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Semiology second semester > Ischemia sdr > Flashcards

Ischemia sdr Flashcards

1
Q

HYPOXIA

A

= metabolic impairment of cell function due to a

decreased oxygen supply

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2
Q

ISCHEMIA

A

= Hypoxia + Decreased cleansing of metabolic waste
→ For the myocite
• Lactate ↔ Piruvate
• H+

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3
Q

ISCHEMIC HEART DISEASE

A

= a syndrome
→ characterized by ischemia of the myocyte cells & interstitium as a consequence of an impaired coronary flow (macro and/or microvascular)
→ inadequate supply of blood and oxygen to an area of the myocardium due to the occurrence of an imbalance between myocardial oxygen supply and demand.

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4
Q

Myocardial ischemia syndromes

CAUSES

A
  1. Nonatherosclerotic

2. Atherosclerosis

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5
Q

Nonatherosclerotic Causes of IHD

A

slide 3

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6
Q

ATHEROSCLEROSIS

A

“The most common cause of myocardial ischemia is atherosclerotic disease of an epicardial coronary artery (or arteries) sufficient to cause a regional reduction in myocardial blood flow and inadequate perfusion of the myocardium supplied by the involved coronary artery.”

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7
Q

Coronary artery disease- (CAD)
Definition
Pattern

A

Definition ( European Society of Cardiology 2019)
CAD “is a pathological process characterized by
atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or non-obstructive ”
Pattern:
 progressive
 various clinical presentations

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8
Q

ATHEROSCLEROTIC PLAQUES
Plaques stability, activity and vulnerability
Stable atherosclerotic plaques
Composition

A
  1. Fibrous cap between intima and media
  2. Lipid core
  3. Hypocellularity
    Stable when
     Fibrous tissue exceed the lipids
     Noninflammatory cells&raquo_space; inflammatory cells
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9
Q

ATHEROSCLEROTIC PLAQUES
Plaques stability, activity and vulnerability
Unstable plaque

A

= culprit lesion for an acute vascular event
─ Fibrous cap: Thikness ↓→ cap Inflammation & Rupture &Thrombus formation
[Macrophages↑(~1/4of cap), Smooth muscle cells ↓, apoptosis ↑]
─ Necrotic Core↑ → Lipids&raquo_space; Fibers
─ Plaque size ↑
─ Neovascularization ↑ + Intraplaque hemorrhage ↑
─ Perivascular inflammation
─ ↑ Paradoxical remodeling (stenosis ↓)

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10
Q

Pathogenesis of Atherosclerotic Plaques

A
  1. Endothelial damage
  2. Protective response results in production of
    cellular adhesion molecules
    3.Monocytes and T lymphocytes attached to
    ‘sticky’ surface of endothelial cells
    4.Migrate through arterial wall to subendothelial space
    5.Macrophages take up oxidised LDL cholesterol
  3. Lipid-rich foam cells
  4. Fatty streak and plaque
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11
Q

Results of myocardial ischemia

Conclusions:

A 
take a look at slides 5,6,7
─ Acidosis → Pain
─ Mechanical inhomogeneity→ mechanical remodeling
↓
• diastolic dysfunction
• systolic dysfunction
• dilatation
• HF
• myocardial ruptures
─ Electrical inhomogeneity → electrical remodeling

↓
• rhythm disorders
• conduction disorders
• SCD

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12
Q

Ischemic heart disease (IHD)
Classification
Chronic coronary syndromes

A
  • Chronic stable angina
  • Asymptomatic and symptomatic pts with stabilized symptoms < 1 year after an ACS Or
    patients with recent revascularization
  • Asymptomatic and symptomatic pts >1 year after initial diagnosis or revascularization
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13
Q

Ischemic heart disease (IHD)
Classification
Acute coronary syndromes (ACS)

A
  1. Unstable angina
  2. ST elevation myocardial infarction
  3. Non ST elevation myocardial infarction
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14
Q

