment depression in leads V5 and V6 reflect in patient
with signs of left ventricle hypertrophy? (1) What changes are observed in leads V1 and
V2 in this case? (1)
• Low lateral subendocardial ischemia

• Deep S in V1 and V2
37. ECG example: R wave amplitude in V6 lead is 20 mm, in V1 lead S wave depth is 18
mm. Which pathology is indicated by these changes? (2)
• Definite LV hypertrophy ( R V5/V6 + S V1  35 mm)
38. Complete left bundle branch block (LBBB), name the changes on ECG! (2)
• Wide, large R waves in left leads ( I, aVL, V5, V6) and large, wide S waves in right leads
(V1, V2)
• QRS becomes wider > 0.12 s
• Discordant ST-T changes!!
39. Complete right bundle branch block (RBBB), name the changes on ECG! (2)
• M-shaped R waves in V1 and wide S waves in left leads (I, aVL, V5, V6)
• Discordant ST-T changes
40. What does new onset complete left bundle block point to, if patient is complaining of
chest pain more than one hour? (2)
• Lateral MI
• Hypertension
• Cardiomyopathy
41. What is the QRS complex width in case of complete right or left bundle branch block?*
(1)
• QRS  0.12 s
42. Describe discordant ST-T changes on ECG in case of complete left bundle branch block!
(2)
43. Describe discordant ST-T changes on ECG in case of right bundle block! (2)
44. What are the changes on ECG in case of subendocardial ischemia?* (1)
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• ST depression  0.5 mm
• Horizontal or downsloping depression
45. What are the changes on ECG in case of transmural ischemia?* (1)
• ST elevation  1 mm
• Horizontal, upsloping or conves
• Reciprocal changes are present
46. In which cases the transmural ischemia signs appears on ECG? (1)
• Typically, in acute stage of MI
47. In which cases the subendocardial ischemia signs can be present on ECG (write three
possible clinical diagnosis)? (2)
• During angina attack

• During ischemia provoked by exercise test
• ACS without ST elevation (unstable angina or AMI)
48. Hyperacute phase of myocardial infarction, describe ECG changes!(2)
• High positive, symmetric T waves (no ST elevation yet)
49. Acute phase of myocardial infarction, describe ECG changes! * (2)
• ST elevation and positive T waves

• Development of necrosis as a decrease of R wave and development of pathologic Q wave
50. Subacute phase of myocardial infarction, describe ECG changes! (2)
• ST elevation and inverted T waves

• Development of necrosis as a decrease of R wave and development of pathologic Q wave
51. Scar (repair) phase of myocardial infarction, describe ECG changes! (2)
• ST segment returns to isoelectric line, negative T waves may remain

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52. Explain “reciprocal changes” on ECG (what does it mean?)! (1)
• Mirror image in the opposite wall seen as depression

• NOT ischemia
53. In which leads the reciprocal changes will be visible, if the direct changes are in I, aVL
leads? (1)
• II, III, aVF
54. In which leads the reciprocal changes will be visible, if the direct changes are in II, III,
aVF leads? (1)
• I, aVL
55. What are possible ECG changes in the case of acute pericarditis? (2)
• ST elevation  1 mm in mostly all leads

• No reciprocal changes
56. What are possible ECG changes in the case of hyperkaliemia? (2)
• Tall and narrow T wave

• Wide, flat P wave
• Prolonged PR interval
• Decreased R wave amplitude
• Widened QRS
• Depressed ST segment
57. Why is prolonged QT interval dangerous? (2)
• Heart rate dependent

• Long QT is associated with increased risk of Torsades de pointes
• Ventricular tachycardia
• Ventricular arrhythmia
58. Name possible the ECG changes in case of pulmonary embolism! (2)
• S1, QIII, TIII (inverted T in lead III)

• Right axis deviation, RBBB
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• Shift in the transition zone (R=S) to the left (V3  V5)

• Inverted T waves in V1-V3 (and tendency of ST elevations)
• Tendency of ST depression in V4-V6
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CHD. Stable angina. CVD prevention.
1. Please name at least six risk factors of coronary heart disease!* (1)
• Age and gender

o Men > 45 years
o Females >55 years
• Dyslipidemias
o TC > 5mmol/l
o LDL > 3mmol/l
o TG > 1.7 mml/l
o HDL < 1.0 mmol/l
• Hypertension
• Diabtes, particularly type II (metabolic syndrome, obesity, decreased physical activity,
diet)
• Smoking, alcohol
• Positive family history of
o MI
o Sudden cardiac death in 1st degree relatives
o Male (father, brother) < 59 years
o Females (mother, sister) < 65 years
2. Which four lipid fractions are usually determined in clinical practice?* (0.5)
• Total cholesterol > 5.0 mmol/L

• LDL-cholesterol > 3.0 mmol/L
• Triglycerides > 1.7 mmol/L
• HDL-cholesterol < 1.0 mmol/L
3. Which of four lipid fractions is (are) dependent on meal? (0.5)
• Triglycerides
• Total cholesterol
• HDL
• LDL
4. Which of these four lipid fractions is (are) related with high cardiovascular risk
and which – with lower cardiovascular risk?* (0.5)
• High are associated with cholesterol and LDL

• Low is associated with HDL
5. Which medication group most effectively lowers the levels of total cholesterol
and LDL cholesterol?* (1)
• Statins are the most powerful
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o Atorvastatin 10 – 80 mg x 1
o Simvastatin 20 – 40 mg x 1
o Pravastatin 20 – 40 mg x 1
o Rosuvastatin 5 – 40 mg x 1
o Fluvastatin XL 80 mg x 1
6. What physical signs are characteristic for patients with familial

hypercholesterolemia? (1)
• TC > 7-8 mmol/l

• LDL > 5-6 mmol/l
• Tuberous and tendon xantomata
• Arcus senilis/cornealis and xantelasms which are not specific to FH but can be a reason
to suspect it
7. Describe signs of familial hypercholesterolemia (clinical, anamnestic etc) (2)
Risks of hyperlipidemia
• Family history of hyperlipidemia
• Arcus senilis < 50 years
• Xanthomata/xanthelasmas
Risk of CVD
• Known CVD
• Family history of CVD < 65 years
• DM or impaired glucose tolerance
• Hypertension
• Smoker
• High BMI
• LDL receptor defect  Increased LDL  Hyperlipidemia
8. Explain familial hypercholesterolemia cascade screening! (1)
• Relatives of people with a confirmed diagnosis of mono—FH are offered DNA testing,
through a nationwide systematic cascade process
• Most people in UK with FH are undiagnosed
• Nationwide ensures all family members can access DNA testing wherever they live
• Local data collection  database
9. Name examples of statins! (1) Explain the mechanism of action? (1)
Competitive inhibition of HMG-CoA reductase → reduced intrahepatic cholesterol

biosynthesis → upregulation of expression of LDL receptor genevia sterol regulatory element-
binding protein (SREBP) → Reduced LDL levels and increased HDL
HMG-CoA reductase is unable to convert HMG-CoA to mevalonate, which is the rate-
limiting step of cholesterol synthesis.
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4th & 6th course 2012/2013
• Atorvastatin 10 – 80 mg x 1
• Simvastatin 20 – 40 mg x 1
• Pravastatin 20 – 40 mg x 1
• Rosuvastatin 5 – 40 mg x 1
• Fluvastatin XL 80 mg x 1
10. Name most common adverse effects of statins! (1)
• Myalgia (muscle pain)/ rhabdomyolysis

• Liver damage  increased production of liver enzymes
• General: headache, GI symptoms (diarrhoea, constipation, flatulence)
• Neurological: memory loss or confusion
11. What other groups of drugs apart from statins can lower total and LDL cholesterol
levels? (1)
• Cholesterol absorption inhibitors e.g. Ezetimibe

• Fibrates e.g. Ciprofibrate, Gemfibrozil
• Omega-3 fatty acids in large doses �
• [Nicotinic acid, niacin]
• [Bile acid sequestrates] �
• Others�
o PCSK9 inhibitors�
o ApoB antisense therapy
o CETP inhibitors�
o LDL apheresis in HoFH
12. What group of drugs most effectively lower the levels of triglycerides? Name at
least one example! (1)
• Fibrates
o Fenofibrate micronized 200 mg x 1
o Ciprofibrate, Gemfibrozil
13. Which is the main lipid parameter that is used as a guideline to reduce
cardiovascular risk? (1) What is the target level (how low it should be) in a patient
with established coronary heart disease? * (1)
• In patients with very high CV risk the LDL-C goal

o < 1.8 mmol/l
o Or > 50% LDL-C reduction when target level cannot be reached
• In patients with high CV risk
o < 2.5 mmol/l
• In patients with moderate risk
o < 3.0 mmol/l
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14. Describe primary and secondary cardiovascular disease prevention!* (1)
Primary
• To prevent the development of the CV event in the apparently healthy individuals
• Population and individual levels
• Needs risk estimation to decide if indicated and how aggressively should be managed for
an individual
• No smoking, no secondary smoke
• Healthy food
• Regular physical activities
• Avoid and reduce overweight, obesity
• Restrict alcohol
• Regular control of BP and lipids, treat them if above targets
• Pharmacotherapy: Statins, Antihypertensive therapy, treatment of diabetes (aspirin in
high risk individuals)
Secondary
• To prevent further events and progression if CVD in patients with established disease
• Prevention is absolutely indicated and should be initiated in all patients – those with
established atherosclerotic disease
• Pharmacotherapy: lipid-lowering drugs (statins in maximal doses), aspirin 75-100 mg/d,
clopidogrel if aspirin not tolerated, antihypertensive therapy, treatment of diabetes
15. What signs indicate very high cardiovascular risk? (2)
• Documented CVD by invasive or non-invasive testing

o Previous MI
o ACS
o Coronary revascularization (PCI, CABG) and other arterial revascularization
procedures
o Ischaemic stroke
o Peripheral artery disease (PAD)
• Diabetes mellitus with one or more CV risk factors and/or target organ damage
• Severe chronic kidney disease (GFR < 30 mL/min)
• A calculated SCORE > 10 %
16. What signs indicate high cardiovascular risk? (2)
• Markedly elevated single risk factors such as familial dyslipidemias and severe
hypertension
• Diabetes mellitus but without CV risk factors or target organ damage
• Moderate chronic kidney disease (GFR 30-59 mL/min)
• A calculated SCORE of 5-9 % for a 10-year risk of fatal CVD
17. What signs indicate average cardiovascular risk? (1)
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• Subject are considered to be at moderate risk when their SCORE 1-4 % at 10 years
18. What signs indicate low cardiovascular risk? (1)
• Individuals with a SCORE < 1 %
19. What fatal cardiovascular risk score is considered to be high (% in 10 years

according to SCORE tabs) (in order to start primary prevention)? (1)
• A calculated SCORE of 5-9 %
20. What fatal cardiovascular risk score is considered to be very high (% in 10 years
according to SCORE tabs) (1)
• A calculated SCORE ≥10% �
21. What kind of lifestyle modifications should be performed in order to reduce

cardiovascular risk (to perform prevention of cardiovascular disease)? (2)
• Stop smoking
• Decrease BP < 130/80 mmHg
• Decrease lipids
o LDL < 1.8 mmol/l
o Total cholesterol <4.0 mmol/l
• Diet: reduction of calories and carbohydrates
• Exercise
• Reduction of weight
22. Which medication is required for a person with very high cardiovascular risk in
primary prevention? (2)
• Lipid-lowering treatment (statins)

