cvs 6

1. Lecture №6. The acute and chronic
coronary syndrome.
Lecture №7. The syndrome acute
and chronic cardiac failure.
Acute and chronic coronary
syndrome.
Acute and chronic cardiac failure.
1

2. Unstable Angina and Non-ST-Elevation
Myocardial Infarction.
• Patients with ischemic heart disease fall into two large
groups:
• patients with chronic coronary artery disease (CAD)
who most commonly present with stable angina
• and patients with acute coronary syndromes (ACSs).
• The latter group, in turn, is composed of patients with
acute myocardial infarction (MI) with ST-segment
elevation on their presenting electrocardiogram
• and those with unstable angina and non-ST-segment
elevation MI (UA/NSTEMI).
2

3. Definition
• The diagnosis of UA is based largely on the clinical
presentation.
• Stable angina pectoris is characterized by chest or arm
discomfort that may not be described as pain but is
reproducibly associated with physical exertion or stress and
is relieved within 5–10 min by rest and/or sublingual
nitroglycerin .
3

4. Definition
• UA is defined as angina pectoris or equivalent ischemic
discomfort with at least one of three features:
(1) it occurs at rest (or with minimal exertion), usually
lasting >10 min;
 (2) it is severe and of new onset (i.e., within the prior
4–6 weeks);
and/or (3) it occurs with a crescendo pattern (i.e.,
distinctly more severe, prolonged, or frequent than
previously).
The diagnosis of NSTEMI is established if a patient with
the clinical features of UA develops evidence of
myocardial necrosis, as reflected in elevated cardiac
biomarkers.
4

5. Pathophysiology
• UA/NSTEMI is most commonly caused by a reduction in oxygen
supply and/or by an increase in myocardial oxygen demand
superimposed on an atherosclerotic coronary plaque, with varying
degrees of obstruction.
• Four pathophysiologic processes that may contribute to the
development of UA/NSTEMI have been identified:
• (1) plaque rupture or erosion with superimposed nonocclusive
thrombus, believed to be the most common cause—NSTEMI may
occur with downstream embolization of platelet aggregates and/or
atherosclerotic debris;
• (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's
variant angina;
• (3) progressive mechanical obstruction [e.g., rapidly advancing
coronary atherosclerosis or restenosis following percutaneous
coronary intervention (PCI)];
• and (4) secondary UA related to increased myocardial oxygen
demand and/or decreased supply (e.g., tachycardia, anemia).
More than one of these processes may be involved. 5

6. Pathophysiology
• Among patients with UA/NSTEMI studied at
angiography, approximately 5% have left main stenosis,
15% have three-vessel CAD, 30% have two-vessel
disease, 40% have single-vessel disease, and 10% have
no critical coronary stenosis;
• some of the latter have Prinzmetal's variant angina
• The "culprit lesion" on angiography may show an
eccentric stenosis with scalloped or overhanging edges
and a narrow neck.
• Angioscopy may reveal "white" (platelet-rich) thrombi,
as opposed to "red" thrombi, more often seen in
patients with acute STEMI. Patients with UA/NSTEMI
often have multiple plaques vulnerable to disruption.
6

7. Clinical Presentation
History and Physical Examination
• The clinical hallmark of UA/NSTEMI is chest pain,
typically located in the substernal region or
sometimes in the epigastrium, that radiates to the
neck, left shoulder, and left arm.
• This discomfort is usually severe enough to be
considered painful.
• Anginal "equivalents" such as dyspnea and
epigastric discomfort may also occur, and these
appear to occur more often in women.
7

8. Clinical Presentation
History and Physical Examination
• The examination resembles that in patients with stable
angina and may be unremarkable.
• If the patient has a large area of myocardial ischemia
or a large NSTEMI, the physical findings can include
• diaphoresis,
• pale cool skin
• sinus tachycardia
• a third and/or fourth heart sound,
• basilar rales
• and sometimes hypotension, resembling the findings of
large STEMI.
8

9. Electrocardiogram
In UA,
• ST-segment depression,
• transient ST-segment elevation,
• and/or T-wave inversion occur in 30–50% of patients,
depending on the severity of the clinical presentation.
• In patients with the clinical features of UA, the
presence of new ST-segment deviation, even of only
0.05 mV, is an important predictor of adverse outcome.
• T-wave changes are sensitive for ischemia but less
specific, unless they are new, deep T-wave inversions
(0.3 mV).
9