Other IHD Forms in which pain is not a dominant symptom

A
  1. Asymptomatic subjects in whom CAD is detected at screening
  2. Ischemic dilated cardiopathy with progressive heart failure
  3. Ischemic mitral regurgitation
  4. Rhythm and conduction disturbances
  5. Sudden cardiac death
  6. Vasospastic (Prinzmetal) and microvascular angina
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15
Q

Ischemic syndromes

Clinical Pattern

A

CAD
- Chronic coronary sdr. (Former stable CAD) =>
1.Chronic stable angina
2.Asymptomatic (Silent)
Ecg ischemia
- Acute, unstable(due to aterotrombosis)ACS :
>Without necrosis -> Unstable anginaTn (–)
>With necrosis =>
1. ST elevation MI= STEMI
2. Non-ST elevation MI= NTEMI
- Sudden cardiac death

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16
Q

Ischemic syndromes

Symptoms

A

 Chest pain
 Diaphoresis
 Anginal equivalents (dyspnea, faintness, fatigue, and frequent belching)
 Non–chest locations of discomfort (either exertional or at rest)
- Neck or mandibular discomfort or pain
- Throat tightness
- Shoulder discomfort
- Interscapular or infrascapular discomfort
- Upper arm or forearm discomfort (more often left-sided)
- Mid-epigastric burning
 Nausea or vomiting (due to increased vagal tone secondary to inferior
myocardial ischemia or infarction)
 Symptoms Determined by complication
> heart failure symptoms
− Dyspnea on exertion, Dyspnea at rest, Paroxysmal nocturnal dyspnea
− Gradual↑of exertional dyspnea with ↓effort tolerance)
> Dizziness and syncope

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17
Q

Ischemic syndromes

Signs /Physical examination

A
  • normal physical findings OR

* findings related to the the consequences of myocardial ischemia or evidence of risk factors

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18
Q

Ischemic syndromes

Cardiovascular characteristic signs when present

A

Auscultation

  • S3 may be present
  • transient apical Mitral systolic murmur (holosystolic or mid- late) due to reversible papillary muscle dysfunction that results in mitral regurgitation
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19
Q

Ischemic syndromes

Nonspecific signs

A

Pulse: normal (n)/ abnormal
Systolic blood pressure: n /↑ / ↓
Inspection, Palpation, Percussion- not relevant for IHD
Inspection: no facies
Palpation: the point of maximal impulse: variable with coexistent cv conditions
Percussion: cardiac dull area - variable with coexistent cv conditions

20
Q

Mechanisms of Anginal Pain

A

 Not known
 Presumed: ischemic episodes might excite chemosensitive and mechanosensitive receptors → release of adenosine, bradykinin, and other
substances → excite the sensory ends of sympathetic and vagal afferent fibers→ afferent fibers traverse the nerves that connect to the upper five thoracic sympathetic ganglia and the upper five distal thoracic roots of the spinal cord→ Impulses are transmitted by the spinal cord to the thalamus and then to the neocortex
 referred cardiac pain →within the spinal cord, cardiac sympathetic afferent impulses possibly will converge with impulses from somatic thoracic structures

21
Q

CHRONIC STABLE ANGINA
DEFINITION
DIAGNOSTIC TOOLS

A

Angina pectoris is a discomfort in the chest or adjacent areas
caused by myocardial ischemia.
Generally it is the initial form of IHD presentation in > 1/2 of patients

DIAGNOSIS tools
Clinical = typical CHEST PAIN
+ Noninvasive Testing
Ecg: Rest / effort
Echocardiography: contractility → segmental abnormality
Scintigraphy 201Tl, 99mTc , / SPECT / PET
Invasive Assessment
Coronary Angiography
Other
Biomarker for necrosis: absent
Assesing risk factor for ATS: Lipid profile, Glycemia

22
Q

CHRONIC STABLE ANGINA PECTORIS

Classical criteria described by Heberden “as conveying a sense of strangling and anxiety”

