Prepared by Marta R. Gerasymchuk, M.D., Ph.D., Associate Professor of PATHOPHYSIOLOGY DEPARTMENT, IFNMU

2. Plan of the lecture
1. Organization of the circulatory
system.
2. Cardiac cycle.
3. Conductive system of the heart.
4. Mechanisms of compensation
5. Arhytmias of the heart. Deffinition.
Classification. Pathogenesis.
6. Ischaemic heart disease.
7. Heart failure.

3. Actuality of the lectureActuality of the lecture
The disorders of cardiac rhythm concern to complex
manifestations of pathology of heart. Its can arise in rather
small damage of the conducting system, and in some cases
in structural changes. More often arrythmia arise with
infectious illnesses and intoxications as consequence of
miocarditis or dystrophy processes in cardiac muscle, and
also in heart ishemic disease, cardiosclerosis.
Arrythmia can be result in development of cardiac
insufficiency.
Arterial hypertension is a very common condition. Cerebral,
coronary and renal vessels are mainly affected by the
deleterious effect of this condition, and both acute and
chronic organ failure may ensue.
Exacerbation of underlying pathophysiologic conditions or
new precipitating factors can lead to hypertensive crisis,
either urgencies or emergencies.

4. FUNCTIONAL ORGANIZATION
OF THE CIRCULATORY SYSTEM
■ The circulatory system consists of the heartheart,
which pumps blood; the arterial systemarterial system,
which distributes oxygenated blood to the
tissues; the venous systemvenous system, which collects
deoxygenated blood from the tissues and
returns it to the heart; and the capillariescapillaries,
where exchange of gases, nutrients, and
wastes occurs.
■ The circulatory system is divided into two
parts: the low-pressure pulmonarylow-pressure pulmonary
circulationcirculation, linking the transport function of
the circulation with the gas exchange
function of the lungs; and the high-pressurehigh-pressure
systemic circulationsystemic circulation, providing oxygen and
nutrients to the tissues.
■ The circulation is a closed system, so the
output of the right and left heart must be
equal over time for effective functioning of
the circulation.

5. Electrocardiogram (ECG)Electrocardiogram (ECG)

7. (Frank-) Starling Law(Frank-) Starling Law
• Within limits, the greater the stretching of the
muscle fibers (preload), the greater the force of
contraction.
• The extra force of contraction is necessary to
pump the increased volume of blood from the
ventricle.
• Cardiac output increases
Neural reflexesNeural reflexes
• Bainbridge reflex – increased heart rate due to
increased right atrial pressure
• Increased pressure in arteries stimulates a
baroreceptor reflex that decreases heart rate.

8. Cardiac ConductionCardiac Conduction
SystemSystem

9. ARRHYTHMIAS OFARRHYTHMIAS OF
HEARTHEART Violation of rhythm of heartViolation of rhythm of heart accompanies aaccompanies a
number of diseases of the cardio-vascular system.number of diseases of the cardio-vascular system.
Most often they are observed at coronaryMost often they are observed at coronary
insufficiency.insufficiency. Arrhythmia registeredArrhythmia registered inin the acutethe acute
period of heart attack of myocardium in 95-100 %period of heart attack of myocardium in 95-100 %
patientspatients..
 In most world countriesIn most world countries sudden cardiac death issudden cardiac death is
about 15 %about 15 % from all cases of «natural» death. Thefrom all cases of «natural» death. The
main reason of sudden death at cardiac pathologymain reason of sudden death at cardiac pathology
in 93 % is arrhythmias.in 93 % is arrhythmias.
Arrhytmias are violation of frequency, rhythm,Arrhytmias are violation of frequency, rhythm,
co-ordination and sequence of heartbeatco-ordination and sequence of heartbeat..

10. Etiology of heart rhythm disorderEtiology of heart rhythm disorder
The rhythm violations arise under the influence of different pathologicalThe rhythm violations arise under the influence of different pathological
agents, which can be divided on such groups:agents, which can be divided on such groups:
 Functional violationsFunctional violations andand influencesinfluences, for example:, for example: violation ofviolation of
vegetative nerves systemvegetative nerves system condition (sympathetic or parasympatheticcondition (sympathetic or parasympathetic
link hyperactivity),link hyperactivity), physical workphysical work,, physical overloadphysical overload,, body temperaturebody temperature
changeschanges,, the increase of intracranium pressurethe increase of intracranium pressure,, respirationrespiration (especially(especially
in children);in children);
 Organic injury of myocardiumOrganic injury of myocardium , for example:, for example: inflammation ofinflammation of
myocardiummyocardium (as the result of infection), the(as the result of infection), the myocardium dystrophymyocardium dystrophy (in(in
the result of hypoxia, ischemia or amiloidosis),the result of hypoxia, ischemia or amiloidosis), necrosis ofnecrosis of
myocardiummyocardium;;
 Influences of toxic substances on the myocardiumInfluences of toxic substances on the myocardium (alcohol,(alcohol,
drugs, big dose adrenalin and noradrenalin, glucocorticoids, bacterialdrugs, big dose adrenalin and noradrenalin, glucocorticoids, bacterial
toxins, phosphororganic substances);toxins, phosphororganic substances);
 Hormone balance disorderHormone balance disorder (hyperthyroidism, hypothyroidism,(hyperthyroidism, hypothyroidism,
hyperfunction of supranephral glands);hyperfunction of supranephral glands);
 Violation of intracellular or extracellular ions balanceViolation of intracellular or extracellular ions balance
(changes of sodium, potassium, calcium, magnesium and chlorine(changes of sodium, potassium, calcium, magnesium and chlorine
concentration);concentration);
 Mechanical influences on the heartMechanical influences on the heart (catheter using for the(catheter using for the
diagnosis and treatment heart diseases, operation on the heart, chestdiagnosis and treatment heart diseases, operation on the heart, chest
trauma).trauma).