10. Cardiac Biomarkers
• Patients with UA who have elevated biomarkers of
necrosis, such as CK-MB and troponin (a much more
specific and sensitive marker of myocardial necrosis),
are at increased risk for death or recurrent MI.
• Elevated levels of these markers distinguish patients
with NSTEMI from those with UA.
• There is a direct relationship between the degree of
troponin elevation and mortality.
• However, in patients without a clear clinical history of
myocardial ischemia, minor troponin elevations have
been reported and can be caused by congestive heart
failure, myocarditis, or pulmonary embolism, or they
may be false-positive readings.
• Thus, in patients with an unclear history, small troponin
elevations may not be diagnostic of an ACS. 10

11. Diagnostic Evaluation
• The first step in evaluating patients with possible
UA/NSTEMI is to determine the likelihood that CAD
is the cause of the presenting symptoms.
• The American College of Cardiology/American Heart
Association (ACC/AHA) Guidelines include, among
the factors associated with a high likelihood of ACS,
• a clinical history typical of ischemic discomfort,
• a history of established CAD by angiography,
• prior MI,
• congestive heart failure,
• new electrocardiographic (ECG) changes,
• or elevated cardiac biomarkers. 11

12. Diagnostic Evaluation
• Factors associated with an intermediate likelihood
of ACS in patients with the clinical features of this
condition but without the above high-risk factors
are:
• age >70 years,
• male gender,
• diabetes mellitus,
• known peripheral arterial or cerebrovascular
disease,
• and old ECG abnormalities.
12

13. Diagnostic Pathways
• Four major diagnostic tools are used in the
diagnosis of UA/NSTEMI in the ED:
• the clinical history,
• the ECG,
• cardiac markers,
• and stress testing.
13

14. The goals are
• to (1) recognize or exclude MI (using cardiac
markers),
• (2) evaluate for rest ischemia (chest pain at rest,
serial or continuous ECGs),
• and (3) evaluate for significant CAD (using
provocative stress testing).
• Typical pathways begin with assessment of the
likelihood that the presenting symptoms are due to
ischemia.
14

15. Diagnostic Pathways
• Patients with a low likelihood of ischemia are usually
managed with an ED-based critical pathway (which in
some institutions is carried out in a "chest pain unit”.
• Evaluation of such patients includes clinical monitoring
for recurrent ischemic discomfort, serial ECGs, and
cardiac markers, typically performed at baseline and at
4–6 h and 12 h after presentation.
• If new elevations in cardiac markers (CK-MB and/or
troponin) or ECG changes are noted, the patient is
admitted to the hospital.
• If the patient remains pain-free and the markers are
negative, the patient may go on to stress testing. This
may be performed as early as 6 h after presentation in
the ED or chest pain center, or on an outpatient basis
within 72 h. 15

16. Diagnostic Pathways
• For most patients, standard treadmill ECG stress testing
is used, but for patients with fixed abnormalities on the
ECG (e.g., left bundle branch block), perfusion or
echocardiographic imaging is used.
• For patients who cannot walk, pharmacologic stress is
used.
• By demonstrating normal myocardial perfusion,
sestamibi or thallium imaging can reduce unnecessary
hospitalizations by excluding acute ischemia.
• CT angiography is used with increasing frequency to
exclude obstructive CAD.
16

17. 17

18. Diagnostic evaluation of patients
presenting with suspected UA/NSTEMI.
• The first step is to assess the likelihood of
coronary artery disease (CAD). Patients at high or
intermediate likelihood are admitted to the
hospital. Those with clearly atypical chest pain are
sent home.
• Patients with a low likelihood of ischemia enter
the pathway and are observed in a monitored bed
in the emergency department (ED) or observation
unit over a period of 6 h, and 12-lead
electrocardiograms are performed if the patient
has recurrent chest discomfort.
18

19. Diagnostic evaluation of patients
presenting with suspected UA/NSTEMI
• A panel of cardiac markers (e.g., troponin and CK-MB) is
drawn at baseline and 6 h later.
• If the patient develops recurrent pain, has ST-segment or T-
wave changes, or has positive cardiac markers, he/she is
admitted to the hospital and treated for UA/NSTEMI.
• If the patient has negative markers and no recurrence of
pain, he/she is sent for exercise treadmill testing, with
imaging reserved for patients with abnormal baseline
electrocardiograms (e.g., left bundle branch block or left
ventricular hypertrophy).
• If positive, the patient is admitted; if negative, the patient is
discharged, with follow-up to his/her primary physician. ETT,
exercise tolerance test; MI, myocardial infarction.
19