A

Chest pain characteristics:
1. Type: ” intermittent claudication”
2. Precipitated/ Provoked by: effort, cold, walking uphill, emotional distress
3. Relived promptly by
 Rest (pts. prefer to rest, sit, or stop walking during episodes)
 Nitroglicerin (but esophageal spasm relived also)- eventually helpful)
4. Reproducible
5. Periodicity (number / day/ week/ month)
6. Location : anterior thoracic (substernal) -discomfort above mandible or below diafragm/ epigastrium is rare
7. Duration : 5-10 min; < 20 minutes→ generally shorter
8. Intensity: mild, moderate
9. Quality : constricting, suffocating, crushing, heavy, and squeezing OR sensation can be vague and described as a mild pressure-like discomfort, tightness, an uncomfortable numbness, or a burning sensation
10. Radiated to mandible, left ear, shoulder, scapula, both arms, both wrists, down the ulnar surface of the left arm, Rarely: left laterothoracic
11. Tyme of onset (Postprandial → presumably caused by redistribution of coronary blood flow to the splanchnic circulation)
12. Evolution: usually begins gradually and reaches its maximum intensity over a period of minutes before dissipating.

23
Q

Chest pain definition as instrument of diagnosis used in guidelines
+
Canadian Cardiovascular Society
Classification System

A

slide 12

24
Q

CHRONIC STABLE ANGINA PECTORIS

slide 13

A 
History taking about:
1. Current symptoms
 “Typical” chest pain
 Change in pattern over prior 24 hr
 If similar to prior ischemic events
 Worse with decreased effort
 Radiation to neck or jaw
 Recent episode of similar pain
 Radiation to left arm
 Radiation to right arm
 Associated diaphoresis
 Associated dyspnea
 Abrupt onset
 Any improvement with nitroglycerin
 “Typical” radiation
 Burning pain
 Associated nausea/vomiting
 Associated palpitations
 Associated syncope
 Pain reproduced on palpation/respiration
exclude coronary origin
2. Family history assesment
3. Checking for Risk factors for atherosclerosis
25
Q

Risk factors for atherosclerosis

A 
Modificable
Dislipidemia
↑ LDL-Cholesterol, ↑ Total Cholesterol
↓ HDL-Cholesterol
↑ Triglicerides
Hypertension
Smoking
Diabetes, insulin resistance and metabolic syndrome
Not Modificable
Male sex
Advanced age
Family history of premature atherosclerosis
Obesity and decreased physical activity
Poverty, Psychosocial factors

Non-traditional risk factors:
Rheumatoid arthritis,
Collagen vascular disorders

Other
↑ Inflammation(hs-CRP, fibrinogen,IL-6, ICAM), etc.
↑ Prothrombotic factors
↑ Homocisteine
↑ Lipoprotein (a)
26
Q

PRINZMETAL’S VARIANT ANGINA

A

Definition: a syndrome characterized by
 severe ischemic pain that usually occurs at rest
 associated with transient Ecg ST-segment elevation caused by focal spasm
of an epicardial coronary artery with
 Coronary spasm results in ischemia and abnormal LV function
 may lead to acute MI, ventricular arrhytmias, and sudden cardiac death
 more frequent in Japan than in North America or Western Europe

Patients profile
 young
 smoker
 fewer coronary risk factors than do patients with NSTE-ACS

Cardiac examination
 Usually unremarkable in the absence of ischemia
 Few patients associate migraine and/or Raynaud’s phenomenon

Angiography + Hyperventilation or intracoronary acetylcholine
→ rest angina with transient ST-segment elevation on Ecg during pain
 Atherosclerotic plaques in at least one proximal coronary artery occur in about
1/2 of patients

27
Q

Unstable IHD

Chest pain characteristics

A
  1. Type: sudden
  2. Occurrence: at rest (Nocturnal angina may be a manifestation of unstable angina )
  3. Duration : > 20 (30) minutes
  4. Intensity: mild, moderate, severe- not specific
  5. Relived by nitroglicerin- generally NOT
  6. Location : anterior thoracic (substernal) or on radiation area
  7. Radiated to mandible, left ear, shoulder, scapular, both arms, both wrists