11. • Development of arrhythmiasDevelopment of arrhythmias can be related tocan be related to
violations of basic functions of the conductingviolations of basic functions of the conducting
system of heart:system of heart:
1) automatism1) automatism,,
2)2) excitabilityexcitability andand
3)3) conductivity.conductivity.
• Classification of arrhythmias:Classification of arrhythmias:
I. Arrhythmias, related with violations of automatism.I. Arrhythmias, related with violations of automatism.
II. Arrhythmias, related with violations of excitability.II. Arrhythmias, related with violations of excitability.
III. Arrhythmias, related with violations ofIII. Arrhythmias, related with violations of
conductivity.conductivity.
IV. Arrhythmias, related with violations of excitabilityIV. Arrhythmias, related with violations of excitability
and conductivity.and conductivity.

12. Normal Rhythms

13. Arrhythmias, related with violationArrhythmias, related with violation
ofof automatismautomatism of heartof heart
 Distinguish two groups of arrhythmiasDistinguish two groups of arrhythmias, related with, related with violationviolation
of automatism of heart.of automatism of heart.
1)1) Nomotopic arrhythmiasNomotopic arrhythmias -- the generation of impulsesthe generation of impulses, as well, as well
as in a norm,as in a norm, takes place bytakes place by pacemaker cells (P-cells) inpacemaker cells (P-cells) in
sinoatrial [sinus] node, [nodus sinuatrialis]sinoatrial [sinus] node, [nodus sinuatrialis]. To them belong:. To them belong:
 a)a) sinus tachycardiasinus tachycardia is multiplying frequency of cardiacis multiplying frequency of cardiac
reductions;reductions;
 b)b) sinus bradycardiasinus bradycardia is diminishing of frequency of cardiacis diminishing of frequency of cardiac
reductions;reductions;
 c)c) sinus (respiratory) arrhythmiasinus (respiratory) arrhythmia is a change of frequency ofis a change of frequency of
heartbeat in the different phases of respiratory cycleheartbeat in the different phases of respiratory cycle
(become more frequent at inhalation [breath] and(become more frequent at inhalation [breath] and
diminishing is at exhalation [outward breath]).diminishing is at exhalation [outward breath]).

14. Arrhythmias, related withArrhythmias, related with
violation of automatismviolation of automatism

15. Heterotopic ArrhythmiasHeterotopic Arrhythmias
2)2) heterotopic arrhythmiasheterotopic arrhythmias areare a syndrome ofa syndrome of weakness of sinusweakness of sinus
nodenode.. The generation of impulses appears into other structures ofThe generation of impulses appears into other structures of
the conducting system. A syndrome develops as a result ofthe conducting system. A syndrome develops as a result of
diminishing of activity or stopping of activity of sinus node at thediminishing of activity or stopping of activity of sinus node at the
damage of it cells or primary functional violations. The followingsdamage of it cells or primary functional violations. The followings
types of pathological rhythms of heart can develop:types of pathological rhythms of heart can develop:
 a)a) atrium slow rhythmatrium slow rhythm - a driver of rhythm is in the structures of- a driver of rhythm is in the structures of
left atrium, frequency of heartbeat lesser than 70 per 1 min;left atrium, frequency of heartbeat lesser than 70 per 1 min;
 b)b) atrio-ventricular rhythmatrio-ventricular rhythm - the source of impulses are drivers of- the source of impulses are drivers of
rhythm of the II order (overhead, middle or lower part of atrio-rhythm of the II order (overhead, middle or lower part of atrio-
ventricular node), frequency of heartbeat in dependence on theventricular node), frequency of heartbeat in dependence on the
place of generation of impulses diminishes from 70 to 40 perplace of generation of impulses diminishes from 70 to 40 per
minute ;minute ;
 c)c) idioventricular rhythmidioventricular rhythm - the generation of impulses appears in- the generation of impulses appears in
the drivers of rhythm of the III order (His' bundle, atrioventricularthe drivers of rhythm of the III order (His' bundle, atrioventricular
fascicle, fasciculus atrioventricularis and pedunculi of it),fascicle, fasciculus atrioventricularis and pedunculi of it),
frequency of heartbeat lesser than 40 per minute.frequency of heartbeat lesser than 40 per minute.

16. Reason and mechanisms of development ofReason and mechanisms of development of
sinus tachy- and bradycardiasinus tachy- and bradycardia
 Increase generating of impulsesIncrease generating of impulses .. Reasons:Reasons:
a) at diminishing of level of maximal diastolic potential of cells of sinus nodea) at diminishing of level of maximal diastolic potential of cells of sinus node
b) at approaching to it of maximum critical potential,b) at approaching to it of maximum critical potential,
c) at multiplying speed of slow diastolic depolarization.c) at multiplying speed of slow diastolic depolarization.
 Such phenomenon is observed:Such phenomenon is observed:
a) under act of the promoted temperature of bodya) under act of the promoted temperature of body
b) stretching areas of sinus node,b) stretching areas of sinus node,
c) under act of mediators of sympathetic system.c) under act of mediators of sympathetic system.
 Opposite,Opposite,
a) diminishing of speed of slow diastolic depolarization,a) diminishing of speed of slow diastolic depolarization,
b) hyperpolarization in a diastole andb) hyperpolarization in a diastole and
c) the decreasing of critical maximum potential, as it is observed at annoying ac) the decreasing of critical maximum potential, as it is observed at annoying a
vagus nerve, are accompanied deceleration of generation of impulses, andvagus nerve, are accompanied deceleration of generation of impulses, and
consequently -consequently -
 The instability [fluctuation, variation] of tone of vagus nerve during the act ofThe instability [fluctuation, variation] of tone of vagus nerve during the act of
breathing predetermine respiratory arrhythmia (become more frequentbreathing predetermine respiratory arrhythmia (become more frequent
palpitation at inhalation, deceleration - at exhalation).palpitation at inhalation, deceleration - at exhalation).
 Children have respiratory arrhythmia in a normChildren have respiratory arrhythmia in a norm , sometimes it also, sometimes it also
observed for adults.observed for adults.
Tachycardia developsTachycardia develops
Bradycardia developsBradycardia develops