20. Risk Stratification and Prognosis
• Patients with documented UA/NSTEMI exhibit a wide
spectrum of early (30 days) risk of death, ranging from 1 to
10%, and of new or recurrent infarction of 3–10%.
• Assessment of "global risk" can be accomplished by clinical
risk scoring systems such as that developed from in the
Thrombolysis in Myocardial Infarction (TIMI) Trials, which
includes seven independent risk factors: age 65 years, three
or more risk factors for CAD, documented CAD at
catheterization, development of UA/NSTEMI while on
aspirin, more than two episodes of angina within the
preceding 24 h, ST deviation 0.5 mm, and an elevated
cardiac marker
• Other risk factors include diabetes mellitus, left ventricular
dysfunction, and elevated levels of creatinine, atrial
natriuretic peptides, and C-reactive protein. 20

21. Early risk assessment
• Early risk assessment (especially using troponin, ST-
segment changes, and/or a global risk scoring system)
is useful both in predicting the risk of recurrent cardiac
events and in identifying those patients who would
derive the greatest benefit from antithrombotic
therapies more potent than unfractionated heparin,
such as low-molecular-weight heparin (LMWH) and
glycoprotein (GP)IIb/IIIa inhibitors, and from an early
invasive strategy.
• For example, in the TACTICS-TIMI 18 Trial, an early
invasive strategy conferred a 40% reduction in
recurrent cardiac events in patients with a positive
troponin level, whereas no benefit was observed in
those with a negative troponin level. 21

22. Early risk assessment
• C-reactive protein, a marker of vascular
inflammation, and B-type natriuretic peptide, a
marker of increased myocardial wall tension,
correlate independently with increased mortality
(and, in some studies, recurrent cardiac events) in
patients presenting with UA/NSTEMI.
• Multimarker strategies are now gaining favor both
to define the pathophysiologic mechanisms
underlying a given patient's presentation more fully
and to stratify the patient's risk further.
22

23. Plate 28 T
23

24. Plate 28 B
24

25. Plate 24
Myocardial
25

26. Plate 24
Myocardial
26

27. Plate 24
Anterolateral
27

28. Plate 25
Myocardial
28

29. Plate 25
Posterior
29

30. The syndrome of coronary failure
• The syndrome coronary failure being due to
myocardial ischemia ( narrowing of coronary
vessels).
• Causes: atherosclerosis, sometimes without
organic changes in vessels in result vasospasm.
• Different acute and chronic coronary failure.
• Acute coronary syndrome its acute condition of
cardiac diseases, which include Q-wave
dependent myocardial infarction, non-Q-wave
myocardial infarction, unstable angina pectoris.
• Chronic coronary failure manifestation
development atherosclerotic cardiosclerosis(
arrhytmias, signs of cardiac failure).
30

31. • Acute coronary syndrome manifestation chest pain with
irradiation to the left hand, shoulder, neck, superior part of
the stomach. The chest pain beginning after physical activity.
The patient is frightened of death, pallor of skin, cold sweat.
Border of heart expansion, sound of heart weakened, may be
arrhythmias, pericardial rub at myocardial infarction ( first-
second days).
• ECG: depression of s.ST and inversion T wave or elevation of
s.ST (in angina pectoris). Presence pathological large Q wave
and elevation of s.ST with negative T wave (myocardial
infarction).
• Common blood count: leucocytosis, increase ESR, increase of
enzymes.
31

32. Ischemic heart disease
Myocardial ischemia develops when there is an imbalance between supply of oxygen and the
myocardial demand.
ETIOLOGY :
1. Decreased coronary blood flow due to mechanical obstruction such as:
• Atheroma - occluding one or more major coronary arteries.
• Spasm of coronary artery
• Thrombosis
• Embolus
• Coronary arteritis (e.g. in SLE)
• Congenital abnormalities of coronary artery.
2 Increased myocardial oxygen requirement
• Increased cardiac output: in thyrotoxicosis
• Myocardial hypertrophy: usually from aortic stenosis or hypertension.
3. Decreased flow of oxygenated blood to myocardium
• Anemia
• Hypotension - causing decreased coronary perfusion pressure.
4. Cardiac syndrome X
• Angina occurring in patient with normal coronary arteries, resulting from disease of coronary
microcirculation is called syndrome X. This is also called microvascular angina.
32

33. Atherosclerosis
• The most common cause of myocardial ischemia
and angina is the formation of atheroma.
Atheroma is a fibrofatty plaque in the intima of
large and medium size arteries producin
narrowind of the lumen of the vessels. Exact
causc of atheroma formation is not known. A
50%r reduction in reduction in luminal diameter
produces a reduction in luminal cross- sectional
area of approxymately 70%. Tis is considered
significant obstruction and patient becomes
symptomatic on exertion whenincreased blood
flow is required that can not be supplied
according to the demand.
33