Rarely: left laterothoracic

28
Q

Non-ST-Segment Elevation Acute Coronary Syndrome

Unstable angina and Acute MI

A

History and Physical Examination
CHEST DISCOMFORT is typically severe and has at least 1 of 3 features:
 Occurrence at rest (or with minimal exertion)
 Lasting >10 min
 relatively recent onset (i.e., within the prior 2 weeks)
and/or
 a crescendo pattern (distinctly more severe, prolonged, or frequent than previous
episodes) NSTEMI → any of these features (without Ecg ST segment elevations)
+ evidence of myocardial necrosis=abnormally elevated levels of biomarkers

 Located in the substernal region
 Radiates to the left arm, left shoulder, and/or superiorly to the neck and jaw
Anginal equivalents: dyspnea, epigastric discomfort, nausea, or weakness may occur
instead of chest discomfort→ more frequent in: women, elderly, diabetes

Physical examination
 resembles that in patients with stable angina and may be unremarkable
 large NSTEMI→ diaphoresis; pale, cool skin; sinus tachycardia; S3 and/S4; basilar rales; sometimes, hypotension.

29
Q

PATHOPHYSIOLOGY of NSTE-ACS

A

Imbalance between myocardial oxygen supply and demand
Thrombus formation: 4 processes that lead to that
(1) disruption of an unstable coronary plaque due to:
 Plaque rupture
 Erosion
 a calcified protruding nodule that leads to intracoronary thrombus formation
(2) Coronary arterial vasoconstriction
(3) Gradual intraluminal narrowing
(4) Increased myocardial oxygen demand produced by conditions such as
 Fever
 Tachycardia
 Thyrotoxicosis
in the presence of fixed epicardial coronary obstruction

30
Q

DIAGNOSTIC EVALUATION of NSTE-ACS

A
  1. Chest pain
  2. Clinical examination
  3. 3 noninvasive tools
     ECG
     cardiac biomarkers
     stress testing
     coronary computed tomographic angiography CCTA may improve the accuracy
    Goals
    (1) Recognize or exclude myocardial infarction (MI)
    [ ↑cTn (cardiac troponin)=MI]
    (2) Detect rest ischemia (using serial or continuous ECGs)
    (3) Detect coronary obstruction at rest with CCTA and/ or myocardial ischemia using stress testing
31
Q

UNSTABLE ANGINA

A

UA is usually secondary to abrupt reduction in myocardial perfusion as a result of nonocclusive coronary thrombosis in which the nonocclusive
thrombus that developed on a disrupted atherosclerotic plaque does not result
in biochemical evidence of myocardial necrosis
UA must be diagnosed from the clinical history (based on anamnesis) and negative biomarker
3 principal presentations of UA:
(1) rest angina or angina with minimal exertion usually lasting at least 20 minutes
(2) new-onset severe angina (Canadian Cardiovascular Society grade III or higher; Table 36–1)
(3) crescendo angina, defined as previously diagnosed angina that has become distinctly more frequent, precipitated by less severe degrees of exertion, or
more severe

32
Q

NSTEMI is also termed non–ST-segment elevation

ACS (NSTE-ACS)

A

Definition: Angiographic, intravascular ultrasound (IVUS), and angioscopic studies indicate that acute NSTEMI usually results from the disruption of an
atherosclerotic plaque with a subsequent platelet-rich thrombus that obstructs microvascular blood flow and may transiently or partially obstruct epicardial
blood flow.

Diagnosis is based on cardiac chest pain from myocardial ischemia + the presence of abnormal concentrations of biomarkers indicative of myocardial
necrosis, either the troponins (which are structural proteins) or creatine kinase- MB (which is a cardiac enzyme)

The clearest separation between this end of the spectrum and ST-segment elevation myocardial infarction (STEMI) is made by the electrocardiogram (ECG).