17. Arrhythmias, related to violations of excitabilityArrhythmias, related to violations of excitability
The main reason is appearance so-called ectopic hotbed of
excitations which generate premature impulsespremature impulses.
The most widespread arrhythmias of this group are:
a) extrasystole [beat]a) extrasystole [beat] andand
b) paroxysmal [recurrent, reentrant] tachycardia.b) paroxysmal [recurrent, reentrant] tachycardia.
Extrasystole is a type of arrhythmias, which are stipulated
violations of function of excitability which shows up the origin
of premature contraction of heart or only ventricles.
In dependence on localization of hotbed which an premature
impulse goes out from, distinguish the followings types of
extrasystole:
a)a) sinussinus (or nomotopic),(or nomotopic),
b)b) atrialatrial,,
c)c) atrio-ventricularatrio-ventricular andand
d)d) ventricular [ventricular premature beats].ventricular [ventricular premature beats].
As a wave of excitation, which arose up in an unusual place,
spreads in the changed direction, it is reflected on the
structure of the electric field of heart and finds a reflection on
an electrocardiogram.

18. Sinus extrasystoleSinus extrasystole
• Sinus extrasystole arises up
as a result of premature
excitation part of cells of
sinus node. On ECG:
shortening interval TP. As a
result shortening of diastole
and diminishing of filling of
ventricles a pulse wave is
diminished too.

19. Atrial extrasystolesAtrial extrasystoles
• Atrial extrasystolesAtrial extrasystoles are
observed at presence of heart
beat of ectopic excitation in the
different areas of atrium and are
characterized:
a) change the form P-waveform P-wave
(reduced, two-phase, negativereduced, two-phase, negative);
b) at the stored complex QRS and
c) some lengthening of diastolic
interval after extrasystole (an
incomplete compensate pauseincomplete compensate pause).

20. Atrio-Atrio-
ventricularventricular
extrasystoleextrasystole
• Atrio-ventricular extrasystole is observed in case of occurring of
additional impulse in atrio-ventricular node.
• The wave of excitation, which goes out from overhead and middle
parts of node, spreads in two directions:
a) into ventricles - as normal
b) into atrium - retrograde direct. Thus:
a) the negativenegative P-waveP-wave can be present before or laybefore or lay on complex QRSon complex QRS;
b) diastole interval after a extrasystole is a little prolonged.
A extrasystole can be accompanied simultaneous beat of atrium and
ventricles.
• At a atrio-ventricular extrasystole which goes out from lower part of
node, there is a compensate pause, the same, as well as at a
ventricular extrasystole and P-wave is negative and situated after
complex QRS.

21. Ventricular extrasystoleVentricular extrasystole
• Ventricular extrasystoleVentricular extrasystole are
characterized presence of a completecomplete
compensate pausecompensate pause after premature
heartbeat and deformation complex
QRS.
• Next beat of ventricles arises up onlyNext beat of ventricles arises up only
after arrival to them of duty normalafter arrival to them of duty normal
impulseimpulse.. That is why duration of a
compensate pause equals duration of
two normal diastolic pauses. However if
reductions of heart are so rare that to the
moment of arrival of duty normal impulse
ventricles have time to go out from the
state of adiphoria, a compensate pause
is absent. Premature heartbeat gets in an
interval between two normal and in this
case called the inserted extrasystole.

22. • 1) Atrial ectopic beatsAtrial ectopic beats appear as early
(premature extrasystoles) and abnormal
P-waves in the ECG; they are usually
followed by normal QRS-complexes.
Following the premature beat there is
often a compensatory interval. A
premature beat in the left ventricle is weak
because of inadequate venous return, but
after the long compensatory interval, the
post-extrasystolic contraction (following a
long venous return period) is strong due
the Starling´s law of the heart. -
Adrenergic b-blockers are sometimes
necessary.
• 2) Ventricular ectopic beatsVentricular ectopic beats
(extrasystoles) are recognized in the ECG
by their wide QRS-complex (above 0.12
s), since they originate in the ventricular
tissue and slowly spread throughout the
two ventricles without passing the Purkinje
system. The ventricular ectopic beat is
recognized by a double R-wave. The
classical tradition of simultaneous cardiac
auscultation and radial artery pulse
palpation eases the diagnosis. Now and
then a pulsation is not felt, and an early
frustraneous beat is heard together with a
prolonged interval. A beat initiated in the
vulnerable period may release lethal
ventricular tachycardia, since the tissue is
no longer refractory.

23. Paroxysmal tachycardiaParoxysmal tachycardia
• Paroxysmal tachycardiaParoxysmal tachycardia is arrhythmia, which is stipulated
violations of function of excitability, which shows up the
origin of group of extrasystoles which fully repress a
physiology rhythm.
• At paroxysmal tachycardia the normal rhythm of heart isnormal rhythm of heart is
suddenly brokensuddenly broken by attack of beats with frequency from 140
to 250 shots per minute.
• Duration of attack can be different - from a few secondsfew seconds to a
few minutesfew minutes. It is suddenly stopped and recommences
normal rhythm.
Paroxysmal supraventrical
tachycardia
Paroxysmal supraventricular tachycardia: note accelerated
rate and narrow QRS complexes.

24. Arrhythmias, related to violation ofArrhythmias, related to violation of
conductivity of impulsesconductivity of impulses
 Select two groups of such arrhythmias:Select two groups of such arrhythmias:
1) Heart block.1) Heart block.
2) Increased conducting of impulses –2) Increased conducting of impulses – WPW-syndromeWPW-syndrome (Wolf-Parkinson-(Wolf-Parkinson-
White block)White block)
 Heart blocksHeart blocks are arrhythmias, conditionedare arrhythmias, conditioned deceleration or completedeceleration or complete
stopped conducting of impulsesstopped conducting of impulses on the conducting system.on the conducting system.
 ReasonsReasons::
a)a) the damage of conductive ways,the damage of conductive ways,
b)b) worsening of other functional descriptionsworsening of other functional descriptions, which is accompanied, which is accompanied
deceleration or complete stopped conducting of impulse.deceleration or complete stopped conducting of impulse.
 Violations of conductivity canViolations of conductivity can arise up:arise up:
a)a) between a sinus node and atriumsbetween a sinus node and atriums
b)b) inwardly atriums,inwardly atriums,
c)c) between atriums and ventricles andbetween atriums and ventricles and
d)d) in one of legs of His' bundle.in one of legs of His' bundle.
 Followings types of blockades select:Followings types of blockades select:
1)1) intraatrialintraatrial;;
2)2) atrio-ventricular;atrio-ventricular;
3)3) intraventricularintraventricular..