• Antihypertensive therapy
• Treatment of diabetes
• Aspirin 75-100 mg/d in very high-risk individuals
23. What are the main principles of healthy diet to reduce cardiovascular risk? (2)
• Type of fat
o Concentrate on MUFA, PUFA and Omega 3  unsaturated fatty acids
o Avoid saturated and trans-fatty acids
• Vegetables, fruits (400-500 g per day)
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o 5 portions (3 vegetables + 2 fruits)

• Proteins
o Legumes vs animal proteins
• Carbohydrates
• Decrease salt intake
• 1 alcohol unit
24. Describe principles of Mediterranean diet! (1)
• Vegetables, fruits, legumes, cereals/wholegrains, fish, high MUFA:SFA ration, and

moderate intake of alcohol (red wine during meals)
• Less red meat and dairy fat
25. Which fatty acids raise cardiovascular risk and should be decreased in a diet for a
high risk individual? What products contain them? (1)
• Saturated fatty acids  dairy products and animal fat

• Trans-fatty acids  semi-solid fats, margarine, cakes, pastries
26. Which fatty acids are recommended more for a person with high cardiovascular
risk? What products contain them? (1)
• Monounsaturated fatty-acids  olive oil, rapeseed oil, almond, nuts

• Polyunsaturated fatty-acids  other liquid vegetable oils
• Omega-3  sea food, oily fish, nuts, seeds
27. What products contain omega-3 fatty acids and what is their effect on
cardiovascular system (positive/negative)?* (1)
• Found in oily fish eg. salmon, herring

• Found also in nuts and seeds
• Decrease total cholesterol, LDL and TGs and increase HDL
• Anti-arrhythmic  reduce risk of sudden death
28. What products contain saturated fatty acids and what is their effect on
cardiovascular system (positive/negative)?* (1)
• Found in dairy products, processed meats, fatty meat products, cakes, biscuits, chips
• Negative effect, raise total cholesterol, LDL and risk of CVD
29. What products contain monounsaturated fatty acids and what is their effect on
cardiovascular system (positive/negative)? (1)
• Olive oil, sunflower oil, rapeseed oil, meats, almonds, nuts

• Positive effect, decrease LDL cholesterol
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30. What products contain polyunsaturated omega-6 fatty acids and what is their
effect on cardiovascular system (positive/negative)? (1)
• Vegetable oils, oily fish

• Seeds
• Positive effect decrese LDL
31. What products contain trans-fatty acids and what is their effect on cardiovascular
system (positive/negative)? (1)
• Semi-solid fats, margarine, cakes, pastries

• Negative, increase LDL and risk of heart disease
32. What is the advisable amount of physical activities (in hours) for cardiovascular
prophylaxis in case of no contraindications for exercise? (1)
• 2.5 – 5 hours of aerobic exercise at least moderate intensity

• 1- 2.5 hours of vigorous intensity
33. How is maximal pulse calculated? How is submaximal pulse calculated? (1)
• Maximal pulse = 220 – age

• Submaximal pulse = 85% of maximal pulse
34. Describe symptoms of stable angina functional class I!* (1)
• Ordinary physical activity doesn’t cause angina such as walking, climbing stairs
• Angina occurs with strenuous, rapid, prolonged exertion at work or recreation
35. Describe symptoms of stable angina functional class II!* (1)
• There is slight limitation of ordinary activity

• Angina occurs on walking or climbing stairs climbing stairs rapidlt, walking uphill,
walking or stair climbing after meals or in cold, or in wind, or under emotional stress, or
during the few hours after awakening
• Angina occurs on walking more than 2 blocks on the level and climbing more than one
flight of ordinary stairs at normal pace and in normal conditions
36. Describe symptoms of stable angina functional class III!* (1)
• There is marked limitation of ordinary physical activity

• Angina occurs on walking one or two blocks on the level and climbing one flight of stairs
in normal conditions and at a normal pace
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37. Describe symptoms of stable angina functional class IV!* (1)
Inability to carry on any physical activity without discomfort – angina symptoms may be present
at rest
38. Which medications (names and administration form) and in which period of time
relieve/ discontinue attack of angina?* (1)
• Beta blockers
o Bisoprolol p.o. 2.5 – 10 mg x 1
• Ion channel inhibitors
o Ivabradine p.o. 5 -7.5 mg x 2
• Calcium channel blockers
o Amlodipine 5 – 10 mg x 1
• Long-acting nitrates
o ISMN p.o. 30 – 60 mg x 1
• Ranolazine 375 – 750 mg x 2
• Nitroglycerine sublingually
39. What type of pain is typical for angina pectoris (describe the character of pain)?*
(2)
• Pressure/squeezing/ grip-like/ heavy/ suffocating

• Sensation of discomfort, not pain
• Never sharp/stabbing
• Doesn’t change with position
40. When else (in which disease, except coronary atherosclerosis) angina can be
observed? (1)
• Oesophageal disorders
• GERD
• Hyperthyroidism
• Profound anaemia
• Uncontrolled hypertension
• Valvular heart disease
• Bradyarrythmia
• Tachyarrythmia
41. Explain microvascular angina! (1)
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Spasms within the walls of these very small arterial blood vessels and failure of causes reduced
blood flow on vasodilation to the heart muscle leading to a type of chest pain referred to as
microvascular angina.
42. How long typically does an angina episode last? (1)
• Lasts 5 – 15 minutes with gradual onset and disappearance
43. What are the most common provoking factors of stable angina*? (1)
• Physical exertion
• Emotional stress
• Cold/ wind
• Heavy meals
• Uncommon
o lying flat  decubitus angina
o vivid dreams  nocturnal angina
44. What are the most common relieving factors of stable angina?* (1)
• Rest
• Termination of physical exertion
• Nitroglycerin sublingually 1 tab 0.5 mg  30 seconds
• ISDN 1 tab 10 mg  5 minutes
45. Describe possible irradiation of angina pain! (1)
• Left shoulder/arm (ulnar part of the hand)

• Both shoulders/arms
• Lower jaw
• Does not irradiate higher than lower jaw and lower than navel
• Less frequently, left scapula and epigstrium
46. What laboratory tests should be performed in a patient with suspicion of stable
angina? (2)
• Blood biochemistry
o Lipid fractions
o Glucose
o Creatinine
o Potassium
o AST/ALT
o ESR  to exclude arteritis
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• Full blood count
47. What non-invasive tests are used to diagnose myocardial ischemia (name all
possible)? (2)
• Stress ECG + VEM

• MPS
• Stress Echocardiography
48. What additional tests (except laboratory) should be performed in patient with
suspicion of stable angina (name particularly)? (2)
• Rest ECG
• Exercise ECG
• MPS
• Stress EchoCG
• Coronary angiography
49. What ECG signs on veloergometry confirm stress induced myocardial ischemia?
(1)
• Horizontal or down-sloping ST depressions

• Typical angina + ST depression  1 mm ( 2 leads)
• OR
• ST depressions  2 mm ( 2 leads)
50. What cases veloergometry test is considered positive ? (1)
• Typical angina + ST depression  1 mm ( 2 leads)

• OR
• ST depressions  2 mm ( 2 leads)
51. Explain stress echocardiography! Briefly describe the method! How is stress
induced ischemia diagnosed? (2)
• It is done during rest and exertion

• Either the patient exercises or is given dobutamine which induces stress
• During the maximal stress look for the region in the left ventricle which is contracting
less or not contracting  akinesia/hypokinesia which is most likely due to ischemia
52. Explain myocardial perfusion scintigraphy (SPECT)! Briefly describe the method!
How is stress induced ischemia diagnosed? (2)
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• IV injection a molecule linked with a radioactive tracer, done at rest and during maximal
exercise, radionuclide isotope 99mTc vai 201Tl
• Tracers stick to viable and perfused myocardial cells

• Wherever the myocardiam is viable and perfused with blood and with SPECT you
analyze depending on tracer signal
• Perfusion intensity is quantified  the lighter the better the perfusion
• EF and LV dimensions are measured (at exertion and rest)
• If as bad during stress and excersice  Scar
• Worse during the stress  stress-induced ischemia
53. Name non-invasive image diagnostic method for diagnosis of coronary

atherosclerosis! (1)
• MS-CT
• Coronary CMR
54. Which test nowadays is a „gold standard” in diagnosis of coronary artery

disease?* (1)
55. Please describe coronary angiography!* (1)
• Coronary angiography is a procedure that uses contrast dye, usually containing iodine,
and x ray pictures to detect blockages in the coronary arteries that are caused by plaque
buildup
• Golden standard
• Done in radial artery, previously femoral
56. Explain how FFR (fraction flow reserve) is measured! (1) What is normal
measurement result? What do changes in FFR indicate? What are borderline
results? (1)
• Invasive method which estimates physiologic significance of a lesion �

• Difference between two pressures is measured: – coronary pressure distal to stenosis
(Pd)�– aortic pressure (PAo) �
• Maximal hyperemia (i.v. or i.cor. adenosine) �
• Significant stenosis, if FFR<0.75 [<0.80] �
• Gray zone’, if FFR 0.76-0.79 (unless LM lesion – �then it is significant) �
• Not significant, if FFR >0.80 �
57. Name intravascular image diagnostic methods! (1)
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• For ischemia
o FFR
o iFR
• For atherosclerosis
o Coronary angiography
o IVUS (intravascular ultrasound)
o (VH, iMAP)
58. Please describe – “stenosis” and “occlusion” of coronary artery!* (0.5)
• Stenosis refers to the narrowing of the coronary artery meanwhile occlusion refers
to the complete blockage of the artery
59. Which degree stenosis (in percent) is considered to be hemodynamically

significant? (1)
• More than 70 %
60. Please name all three (or four) main coronary arteries! (1)
• LM, supplies 75-100 % of left ventriculum

• LAD, supplies anterior wall of LV
• LCX, supplies LV posterior wall, sometimes inferior wall
• RCA, supplies LV inferior wall
61. Name the main groups of anti-anginal drugs! (1) Give an example for each group!
(1)
• Beta blockers
o Bisoprolol
• Ion channel inhibitor
o Ivabradine
o Amlodipine
o ISMN
• Other agents
o Ranolazine
62. Describe principles of stable angina treatment! (2)
• Secondary prevention
o Lifestyle
o Aspirin
o Statins
o DM treatment
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o Antihypertensive therapy
• Antianginal therapy
• Revascularization
63. Name most frequently used beta-blockers* with dosage! (1)
• Bisoprolol 2.5 – 10 mg x 1
• Metoprolol succinate 25 – 100 mg x 1
• Nebivolol 2.5 – 5 mg x 1
64. Name selective beta-blockers!* (1)
• Atenolol
• Acebutolol
• Metoprolol
• Bisoprolol
• Nebivolol
• Betaxolol
• Esmolol
65. Name non-selective beta-blocker! (1)
• Propranolol
• Sotalol
• Timolol
• Nadolol
• Penbutolol
• Oxprenolol
66. Name beta-blocker(s) with alfa-blocker properties! (1)
• Nebivolol
• Carvedilol
• Labetalol
67. Name beta- blocker(s) with vasodilating properties! (1)
• Carvedilol
• Labetalol
68. Name absolute contraindications for beta-blocker use! (1)
• Symptomatic bradycardia
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• Cardiogenic shock and hypotension

• Decompensated heart failure
• Asthma
• Pheochromocytoma
69. Name most frequently used dihydropyridine calcium channel blockers* with
dosage! (2)
• Amlodipine 5 – 10 mg x 1
• Lacidipine 4 – 6 mg x 1
• Felodipine 5 – 10 mg
70. What is the most common adverse effect of amlodipine and felodipine? (1)
• Peripheral/ankle edema
• Reflex tachycardia
• Facial flushing
• Headaches
71. Name most frequently used non-dihydropyridine calcium channel blockers! (1)
• Dilitiazem
• Verapamil
72. Please name three calcium channel blockers from different groups and describe
their pharmacodynamic differences! (2)
73. Please name most frequently used long acting nitrates!* (1)
• ISMN
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• ISDN
74. Explain nitrate tolerance and how to avoid it! (1)
• Over time, the effectiveness of nitrates declines

• 6 – 8 hour nitrate free period
• Best achieved at night
75. What is the most common adverse effect of nitrates? (1)
• Circulatory dysregulation: hypotension, reflex tachycardia

• Headache
• GERD
• Tolerance
76. Name an anti-anginal drug which selectively slows sinus rhythm but does not
affect any other structure of the heart (has no effect on atrioventricular
conduction)? (1)
Ivabradine
77. Name anti-anginal drugs which reduce ischemia by direct impact on

cardiomyocites!
• Ranolazine,
• Meldonium
• Trimetazidine
78. Which are the most effective antianginal drugs for the treatment of vasospastic
angina? (1)
• Ranolazine
79. Which anti-anginal drugs are contraindicated in patient with bronchial asthma?
Which are allowed to use in this case? (1)
• Beta blockers are contraindicated

• Calcium channel blockers and ion channel inhibitors are allowed
80. Which anti-anginal drugs are contraindicated in patient with bradycardia? Which
are allowed to use in this case? (1)
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• Beta blockers contraindicated

• Long-acting nitrates and DHP are allowed
81. Which anti-anginal drugs induce bradycardia but are not contraindicated in patient
with bronchial asthma? (1)
• Verapamil
• Diltiazem
82. Which anti-anginal drugs can cause headache? (1)
83. Name two main methods of revascularization!* (1)
• PCI/PCTA (percutaneous coronary intervention)

• CABG (coronary artery bypass grafting)
84. Explain PTCA/ PCI, briefly describe the method !* (2)
85. Explain BMS! (1)
• Bare metal stent

• No drug elution
• Endothelization within a month
• Clopidogrel should be taken 1 month
• Higher risk of in-tent restenosis
86. Explain DES! Name the advantages and disadvantages of these stents! (2)
• Drug-eluting stents
• Default stents
• Eluting of cytotoxic drugs inhibiting neointimal growth/proliferation (tacrolimus,
everolimus)
• Low risk of restenosis
• Slower endothelizayion
• Clopidogrel should be taken 6 months (3 – 12 months on individual basis)
87. Explain BVS (type of stent)! (1)
• Bioresorbable vascular scaffold

• Dissolves within 2-3 years after implantation
• MRI/CT compatibility
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• More even support of arterial wall
88. Explain coronary artery bypass grafting (CABG) , briefly describe the method!*
(2)
• Coronary artery bypass graft

• Performed by a cardiac surgeon
• On/ off pump surgery
• Access is usually by sternotomy, rarely lateral
• Grafts:
o Vena saphena magna (SVG – saphenous vein graft)
▪ 10% occluded after one year,
▪ May be affected by atheroma!
o LIMA / LITA (left internal mammary/thoracic artery) • The best long-term
patency – 90% open after 10 years
▪ Usually anastomosis to LAD
▪ RIMA / RITA (right artery) is also used
o Radial and other arteries less frequently used
• It is not mandatory to use clopidogrel or warfarin after CABG! The usual prevention!
Warfarin only after valve replacement, if indicated
89. What kind of material(s) coronary artery shunts are made of? (1)
• BMS
o Stainless steel
o Cobalt chromium
• Bioresorbable
o Polylactate
o Magnesium
• DES
o Tacrolimus
o Everolimus
o Sirolimus
90. Which drugs must be used in order to prevent stent thrombosis after PCI? (1)
• Antiplatelet
o Clopidogrel
91. What antiplatelet drug (name, dosage and duration of use) should be used in
patient with confirmed coronary artery disease? (1)
• Aspirin 75 mg
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• Clopidogrel 75 mg, taken 1 month in BMS revascularization and 6 months in DES

revascularization
92. Patient (54 years old man) complains of stubbing pain at ictus cordis region
appearing independently on physical activity. Pain may occur for a few seconds
and may last for 2-3 hours. Such complaints exist already one month, but durung
last 48 hours are appearing at rest. Which diagnosis is most probable – toracalgia,
stable angina or unstable angina?* (0.5) Is coronary angiography indicated due to
these complaints?* (0.5) (1 point)
93. Patient (62 years old man) complains of squeezing chest discomfort, which lasts
for half a year. Complaints typically appear in the morning, when he starts to
walk, but pain does not repeat during the day. Patient is smoking one cigarette
pack daily for 40 years. What other risk factors should be clarified? (1) What is
your primary diagnosis (formulate correctly!)? (1) Which investigations should be
performed? (2) (4 points)
94. Please write the scheme of medical treatment for patient with stable angina
functional class II, heart rate 84x’, TA 162/94 mmHg, TC 6.0 mmol/l, TG 1.8
mmol/l, HDL 1.2 mmol/l, LDL 3.98 mmol/l. (3)
• For HR beta blocker Bisoprolol 2.5 – 10 mg x 1

• For BP calcium channel blockers Amlodipine 5 – 10 mg x 1
• Atorvastatin 10 – 80 mg x 1 to lower total and LDL-cholesterol
• (For angina pain relief long-acting nitrates ISMN 30 – 60 mg x 1, avoid tolerance)
95. Please write the scheme of medical treatment for patient with stable angina
functional class III, heart rate 56x’, TA 174/92 mmHg, TC 6.0 mmol/l, TG 1.8
mmol/l, HDL 1.2 mmol/l, LDL 3.98 mmol/l. (3)
Amlodipine 5 – 10 mg x 1 for BP and Atorvastatin 10 – 80 mg x 1

(For angina pain relief long-acting nitrates ISMN 30 – 60 mg x 1, avoid tolerance)
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Arterial hypertension
1. What is the correct patient position during arterial pressure measurement? (1)
• Patient is sitting comfortably in a warm room

• Clothes with sleeves are taken off
• Arm chair should be used
• Forearm lies freely on a hard surface and hand is relaxed
2. How much cuff inflation is required during arterial pressure measurement? (1)
• Inflate while palpating radial pulse  until it disappears

• Additional 20 mmHg
3. Which device (meter) is considered to be the “gold standard” for arterial

pressure measurement?* (1)
• Mercury sphygmomanometer
4. What does orthostasis mean?* How is it checked? (2)
• Decrease in blood pressure that happens soon after standing

• Patient being in upright/ standing position and measure BP after one minute
• Postural hypotension
o Drop in systolic BP > 20 mmHg
o Drop in diastolic BP > 10 mmHg
5. What are the conditions from patient side for correct blood pressure
measurement? (2)
• Consider recent use of medication

• No coffee, tea, coke, cigarette within previous 30 mins, ideally 2 hours
6. How systolic and diastolic blood pressure is detected by auscultation?* (1)
• Systolic BP  appearance of Korotkoff sounds

• Diastolic BP  disappearance of Korotkoff sounds
7. First degree of arterial hypertension – what are systolic and diastolic

measurements?* (1)
• BP 140 – 159/ 90 – 99 mmHg
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8. Second degree of arterial hypertension – what are systolic and diastolic

measurements? (1)
• BP 160 – 179 / 100 – 109 mmHg
9. Third degree of arterial hypertension – what are systolic and diastolic

measurements? (1)
• Systolic  180 mmHg

• Diastolic  110 mmHg
10. What does isolated systolic hypertension mean? (1)
• Systolic  140 mmHg