33
Q

ST-SEGMENT ELEVATION MYOCARDIAL

INFARCTION

A
  • ~1/2 of AMI-related deaths occur before the patient reaches the hospital
  • ECG is a pivotal diagnostic and triage tool

PATHOPHYSIOLOGY: ROLE OF ACUTE PLAQUE RUPTURE
 occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a
coronary artery previously affected by atherosclerosis
 Vulnerable plaques prone to disruptionare have a rich lipid core and a thin fibrous cap
 Evolving precesses: platelet deposition and activation→conformational change in the
glycoprotein IIb/IIIa receptor → high affinity for soluble adhesive proteins → activate
fibrinogen& coagulation cascade → culprit coronary artery is occluded by a thrombus
containing platelet aggregates and fibrin strands

Rare etiology
 coronary emboli
 congenital abnormalities
 coronary spasm
 inflammatory—diseases
34
Q

Definition of Myocardial Infarction

Criteria for Acute Myocardial Infarction

A

The term acute myocardial infarction should be used when
- there is acute myocardial injury with clinical evidence of acute myocardial ischaemia and
- with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following:
 Symptoms of myocardial ischaemia
 ECG changes indicative of new ischemia (new ST/T-wave changes or new left bundle branch block [LBBB])
 Development of new pathological Q waves
 Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology
 Identification of a coronary thrombus by Angiography or Autopsy (not for types 2 or 3 M )

35
Q

Classification of Myocardial Infarction

A

Type I: Spontaneous Myocardial Infarction related to complicated atherosclerosis with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis.
Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance myocardial injury with necrosis where a condition other than CAD contributes to an
imbalance between myocardial oxygen supply and/ or demand
Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable:
Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic electrocardiogram (ECG) changes or new left bundle branch block (LBBB), but death occurring before blood samples

Type 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention (PCI)
Type 4b: Myocardial Infarction Related to Stent Thrombosis
Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting (CABG)

36
Q

STEMI CLINICAL PRESENTATION

A

 History
 Prodromal Symptoms = Chest discomfort resembling classic angina pectoris, but it
occurs at rest or with less activity than usual. A feeling of general malaise or frank exhaustion frequently accompanies other symptoms preceding STEMI
 Predisposing Factors are present in 1/ 3- 1/2 of cases (vigorous physical exercise, emotional stress, or a medical or surgical illness)
 Circadian periodicity especially in the morning within a few hours of awakening
CHEST PAIN
 deep and visceral (heavy, squeezing, and crushing; occasionally, it is described as stabbing or burning )
 similar in character to the discomfort of angina pectoris but
 commonly occurs at rest
 is usually more severe
 lasts longer
 Location:
 central portion of the chest and/or the epigastrium, and,
 The frequent location of the pain beneath the xiphoid and epigastrium
→mistaken impression of indigestion

 Radiates
 to the arms (on occasion)
 Less common sites of radiation include the abdomen, back, lower jaw, and neck
 The pain of STEMI may radiate as high as the occipital area but not below the
umbilicus

37
Q

STEMI CLINICAL PRESENTATION

A

CHEST PAIN
 Onset
 at rest ussually
 when it begins during a period of exertion, it does not usually subside with
cessation of activity
 painless STEMIs: patients with diabetes mellitus; elderly

Accompaniing factors:
 Anxiety
 Sweating(diaphoresis)
 Weakness
 Nausea, Vomiting
 a sense of impending doom
 The respiratory rate may rise slightly soon after the development of STEMI; in
patients without heart failure (HF) because of anxiety

Other presentation symptoms:
sudden-onset dyspnea → may progress to pulmonary edema
sudden loss of consciousness, a confusional state, a sense of profound weakness
the appearance of an arrhythmia
evidence of peripheral embolism
an unexplained drop in arterial pressure

38
Q

PHYSICAL FINDINGS (I)

A

 Anxiety and restless
 Altering their position
 Moving about in bed
 Stretching
 Pallor + perspiration and coolness of extremities
 The combination of substernal chest pain persisting for >30 min and
diaphoresis strongly suggests STEMI
 Vegetative manifestations of
- sympathetic nervous system: hyperactivity (tachycardia and/or hypertension) → common with anterior infarct
- parasympathetic hyperactivity (bradycardia and/or hypotension) → common with inferior infarction show evidence of
 Apical impulse may be difficult to palpate
 An abnormal systolic pulsation caused by dyskinetic bulging of infracted myocardium→ with anterior wall infarction (may develop in the periapical area within the first days of the illness and then may resolve