34. Risk factors for atherosclerosis
Fixed risk factors
Age:
• Risk increases with age, rare in childhood except in familial
hyperlipidemia.
Male sex:
• Men have higher incidence of ischemic heart disease than
premenopausal women. After menopause the incidence of
atherosclerosis in women reaches that in men. This
protection in premenopausal women is probably due to
estrogen..
Family history:
• A positive family history means ischemic heart disease in
first-degree relatives before the age of 45 years in male and
before 50 years in female.
•
34

35. Modifiable risk factors
• (Changeable with treatment)
Strong association:
• Hyperlipidemia:
High scrum cholesterol especially increased low –density lioprotein
(LDL) and decreased high-density lioproteins (HDL) is strongly
associated with coronary atheroma.
• Hypertension
Both systolic and diastolic hypertension are associated with increased
risk of coronary artery disease. The risk is same for men and
women.
• Cigarette smoking
Risk of coronary artery is directly related to number of cigarette
smoked. The risk from smoking declines to almost normal after ten
years of quitting.
• Diabetes mejlitus
Diabetes or even just an abnormal glucose tolerance test is strongly
associated with vascular disease.
35

36. ANGINA PECTORIS
Angina pectoris is a clinical syndrome characterized
by paroxysmal chest pain due to transient
myocardial ischemia. It may occur whenever
there is imbalance between myocardial oxygen
supply and demand. The most common cause is
atherosclerosis; however angina may also
develop in aortic stenosis (AS) and hypertrophic
cardiomyopathy (HOCM) even there is no
coronary atheroma.
36

37. PATHOPHYSIOLOGY OF STABLE ANGINA, UNSTABLE ANGINA AND
MYOCARDIAL INFARCTION
• Stable angina:
Stable angina is the angina that occurs when coronary perfusion is
impaired by fixed or stable atheroma of coronary arteries i-c patient
has fixed capacity of exertion after that he starts feeling chest pain.
• Unstable angina:
Unstable angina is the angina that is characterized by rapidly
worsening chest pain, pain on minimal exertion or pain at rest. The
culprit lesion is usually a complex ulcerated or fissured atheroma
with adherent platelet - rich thrombus and local coronary spasm.
Unstable angina = ulcerated atheroma + thrombus formation
abrupt reduction of blood flow caused by thrombus formation
angina at rest.
• Myocardial infarction
Pathophysiology of unstable angina and myocardial infarction is same
(i-e thrombus formation on atherosclerotic plaque) however in
unstable angina obstruction of artery is incomplete while in Ml
there is total obstruction.
37

38. Prinzmetal’s angina
Atherosclerotic plaque
Myocardial
infarction
Thrombosis with
total occcluding of
the lumei
Ulcerated
fibrous cap
Necrotic
centre
Sub-totial
occlusive
thrombus
Stable angina pectoris Unstable angina pectoris
Endothelium
Lumen
38

39. TYPES OF ANGINA
1. Classical or exertional angina
It occurs due to increased myocardial oxygen demand during exertion or
emotion in a patien narrow coronary arteries. It is relieved promptly by
rest and by nitroglycerine.
2. Variant or Prinzmetal's angina
It Occurs at rest and is not a result of increasec myocardial demand. It is
produced by the episodic reduction of myocardial blood supply due to
coronary artery spasm. Underlying atherosclerotic disease may or may not
be present. This type of angina occurs more frequently in women (under
age 50 years) especially early in the morning awakening patients from
sleep and the pain is usually more severe and more prolonged than i
classical angina. It tends to involve right coronary artery. It is
characteristically associated with ST elevation rather than depression (as
seen classical angina).
3. Unstable angina
Unstable angina refers to angina of recent onset (less than one month),
worsening angina characterized by increased frequency and duration of
episode, or angina at rest not responding readily to therapy. 39

40. • 4. Decubitus angina
This is angina that occurs when the patient lies down. . it
usually occurs in association with impaired left
ventricular function. Patient with this symptoms
usually has severe coronary artery disease.
• 5. Nocturnal angina.
This is the angina that awakes the patient from sleep. It
may be provoked by vivid dreams. It may occur due to
critical coronary artery obstruction or coronary spasm.
• 6. Cardiac syndrome X
Patient presents with angina, positive exercise test (ETT)
and angiographically normal coronary arteries. It may
be because of functional abnormalities of coronary
microcirculation (no dilatation of arterioles at the time
of stress).
40