• Diastolic < 90 mmHg
11. What blood pressure is considered as arterial hypertension when measured in

in outpatient conditions by patient him/herself? (1)
• Systolic BP  135 mmHg and/or  85 mmHg diastolic
12. What blood pressure during daytime is considered as arterial hypertension

when measured in 24 hour ambulatory monitoring? (1)
• Systolic BP  130 and/or  80 mmHg diastolic
13. What is “white coat hypertension”? (1)
• Elevated blood pressure on clinical setting usually in presence of physician but

not in other settings outside the clinic
• Nevertheless it points to possible tendency for HTN
• Observed in many true hypertensives as well
14. What additional examinations are needed to diagnose white coat

hypertension? (1)
• Repeated measurements (the same visit and repeated visits)

• Nurse measurements
• Unattended measurements
• Self measurements at home
• 24 hour ambulatory monitoring
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15. What is masked hypertension? (1)
• Elevation of BP in daily measurements at home

• BP is not elevated in clinical setting
16. What is spurious hypertension? (1)
• Spurious HTN, can be observed in young tall males and only systolic isolated
HTN, the explanation could be because the arteries are longer, wider and more
elastic this causes an increase in the pulse pressure amplification.
17. Is there a difference between central and brachial blood pressure? If yes,
explain! (1)
• The central blood pressure is lower than the brachial blood pressure due to
pulse pressure amplification as pulse wave travel down the arterial wall.
18. What is pulse wave? (1). What does pulse wave velocity indicate? (1)
Pulse wave is the wave propagating along the blood vessels wall during systole.
Measure of arterial stiffness, or the rate at which pressure waves move down the
vessel.
19. What is pulse pressure? (1)
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Pulse pressure= systolic – diastolic pulse pressure
20. What is augmentation pressure? (1)
Augmentation pressure is the reflected wave pressure added to the systolic pressure
21. Characterize malignant hypertension! (1)
• Extremely adverse development of arterial HTN with very elevated blood

pressure and early manifestation of severe complications:
o Encephalopathy or retinopathy with accompanying papilledema
o Also eg. stroke, LV acute failure, cardiogenic pulmonary edema
• Often  180/120 mmHg
22. Please explain primary and secondary arterial hypertension!* (0.5) What is the
prevalence of them? (0.5) (1 point)
• Primary HTN 90 – 95 %
o Mechanism still unclear
o Tends to be familial and as a consequence of interaction between
environmental and genetic factors
• Secondary HTN 5 %
o Renal disease
o Endocrine disorder
o Medications
o Obstructive sleep apnoea
23. What clinical signs indicate possible secondary hypertension? (2)
• Early onset age < 40

• Sudden onset or sudden worsening of HTN in patients with well controlled BP
• Severe, or hypertensive crisis, malignant HTN
• Severe HMOD
24. Name possible causes of secondary hypertension! (2)
Renal (renal vascular stenosis, PCKD, chronic renal failure), endocrine, others
(Scleroderma, Obstructive sleep apnea, coarctation of aorta, anemia)
25. What endocrine pathologies may cause arterial hypertension? (2)
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Conn’s syndrome
Pheochromocytoma
Hyperthyroidism
Oestrogen birth control pills
Acromegaly
Primary hyperaldosteronism
Cushing’s syndrome
26. What renal pathologies may cause secondary hypertension? (2)
Renal vascular stenosis, PCKD, renal tumors, diabetic nephropathy, renal hypoplasia,
vasculitis, glomerulonephritis
27. What does coarctation of the aorta mean?* (1) Why and how this pathology
can influence blood pressure? (1)
• Localized narrowing of descending aorta

• Usually distal to the origin and left subclavian artery
• Normally systolic BP is 20 mmHg higher than BP measured at a. brachialis
and distal BP is equal
• But in coarctation
o BP is higher and can cause secondary hypertension
o Heart failure
o Weak femoral pulse
o Systolic murmur  posteriorly over coarctation
o Ejection click/systolic murmur
o Collaterals form in periscapular/internal/mammary/intercostal arteries
28. Name the criteria of metabolic syndrome! (2)
• Insulin resistance
• Abdominal obesity
• Primary HTN
• Dyslipidemia
• Extremely high risk of atherosclerotic diseases
29. Please name “target organs”, which are damaged in case of long-lasting
arterial hypertension! (1)
• Heart
• Kidneys
• Eyes
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• Brain
• Large arteries
30. Please name characteristic target organ damage signs and explain how it can
be diagnosed? (2)
LVH  overload, heart failure  EchoCG

Hypertensive nephropathy  microalbuminuria, proteinuria
Hypertensive nephropathy  visual inspection  Bleeding or exudates, papilledema
Hypertensive encephalopathy  impaired mental function, dementia
Atherosclerosis  CDH, ischemic stroke, claudication, intestinal ischemia
31. What cardiac damage does hypertension cause? (2)
• LVH  overload  LV failure  Pulmonary congestion  Right atrium and

ventricule overload  oedema
32. What ECG changes can be found in a patient with long-lasting elevated
arterial pressure? (1) Describe these ECG changes (what exactly changes)! (1)
(2 points)
Persistent high voltage QRS is usually indicative of LVH, widening of P wave is

suggestive of left atrial enlargement and changes in S-T segment and T wave is
mostly due to myocardial ischemia and injury with or without LVH
Depending of the grade of HTN it can be as well asymptomatic.
33. What changes on echocardiography may be present in a patient with long-

lasting arterial hypertension?* (1)
• LVH
• Dilation
• EF
34. What are the manifestations of kidney damage in case of arterial

hypertension? (please describe chronologically) (2)
• Systolic murmur in renal artery stenosis

• Atherosclerosis
• Hypertensive nephropathy
• Microalbuminuria
• Proteinuria
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• Chronic renal failure

• Edema
35. What is the earliest sign of renal damage (diagnosed in clinical practice) in
case of primary arterial hypertension? (1)
• Slow decrease in renal function

• Blood test  GFR, serum creatinine  uremia and azotemia
• Protein, sugar, blood in urine
• Increased urination frequency, nocturia, polyuria
36. Which changes in what tests indicate renal damage in a patient with arterial
hypertension (name investigations and abnormal findings)? (2)
Blood analysis
Proteinuria
Microalbuminuria (30-300mg)
Decreased GFR <60
Increased urination frequency, nocturia, polyuria
37. What method is used for evaluation of carotid artery damage in patients with
hypertension? What is measured? (1)
CT angiography with visualization of carotid artery stenosis
38. What changes in urinalysis can be explained by primary arterial hypertension?

(1)
• Protein, blood, glucose in urine

• Reduced GFR  increased pressure  increased flow  decreased filtration
• Proteinuria
o Injury to podocytes
o Scarring
o Depositions in the matric
• Hematuria
o Inflammation
39. What changes and in which arterial beds will be found in case of arterial
hypertension? (1) What complications can be caused ? (1)
• Coronary arteries  CHD
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• Carotid arteries  ischemic stroke

• Aorta/ leg arteries  claudication/ gangrene
• Renal arteries  vasorenal mechanism of HTN
• Mesenterical arteries  intestinal ischemia
40. Describe the degrees of hypertensive retinopathy! (1)
1. Mild narrowing of arterioles

2. Constriction of veins at arterial crossings  AV nipping
3. Bleeding and/or exudate “cotton wool”
4. Papilloedema
41. What examinations will you perform for a patient with possible primary
arterial hypertension? Why? (2)
Blood pressure measurement

If severe immediately or not  2nd type HTN
HTN before 30yo  2nd HTN
Blood test for excluding 2ndary causes of HTN
Ie: hyperaldosteronism = hypokalemia
42. What blood biochemical tests will you perform for a patient with possible
primary arterial hypertension? Why? (1)
Sodium, potassium
Creatinine with GFR
Blood glucose
Lipids
43. What is ankle-brachial index? What does it indicate? How is it measured? (1)
The ankle-brachial index test compares the blood pressure measured at your ankle
with the blood pressure measured at your arm. A low ankle-brachial index number
can indicate narrowing or blockage of the arteries in your legs.
ABI<0,9  Indicate PAD
From 0,91 to 0,99 = borderline PAD
From 1 to 1,4 = No PAD
44. Formulate diagnosis in patient with blood pressure usually 190-200/100-106

mmHg and with no evidence of secondary causes! (1)
• Grade 3 /severe primary hypertension
1
0
0
45. Formulate diagnosis in a patient with blood pressure ordinarily 172/94 mmHg
and with no evidence of secondary causes! (1)
• Grade 2 primary hypertension
• Isolated systolic hypertension
• High normal prehypertension
48. Formulate diagnosis in a patient with blood pressure ordinarily 164/100

mmHg and with no evidence of secondary causes! (1)
• Grade 2 primary hypertension
49. Formulate diagnosis in a patient with known membranoproliferative

glomerulonephritis and blood pressure usually 164/100 mmHg! (1)
• Grade 2 hypertension secondary to glomerulonephritis
50. Formulate diagnosis in patient with Cushing syndrome and blood pressure
usually 142/92 mmHg! (1)
• Grade 1 hypertension secondary to Cushing’s syndrome

51. Which minerals are advised to intake more and which less in case of arterial
hypertension? (1)
• Less Na+ and more K+, Mg2+, Ca2+
52. Basic principles of therapy in asymptomatic patient with blood pressure

142/82 mmHg and low cardiovascular risk? (2)
• Lifestyle advice, no medical therapy
• Diet
• Cessation of smoking and excessive alcohol use
• Exercise
• Weight reduction
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0
1
53. Basic principles of therapy in asymptomatic patient with blood pressure

146/92 mmHg and high cardiovascular risk? (2)
• Medical therapy required

• ACE inhibitors or angiotensin receptor blockers
• Diuretics
• Beta blockers
54. Please name first-line medications (five groups) in the treatment of arterial
hypertension (name at least one example of each group)! (2 points)
• Diuretics
o Indapamide
• Beta blocker
o Bisoprolol
• CCB
o Nifedipine
• ACE inhibitor
o Lisinopril
• ARB
o Candesartan
55. Please name second-line medications in the treatment of arterial hypertension

