ARRHYTHMIA

Petr Nachtigal
 Conduction system and pacemaker

 Participate on inherent and rhythmical electrical

activity, which is followed by the rhythmical
mechanical work of the myocardium (pumping of the
blood)

 This electrical activity is influenced by nervous system

and hormones but they do not establish the
fundamental rhythm
 Conduction system and pacemaker
 Sinoatrial node
 Located in the right atrium under the opening of superior vena
cava

 Atrioventrical node
 Located in the septum between the two atria

 Atrioventrical bundle (bundle of His)

 Only electrical connection between atrium and ventricle

 Right and left bundle branches

 Runs in the interventricular septum towards the apex

 Conduction myofibers (Purkinje fibers)

 Conduct the impulse into the mass of ventricular muscle
tissue
 Blood flow through the heart
 The right atrium receives deoxygenated blood from superior vena cava and

inferior vena cava

 Coronary sinus located in the right atrium receives blood from the vessels that

supplying the heart wall

 From the right atrium blood flows into the right ventricle and then it is pumped

via pulmonary trunk into the lungs

 Oxygenated blood from the lungs returns to the heart via four pulmonary veins

that empty the left atrium.

 Blood then passes into the left ventricle and than it is pumped into the coronary

arteries and aorta.

 Cardiac output
 the volume of blood being pumped by the heart, in particular by the left

or right ventricle, per unit time.

 Cardiac output is the product of the heart rate (HR), or 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

 For a healthy person weighing 70 kg, the cardiac output at rest averages

about 5 L/min; assuming a heart rate of 70 beats/min, the stroke

volume would be approximately 70 mL.

 ARRHYTHMIA
• disturbance in the heart rhythm

Causes of arrhytmmia:

Abnormal rate of impulse generation in sinoatrial node or

other pacemaker cells
Causation
• hypoxia, ischemia, drug toxicity, vagal hyperactivity, acidosis
 ARRHYTHMIA
• disturbance in the heart rhythm

Causes of arrhytmia:

Abnormal conduction of impulses

Causation
• rheumatic fever, viral myocarditis
• hypertension, valvular dysfunction → calcification and fibrosis
of conduction system
 ARRHYTHMIA
Abnormal rate of impulse generation :

• Sinus bradycardia
• heart rate 60 or less
• decreased filling of the ventricle → decreased cardiac output

• Sinus tachycardia
• heart rate 100 – 150
• caused by hypoxia, fever

• Atrial tachycardia
• heart rate 150 – 250
• decreased cardiac output → decreased mean arterial pressure
• increased myocardial demand
 ARRHYTHMIA
Abnormal rate of impulse generation :

• Atrial, ventricular flutter

• 251 – 300
• decreased filling of the ventricle → decreased cardiac output

• Atrial, ventricular fibrilation

• heart rate more than 300
• decreased filling of the ventricle → decreased cardiac output
 ARRHYTHMIA
Disorders of impulse conduction :

• Sinus block
• Resulting in decreased cardiac output

• Atriventricular dissociation
• Decreased cardiac output from loss of atrial distribution to
ventricular preload
 Clinical symptoms of arrhytmia
 Palpitations

• are the perceived abnormality of the heartbeat characterized by awareness of cardiac

muscle contractions in the chest

• might occur during volume overload of the heart

 Heart valve disorders

 Decrease of cardiac output

• Syncope, fainting

• Chest pain

• Tiredness

• Dyspnea – shortness of breath

 Clinical symptoms of arrhytmia

 Thromboembolic complications

 Thrombus moving from the heart in the brain – stroke

 Thrombi in other organs - kidney

 Heart failure

 Sudden cardiac arrest

 Valves of the heart

 The valves prevent back flow of the blood

 The valves are composed of dense connective

tissue that is covered by endothelium.
 Valves of the heart

Atrioventricular valves
 Tricuspid valve
 It is located between right atrium and ventricle

 It is consist of three cuspids (flaps) that are anchored to the

tendonlike structures called chordae tendinae that are anchored via
papillary muscles into the muscle tissue of the ventricle
 Valves of the heart

