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STEP 4: Cardio PATHOMA FA > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

ANGINA 1: What is the hallmark of REVERSIBLE myocyte injury in STABLE ANGINA?

A

CELLULAR SWELLING

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2
Q

ANGINA 1:What is the maximum time frame that the myocardium can withstand lack of blood flow before IRREVERSIBLE injury and cell death occur?

A

20 MINUTES

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3
Q

UW**: ANGINA 1: Where is the most susceptible location of STABLE ANGINA? Why is it the most susceptible location? What is the associated EKG finding?

A

SUBENDOCARDIAL ISCHEMIA
Reason: SUBENDOCARDIUM = Area of HIGHEST INCREASED INTRAVENTRICULAR PRESSURE + LV WALL TENSION during systole = Increased myocardial O2 demand

Associated Finding = ST DEPRESSION

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4
Q

ANGINA 1: How long does the chest pain of STABLE ANGINA last? What are the other clinical Sx of stable angina?

A

Stable angina chest pain

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5
Q

ANGINA 1: How is STABLE ANGINA relieved? (1 med, 1 not)

A

Relieved by 1) REST - Decrease myocardial O2 demand
2) NITROGLYCERIN - BOTH venodilates + coronary artery vasodilation
VENODILATION - Decreases preload -> Decreases myocardial O2 demand
CORONARY ARTERY VASODILATION - Increases O2 supply

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6
Q

ANGINA 1: What differentiates STABLE ANGINA from UNSTABLE ANGINA?

A

STABLE ANGINA: Chest pain elicited by exertion or emotional stress
UNSTABLE ANGINA: Chest pain at REST

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7
Q

ANGINA 2: Where is the most susceptible location of UNSTABLE ANGINA? What is the associated EKG finding?

A

SUBENDOCARDIAL ISCHEMIA
ST DEPRESSION
Same as STABLE ANGINA

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8
Q

ANGINA 2: Describe why UNSTABLE ANGINA has a high risk of progression to MI.

A

UNSTABLE ANGINA: Rupture of atherosclerotic plaque -> Exposure of sub-endothelial collagen -> Thrombosis -> INCOMPLETE CA occlusion

High risk of COMPLETE CA occlusion = MI

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9
Q

ANGINA 2: Is there REVERSIBLE or IRREVERSIBLE injury to myocytes in UNSTABLE ANGINA?

A

REVERSIBLE still

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10
Q

ANGINA 2: Is there REVERSIBLE or IRREVERSIBLE injury to myocytes in PRINZMETAL ANGINA?

A

REVERSIBLE injury = Cellular Swelling

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11
Q

ANGINA 2: How is UNSTABLE ANGINA relieved?

A

NITROGLYCERIN

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12
Q

ANGINA 3: What is PRINZMETAL ANGINA? Is it related to exertion?

A

Chest pain due to CORONARY ARTERY VASOSPASM that clamps down on the ENTIRE vessel occluding blood supply to EPI, MYO, and ENDOCARDIUM
UNRELATED to exertion

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13
Q

ANGINA 3: How is PRINZMETAL ANGINA relieved?

A

Nitroglycerin

Ca2+ channel blockers - Relieve CA vasospasm

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14
Q

What differentiates ANGINA (3 types) from MYOCARDIAL INFARCTION?

A 
ANGINA = Reversible injury to myocytes = Cellular swelling 
MI = Irreversible injury to myoctyes = NECROSIS = Membrane damage = Release of cardiac enz
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15
Q

What are the possible causes of an MI = COMPLETE OCCLUSION of CA?

A
  1. Rupture of atherosclerotic plaque
  2. CA vasospasm - clamping down on vessel entirely [Due to PRINZMETAL ANGINA or cocaine usage]
  3. Emboli
  4. Vasculitis [KAWASAKI - age of 5, preferentially affects coronary artery]
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16
Q

How long does the chest pain of an MI last? What are the other clinical Sx?

A

Chest pain >20min (IRREVERSIBLE injury to myocytes), radiates to left arm and jaw
Diaphoresis, Dyspnea (pulmonary congestion)

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17
Q

Which chamber does the MI most commonly affect? Which chambers are generally spared?

A

LV - most affected

RV, LA, RA - generally spared

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18
Q

Which is the most commonly occluded CA resulting in an MI? Which portions of the heart are infarcted? What leads are these detected in?

A

LAD - Anterior wall (LV) + Anterior septum (LV)

Detected in Leads V1-V4

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19
Q

Which is the 2nd most commonly occluded CA resulting in an MI? Which portions of the heart are infarcted? What leads are these detected in?

A

RCA - Infarctions of posterior inferior wall (LV) + posterior interventricular septum (LV) + Papillary muscles (LV) + AV node/SA node (can cause BRADYCARDIA/ HEART BLOCK)
Detected in leads V1 (opp), II, III, avF

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20
Q

Which is the 3rd most commonly occluded CA resulting in an MI? Which portions of the heart are infarcted? What leads are these detected in?