(with examples of drugs)! (2)
• Alpha blockers
o Phentolamine (non-selective)
• Centrally active alpha 2 agonist
o Clonidine
o Methyldopa
• Centrally acting imidazoline receptor agonists
o Moxonidine, rilmenidine
56. What is the mechanism of action of ACEI? (1) Please name at least two
examples (preferable with doses)! (1) (* at least one)
• Inhibit conversion of Ang I to Ang II which decreases vasoconstriction and in
turn decreases BP
• Decreased secretion of aldosterone  decreased Na and reabsorption
• Lisinopril
• Ramipril 5 – 10 mg
• Enalapril
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2
57. What are the contraindications for ACEI? (1)
• Pregnancy
• Bilateral renal artery stenosis
• Hyperkalemia
• Quinke’s edema
58. Please name the most common side-effects of ACEI! (1)
• Cough
• Rash
• Hypotension
• Hyperkalemia
• Renal dysfunction
59. Please name non-dihydropyridines! (1) What are the pharmacodynamic

differences between them (effect on myocardium and arteries)? (1)
Phenylakylamines
• Verapamil
• Decrease contractility of heart, slows down AV conduction and sinus rhythm
• Potent myocardial depressant activity
• Weak natriuretic/diuretic effect
Benzothiazepines
• Ditiazem
• Moderate vasodilator
• Moderate myocardial depressant activity
• Decreases peripheral resistance
60. Please name dihydropyridines* (preferable with doses)! (1) What is their
effect on myocardium and arteries? (1) (2 points)
• Amlodipine 5 -10 mg
• Felodipine 2.5 – 10 mg
• Lacidipine 4 – 6 mg
• Potent vasodilator
• Minimal myocardial depressant activity
• Weak diuretic effect
61. What are the contraindications for calcium channel blockers? (1)
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0
3
Verapamil
• II/III degree AV block
• CHF
• WPW syndrome
• Therapy with BB
Dihydropyridines
• Hypotension
62. What are possible side-effects of calcium channel blockers? (1)
• Tachyarrythmia
• Flushing/palpitations
• Peripheral edema
• Sympathoadrenal activity
• CHF
63. Which calcium channel blockers have bradycardizing effect? (1)
• Verapamil and diltiazem
64. What are “tropic” effects in heart of beta-blockers? (0.25 for each) (1 point)
• Negative chronotropic
• Negative inotropic effect
• Negative bathmotropic
65. What are the contraindications for beta-blockers? (1)

• Symptomatic bradycardia
• Cardiogenic shock and hypotension
• Decompensated heart failure
• Asthma
• Pheochromocytoma
66. What are the side-effects of beta blockers? (1)
• Bronchospasm
• Heart failure
• Lethargy
• Impotence
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0
4
67. Please name at least one selective and one non-selective beta-blocker
(preferable with doses)!* (1)
• Selective: Bisoprolol 5 – 10 mg
• Non-selective: Propranolol 120 – 320 mg
68. Which beta receptors are prevalent in myocardium? (0.5)
• Beta 1 receptors
69. Does metoprolol (and how) effect heart rate? (0.5) Does ramipril (and how)
effect heart rate? (0.5) (1 point)
• Metoprolol affects, negative inotropic, negative chronotropic

• Ramipril doesn’t
70. Does perindopril (and how) effect heart rate? (0.5) Does bisoprolol (and how)
• Perindopril doesn’t
• Bisoprolol does, negative inotropic, chronotropic
71. Does bisoprolol (and how) effect heart rate? (0.5) Does indapamide (and how)

• Indapamide doesn’t
72. Does indapamide (and how) effect heart rate? (0.5) Does losartan (and how)
• Indapamide doesn’t
• Losartan doesn’t
73. Does candesartan (and how) effect heart rate? (0.5) Does amlodipine (and
how) effect heart rate? (0.5) (1 point)
• Candesartan doesn’t
• Amlodipine does, reflex tachycardia
1
0
5
74. Does diltiazem (and how) effect heart rate? (0.5) Does lacidipine (and how)
• Diltiazem does, decrease contractility, slows AV conduction and weakens

sinus rhythm
• Lacidipine does, reflex tachycardia
75. Does verapamil (and how) effect heart rate? (0.5) Does bisoprolol (and how)
• Verapamil does, reflex tachycardia

76. Does perindopril (and how) effect heart rate? (0.5) Does amlodipine (and
how) effect heart rate? (0.5) (1 point)
• Perindopril doesn’t
• Amlodipine does, reflex tachycardia
77. Please name beta-blockers with vasodilator’s properties! (1)

• Carvedilol
• Labetalol
78. Please name AT II receptors blockers (ARBs)! (1)
• Candesartan
• Valsartan
79. What are the contraindications for ARBs? (1)
• Similar to ACE inhibitors

• Pregnancy
• Bilateral renal artery stenosis
• Hyperkalemia
• Quinke’s edema
80. Name diuretics used as first-line medication in arterial hypertension (at least
1) (2)
• Indapamide
• Furosemide
• Hydrochlorthiazide
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0
6
81. In what cases loop diuretics are used in arterial hypertension patients? (1)
• Renal failure
• CHF
82. Which diuretics are used in patients with severe renal failure (GFR < 30
ml/min) in case of arterial hypertension? (1)
• Loop diuretics
o Furosemide
83. Which diuretics are used in patients with heart failure in case of arterial
hypertension? (1)
• Thiazides
o Hydrochlorthiazide
o Indapamide
84. Name potassium sparing diuretics (0.5). Which of them are aldosterone
antagonists? (0.50 (1 point)
• Amiloride
• Spironolactone  aldosterone antagonist
85. What are the contraindications for diuretics? (1)
• Gout
• Pregnancy
86. What are the side-effects of diuretics? (1)
• Hypokalemia risk
• Can increase insulin resistance
• Increase uric acid levels
• Hypersensitivity
87. Please name central-acting antihypertensive agents (the group and example)!
(1)
• Centrally active alpha 2 agonist

o Clonidine
o Methyldopa
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7
• Centrally acting imidazoline receptor agonists

o Moxonidine, rilmenidine
88. Please name alpha-blockers! (1) In what other disease treatment are they used?
(1) (2 points)
• Phentolamine (non-selective)
• Doxazosin
• Prazosin
• Benign prostate hyperplasia
89. What are the contraindications for alpha-blockers treatment?
• Orthostatic hypotension
• Not advisable in patients with CHF
1
0
8
Basic principles of cardiovascular system investigation.
• Describe the principles of jugular vein inspection! (1)
• JVP can be used as substitute marker for central pressure

• Measure by observing level of pulsation of internal jugular vein
• JVP reflects rx atrial pressure
• Patient reclining with head elevated 45°, neck muscles relaxed. If JVP is low: patient
should lay down, if JVP is high: patient should sit upright
• measure elevation of neck veins above the sternal angle (Lewis method).
• Normal CVP <= 4 cm above sternal angle (<7mmHg/9cmH2O)
• What does jugular vein pulsation indicate? (1)

High pressure in internal jugular vein high central venous pressure
• Describe what is hepatojugular reflux! (1)

Pressing on abdomen causes increase in JVP: if rise persists >15s the sign is positive.
Causes: LVF, inability to eject increased venous return
• What is the correct doctor’s and patient’s position during the heart auscultation?
(1)
Doctor on patient rx side, patient sitting or standing.
• What is the sequence of auscultation of the valves?* (2)

Mitral, Aortic, Pulmonary, Tricuspid, Erb’s point.
• What is the suspected diagnosis in a case of systolic murmur heard at the back
between scapulae? (1)
• Coarctation of aorta
• Mitral valve prolapse with moderate regurgitation
• What is the possible aetiology of systolic murmur heard over the carotid artery (-
ies)? * (1)
• Aortic valve stenosis
• Aortic supravalvular stenosis
• Carotid bruit
• What is the possible aetiology of the murmur over the abdominal aorta? (1)
• Abdominal aorta aneurysm or dissection
• Aortic sclerosis (arteriosclerosis obliterans)
• Peripheral vascular disease
• What is the possible aetiology of the murmur over the femoral artery (-ies)? (0.5)
• Aortic regurgitation-insufficiency
• Aortic aneurysm
• Lead intoxication
• Chlorosis
• Thyphoid fever
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• What kind of the murmur is auscultated in a patient with aortic stenosis?* (1)
Mesosystolic ejection murmur, diamond, loud and rasping. Radiate to carotid.
• What kind of the murmur is auscultated in a patient with mitral regurgitation ?* (1)
Pansystolic murmur, blowing.
• What kind of the murmur is auscultated in a patient with aortic regurgitation?* (1)
Systolic ejection murmur, decrescendo, and Austin Flint murmur.
• What kind of the murmur is auscultated in a patient with tricuspid regurgitation?

(1)
Pansystolic, blowing.
• What kind of the murmur is auscultated in a patient with mitral stenosis?* (1)
Mid-diastolic, rambling, low pitch.
• Auscultation site of the aortic valve?* (1)

2nd right ICS, right sternal border.
• Auscultation site of the mitral valve?* (1)

1-1,5cm medially from L.Medioclavicularis in 5th ICS.
• Auscultation site of the tricuspid valve?* (1)

• 4th left ICS
• lower 1/3 of sternum
• Proc. Xyphoideus
• 4th right ICS, right sternal border
• Auscultation site of the pulmonary valve?* (1)

2nd left ICS.
• Auscultation site of Erb’s point? What is auscultated in Erb’s point?* (1)

3rd left ICS, for ausculation of aortic valve insufficiency and rx side pathologies.
• What is the transmission (irradiation) site of the murmur in aortic stenosis? (1)
To the carotid.
• What is the transmission (irradiation) site of the murmur in mitral regurgitation?

(1)
To axilla.
• In which patient position mitral murmurs are louder on auscultation? (1)

• Left lateral decubitus in expiration
• Mitral valve prolapse: standing
• In which patient position pericardial friction rub is louder on auscultation? (1)

Sitting forward, in expiration.
• In which patient positions murmur of aortic regurgitation is louder on auscultation?