25. SA BLOCKSA BLOCK
Rate normal or bradycardia
P wave those present are normal
QRS normal
Conduction normal
Rhythm basic rhythm is regular*

26. Atrio-ventricularAtrio-ventricular
blockblock
 Four typesFour types of atrio-of atrio-
ventricular (AV)-ventricular (AV)-
block. From aboveblock. From above
downwards:downwards:
 First-degree AV-First-degree AV-
block,block,
 Second-degreeSecond-degree
Mobitz I blockMobitz I block
(Wenchebach),(Wenchebach),
 Second-degreeSecond-degree
Mobitz II block,Mobitz II block,
andand
 Complete AV-Complete AV-
block.block.

27. Increase conductingIncrease conducting
of impulsesof impulses
• WPW-syndrome –
characterized the
speed-up
conducting of
impulses from
atriums to the
ventricles, as a
result there is
premature
excitation of the
last, tachycardia
develops, the
interval of PQ
diminishes on an
electrocardiogram.

28. Re-entry mechanismRe-entry mechanism
Under normal conditions, anUnder normal conditions, an
electrical impulse is conductedelectrical impulse is conducted
through the heart in an orderly,through the heart in an orderly,
sequential manner. Thesequential manner. The electricalelectrical
impulse then dies out and does notimpulse then dies out and does not
reenter adjacent tissuereenter adjacent tissue becausebecause thatthat
tissue has already been depolarizedtissue has already been depolarized
and is refractory to immediateand is refractory to immediate
stimulationstimulation. However, under certain. However, under certain
abnormal conditions, an impulse canabnormal conditions, an impulse can
reenter an area of myocardium thatreenter an area of myocardium that
was previously depolarized andwas previously depolarized and
depolarize it again. There threedepolarize it again. There three
conditions are the necessary for thisconditions are the necessary for this
mechanism beginning:mechanism beginning:
1 – two conductive ways are the1 – two conductive ways are the
functionally or anatomicallyfunctionally or anatomically
disconnected;disconnected;
2 – some conductive way is2 – some conductive way is
blocked;blocked;
3 – the antegrade conductive way3 – the antegrade conductive way
is blocked, but the retrograde oneis blocked, but the retrograde one
is preserved.is preserved.
So, in that condition impulse (orSo, in that condition impulse (or
impulses) travels numerous throughimpulses) travels numerous through
some area of conductive system andsome area of conductive system and
returns through another pathway toreturns through another pathway to
the reactivated myocardiocytes.the reactivated myocardiocytes.

29. Arrhythmias with violation of functions ofArrhythmias with violation of functions of
excitability and conductivityexcitability and conductivity
1)1) atrial flutteratrial flutter (frequency of(frequency of
atrium beats -atrium beats - 250-400250-400 //
min).min).
2)2) Atrial fibrillationAtrial fibrillation (frequency(frequency
of impulses which arise upof impulses which arise up
in atrium isin atrium is 400-600400-600 / min)./ min).
► Atrial flutterAtrial flutter andand
fibrillation have identicalfibrillation have identical
reasons of developmentreasons of development
and can pass one toand can pass one to
another. So, these twoanother. So, these two
types of violation of rhythmtypes of violation of rhythm
of heart combine into oneof heart combine into one
and called isand called is fibrillationfibrillation..
3)3) ventricle flutterventricle flutter (frequency(frequency
of ventricle beat isof ventricle beat is 150-150-
300300/m)./m).
4)4) FibrillationFibrillation of ventriclesof ventricles
(frequency of impulses in(frequency of impulses in
ventricles isventricles is 300-500300-500 / min)./ min).
► ArrhythmiasArrhythmias which arise up as a result of simultaneous violation of functionswhich arise up as a result of simultaneous violation of functions
ofof excitabilityexcitability andand conductivityconductivity.. To them belong:To them belong:

30. Even when the stimulus
formation in the sinus
node is normal,
abnormal ectopic
excitations can start
from a focus in an
atrium (atrial), the AV
node (nodal), or a
ventricle (ventricular).

32. Coronary Heart
Disease The term coronary heart disease
(CHD) describes heart disease
caused by impaired coronary blood
flow.
 In most cases, CHD is caused by
atherosclerosis.
 Diseases of the coronary arteries can
cause angina, myocardial infarction
or heart attack, cardiac dysrhythmias,
conduction defects, heart failure, and
sudden death.
 Heart attack is the largest killer of
American men and women, claiming
more than 218,000 lives annually.
Each year, 1.5 million Americans
have new or recurrent heart attacks,
and one third of those die within the
first hour, usually as the result of
cardiac arrest resulting from
ventricular fibrillation.

33. Pathogenesis of CoronaryPathogenesis of Coronary
Heart DiseaseHeart Disease
• HDL (good)HDL (good)
cholesterol removescholesterol removes
excess cholesterol inexcess cholesterol in
the blood stream.the blood stream.
• LDL (bad)LDL (bad) cholesterolcholesterol
enters the arterial wallenters the arterial wall
andand is taken up by ouris taken up by our
body’s scavenger cells.body’s scavenger cells.
• Subsequently, they willSubsequently, they will
turn into fatty streaksturn into fatty streaks
which progress intowhich progress into
atheromatous plaques.atheromatous plaques.
• Hence, LDLHence, LDL
cholesterol is said tocholesterol is said to
promotepromote
atherosclerosis.atherosclerosis.