A

LCX - Infarction of LV lateral wall

Detected in leads I, aVL , V5-V6

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21
Q

What are the two phases of an MI and the associated EKG findings?

A

PHASE 1: Sub-endocardial Ischemic Necrosis/Infarction (Involving

22
Q

What is the hallmark of IRREVERSIBLE damage to myocytes in an MI?

A

MEMBRANE DAMAGE

23
Q

What is the most Se and Sp marker of an MI? What is the time pattern of this marker?

A

TROPONIN I = GOLD STANDARD

Rises 2-4hrs after infarction, Peaks at 24hrs, Returns to nl (7-10d)

24
Q

Which is a good marker for detecting RECURRENT MIs after the initial MI [72hrs > recurrent > 7-10d]? Why would troponin I not be useful for detecting a RECURRENT MI 5days after first MI?

A

CK-MB: Rises 4-6hrs after infarction, Peaks at 24hrs, Returns to nl at 72hrs
Troponin I would NOT be useful in detecting this, since Troponin I levels would still be ELEVATED from the first MI (Stay elevated for 7-10d)

25
Q

How does ASA/HEPARIN work to treat an MI?

A

Both act to LIMIT initial THROMBOTIC event that resulted in complete CA occlusion for >20min, resulting in IRREVERSIBLE damage.

ASA = Irreversible COX1 > COX2 inhibitor -> Preferential decrease in TXA 2 -> Preferential decrease in Platelet aggregation/vascular tone

HEP = Binds and ACTIVATES anti-thrombin III -> Inactivates Thrombin + FXa (ANTI-COAGULANT)

26
Q

Which other medications are given to treat an MI?

A

NITRATES: Venodilation + Coronary arterial vasodilation = Decrease myocardial O2 demand + Increase myocardial O2 supply

BETA BLOCKERS: Decrease HR -> Decrease myocardial O2 demand + Decrease risk of ARRHYTHMIA (feared complication of MI)

ACE INHIBITORS: Decrease AngII-mediated peripheral vasoconstriction (Afterload) + Decrease AngII-aldosterone-mediated volume retention. BOTH act to DECREASE LV Dilation - Less volume = Less myocardial O2 demand

27
Q

What is the surgical Tx option of an MI? What is the overall goal of this?

A

FIBRINOLYSIS or ANGIOPLASTY - To open up the blocked vessel

28
Q

What are two possible complications of FIBRINOLYSIS or ANGIOPLASTY in treating the MI?

A

COMPLICATION 1: Contraction Band Necrosis - Reperfusion of irreversibly damaged myocytes -> Ca2=influx -> Myofibril contraction (Bands)

COMPLICATION 2: Reperfusion injury - Reperfusion -> Return of O2 + Inflammatory cells -> Free radical damage -> Greater myocyte death

29
Q

Pt had an MI 5days ago. He receives a FIBRINOLYSIS/ANGIOPLASTY procedure to open up the blocked LAD vessel. However, Troponin I/CK-MB continued to rise after 10days. Why are his cardiac enzyme levels still continuing to rise?

A

REPERFUSION INJURY
Surgical procedure opened up the blocked LAD -> Reperfusion -> O2 and inflammatory cell return -> Free radical damage -> Further damage to myocytes

30
Q

What are the 3 key phases of morphologic changes of an MI?

A

PHASE 1: COAGULATIVE TISSUE NECROSIS
PHASE 2: ACUTE INFLAMMATION (Neutrophils -> Macrophages) - Remember tissue necrosis = stimulus of acute inflammation
PHASE 3: WOUND HEALING - Repair of PERMANENT tissue (cardiac muscle granulation tissue -> Fibrosis and scar formation)

31
Q

Within the first 4 hours of an MI, what are the 3 types of complications?
HINT: Think systemically, think Decreased Ejection fraction, and early complication of rate/rhythm

A
  1. CARDIOGENIC SHOCK - Decreased systemic BP -> Decreased blood flow to organs
  2. CONGESTIVE HEART FAILURE - Backup of blood flow and inability to eject out proper stroke volume (DECREASED EF)
  3. ARRHYTHMIA
32
Q

Within the first 4-24hrs of an MI, what injury process is occurring? What is the gross change? What is the feared complication?

A

COAGULATIVE NECROSIS
Dark discoloration of heart

Complication = ARRHYTHMIA - Due to irreversible damage of conducting systems (would be present within the first 24hrs)

33
Q

Within the first 1-3days of an MI, what injury process is occurring? What is the gross change? What is the feared complication?

A 
ACUTE INFLAMMATION (specifically neutrophils) 
Yellow pallor (WBC infiltrate within myocardium)

Complication = FIBRINOUS PERICARDITIS (exudate infiltrating surrounding pericardium) = CHEST PAIN + Friction Rub

34
Q

Which ONLY ONE TYPE of myocardial infarction will result in a complication of FIBRINOUS PERICARDITIS?

A

***TRANSMURAL INFARCTION
NOT subendocardial infarction - exudate is not present in the epicardium that would extend into the pericardium as in fibrinous pericarditis

35
Q

Within the first 4-7days of an MI, what injury process is occurring? What is the gross change?