(1)
Sitting forward in expiration-
1
1
0
• Definition of protosystolic murmur! (0.5)
Ocurring early systole (fisrt 1/3), decrescendo.
• Definition of mesosystolic murmur! (0.5)

Occurring in mid systole (second 1/3), diamond.
• Definition of pansystolic murmur! (0.5)

Lasting through the whole systole.
• Definition of telesystolic murmur! (0.5)

Occurring in late systole (last 1/3).
• Definition of holosystolic murmur! (0.5)

As pansystolic.
• Definition of presystolic murmur! (0.5)

In last 1/3 of diastole.
• Definition of protodiastolic murmur! (0.5)

In first 1/3 of diastole.
• Definition of mesodiastolic murmur! (0.5)

In second 1/3 of diastole
• Definition of pandiastolic murmur! (0.5)

During whole diastole.
• Definition of telediastolic murmur! (0.5)

In last 1/3 of diastole.
• Definition of holodiastolic murmur! (0.5)

As pandyastolic.
• Which murmurs are better auscultated on inspiration? (1)

Rx heart side (Tricuspid, Pulmonary)
• Which murmurs are better auscultated on expiration? (1)

Lx heart side (Mitral, Aortic)
• Define A2! In which cases is it auscultated? (1)

• Systemic hypertension
• Accented aortic valve closure
• Define P2! In which cases is it auscultated? (1)

• Pulmonary HT, mitral stenosis, mitral regurgitation
• Accented pulmonary valve closure
• What does S3 gallop rhythm indicate? (1)

LV failure, Mitral regurgitation. May be normal in young adults, athletes, pregnancy,
fever.
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1
• What does S4 indicate? (1)
Strong atrium contraction against on compliant ventricles, usually in LVH.
• What kind of murmur is auscultated in a patient with hypertrophic obstructive

cardiomyopathy (HOCMP)? (2)
Outflow obstruction: harsh ejection/mid systolic murmur.
• Describe acrocyanosis! (1) What does it indicate? (1) (2 points)

• Cyanosis of extremities
• Rx heart failure
• Polycytemia
• Lung disease
• Slow blood flow-cogestion
• Describe central cyanosis! (1) What does it indicate? (1) (2 points)

• Tongue, lips, cheeks
• Lx heart failure
• Low O2 sat
• What location of edema is characteristic for a walking patient with congestive heart
failure? (1)
Sacral area.
• What location of edema is characteristic for a recumbent patient with congestive

heart failure? (1)
Lower legs, medial ankles, feet.
• Ictus cordis location? (0.5) In which cases and how can ictus cordis be deviated? (0.5)
(1 point)
• 1-1,5cm from Linea Medioclavicularis Sx in 5th ICS. (higher and more lateral in
children)
• Deviation: laterally and downward in LVH; lateral and/or downwards in
cardiomegaly; pleural or pulmonary diseases; chest deformity.
• Define thrill of the chest wall! (1) When is it observed?

• Vibration-tactile equivalent of murmur.
• Most common causes: aortic stenosis, pulmonary stenosis, mitral
regurgitation, ventricular septal defects.
• Palpation sites of central pulse?* (1)

• Carotids
• Femoral arteries
• Palpation sites of periferal pulse? (1)

• Radial A.
• Brachial A.
• Temporal A.
• Popliteal A.
• Post. Tibial A.
• A. Dorsalis Pedis
1
1
2
• Define pulse deficiency! (1)
Difference between central and peripheral pulse (central higher than peripheral), ususlaly
due to Afib or frequent extrasystoles.
• In which cases pulsus celer et altus is palpable? (2)

Aortic regurgitation, aortic insufficiency
• In which cases pulsus tardus et parvus is palpable? (2)

Aortic stenosis
• Define pulsus paradoxus! What pathology does it indicate ? (2)

• Abnormal decrease of stroke volume, BP, pulse amplitude during
inspiration
• Causes: cardiac tamponade, sleep apnoe, COPD.
• Define pulsus alternans! (2)

• Alternation of strong and weak beats
• CHF, cardiac insufficiency
• Define dyspnoe!* (1)

Sense of breathlessness-breathing difficulty-perception of effort to breathe.
57. Define inspiratory dyspnoe! What cardiovascular pathologies does it indicate? (1)
Diffculty of breathing in inhalation phase, common in CHF, Lx heart failiure with
pulmonary edema and cardiac tamponade.
58. Define exspiratory dyspnoe! Is it characteristic to cardiovascular pathology? (1)

Diffculty of breathing in exhalation, usually asthma or COPD.
59. Define orthopnoe!* (1) What does it indicate?* (1) (2 points)

Dyspnoe lying flat, indicates advanced HF.
60. Define cardiac asthma ! (1) What are the symptoms? What does it indicate? (1) (2
points)
Syndrome of coughing, wheezing and dyspnoe resembling asthma but caused by
pulmonary edema in result of Lx heart failure.
61. What pulmonal auscultation finding is characteristic to left ventricle failure? (1)
Crackles on inspiration.
62. Describe the nature of the pain in a patient with angina!* (1)
Hypoxia of cardiac muscle due to reduced blood flow.
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CHD. Acute coronary syndromes.
1. Explain the pathogenesis of acute coronary syndrome!* (1)
Atherosclerotic plaque rupture and coronary artery (partial or complete) occlusion

Platelet aggregation  coagulation cascade  Thrombus
TXA2 release  Coronary vasoconstriction
Critical stenosis
2. What are the typical clinical symptoms of myocardial infarction?* (2)
Squeezing pain in the chest  Pressure like, burning, lacerating pain

Sweating, breathlessness, nausea, vomiting
Feeling of impending death (angor animi)
3. What is the typical character of pain in the case of myocardial infarction?*

(1)
Constricting, heavy  Squeezing
4. What is the typical localization and irradiation of pain in a case of

myocardial infarction?* (1)
Retrosternal (more wide-spread than angina)

Irradiating to = arms, neck, jaw, sometimes epigastrium
5. What is the typical duration of pain in a case of myocardial infarction? *

(0.5)
Prolonged = more than 30 minutes (up to 60 minutes)
6. What other complaints (except pain) may occur in a case of myocardial

infarction? (1)
Cold sweat, nausea, vomiting, weakness and fatigue (hypotension), arrhythmia

(syncope), asymptomatic
7. Name atypical localization of pain in a case of myocardial infarction! (1)
Abdominal, peripheral, asymptomatic
8. Explain the difference between unstable angina and stable angina?* (1)
Stable angina (stable fibrous plaque) = predictable, symptoms over long term, related
to effort, demand-led ischaemia
Unstable angina (ruptured, unstable plaque) = Unpredictable, symptoms at rest,

supply-led ischaemia, frequent and nocturnal symptoms, symptoms over short terms
Risk of developing MI/Cardiac death
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9. Name four main clinical forms of unstable angina! (2)
Rest, new onset, increasing and early post-infarction
10. Describe clinical signs and criteria of unstable angina at rest! (2)
Angina occurring at rest and usually prolonged >20 minutes occurring within a week
of presentation
11. Describe clinical signs and criteria of unstable increasing angina! (2)
Previously diagnosed angina that is distinctly more frequent, longer in duration or

lower in threshold (i.e., increased by at least one CCSC class within 2 months of
initial presentation to at least CCSC III severity).
12. Describe clinical signs and criteria of new onset unstable angina! (2)
Angina of at least CCSC III severity with onset within 2 month of initial presentation.
13. Describe clinical signs and criteria of early post-infarction unstable angina!
(2)
Angina that occurs during first 2 weeks after myocardial infarction.
Only thing I was able to find about these 4 questions
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14. Which is first and most significant additional investigation that should be
performed in patient with suspicion of acute coronary syndrome (ACS) in
order to choose optimal treatment strategy?* (0.5)
ECG
15. Describe the classification of acute coronary syndromes by ECG criteria

(which is important in a case of acute phase of ACS)?* (1) In which case is
the strongest possibility that the diagnosis is myocardial infarction?* (1) (2
points)
ST depression, T wave inversion, no changes in concerned leads where

subendocardial ischaemia happens  ACS without ST elevation
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ST elevation >1mm or >2mm in V2, V3  ACS with STE (Highest possibility for
diagnosis MI)
16. Name the two main forms of acute coronary syndromes (written as a final
diagnosis on patient discharge)!* (1)
CHD. Acute coronary syndrome without ST elevation. (Unstable angina, non Q non
STEMI).
CHD. Acute coronary syndrome with ST elevation in (…) wall of left ventricule.
STEMI.
17. Do all the patients with acute myocardial infarction have ST elevations on
ECG?* (1)
No  Non Q non STEMI.
18. Which ECG signs are typical: myocardial infarction in hyperacute phase in
anterior wall of the left ventricle?* (2)
High positive, symmetric T waves in V2, V3 (V1, V4 as well) (no ST elevations)
19. Which ECG signs are typical: myocardial infarction in acute phase in
ST elevations and positive T waves in V2, V3 (also V1, V4) with reciprocal changes
in posterior leads
20. Which ECG signs are typical: myocardial infarction in acute phase in lateral
wall of the left ventricle?* (2)
ST elevations and positive T waves in V5, V6, I, avL and reciprocal changes in
posterior leads
21. Which ECG signs are typical: myocardial infarction in acute phase in inferior
wall of the left ventricle?* (2)
ST elevations and positive T waves in II, III, avF leads and reciprocal changes in high
lateral leads
22. Which ECG signs are typical: myocardial infarction in acute phase in inferior
and posterior wall of the left ventricle? (2)
ST elevations and positive T waves in II, III, avF and V7-V9 and reciprocal changes
in high lateral and anterior leads (V1-V4)
23. Which ECG signs are typical: myocardial infarction in acute phase in
posterior (basal) wall of the left ventricle? (2)
ST elevations and positive T waves in V7-V9 and reciprocal changes in anterior leads
(V1-V4)
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24. Which ECG signs are typical: myocardial infarction in subacute phase in
ST elevations and inverted T waves in V2, V3 (V1 and V4) and reciprocal changes in
posterior leads
lateral wall of the left ventricle?* (2)
ST elevations and inverted T waves in I, avL, V5, V6 and reciprocal changes in

inferior leads
inferior wall of the left ventricle?* (2)
ST elevations and inverted T waves in II, III and avF and reciprocal changes in high
lateral leads
inferior and posterior wall of the left ventricle? (2)
ST elevations and inverted T waves in II, III, avF + V7-V9 and reciprocal changes in
high lateral leads and anterior leads
28. Which ECG signs are typical: myocardial infarction in scar phase in posterior
(basal) wall of the left ventricle? (2)
ST segment on isoelectric line and negative T wave in V7-V9
29. Which ECG signs are typical: myocardial infarction in scar phase in anterior
wall of the left ventricle? (2)
ST segment on isoelectric line and negative T wave in V2, V3 (V1 and V4 as well)
30. Which ECG signs are typical: myocardial infarction in scar phase in lateral
ST segment on isoelectric line and negative T wave in V5, V6, I, avL
31. Which ECG signs are typical: myocardial infarction in scar phase in inferior
ST segment on isoelectric line and negative T wave in II, III, avF
32. Which ECG signs are typical: myocardial infarction in scar phase in inferior
and posterior wall of the left ventricle? (2)
ST segment on isoelectric line and negative T wave in II, III, avF and V7-V9
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33. Which ECG signs are typical: myocardial infarction in scar phase in posterior
(basal) wall of the left ventricle? (2)
ST segment on isoelectric line and negative T wave in V7-V9
34. What are the criteria of pathologic Q wave?(2)
Q width > 0,03

Q depth > ¼ of R depth in the same lead
Q wave present in V2-V3
35. Which ECG signs are typical for acute coronary syndrome without ST-
segment elevations? Which of them are more specific? (2)
ST depression (horizontal, downsloping) >0,5mm in two consecutive leads (MOST

TYPICAL+++)
T wave inversion >1mm in two contiguous leads with dominant R>S
No changes
36. For which coronary artery occlusion left ventricle anterior wall infarction is
typical?1 (1)
LAD
37. For which coronary artery occlusion left ventricle inferior wall infarction is
typical?1 (1)
RCA
38. What shape of ST elevation is characteristic for acute transmural ischemia?