34. Cholesterol readings includes:Cholesterol readings includes:
Total cholesterolTotal cholesterol
DesirableDesirable : < 5.2 mmol/L: < 5.2 mmol/L
Borderline HighBorderline High : 5.2: 5.2 –– 6.2 mmol/L6.2 mmol/L
HighHigh : ≥ 6.2 mmol/L: ≥ 6.2 mmol/L
LDL cholesterolLDL cholesterol
DesirableDesirable : < 3.3 mmol/L: < 3.3 mmol/L
Borderline HighBorderline High : 3.3: 3.3 –– 4.1 mmol/L4.1 mmol/L
HighHigh : ≥ 4.1 mmol/L: ≥ 4.1 mmol/L
Well-Balanced Cholesterol Levels :Well-Balanced Cholesterol Levels :
Healthy LifestyleHealthy Lifestyle

36. Types of chronic ischemic heart diseaseTypes of chronic ischemic heart disease
and acute coronary syndromesand acute coronary syndromes
Coronary heart diseaseCoronary heart disease
Chronic ischemic heart disease Acute coronary syndrome
StableStable
anginaangina
Silent myocardial
ischemia
Variant
angina
No ST-segment
elevation
Q-wave
AMI
Unstable
angina
Non-ST-segment
elevation AMI
ST-segment
elevation

37. Atherosclerosis:
A Progressive Process
Disease progression
PHASE I: Initiation PHASE II: Progression PHASE III: Complication
Normal
Fatty
Streak
Fibrous
Plaque
Occlusive
Atherosclerotic
Plaque
Plaque
Rupture/
Fissure &
Thrombosis
MI
Stroke
Critical Leg
Ischemia
Coronary
Death
Unstable
Angina
Libby P. Circulation. 2001;104:365-372.
Ischemia
Thrombus formation
Coronary vasospasm

38. 1) FATTY
STREAK
(non-
palpable, but
a visible
YELLOW
streak)
2) ATHEROMA
(plaque)
(palpable)
3) THROMBUS
(non-
functional,
symptomatic)

39. ANGINA PECTORIS
• Paroxysmal (sudden)
• Recurrent
• 15 sec.15 min.
• Reduced perfusion, but NO infarction
• THREE TYPES
• STABLE:STABLE: relieved by rest or nitroglycerin
• PRINZMETAL:PRINZMETAL: SPASM is main feature, responds to
nitro, S-T elevation
• UNSTABLEUNSTABLE (crescendo, PRE-infarction, Q-wave
angina): perhaps some thrombosis, perhaps some
non transmural necrosis, perhaps some
embolization, but DISRUPTION of PLAQUE is
universally agreed upon

40. Chest PainChest Pain
 First symptom of those suffering myocardialFirst symptom of those suffering myocardial
ischemia.ischemia.
 Called angina pectoris (angina – “pain”)Called angina pectoris (angina – “pain”)
 Feeling of heaviness, pressureFeeling of heaviness, pressure
 Moderate to severeModerate to severe
 In substernal areaIn substernal area
 Often mistaken for indigestionOften mistaken for indigestion
 May radiate to neck, jaw, left arm/ shoulderMay radiate to neck, jaw, left arm/ shoulder
Due to :Due to :
Accumulation of lactic acid inAccumulation of lactic acid in
myocytes or stretching of myocytesmyocytes or stretching of myocytes

41. Stable angina pectoris
 Caused by chronic coronary obstruction
 Recurrent predictable chest pain
 Gradual narrowing and hardening of
vessels so that they cannot dilate in
response to increased demand of physical
exertion or emotional stress
 Lasts approx. 3-5 minutes
 Relieved by rest and nitrates
Stress testStress test
showsshows
ST segmentST segment
depressiondepression
> 1mm> 1mm

42. Prinzmetal angina pectorisPrinzmetal angina pectoris
(Variant angina)(Variant angina)
 Caused by abnormal vasospasm of normal vessels (15%) orCaused by abnormal vasospasm of normal vessels (15%) or
near atherosclerotic narrowing (85%)near atherosclerotic narrowing (85%)
 Occurs unpredictably and almost exclusively at rest.Occurs unpredictably and almost exclusively at rest.
 Often occurs at night during REM sleepOften occurs at night during REM sleep
(rapid eye movement)(rapid eye movement)
 May result from hyperactivity of sympathetic nervous system,May result from hyperactivity of sympathetic nervous system,
increased calcium flux in muscle or impaired production ofincreased calcium flux in muscle or impaired production of
prostaglandinprostaglandin
 Vasoconstriction is due to platelet thromboxane AVasoconstriction is due to platelet thromboxane A22 or anor an
increase in endothelinincrease in endothelin
This causes a pattern of ST elevationST elevation that is very similar to acute STEMI
— i.e. localised ST elevation with reciprocal ST depression occurring
during episodes of chest pain. However, unlike acute STEMI the ECG
changes are transient, reversible with vasodilators and not usually
associated with myocardial necrosis. They may be impossible to
differentiate on the ECG.
ST elevation myocardial infarction (STEMI)

43. Silent IschemiaSilent Ischemia
• Totally asymptomaticTotally asymptomatic
• May be due abnormality inMay be due abnormality in
innervationinnervation
• Or due to lower level ofOr due to lower level of
inflammatory cytokinesinflammatory cytokines

45. Unstable Angina pectorisUnstable Angina pectoris
Lasts more than 20 minutes at rest,Lasts more than 20 minutes at rest,
or rapid worsening of a pre-existingor rapid worsening of a pre-existing
anginaangina
May indicate a progression to M.I.May indicate a progression to M.I.
Pathogenesis:Pathogenesis:
Severe, fixed, multivesselSevere, fixed, multivessel
atherosclerotic diseaseatherosclerotic disease
Disrupted plaques with or withoutDisrupted plaques with or without
platelet nonocclusive thrombiplatelet nonocclusive thrombi