A 
ACUTE INFLAMMATION (Specifically macrophages - eat up all the necrotic debris = Wall is WEAKEST AT THIS POINT) 
YELLOW PALLOR (WBC infiltrate in myocardium)
36
Q

Within the first 4-7days of an MI, what are the 3 possible complications?

A

MACROPHAGE ACUTE INFLAMMATION PHASE = clean up all necrotic debris = Weakest point of muscle repair

COMPLICATION 1: RUPTURE ventricular free wall -> Blood enters pericardial sac -> Compresses heart = CARDIAC TAMPONADE
COMPLICATION 2: RUPTURE of interventricular septum: L->R SHUNT
COMPLICATION 3: RUPTURE of papillary muscle: Chordae tendinae of mitral valve no longer anchored to papillary muscle -> MITRAL REGURG during systole

37
Q

Which vessel occlusion MI will result in a complication of MITRAL INSUFFICIENCY/REGURG during systole? What phase of MI will this occur in?

A

RCA (specifically POSTERIOR DESCENDING ARTERY branch)**
Work backwards: Complication of mitral insufficiency - Due to RUPTURE of papillary muscle - Supplied by PDA branch of RCA (in addition to posterior inferior wall/posterior septum)

Occurs 4-7d after MI during acute inflammation (macrophages)

38
Q

Within the first 1-3wks of an MI, what injury process is occurring? What is the gross change?

A 
FIRST PORTION of WOUND HEALING [repair] = GRANULATION TISSUE 
RED BORDER (as new blood vessels of granulation tissue enters around the borders of the infarct)
39
Q

Within >1mo of an MI, what injury process is occurring? What is the gross change? What are the 3 complications?

A

Second phase of WOUND HEALING [repair] - Scar formation
White fibrotic scarring
Scar - Not as strong as original myocardium resulting in 3 possible complications

COMPLICATION 1: ANEURYSM=Balloon dilatation of weakened wall
COMPLICATION 2: MURAL THROMBUS= Stasis following weakened wall
COMPLICATION 3: DRESSLER SYNDROME

40
Q

What is DRESSLER SYNDROME? When do you see it most commonly?

A

DRESSLER SYNDROME: Autoimmunity against host pericardium as a complication, 6-8wks after an MI
Pathophys: Transmural infarction extended out of the epicardium into the pericardium -> Pericarditis -> Immune system makes auto-Abs against self pericardial Ags

41
Q

How does SUDDEN CARDIAC DEATH usually occur? What are the two possible clinical presentations?

A

SUDDEN CARDIAC DEATH - Usually due to FATAL VENTRICULAR ARRHYTHMIA

Without clinical sx OR death occurs

42
Q

What is the most common cause of SUDDEN CARDIAC DEATH? What is the main predisposition factor?

A

ACUTE ISCHEMIA

90% of these pts have pre-existing severe atherosclerosis

43
Q

What are the less common causes of SUDDEN CARDIAC DEATH?

A
  1. MVP
  2. HCM
  3. Cocaine abuse
44
Q

ANGINA 3: Where is the most susceptible location of ischemia of PRINZMETAL ANGINA? What is the associated EKG finding?

A

TRANSMURAL ISCHEMIA - Complete CA occlusion supplying epicardium, myocardium, and endocardium

Associated EKG finding = ST ELEVATION

45
Q

What is the gold standard of diagnosing a MI in the first 6hrs?

A

EKG

46
Q

UWORLD: What is the PREFERRED METHOD OF TREATMENT of a STEMI if a pt presented to the ER within 12hrs of Sx onset? Why is this treatment preferred?

A

PERCUTANEOUS CORONARY INTERVENTION (PCI)

Preferred over fibrinolysis due to LOWER RATES of INTRACEREBRAL HEMORRHAGE and recurrent MI

47
Q

**UW: What are some clinical manifestations of MYOCARDIAL REPERFUSION INJURY after PCI procedure?

A

ARRHYTHMIA
MYOCARDIAL STUNNING (Prolonged but reversible cardiac dysfn)
MYOCYTE DEATH

48
Q

Formulation of cardiac LV wall tension:

A

LAPLACE LAW

LV Tension = (PRESSURE x RADIUS) / (2 x wall thickness)

49
Q

**UW: What are the sequential EKG changes seen for an acute TRANSMURAL MI?

A
  1. Peaked T-waves (localized hyperkalemia)
  2. ST elevation
  3. Pathologic Q waves
50
Q

**UW: Timeline of macrophage-mediated destruction of a TRANSMURAL MI

A
  1. 3-5d: RUPTURE OF PAPILLARY MUSCLE - Mitral regurg
  2. 3-5d: RUPTURE OF INTERVENTRICULAR SEPTUM - VSD
  3. 5-14d: RUPTURE OF FREE WALL - Pericardial tamponade (JVD, Distant heart sounds)

STEP 4: Cardio PATHOMA FA (6 decks)

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