41. SYMPTOMS
• Chest pain Site, radiation, character, duration,
precipitation factors)
• dyspnea
• Associated symptoms
SIGNS
• During attack patient looks anxious. Dyspnea,
pale face, and cold sweats may also be
present. In between attacks, physical
examination is frequently negative except
findings of risk factors.
41

42. Investigations
• ECG
• Exercise tolerance test
• Isotope scanning
• EchoCG
• Coronary angiograthy
42

43. MYOCARDIAL INFARCTION (MI)
Acute ischemic necrosis of an area of myocardium is known as
myocardial infarction or myocardial necrosis occurring as a result of
critical imbalance between coronary blood supply and myocardial
demanad is called MI. I majority of patients Ml devclops in left
ventricle: right ventricular infarction frequently accompanies left
ventricular inferior wall MI.
PREDISPOSING FACTORS
• Myocardial infarction result from prolonged ischemia precipitated
in most cases by formation of occlusive thrombus at the site of
rupture of an atheromatous plaque in coronary artery.
• Rarely infarction may_result from prolonged vasospasm,
jnadequate myocardial blood flow e.g. hypotension) or excessive
metabolic demand. ~
• Very rarely myocardial infarction may be caused by embolic
occlusion, vasculitis, aortic root dissection, or aortitis.
43

44. Precipitating factors
• Reduced myocardial perfusion due to
hypotension as a result hemorrhage or septic
shock.
• Increased myocardial oxygen demand
secondary to aortic stenosis, fever and
tachycardia.
• Respiratory tract infections, hypoxemia of any
cause, hypoglycemia, sympathomimetics
drugs.
44

45. CLINICAL FEATURES
Symptoms
• Chest pain
The pain is retrosternal similar to angina in location
and radiation but it occurs at rest or with less
activity and is more severe and lasts longer (> 30
min); Pain may begin with exercise or
psychological stress but may occur at rest without
оbvious precipitating factors. It is not relieved by
nitroglycerine. Some patients note only dull ache
or numbness of the wrists jn association with
severe retrosternal discomfort, pain may also
begin in_epigastrium and simulates abdominal
disorders.
45

46. Associated symptoms
• Nausea and vomiting are more common in inferior wall MI
than in anterior wall MI.
• In some patients diarrhea or a violent urge to evacuate the
bowels during acute phase of MI.
• Severe weakness, dizziness and palpitations may be
associated with chest discomfort.
• There is profuse sweating which may drench the bed
clothes.
• Syncope may develop due to fall in blood pressure or due
to development of serious arrhytmia or heart block.
• Patient is restlessness due to anxiety and pain.
• There may be atypical presentation of MI with stroke or
peripheral embolism, indigestion, acute mania or psychosis.
46

47. On examination:
– General
– Pulse
– Blood pressure
– Temperature
– Respiratory rate
– Examination of precordium
– Lungs
47

48. PHYSICAL SIGNS OF MI
Signs of sympathetic activation:Pallor, sweating, tachycardia
Signs of vagal activation: Vomiting, sometimes bradycardia
Signs of impaired MI: Raised JVP, narrow pulse pressure, 3th
heart sound,
Quiet 1th heart sound, diffuse apical impulse, hypotension,
oliguria, cold peripheries, lung crepitations
Sign of tissue damage: fever.
Complications: arrhytmias, murmur of ventricular septal defect,
mitral regurgitation, pericardial rub.
48

49. Investigations of MI
• A history of ischemic type chest pain.
• ECG changes of myocardial infarction.
• Initially a rise and then fall of cardiac
enzymes.
• ECG:
• Peaked (hyperacute) T waves -> ST segment
elevation -> Formation of Q waves -> T wave
inversion. These changes may occur over a
few hours to several days.
49

50. ECG localization of MI
Infarct location Leads showing changes Likely coronary artery
involved
Inferior wall MI II, III, aVF RCA
Septal MI V1-V2 LAD
Anterior wall MI V3-V$ LAD
Anterioseptal V1-V4 LAD
Extensive anterior wall MI I, aVL, V1-V8 LAD
Lateral wall MI I, aVL, V5-V6 Circumflex
High lateral wall MI I, aVL Circumflex
Posterior wall MI Prominent R in V1 RCA or Circ.
Right ventricular MI ST elevation in V1 and
right- sided V4 with
anterior wall MI
RCA
50