Atrioventricular valves
 Bicuspid (mitral) valve
 It is located between left atrium and ventricle

 It is consist of two cuspids (flaps) that are anchored to the

tendonlike structures called chordae tendinae that are anchored via
papillary muscles into the muscle tissue of ventricle
 Valves of the heart
Semilunar valves

 Located in the emerge of the pulmonary trunk and

aorta

 Prevents blood from flowing backward into the heart

 They are consist of three semilunar (half-moon) cusps

 Blood flow through the heart
 The right atrium receives deoxygenated blood from superior vena cava and inferior vena
cava

 Coronary sinus located in the right atrium receives blood from the vessels that supplying the
heart wall

 From the right atrium blood flows into the right ventricle and then it is pumped via
pulmonary trunk into the lungs

 Oxygenated blood from the lungs returns to the heart via four pulmonary veins that empty
the left atrium.

 Blood then passes into the left ventricle and than it is pumped into the coronary arteries and
aorta.
 Alteration of heart valves
 Valve stenosis
 narrowed opening of the valve

 decreased blood flow through the valve

 Valve insufficiency
 incomplete sealing of the vessel

 regurgitation of the blood in the heart

 Mitral stenosis
Causation:
 rheumatic endocarditis
 alteration of valve structure by inflammation
 decreased diameter of valve openning (below 2 cm2)

Pathophysiology:
 decreased blood flow from left atrium to left ventricle →
 congestion of blood in left atrium
 slowing down of ventricle filling
 Mitral stenosis
Pathophysiology:
 tachycardia or aggravation of stenosis results in
 decreased cardiac output (forward failure)
 hypotension
 decreased perfusion of organs

 increased blood pressure in pulmonary circulation

 formation of lung oedema – dyspnea (shortness of breath)
 compensatory thickening of lung vessel wall
 protection against formation of oedema
 overloading of right heart (right heart failure)
 Mitral stenosis

Clinical manifestation:

 dyspnea, hemoptysis (cough up of blood)

 increased blood pressure in pulmonary capillaries (vessels disruption)

 embolism

 turbulent blood flow and blood stasis in the left ventricle → formation of

thrombi
 Mitral stenosis
Clinical manifestation:

 peripheral cyanosis
 decreased tissue perfusion + blood stagnation → increased levels of reduced hemoglobin

 atrial fibrilation
 increased blood volume in atrium → increased consumption of energy → alteration of

impulse generation

 decreased ventricle filling

 formation of thrombi
 Mitral insufficiency

Causation:
 rheumatic endocarditis
 alteration of valve structure by inflammation
 calcification of valve cusps

 ischemic heart disease

 alteration of papillary muscles (rupture)
 Mitral insufficiency

Pathophysiology:
 Recirculation of blood in the left heart

 increased filling of left atrium + increased blood flow through

left ventricle → volume overload of left atrium and ventricle →
compensatory hyperthrophy

 increased blood pressure in pulmonary circulation only in severe insufficiency

 Mitral insufficiency
Clinical manifestation:
 palpitation
 increased blood flow in the left heart
 arrhythmia

 embolism
 turbulent blood flow and blood stasis in the left ventricle → formation of
thrombi

 peripheral cyanosis
 decreased tissue perfusion + blood stagnation → increased levels of reduced
hemoglobin
 Aortic stenosis

Causation:

 rheumatic fever

 alteration of valve structure by inflammation

 the narrowing of aortic opening

 clinical manifestation when the narrowing is more than 50%

 Aortic stenosis

Pathophysiology:

 increased afterload (pressure overload of heart)

 compensatory hyperthrophy of the left heart

 normal perfusion of peripheral tissues
 Aortic stenosis

Clinical manifestation:

 angina pectoris

 relative deficiency of oxygen (energy)

 increased demand for oxygen

 decreased diastolic pressure in the aorta → decreased perfusion of coronary

circulation
 Aortic stenosis

Clinical manifestation:

 syncope
 very short blackout due to hypoxia of brain

 left heart failure

 sudden cardiac death

 left ventricle fibrilation + hypoxia of brain
 Aortic insufficiency
Causation:
 rheumatic, bacterial endocarditis
 alteration of valve structure by inflammation

 atherosclerosis
 alteration of valve function after ICHS complications

 ascendent aortic aneurysm

 Aortic insufficiency
Pathophysiology:

 blood is returned from aorta to left ventricle during

ventricle diastole
 volume overload of left ventricle

 compensatory hyperthrophy of left heart

 normal perfusion of peripheral tissues
 Aortic insufficiency
Clinical manifestation:
 palpitation

 increased blood flow in the left heart

 arrhythmia

 angina pectoris
 relative deficiency of oxygen (energy)
 increased demand for oxygen – volume overload
 Aortic insufficiency
Clinical manifestation:

 syncope
 very short blackout due to hypoxia of brain

 left heart failure

 sudden cardiac death

 left ventricle fibrilation + hypoxia of brain
 Tricuspid insufficiency
Causation:
 left heart failure + pulmonary hypertension → dilatation of right
ventricle (valve insufficiency)

Pathophysiology:
 blood stasis before right heart
 oedema
 hepatomegaly
 icterus

 ascites
 peripheral cyanosis
 dyspepsia
 Tricuspid stenosis
Causation:
 rheumatic, bacterial endocarditis

Pathophysiology:
 blood stasis before right heart
 oedema
 hepatimegaly
 icterus

 ascites
 peripheral cyanosis
 dyspepsia
PATHOPHYSIOLOGY OF CARDIAC FAILURE

Causation:

Alterations of myocardium

• Ischemic heart disease

• Myocarditis

• Cardiomyopathy
PATHOPHYSIOLOGY OF CARDIAC FAILURE
Causation:
Chronical hemodynamic overloading of the heart
• Pressure overloading
• Arterial hypertension
• Stenosis of aorta
• Pulmonary hypertension

• Volume overloading
• Heart valve dysfunction

Alterations of cardiac rhythm - arrhytmia

PATHOFYSIOLOGY OF CARDIAC FAILURE
Forward failure of the left heart:
• Decreased perfusion and blood supply of organs and
tissues
• Tiredness (fatigue)

• Giddiness (dizziness), fainting

• Oliguria (decreased elimination of urine)

PATHOFYSIOLOGY OF CARDIAC FAILURE
Forward failure of the left heart:
• Decreased perfusion and blood supply of organs and
tissues

• Dyspepsia

• Anareobic glycolysis (lactate, tissue acidosis)

• Increased amount of reduced hemoglobin (less than 50 g/l) in

capillaries → peripheral cyanosis (a dark bluish or purplish coloration
of the skin, nail beds, lips, or mucous membranes due to deficient oxygenation
of the blood)
 PATHOFYSIOLOGY OF CARDIAC FAILURE
Forward failure of the right heart:
• Decreased perfusion and blood supply in lungs

• Shortness of breath - dyspnea

• Central cyanosis (due to the central hypoxia)

 PATHOPHYSIOLOGY OF CARDIAC FAILURE
Backward failure left heart:

• Stasis of blood before left heart

• Stasis of blood in front of the left heart in lung circulation

• ↑ increased pressure in pulmonary vessels
• Stasis of blood in lungs → edema → dyspnea
• ↑ pressure in pulmonary artery → ↑ pressure in right ventricle
→

Shortness of breath, also known as dyspnea, is a feeling like one cannot breathe well
enough.
PATHOPHYSIOLOGY OF CARDIAC FAILURE
Backward failure of the right heart:
• Stasis of blood before right heart

• Stasis of blood in front of the right heart in major circulation

• ↑ pressure in the circulation veins → peripheral edema
• hepatomegaly
• icterus
• ascites
• peripheral cyanosis
• dyspepsia
• slowdown of blood flow → ↑ utilization of oxygen →
formation of reduced hemoglobin → peripheral cyanosis