46. Sudden cardiac deatSudden cardiac deathh (SC(SCDD))
 1. Inexpected death within 1 hour after the onset of1. Inexpected death within 1 hour after the onset of
symptomssymptoms
2. Risk factors2. Risk factors
 a. Obesitya. Obesity
 b.b. GGlucoslucosee intoleranceintolerance
 c. Hypertensionc. Hypertension
 d. Recent non-Q wave myocardial infarctiod. Recent non-Q wave myocardial infarctionn
 e. Smokinge. Smoking
3. Occurs more frequently in the morning hours when3. Occurs more frequently in the morning hours when
hypercoagiilability is ahypercoagiilability is att its peaits peackck
4. Pathogenesis4. Pathogenesis
 a. Severe aa. Severe attheroseleroheroselerottic coronary arteryic coronary artery didiseasesease
 b. Disruptedb. Disrupted filimnsfilimns plaquesplaques
 c. Absence of occlusive vessel thrombus (>80%; of cases)c. Absence of occlusive vessel thrombus (>80%; of cases)
 d. Cause of death is ventricular fibrillation.d. Cause of death is ventricular fibrillation.
 5. Diagnosis of exclusion after the following causes are5. Diagnosis of exclusion after the following causes are
ruled outruled out
 a. Mitral valve prolapse (MVP)a. Mitral valve prolapse (MVP)
 b. Hypertrophic cardiomyopathyb. Hypertrophic cardiomyopathy
 c. Calcific aortic stenosisc. Calcific aortic stenosis
 d. Conduction system abnormalid. Conduction system abnormalitietiess
 e. Cocaine abusee. Cocaine abuse

47. Acute myocardial infarction (Acute myocardial infarction (AMIAMI))
1.1. EEpidemiologypidemiology
 a. Most common cause ofa. Most common cause of
deatdeathh in adults in thein adults in the
United States.United States.
 b. Prominent in malesb. Prominent in males
between 40 and 65 yearsbetween 40 and 65 years
oldold
 c. Nc. Noo predominant sexpredominant sex
predilection after 65 yearspredilection after 65 years
oldold
 d. At least 25% of AMIsd. At least 25% of AMIs
are clinically unrecognized.are clinically unrecognized.

48. Myocardial IschemiaMyocardial Ischemia
 Myocardial cell metabolic demands not metMyocardial cell metabolic demands not met
 Time frame of coronary blockage:Time frame of coronary blockage:
 10 seconds following coronary block10 seconds following coronary block
 Decreased strength of contractionsDecreased strength of contractions
 Abnormal hemodynamicsAbnormal hemodynamics
 See a shift in metabolism, so within minutes:See a shift in metabolism, so within minutes:
 Anaerobic metabolism takes overAnaerobic metabolism takes over
 Get build-up of lactic acid, which is toxic withinGet build-up of lactic acid, which is toxic within
the cellthe cell
 Electrolyte imbalancesElectrolyte imbalances
 Loss of contractibilityLoss of contractibility

49. 20 minutes after blockage20 minutes after blockage
Myocytes are still viable, soMyocytes are still viable, so
If blood flow is restored, andIf blood flow is restored, and
increased aerobic metabolism, andincreased aerobic metabolism, and
cell repair,cell repair,
 →→Increased contractilityIncreased contractility
About 30-45 minutes after blockage, ifAbout 30-45 minutes after blockage, if
no reliefno relief
Cardiac infarct & cell deathCardiac infarct & cell death

50. Myocardial infarctionMyocardial infarction
 Necrosis of cardiac myocytesNecrosis of cardiac myocytes
• IrreversibleIrreversible
• Commonly affects left ventricleCommonly affects left ventricle
• Follows after more than 20 minutes ofFollows after more than 20 minutes of
ischemiaischemia

51. PathogenesisPathogenesis
a. Sequencea. Sequence
 1) Sudden1) Sudden disniptidisniptioonn of an atheromatousof an atheromatous
plaqueplaque
 2) Su2) Subbendothelialendothelial colcoliaiagengen andand thrombogenicthrombogenic
necrotic material are exposed.necrotic material are exposed.
 3) Platelets adhere to the exposed material3) Platelets adhere to the exposed material
and eventually form an occlusiveand eventually form an occlusive plateletplatelet
tthhrombus.rombus.
b. Role of thromboxane Ab. Role of thromboxane A22
 1) Contributes to1) Contributes to fformation oformation of the plateletthe platelet
thrombusthrombus
 2) Causes vasospasm of2) Causes vasospasm of the artery to reducethe artery to reduce
blood flowblood flow

52. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
Coronary artery cannot supply enough blood to the heart inCoronary artery cannot supply enough blood to the heart in
response to the demand due to CADresponse to the demand due to CAD
Within 10 seconds myocardial cells experience ischemiaWithin 10 seconds myocardial cells experience ischemia
Ischemic cells cannot get enough oxygen or glucoseIschemic cells cannot get enough oxygen or glucose
Ischemic myocardial cells may have decreased electrical &Ischemic myocardial cells may have decreased electrical &
muscular functionmuscular function
Cells convert to anaerobic metabolism.Cells convert to anaerobic metabolism.
Cells produce lactic acid as wasteCells produce lactic acid as waste
Pain develops from lactic acid accumulationPain develops from lactic acid accumulation
Pt feels anginal symptoms until receiving demand increasePt feels anginal symptoms until receiving demand increase
OO22 requirements of myocardial cellsrequirements of myocardial cells
MyocardiumInfarction