51. Types of MI
Q-wave infarction (transmural infarction)
• In this type of myocardial infarction pathological Q-waves
develop on ECG. These infarctions result from complete
thrombotic occlusion of coronary artery and manifest on
ECG by symmetrically peaked T waves replaced after
several minutes by ST-segment elevation.
Ngn-Q wave infarction
• It is also called Non- ST elevation infarction (NSTEMI) and
Subendocardial infarctictn.
• Non- Q wave or non- ST elevation MI develops from high-
grade but non-occlusive thrombi (obstruction of coronary
artery is not complete). This infarction is associated
with_ST segment depression an/or T wave inversion
without evolution of pathologic Q waves._There_js__also
some loss R waves in leads facing the infarct.
51

52. CARDIAC ENZYMES
MI leads to detectable rise in the plasma concentration of enzymes
normally confined within cardiac cells. The enzymes most widely
used in the detection of MI are the folloving:
• Cardiac specific troponins
Troponin T and tropon I: These enzymes are highlу specific to cardiac
injury_and can detect small infarctions that are below the detection
limit for CK-MB. Troponin T and I rise early (within 2 -
4 hours) and remains elevated (troponin I, 7- 10 days and troponin
T, 10-14 days).
Therefore these enzymes are especially 2-3 days after infarction
becauseCK-MB reruns to normal till that time while these
enzymes_remain elevated. Although LDH is also elevated for 10 day
but it is non-specific and is also elevated in other conditions, this is
why troponin T or I is preferred. Troponin T kits are available in the
market and this lest can be performed at bedside. It is now most
widely used test for cardiac marker.
52

53. • Creatine Kinase (CK)
It rises within_4 -8 hours, peaks at 24 hours and generally returns to normal
by 2-3 days.
Creatine kinase has three isoenzymes
-CK - MB - Present in heart.
-CK - MM - Present in skeletal muscles
-CK - BB - Present in brain
Therefore CK may be falsely positive in muscle disease, alcohol intoxication,
diabetes, skeletal muscle trauma, exercise, convulsions,
intramuscular injections and pulmonary embolism.
CK-MB is more specific and performed to detect myocardial necrosis.
• Serum myoglobin
Myoglobin released from injured myocardium comes into circulation quite
early and is very sensitrve for detection of infarction (1-4 hours), however
it is not very specific because minor skeletal muscle trauma also releases
myoglobin. In patients presenting less than 6 hours of symptoms onset
and with ST elevation in whom the diagnosis of MI is in doubt,
an_elevated myoglobin level is associated with an increased risk of
mortality.
.
53

54. OTHER SERUM MARKERS
Before availability of troponins several other markers were used for
confirmation of MI, they were non-specific and usually not
performed now except in government hospitals laboratories and in
small centers. You must be aware of these markers' because in viva
exam you may be asked to interpret the report of cardiac enzymes.
1. Asparate aminotransferase (AST) also called serum glutamic
oxaloacetic transaminase (SGOT).
It peaks at 24-48 hours and may fall to normal by 72 hours. It is
nonspecific to heart and may also be released by damaged RBCs,
kidney, liver and lung.
2. Lactate dehydrogenase (LDH)
It peaks at 3-4 days and remains elevated for 10-14 days (important
for the diagnosis of MI in patients presenting after few days of MI).
It is also nonspecific and is also released from damaged liver,
skeletal muscles, and red blood cells.
54

55. • Blood CP/ESR:
-Polymorphonuclear leucocytosis
- Raised ESR
• X-ray chest:
- It may demonstrate pulmonary edema
- Heart size is usually normal
- Enlarged cardiac shadow indicates CCF or
pericardial effusion
• EchoCG: larger the area with wall motion
abnormality, langer is the infarct.
• Radionuclear scan: Technetium-99
pyrophosphate scan can be used to diagnose
acute MI.
55

56. COMPLICATIONS OF MYOCARDIAL INFARCTION
Early complications within first 2-3 days
• Cardiac arrhythmias
• Cardiac failure
• Pericarditis
Later complications
• Recurrent infarction
• Angina
• Thromboembolism
• Mitral valve regurgitation after 3-5 days
• Ventricular septal defect, cardiac rupture (after 3-5 days).
Late complications
• Post-myocardial infarction syndrome
• Shoulder-hand syndrome
• Ventricular aneurysm
• Recurrent cardiac arrythmias
CARDIAC ARRHYTHMIAS
• Ventricular ectopics
• Ventricular tachycardia
• Ventricular fibrillation
• Sinus tachycardia
• Atrial fibrillation
• Sinus bradycardia 56