(1)
Horizontal, upsloping, convex
39. Explain the differentiation of myocardial infarction and unstable angina in a

patient with acute coronary syndrome without ST-segment elevations1* (1)
Cardiac markers elevated in case of non STEMI including hs Troponin I and T
40. In which case myocardial infarction develops more often: 1) ACS with ST
elevations or 2) ACS without ST elevations? (0.5)*
41. In which case Q myocardial infarction develops more often: 1) ACS with ST
elevations or 2) ACS without ST elevations? (0.5)*
42. In which case non-Q myocardial infarction develops more often if there has not
been an appropriate treatment: 1) ACS with ST elevations or 2) ACS without ST
elevations? (1)
43. In which case the possibility of unstable angina as a final diagnosis is higher: 1)
ACS with ST elevations or 2) ACS without ST elevations? (0.5)*
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44. Which tests should be performed immediately in patient with ACS with ST
elevations (name in correct order)? (2)
• Myocardial damage markers
45. Which tests should be performed immediately in patient with ACS without ST
elevations (name in correct order)? (2)
• Response test to antianginal treatment
• Myocardial damage markers (Troponins)
• Repeated ECGs
• EchoCG
46. Name the most specific laboratory marker to diagnose myocardial infarction !* (1)
• Troponins [hs-cTn]
47. When (time in hours) the levels of hs- troponin start to elevate after the onset of
myocardial infarction? (1)
• 2 to 3 hours
48. In what time interval (in hours) hs-troponin has to be repeatedly measured in a
patient with suspicion of
ACS? (1)
• Every 3 hours
49. Please name three

myocardial damage markers
used in clinical practice!
(0.5) Which of them starts to
elevate first (time in hours)?
Which one is most specific?
(0.5)
• Troponin I and
Troponin T  the
most specific
• CK-MB (not
routinely)
• Myoglobin (not
routinely) 
elevates first (around
2 hours)
50. In which chronic pathologies

hs- troponin level can be elevated? (1)
• Heart failure
• Chronic renal failure
• COPD
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51. What pathologies (except myocardial infarction) may cause acute elevation in hs-
troponin level? (1)
52. Please name all changes in laboratory tests (specific and non-specific) typical in a
case of myocardial infarction! Which of them are most specific? (2)
• Elevated cardiac markers - High troponins I and T levels are most specific
– High CK-MB, Myoglobin
• Blood biochemistry – AST is more specific than ALT (both increased)
• Glucose, Creatinine, Potassium, CRP, ESR
• Complete blood cell count – High WBC count
• Lipid levels – High LDL  Non-specific
53. What signs point to very high risk ACS without ST-segment elevations? (1) How
does it influence the treatment strategy? (1) (2 points)
• Picture below
54. Which signs point to high risk ACS without ST-segment elevations? (1) How
does influence the treatment strategy? (1) (2 points)
• Picture below
55. Which signs point to low risk ACS without ST-segment elevations? (1) How does
influence the treatment strategy? (1) (2 points)
• Picture below
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56. Describe prehospital medical treatment in patient with ACS! (2)

• ECG
• Morphine – For pain – 4 to 8 mg IV initially  2 to 8 mg IV every 5 – 15
mins if needed
• Oxygen – Not used routinely – in patients SpO2 <90% - 2-4 L/min
• Nitroglycerin – first dose 0.4-0.5 mg every 5 min
• Aspirin – 300mg to chew OR i.v. 80-150mg
• P2Y12 receptor antagonists – Clopidogril
• Fibrinolysis – Streptokinase
57. Describe MONA therapy in patient with ACS!* Must all components be used in
routine for every patient? (2)
• Morphine – For pain – 4 to 8 mg IV initially  2 to 8 mg IV every 5 – 15
mins if needed
• Oxygen – Not used routinely – in patients SpO2 <90% - 2-4 L/min
• Nitroglycerin – first dose 0.4-0.5 mg every 5 min
• Aspirin – 300mg to chew OR i.v. 80-150mg
58. Name all antithrombotic drugs that can be used in treatment of patient with ACS
with ST elevations (groups and at least one example)! (2)
• Antithrombotic drugs:
o Antiplatelet drugs:
▪ Aspirin
▪ P2Y12 Inhibitors: Clopidogrel
▪ GPI - Eptifibatid
o Anticoagulants:
▪ Heparin (UFH / LMWH)
59. Name all antithrombotic drugs that can be used in treatment of patient with ACS
without ST elevations (groups and at least one example)! (2)
• Antithrombotic drugs:
▪ Aspirin
▪ P2Y12 Inhibitors: Clopidogrel
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▪ GPI - Eptifibatid
o Anticoagulants:
▪ Heparin (UFH / LMWH)
60. Name two main methods of treatment in a case of ACS with ST elevations that
provide effective reperfusion!* (1) Which one is more effective?* (1) (2 points)
• PPCI  reperfusion effective in about 100% of times
• FL  …in about 80% of times – close to 100% if within the first 2h
61. Explain primary PCI/PTCA ! (1) In which patients is it performed? (1) (2 points)
• Percutaneous coronary intervention/Percutaneous transluminal coronary
angioplasty: Accessing the blood stream through the radial artery the
coronary catheterization to visualise the blood vessels on X-ray imaging an
interventional cardiologist can perform a coronary angioplasty a balloon
catheter  stents deployed to keep the blood vessel open.
• Primary PCI is the urgent use of PCI in people with ACS with STE.
o Performed in MI patients ≤90 min since FMC (first medical contact)
o …… ≤60 min since FMC if MI onset <2h ago
o Can still be performed 12-48h since onset, but small benefit.
62. Name indications for thrombolytic (fibrinolytic) therapy in a case of ACS! (2)
• ACS with STE
• If PPCI cannot be performed timely
• within ≤30 min since FMC
63. Name absolute contraindications for thrombolytic (fibrinolytic) therapy! Name

the most severe possible complication! (1)
• Any prior intracerebral haemorrhage (ICH)
• Known structural cerebral vascular lesion
• Known malignant intracranial neoplasm (primary or metastatic)
• Ischemic stroke within 3 months
• Suspected aortic dissection
• Active bleeding
• Significant closed-head or facial trauma within 3 months
o Major bleed/ICH is the most severe complication
64. What is the maximal time after onset of symptoms when the thrombolytic therapy
can be used in patient with ACS (if a patient has indications)?* (1)
• 30 mins
65. Name thrombolytic agents which can be used in treatment of ACS with ST
elevations! (1)
• Streptokinase (SK)
• Alteplase (tPA)
• Reteplase (r-PA)
• Tenecteplase (TNK- tPA)
66. Explain advantages and disadvantages of primary PCI compared with
thrombolytic therapy in treatment of ACS with ST elevations? (2)
• Adv:
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o Higher reperfusion effectiveness – near 100%

o Less systemic complication
o Less contraindications
• Disavd:
o Invasive
o Higher risk – e.g. aortic dissection
o Takes longer time to do
67. Which patients with ACS without ST elevations should undergo emergency
coronary angiography and PCI/PTCA (explain the clinical signs)? (2)
68. Which patients with ACS without ST elevations should undergo urgent coronary
angiography and PCI/PTCA (explain the clinical signs)? (2)
69. Explain rescue PCI/PTCA ! (1)

• If 60 mins after FL in the case of STEMI there was no reperfusion (ST
resolution <50%); then a rescue PCI must be done.
• Rescue (PCI) for (STEMI) is defined as mechanical reperfusion for failed
fibrinolysis. The efficacy of rescue PCI has always been debated. Despite a
high level of immediate technical success and the positive impact on
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ventricular function, conflicting data on mortality have been reported. Several

historical explanations may be given. Initially, rescue PCI was associated with
a high re-occlusion rate and increased mortality if unsuccessful.
70. What is the most likely finding on coronary angiography in patient with ACS with
ST elevations? (0.5)*
• A completely occluded coronary artery
71. What is the most likely finding on coronary angiography in patient with ACS
without ST elevations? (1)*
• A severely stenosed coronary artery
72. What are the signs of successful reperfusion in treatment a patient with ACS with
ST elevations? (1)
• Resolution of angina, dyspnoa, sweats.
73. Name antiaggregants (antiplatelets) of three different groups that are used in
treatment of ACS! (2)
▪ Aspirin
▪ P2Y12 Inhibitors: Ticagrelor
▪ GPI – Eptifibatid
74. Name P2Y12 inhibitors used in ACS treatment! (1)