39
Q

PHYSICAL FINDINGS (II)

A

 Physical signs of ventricular dysfunction include
- fourth and third heart sounds S3/ S4
- decreased intensity of the first heart sound ↓ S1
- paradoxical splitting of the second heart sound
 Midsystolic or late systolic apical systolic murmur (transient ) due to
dysfunction of the mitral valve apparatus may be present
 Pericardial friction rub may be heard in patients with transmural STEMI
 The carotid pulse:
- often decreased in volume, reflecting reduced stroke volume
 Temperature
- elevations up to 38°C )may be observed during the first week after STEMI)
 The arterial pressure is variable
 SBP (systolic blood pressure) declines by ~10–15 mmHg in most patients with transmural infarction

40
Q

LABORATORY FINDINGS

A

STEMI temporal stages:

(1) Acute (first few hours–7 days)
(2) Healing (7–28 days)
(3) Healed (≥29 days)

The laboratory tests

(1) ECG
(2) Serum cardiac biomarkers
(3) Cardiac imaging
(4) Nonspecific indices of tissue necrosis and inflammation

41
Q

ELECTROCARDIOGRAM
Initially presenting with ST-segment elevation
→ ultimately evolve Q waves on the ECG

A

Early Acute Phase
→ begins within minutes, persists, and evolves during hours
T waves
 increase in amplitude and widen over the area of injury (hyperacute pattern)

ST segments
 evolve from concave to straightened to convex upward patterns (acute pattern)
 When prominent, the acute injury pattern of blended

ST-T waves can take on a tombstone appearance
 ST segment depressions that occur in leads opposite those with ST segment elevation are reciprocal changes

42
Q

ELECTROCARDIOGRAM

A

Evolved Acute Phase
 ST segment elevation begins to regress
 T waves in leads with ST segment elevation become inverted
 pathologic Q or QS waves become fully developed (>0.03-second duration or depth >30% of R wave amplitude, or both)

Chronic Phase
 Resolution of ST segment elevation
 Variable
 usually complete within 2 weeks of inferior MI, but it can be delayed further after anterior MI
 Persistent ST segment elevation may freeze with a large anterior MI
 Symmetrical T wave inversions can resolve during weeks to months or can persist for an indefinite period
 Q waves usually do not resolve after anterior MI but often disappear after inferior wall MI

Early reperfusion therapy accelerates the time course of ECG changes
 ST segments recede rapidly
 T wave inversions and loss of R waves occur earlier
 Q waves may not develop or progress and occasionally may regress

43
Q

SERUM CARDIAC BIOMARKERS elevation

A

 Cardiac-derived troponin-I (cTnI) and troponin-T (cTnT) are proteins specific to sarcomeres
 Serial measurement = the preferred approach for differentiating acute MI from unstable angina
 Surrogate biomarkers: CK-MB, AST

44
Q

CARDIAC IMAGING

2-D echocardiography permit evaluation of

A

 Abnormalities of wall motion
 left ventricular (LV) function for prognosis evaluation
 the presence of right ventricular (RV) infarction
 ventricular aneurysm
 pericardial effusion
 LV thrombus
 detection and quantitation of complications (ventricular septal defect & mitral regurgitation)

45
Q

Radionuclide imaging techniques

A

1.Myocardial perfusion imaging with [201Tl] or [99mTc]- sestamibi
 → reveals a defect (“cold spot”) during the first few hours after STEMI
2.Radionuclide ventriculography [99mTc]-labeled red blood cells
 demonstrates wall motion disorders and reduction in the ejection fraction
3.High-resolution cardiac MRI using late enhancement

46
Q

Therapeutic approach in STEMI

A 
slide 25
Rapid reperfusion therapy When
CHEST PAIN
\+
Characteristic ST elevation
Or new LBBB
1. PRIMARY ANGIOPLASTY preferred
2. Fibrinolytic therapy

Semiology second semester (13 decks)

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