57. THE INFORMATION BLOCK
• The syndrome of cardiac failure - the pathological syndrome
developing owing to an inconsistency of contraction functions of a
myocardium on maintenance by oxygen of bodies and tissues of an
organism in rest and at loadings.
• To the factors, influencing on contraction ability of a myocardium
and defining productivity of left ventricule and requirement of a
myocardium in 02, the concern preloading and postloading,
condition contraction of myocardium, HR and a degree of damage
of tissues.
• Preloading, or stretching degree myocardial tissues in rest, is
defined by end-diastolic volume and thickness of a wall of heart. A
chronic stretching and HLV change the end-diastolic pressure. In
clinic a functional condition of ventricule ( contraction condition)
judge on size of cardiac output ( stroke volume of left
ventricules/end-diastolic volume)
57

58. • Postloading, or force of resistance to shortening of
tissues of a myocardium after their stimulation for an
exit from a relaxation condition, is defined by pressure
in a cavity, volume of a cavity and thickness of a wall of
ventricule at the moment of opening of aortic valve.
• Productivity of a myocardium influence availability of
substrata and presence of damages: decrease in
delivery 02 and supply by the basic substrats (fat acids
and glucose) can conduct to damage of a myocardium
with reduction of force of reduction of heart and its
productivity.
• Damage of tissues, acute (caused by a myocardial
infarction) or chronic (with fibrosis, developed as a
result of tissues damage), not only locally breaks
mechanics of a myocardium, but also imposes
additional loading on the tissues which has kept
viability.
58