• Ticagrelor  if PPCI is done but not FL
• Prasugrel
• Clopidogrel  if FL is used
75. Name low-molecular-weight heparins and their way of administration!* Is it

necessary to monitor their efficiency (if yes - which method is used)? (2)
• Dalteparin \
• Enoxaparin  Subcutaneous injection – No, does not require APTT
monitoring.
• Tinzaparin /
76. What is fondaparinux? What is its way of administration? Is it necessary to

monitor its efficiency (if yes - which method is used)? (2)
• It’s an anticoagulant medication chemically related to low molecular weight
heparins.
• It’s given subcutaneously daily.
• No, does not require APTT monitoring
77. Explain unfractionated heparin administration in case of ACS! Is it necessary to

monitor its efficiency (if yes - which method is used)? (2)
• It’s administered parenterally – I.v.
• Yes, activated partial thromboplastin time (aPTT) is used to measure the
anticoagulant effect of unfractionated heparin and to adjust the dose to
maintain levels in the target therapeutic range.
1
2
5
4th & 6th course 2012/2013
78. What is the antidote for unfractionated heparin? (1)

• Protamine sulfate
79. Explain HIT induced by heparins! (1)

• A serious side-effect of heparin is heparin-induced thrombocytopenia (HIT),
caused by an immunological reaction that makes platelets a target of
immunological response, resulting in the degradation of platelets, which
causes thrombocytopenia. This condition is usually reversed on
discontinuation, and in general can be avoided with the use of synthetic
heparins.
80. What medication the patient should use after myocardial infarction for secondary
prevention? Please name groups and examples! (2)
• Antiplatelet drugs: Aspirin 75-100 mg x1
• P2Y12 Inhibitors for 1 year: Ticagrelor 90 mg x2
• Maximum intensity statins: Atorvastatin 80 mg
• ACEI: Perindopril
• Beta blockers: Metaprolol
• Anticoagulant: Rivaroxaban 2.5 mg x2 in selected cases
81. What additional investigation should be performed in order to evaluate the

function of left ventricle after myocardial infarction? Which parameter and how
will be changed? (2)
CLINICAL CASES
82. Male, 54 years old, with “burning” chest pain that irradiates to mandibula
and both shoulders and lasts for three hours. ECG finding – 2-6 mm ST
elevations in I, aVL, V1-V6 leads, TA 150/80 mmHg, heart rate rhythmic, 92
x’. Please formulate diagnosis correctly!* (1) Describe your strategy of
treatment! (2) (3 points)
Dg: ACS with ST elevation in antero-septo-apico-high lateral walls of the left

ventricule (STEMI)
 Repeated ECG + XRay

 hs Tropinin I and T
 Blood analysis (Lipids, Glc, Creatinine, K+, ALAT, ASAT, FBC, Blood group) 
Leukocytosis, CRP and EST increase
Treatment:
PPCI
Followed by: Aspegic 150-300 mg (aspirin) + P2Y12 inhibitors + UFH 70UI/kg iv
bolus + iv morphine IV (pain > 3/10) + benzodiazepine (if stress too important)
After revascularization+++ = Aspirin, ticagrelor, statins, IPP, B blockers +++
1
2
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4th & 6th course 2012/2013
83. Female, 70 years old, with pressure-like retrosternal pain that appeared for
the first time in her life at rest and lasted 15-20 minutes and repeated three
times during the day of hospitalization. Prehospitally ECG showed 1-1.5 mm
ST depressions in leads II, III, aVF which disappeared at the time of arrival
to the hospital. What is your primary clinical diagnosis?* (1) Which
additional investigations should be performed to confirm it? (1) Please write
the treatment plan! (2) (4 points)
Dg: ACS without STE in inferior wall of the LV (Look like UA)
 Repeat ECG in case of symptoms + Continuous monitoring of ST segment
 XRay + EchoCG + blood analysis (Lipids, Glc, Creatinine, K+, ALAT, ASAT,
FBC, Blood group)  eliminate differential diagnoses
 hs Troponin I and T monitoring
Treatment:
Looks like a HIGH RISK PATIENT in case of non STE ACS
 PCI in less than 24h
84. Male, 66 year old, with pressure-like retrosternal pain that was stress
situation induced for the first time in his life and lasts already for 8 hours.
ECG shows 2 mm ST elevations (with positive T waves) in leads II, III
and aVF and downslopping 1 mm ST depressions (with negative T waves) in
leads I and aVL. What is your primary clinical diagnosis?* (1) Which
additional tests are needed to confirm it? (1) Please write the treatment plan!
(2) (4 points)
Dg: ACS with STE in inferior wall of left ventricule (Acute phase of myocardial
infarction)
 Repeated ECG + XRay
 hs Tropinin I and T
 Blood analysis (Lipids, Glc, Creatinine, K+, ALAT, ASAT, FBC, Blood group) 
Leukocytosis, CRP and EST increase
Treatment:
PPCI
Followed by: Aspegic 150-300 mg (aspirin) + P2Y12 inhibitors + UFH 70UI/kg iv
bolus + iv morphine IV (pain > 3/10) + benzodiazepine (if stress too important)
After revascularization+++ = Aspirin, ticagrelor, statins, IPP, B blockers
85. Male, 63 years old, with pressure-like retrosternal pain that periodically
repeated at load and at rest average for 20-30 min in past three days.
Prehospitally ECG - without any pathology. What is your primary clinical
diagnosis?* (1) Which additional investigations should be performed to
confirm it? (1) Please write the treatment plan! (2) (4 points)
Dg: ACS without ST elevation. (look like UA)
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4th & 6th course 2012/2013
 Repeat ECG in case of symptoms + Continuous monitoring of ST segment

Patient considered as LOW RISK if no ST dynamic changes and no elevation of

troponins or presence of other RFs
Treat as STABLE ANGINA
Treatment:
Correction of CV RFs if present
Beta-blockers
Aspirine or Clopidogrel if contraindications for Aspirin
Statins
ACEI if HTN
86. Male, 56 years old, with pressure-like retrosternal pain, which lasts almost
one hour and irradiates to mandibula, for a short moment – cold sweat.
Prehospitally ECG - without any pathology, but ECG on admission shows
negative T waves in chest leads. What is your primary clinical diagnosis?* (1)
Which additional investigations should be performed to confirm it? (1) Please
prescribe the treatment! (2) (4 points)
Dg: ACS without ST elevations (look like MI)

Repeat ECG in case of symptoms + Continuous monitoring of ST segment
If no ST elevations or ST depressions, considered as a high risk non STE

elevation
Treatment:
Acute PCI with DES stent combined with Tirofiban/Eptifibatid
MONA
P2Y12 Rec inhibitors (Ticagrelor 90mg x2)
Anticoagulant treatment (LMWH)
After PCI = Aspirin for life, P2Y12 inhibitors for 6/12 Months, IPP, statins
1
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VT Bradycardias Answ

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VT Bradycardias Answ

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Questions in cardiology

4th & 6th course 2015/2016

Ventricular arrhythmias. Bradycardias.

1. What are the signs of ventricular extrasystoles (premature beats) [PVC=

3. Please explain what does „monomorphic” and “polymorphic” ventricular

4. What are the possible clinical manifestations of ventricular extrasystoles? (1)

5. What is the definition of ventricular tachycardia? (Rate and minimal number

• Brugada sign:distance from the beginning of QRS to S deepest point

7. What does non-sustained and sustained ventricular tachycardia mean? (1)

8. What is the differential diagnosis of wide-QRS complex tachycardias (name what

9. What does „monomorphic” and “polymorphic” ventricular tachycardia mean? (1)

13. What are possible clinical manifestations of ventricular tachycardia?* (2)

15. What kind of additional investigations can be performed to diagnose paroxysmal

21. Which medications are used in long-term ventricular tachycardia treatment

22. What are contemporary long-term treatment methods of ventricular tachycardia

23. What is bradycardia and what is severe bradycardia? (1)

25. What are possible clinical manifestations of bradycardia?* (2)

26. What is Morganji-Adams-Stokes attack? (1)

28. What degree of atrioventricular block may lead to unconsciousness? (1)

29. What is vasovagal syncope (pathogenesis)? In which cases is it observed?

31. What medication overdose may cause severe bradycardia? (1)

32. What is Frederick syndrome?

o dilated cardiomyopathy and arrhythmia are associated with

33. Which methods can be used in bradycardia diagnostics (what kind of

40. What is the difference between electrocardiostimulation (pacemaker) and

• Cardioversion terminates arrhythmias such as, atrial fibrillation, atrial

Valvular heart disease.

2. Please name the indications of transthoracic echocardiography! (2)

• Identification of structural heart diseases  cardiomyopathies, congenital

3. What are the advantages of transesophageal echocardiography compared to

• Transthoracic sometimes produces poor images especially in obesity, thick chest

4. Which parameters can be evaluated on transthoracic echocardiography? (2)

• Heart structure and function  valve stenosis

5. What is vena contracta? How is it measured? In what valvular pathology evaluation

6. Explain facies mitralis! (1)

• Distinctive facial expression associated with mitral stenosis

• Malar flush on the cheeks (due to vasodilation)  rosy cheeks

7. Explain cor bovinum! (1)

• Dilation of both atriums and ventricles due to hypertrophy of the LV due to

8. What parameters are used to evaluate grade

• Echocardiography is the main method to

9. Define valvuloplasty! In which cases is it performed? Define balloon valvuloplasty!

Increase of the LV load (LV outflow obstruction)  LV hypertrophy (concentric)  impaired

13. Name 3 main symptoms of aortic stenosis! (1)

14. Describe auscultative finding in patient with aortic stenosis!(1)

Auscultation on aortic valve or Erb’s point:

16. What pulse is characteristic in patient with aortic stenosis? (1)

• Pulsus parvus et tardus (reduced in amplitude and delayed compared with LV

• Left axis deviation due to left ventricle hypertrophy and overload

18. What echocardiographic finding indicate severe aortic stenosis? (1)

• Severe stenosis: aortic valve area  1.0 cm2

19. Name criteria for surgical therapy of aortic stenosis! (1)

20. Explain TAVI. When is it performed? (1)

• Transcatheter aortic valve implantation (old, damaged valve NOT removed)

21. Which cases balloon valvuloplasty is performed in aortic stenosis? (1)

• In very young patients

• Medical treatment is limited to symptomatic patients with AS who are not

• Progressive exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea

26. Describe auscultative finding in patient with aortic regurgitation! (1)

• Decreased diastolic pressure

30. Describe echocardiographic finding in severe aortic regurgitation. (1)

• Color Doppler evaluation

33. What are the most common causes of mitral

• LA dilation (atriomegaly) → increase of pulmonary venous and capillary pressures →