53. PROGRESSION OFPROGRESSION OF
NECROSISNECROSIS
0-1/2 hr reversible injury

54. Reperfusion injuryReperfusion injury
a. Follows throma. Follows thrombbolytic (fibrinolytic) therapyolytic (fibrinolytic) therapy
b. Early reperfusion salvages some injured butb. Early reperfusion salvages some injured but
viable myocytes but destroys myocytesviable myocytes but destroys myocytes that arethat are
irreversibly damaged.irreversibly damaged.
1) Removal of irreversibly damaged myocytes1) Removal of irreversibly damaged myocytes
improves short- and long-termimproves short- and long-term function andfunction and
survival.survival.
2) Prevents any further damage to myocardial cells2) Prevents any further damage to myocardial cells
3) Limits the size of3) Limits the size of the infarctionthe infarction
c. Reperfusion histologically alters irreversiblyc. Reperfusion histologically alters irreversibly
damaged cells.damaged cells.
1) Produces contraction band necrosis1) Produces contraction band necrosis
2) Caused by2) Caused by hyphypoorcontractionrcontraction of myofibrils in dyingof myofibrils in dying
cellscells
•• Due to the influx of Ca-Due to the influx of Ca-++++ into the cytosolinto the cytosol

55. Types of myocardial infarction
a. Transmural infarction (Qwave infarction)
• 1) Involves the full thickness of the myocardium
• 2) New Q waves develop in an
electrocardiogram (ECG).
b. Subendocardial infarction (non-Q wave
infarction)
• 1) Involves the inner third of the myocardium
• 2) Q waves are absent.

56. Clinical ManifestationsClinical Manifestations
 May hearMay hear
extra, rapidextra, rapid
heart soundsheart sounds
 ECGECG
changes:changes:

T waveT wave
inversioninversion

STST
segmentsegment
depressiondepression

57. Structural, functional changesStructural, functional changes
 Decreased contractilityDecreased contractility
 Decreased LV complianceDecreased LV compliance
 Decreased stroke volumeDecreased stroke volume
 DysrhythmiasDysrhythmias
 Inflammatory response is severeInflammatory response is severe
 Scarring results –Scarring results –
 Strong, but stiff; can’t contract likeStrong, but stiff; can’t contract like
healthy cellshealthy cells

58. Sign and Symptom
 Classic symptom of heart
attack are chest pain radiating
to neck, jaws, back of
shoulder, or left arm
 The pain can be felt like:
 Squeezing or heavy pressure
 A tight band on the chest
 An elephant sitting on the
chest

59. Cont
Other symptoms include:
• Shortness of breath
(SOB)
• Weakness and
tiredness
• Anxiety
• Lightheadedness
• Dizziness
• Nausea vomiting
• Sweating, which may be
profuse

60. Determinants of Blood Pressure
• Components of B/P
– Pressure of blood against the walls of the arteries
– The elasticity of the artery walls
– The volume and thickness of the blood

61. Regulative systemsRegulative systems
Sympathetic Nervous SystemSympathetic Nervous System
 BaroreceptorsBaroreceptors
– Nerve cells in carotid artery & aortic archNerve cells in carotid artery & aortic arch
– Maintain BP during normal activitiesMaintain BP during normal activities
– React to increases & decreases in BPReact to increases & decreases in BP
 BP – impulse to brain to inhibit SNS; HR &BP – impulse to brain to inhibit SNS; HR &
force of contraction; vasodilation of arteriolesforce of contraction; vasodilation of arterioles
 BP – activates SNS; vasoconstriction ofBP – activates SNS; vasoconstriction of
arterioles; HR & heart contractilityarterioles; HR & heart contractility
1. Barroreceptors of aorta arch and sinus caroticus

62. Increase BPIncrease BP
Renin
Angiotensin II
AldosteroneAldosterone
VasoconstrictionVasoconstriction
on systemic andon systemic and
renal vasselsrenal vassels
Left ventricularLeft ventricular
hypertrophyhypertrophy
andand
myocardialmyocardial
ischemiaischemia
Increase leftIncrease left
ventricularventricular
wallwall
tensiontension
Alteration of renalAlteration of renal
arterial andarterial and
capillarycapillary
vessels’ wallvessels’ wall
Glomeruar ischemia,Glomeruar ischemia,
parenchymal damage,parenchymal damage,
proteinuria, end-stageproteinuria, end-stage
renal failurerenal failure
ADHADH
Sodium andSodium and
water renalwater renal
retentionretention
HHypervolemiaypervolemia
Effect of renin-angiotensin systemEffect of renin-angiotensin system
on cardiovascular homeostasison cardiovascular homeostasis
2.2. ReninRenin––angiotensinangiotensin systemsystem

63. Mechanism of Action of AldosteroneMechanism of Action of Aldosterone
Increases CO by increasing blood volume
.

64. Healthy LifestyleHealthy Lifestyle
Maintain a Healthy Blood Pressure:
Blood PressureBlood Pressure
ClassificationClassification
Systolic BPSystolic BP
(mm Hg)(mm Hg)
Diastolic BPDiastolic BP
(mm Hg)(mm Hg)
NormalNormal < 120< 120 < 80< 80
PrehypertensionPrehypertension 120 – 139120 – 139 80 – 8980 – 89
Stage 1 HypertensionStage 1 Hypertension 140 – 159140 – 159 90 – 9990 – 99
Stage 2 HypertensionStage 2 Hypertension 160 – 179160 – 179 100 – 109100 – 109
Stage 3 HypertensionStage 3 Hypertension
(Hypertensive crisis)(Hypertensive crisis)
≥≥ 180180 ≥≥ 110110
Source: Clinical Practice Guidelines Management of Hypertension, 3rd
Ed. 2008
February;MOH/P/PAK/156.08(GU)

65. Hypertension:Hypertension: DefinitionDefinition
Persistent elevation ofPersistent elevation of
 Systolic bloodSystolic blood pressurepressure ≥140 mm Hg≥140 mm Hg
oror
 Diastolic blood pressureDiastolic blood pressure ≥90 mm Hg≥90 mm Hg
 Worldwide an estimatedWorldwide an estimated 1 billion1 billion peoplepeople
have hypertension; about 1 in 3have hypertension; about 1 in 3
Americans affectedAmericans affected
 Direct relationship between hypertensionDirect relationship between hypertension
and cardiovascular disease (CVD)and cardiovascular disease (CVD)

67. ClassificationClassification
Arterial hypotensionArterial hypotension
Arterial hypertensionArterial hypertension
AcuteAcute
ChronicChronic
SecondarySecondary
AP above 139/89 mm HgAP above 139/89 mm Hg
PrimaryPrimary
AP less than 100/60 mm HgAP less than 100/60 mm Hg