59. The causes: the cardiac failure can be caused defeat
of the valvular device (a volume overload,
pressure), coronary vessels or a myocardium.
• The valvular defeats of heart accompanied by
stenoses or regurgitation, increase working
loading by a myocardium, and eventually lead to
its deterioration his contruction conditions.
• Damage of coronary arteries, reducing cardiac
muscle blood supply, causes an ischemia or
infarction with loss as a result of a part of
functionally active myocardium.
• The myocardium deseases consist of the various
conditions, which damages it contraction ability
(myocarditis, myocardium dystrophies)
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60. Due to decrease of contraction abilities of myocardium the left
ventricule it is emptied not complete, that is shown by reduction of
cardiac output. If this indicator decreases on 10 % or more end-
diastolic pressure in the left ventricule, or preloading increases; in
spite of the fact that it the compensate mechanism directed to
increase of efficiency of systolic contraction, as a result leads to
increase of venous and capillary pressure in lungs and haenostasia
develops , thus decrease of cardiac output. The systemtemic
arterial pressure is supported by compensatory growth of
resistance of peripheral vessels, but it leads to the further increase
in postloading and complicates mechanical works of ventricules.
Сoronary failure develops acute and chronically. In typical cases acute
coronary failure develops at the patients who have transferred an
extensive myocardial infarction or after rupture of the valve of
heart. Chronic coronary failure is observed more often at persons
with slowly progressing cardiomyopathy or heart valvular damages.
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61. • At acute coronary failure - sudden reduction cardiac output is often
accompanied by a hypotension without peripheral hypostases.
• At chronic coronary failure - the blood pressure, on the contrary, is
long supported at normal level, but in tissues there is a fluid
accumulation.
The majority of clinical displays of coronary failure develops as a result
of fluid accumulation in system of one or both circles of blood
circulation. This fluid usually accumulation in the vascular channel,
located above the damaged chamber of heart. So, in case of
mechanical overload of left ventricule (aortic stenosis) or its
weaknesses (postinfarction myocardium changes), in result of
haemostasia in lungs develop dyspnea and orthopnea. This
condition called left ventricular coronary failure. If suffer right
ventricule, as in case of a pulmonary hypertensia (for example, at
thomboemboly of pulmonary artery) hypostases, stagnant
hepatomegaly, expansion of veins are expressed. If coronary failure
remains for a long time at patients with damage of valvular
apparats of an aorta or systemic hypertensia at late stages of
disease, develops stagnant hepatomegaly and enlarged of veins.
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62. • Chronic coronary failure. Classification (Strajesco N.D., Vasilenko
V. H, Muharljamov N.M., 1978).
• I stage (initial or hidden): fatigability, dyspnea and tachycardia at
physical activity. In the early (preclinical) period: inadequacy of
functions of heart comes to light only against extreme loadings or
during carrying out of functional tests (three-stage test of the
Master). In the presence of dyspnea, sweating, tremor of fingers,
cyonosis of a nose and lips after 10 minutes and more after loading
the initial condition of the patient is slowly restored.
• II stage (expressed):
A - developments of hypostasis in one of blood circulation circles.
It is clinically shown by a dyspnea, palpitation, fast fatigue at moderate
physical activity, it is accompanied with acrocyonosis, a tachycardia,
increase in the sizes of heart, insignificant increase in a liver,
presence of damp rattles in the inferior departments of lungs; X-ray
- strengthening of pulmonary drawing and roots of lungs of
hypostasis character;
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63. B- proof deep infringements of blood circulation in both circles of
blood circulation. Clinically: the dyrpnea in rest, оrthopnea (the
compelled sitting position), cough in horizontal position, the big
dense liver with the roundish or slightly pointed edge, painful at
palpation, acts under costal edges on 6-8 sm, massive hypostases of
shins and feet, acrocyonosis, is possible etrial fibrillation, heart
borders are expanded, tones of heart are weakened, a tachycardia
«a gallop rhythm», damp rattles in the inferior departments of
lungs, hydrothorax, a hydropericardium, аcytis.
X-ray: consolidation of roots of lungs, pleural and interlobal fluid.
ECHOKG: increase the end-diastolic size of left ventricule, the end-
systolic size of left ventricule, the anterio-posterior size left, - right
atriums, right ventricule , decrease of cardiac output.
• III - stage (final, dystrophic) - an exhaustion of patients (cardiac
kachesia ), orthopnea in rest, a skin flabby, acrocyonosis, massive
hypostases of the inferior finitenesses, аnasarka, the sizes of heart
are increased, tones of heart are weakened, a tachycardia, is
possible atrial fibrillation, considerably increased liver, can be a
jaundice.
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64. • Classification of coronary failure by New-York
Association of heart (NYHA).
• I-FC - patients with disease of heart without
restriction of physical activity, symptomless left
ventricular dysfunction
• II-FC - patients with disease of heart with
restriction of easy physical activity
• II-FC - patients with disease of heart with
considerable restriction of physical activity,
moderate cardiac failure
• IV-FC - patients are incapable to carry out the
easiest loading without sensation of discomfort.
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65. Left ventriacular failure
• Left ventriacular failure is shown by an inadequate tachycardia,
fatigue, dyspnea at easy physical activity. Attacks paroxysmal a night
dyspnea and cough are connected with redistribution of surplus of
a fiuid in lying position. Cough can be very strong and is quite often
accompanied by allocation pink or brownish mucous sputum due to
of an impurity of blood or hemosiderophags.
Survey
• Аcrocyonosis, the compelled position, tachypnea.
Palpation
• Poured and displaced to lateral side an apex beat.
Percussion
Expansion of borders of relative dullness of heart, is more than left.
Dullness sound over the inferior departments of lungs (pleural
effusion).
Auscultation
• Additional III, IV tones, «a gallop rhythm», accent of II tone over a
pulmonary artery. Damp rattles in the inferiof departments of lungs
against rigid breath.
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66. Acute left ventricular failire(a hypostasis of lungs)
Represents display menacing to a life the acute left
ventricular insufficiency, caused suddenly occurrence
of a pulmonary venous hypertensia. Prompt growth of
pressure of filling of left ventricule leads to a fast exit
of a fluid part of plasma through walls of pulmonary
capillaries to in intersticial space and alveoles. At the
patient develop the dificult dyspnea, cyanosis,
tachypnea, the anxiety and fear, appears sensation of
an asthma. Are usual pallor and plentiful sweating.
Pulse can be thready, the blood pressure is sometimes
difficult for defining. Breath is complicated, more of
damp and dry rattles in front and behind in both lungs.
At some patients the strong bronchospasm or stridor (a
cardiac asthma) develops. Heavy hipoxemia and sharp
cuanosis.
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67. Right ventricular failure
Right ventricular failure (with a pulmonary venous hypertensia or
without it). Leading symptoms - fatigue, feeling of burst in a neck,
sensation of completeness in a stomach, morbidity over a liver, a
swelling of anklebones, hypostases of shins, асytes.
• ECG: there are no specific signs of cardiac failure. Changes on an
ECG can specify in causes cardiac failure (hypertrophy of left
ventricular, MI , LBBB of RBBB).
• X-ray of bodies of a thorax: hypostasis in pulmonary veins and
increase of pulmonary drawing. Kerly’s lines reflect long increase of
pressure in left atrium and represent a chronic thickening the
interlobar septs, caused by a hypostasis.
• EchoCG: the sizes of left ventricule and other chambers of heart,
size of cardiac output and infringement of movement of walls. To
define degree of dilatation of left ventricule and hypertrophies of
left ventricule, pathological changes of valves of heart, fluid in
pericardium cavities, intracardiac thrombus and tumours.
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