68. Primary HypertensionPrimary Hypertension
 Etiological TheoriesEtiological Theories
 Inability of kidneys to excrete sodiumInability of kidneys to excrete sodium
 Overactive renin/angiotensin systemOveractive renin/angiotensin system
 Overactive sympathetic nervous systemOveractive sympathetic nervous system
 Decreased vasodilatory reactionDecreased vasodilatory reaction
 Resistance to insulin actionResistance to insulin action
 Genetic Inheritance (polygenic)Genetic Inheritance (polygenic)

69. Risk Factors R/T PrimaryRisk Factors R/T Primary
HypertensionHypertension
Age/HeredityAge/Heredity
SexSex
RaceRace
ObesityObesity
StimulantsStimulants
SodiumSodium
AlcoholAlcohol
StressStress
HyperlipidemiaHyperlipidemia
DiabetesDiabetes
SocioeconomicSocioeconomic
StatusStatus

70. Primary HypertensionPrimary Hypertension
 Water and sodium retentionWater and sodium retention
• AA high sodium intake may resulthigh sodium intake may result
in water retentionin water retention
• Some people are Na sensitiveSome people are Na sensitive
(about 20%) ; not everyone(about 20%) ; not everyone
with high salt diet developswith high salt diet develops
hypertensionhypertension

71. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
• Stress and increased SNS activityStress and increased SNS activity
– Produces increased vasoconstrictionProduces increased vasoconstriction
– ↑↑ HRHR
– ↑↑ Renin releaseRenin release
– Angiotensin II causes direct arteriolarAngiotensin II causes direct arteriolar
constriction, promotes vascularconstriction, promotes vascular
hypertrophy and induces aldosteronehypertrophy and induces aldosterone
secretionsecretion

72. HypertensionHypertension
Clinical ManifestationsClinical Manifestations
often secondary to
target organ disease
Can include:
– Fatigue, reduced
activity tolerance
– Dizziness
– Palpitations, angina
– Dyspnea

73. Target Organ DamageTarget Organ Damage
 Caused by damage to the body’s blood vesselsCaused by damage to the body’s blood vessels
which particularly affect the following organs:which particularly affect the following organs:
 Blood VesselsBlood Vessels
 HeartHeart
 KidneysKidneys
 BrainBrain
 EyesEyes

74. Accelerated-malignantAccelerated-malignant
HTHT
 Fundoscopic changesFundoscopic changes
 Retinal hemorrhagesRetinal hemorrhages
 ExudatesExudates
 PapilledemaPapilledema

75. Secondary HypertensionSecondary Hypertension
►It is caused by another diseaseIt is caused by another disease
process such as:process such as:
►Renal FailureRenal Failure
►Diabetes MellitusDiabetes Mellitus
►Cushing’s SyndromeCushing’s Syndrome
►Primary AldosteronismPrimary Aldosteronism
►Coarctation of the AortaCoarctation of the Aorta
►PheochromocytomaPheochromocytoma
►Sleep ApneaSleep Apnea

76. Hypertensive crisisHypertensive crisis
 DefinitionDefinition

Severe elevation in BP ( >220/120 mmHg)Severe elevation in BP ( >220/120 mmHg)

Sub classified into emergency and urgencySub classified into emergency and urgency
 Hypertensive emergencyHypertensive emergency

Require an immediate reduction in BP ( 1 hr )Require an immediate reduction in BP ( 1 hr )

Rx IV therapy and in ICURx IV therapy and in ICU
 Hypertensive urgencyHypertensive urgency

No evidence of progressive end-organ injuryNo evidence of progressive end-organ injury

Require only gradual reduction in BP in 24-48 hrRequire only gradual reduction in BP in 24-48 hr

77. Collaborative CareCollaborative Care
Lifestyle ModificationsLifestyle Modifications
Physical activity:Physical activity:
– Regular physical (aerobic) activity,Regular physical (aerobic) activity,
– At least 30 min, most days of weekAt least 30 min, most days of week
Avoidance of tobacco productsAvoidance of tobacco products
Stress managementStress management

79. ExperimentalExperimental models of arterialmodels of arterial
hypertensionhypertension..
 Models confirming a role of the nervous factor in increase ofModels confirming a role of the nervous factor in increase of
arterial pressure:arterial pressure:
 1.1. Arterial hypertension owing to an irritation ofArterial hypertension owing to an irritation of
hypothalamus nucleuseshypothalamus nucleuses. The irritation of a back nucleus. The irritation of a back nucleus
frequently resultsfrequently results toto hypertension, connected with increasehypertension, connected with increase
of cardiac output. The irritation of a central nucleus causesof cardiac output. The irritation of a central nucleus causes
hyperensionhyperension due todue to of peripheral resistance increase.of peripheral resistance increase.
Electricity stimulation ventro-medial nucleus givesElectricity stimulation ventro-medial nucleus gives
hypertension, which depends from simultaneoushypertension, which depends from simultaneouslyly increaseincrease
of cardiac output and peripheral resistance.of cardiac output and peripheral resistance.
 2.2. Arterial hypertension from double-side damage nucleusArterial hypertension from double-side damage nucleus
tractus solitarii totractus solitarii to medullamedulla oblongoblongataata of rats, where areof rats, where are
located primary synapsis of sinuaorticus baroreceptors.located primary synapsis of sinuaorticus baroreceptors.
Arterial pressure is increased immediately without changeArterial pressure is increased immediately without change
of frequency of cardiac rof frequency of cardiac rateate. The reason of hypertension is. The reason of hypertension is
the sharp increase of peripheral resistancethe sharp increase of peripheral resistance
 3.3. Reflexogenic hypertensionReflexogenic hypertension,, inin dogs and rabbits adogs and rabbits affterffter
section depressor nerve Ludvig-Cion or sinus nerves Heringsection depressor nerve Ludvig-Cion or sinus nerves Hering
..

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