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CPR Week 3 > 3.3.2. Cardiac Pathology Part 1: Ischemic, CHF, Congenital Defects > Flashcards

3.3.2. Cardiac Pathology Part 1: Ischemic, CHF, Congenital Defects Flashcards

1
Q

Ischemic heart disease is usually due to what?

A

Atherosclerosis of coronary arteries

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2
Q

What is stable angina?

A

Get angina with stress or activity

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3
Q

Why in stable angina do we not always have pain?

A

It’s mild decreased blood flow in the coronary artery, but when we exercise and need more blood to the heart tissue, we can’t get it, it gets a little ischemic, and we feel pain

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4
Q

In Stable Angina, it is due to atherosclerosis of coronary arteries with ____ ____.

A

> 70% stenosis

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5
Q

What type of injury is stable angina?

A

It is reversible!

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6
Q

in Stable Angina, the cells don’t die, hence it being reversible. However, they do do this…

A

Get bigger

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7
Q

Presentation of Stable Angina

A
  1. CP < 20 minutes that radiates to left arm or jaw
  2. Diaphoresis
  3. SOB
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8
Q

What EKG finding do we get with Stable Angina? Why?

A

ST Depression due to subendocardial ischemia

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9
Q

Why is the damage caused by Stable Angina subendocardial?

A

Coronary arteries feed epicardium to endocardium, so if there is a blockage, the most affected portion will be the latest, which typically happens just below the endocardium, or, subendocardial.

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10
Q

Treatment for Stable Angina?

A

Rest or NTG

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11
Q

What is unstable angina?

A

Pain even at rest due to a rupture of an artherosclerotic plaque with thrombosis and incomplete occlusion of the coronary artery.

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12
Q

How is reversibility different between stable and unstable angina?

A

It’s not both irreversible

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13
Q

What is an important note about the occlusion in unstable angina?

A

It is incomplete occlusion

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14
Q

EKG and treatment for unstable angina

A

NTG, EKG shows ST depression

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15
Q

For unstable angina we have a high risk for ____.

A

MI

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16
Q

Prinzmetal angina is what?

A

Vasospasm of the coronary artery

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17
Q

What is different about prinzmetal angina from stable and unstable angina?

A

Prinzmetal is complete and random occlusion, so the chest pain is still episodic, but it is completely unrelated to exertion

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18
Q

EKG for prinzmetal angina? Why?

A

ST elevation because the early part of the coronary artery is clamped in the epicardium, so the blood is lost through the entire vessel whih leads to ST elevation.

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19
Q

Treatment for Prinzmetal Angina

A

NTG and Ca Channel blockers

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20
Q

What is a myocardial Infarction?

A

Necrosis of cardiomyocytes due to a rupture of the atherosclerotic plaque leading to a thrombosis and complete occlusion of the coronary artery

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21
Q

How long does it take for the cardiac tissue to turn necrotic?

A

> 20 minutes

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22
Q

How can vasculitis cause an MI?

A

Inflammed interior wall, coag pathway, thrombus, complete occlusion results.

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23
Q

Presentation for MI

A
  1. Severe crushing chest pain > 20 minutes
  2. Diaphoresis
  3. Dyspnea
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24
Q

Effect of NG on an MI

A

None.

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25
Q

Infarction usually involves the _____

A

Left Ventricle.

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26
Q

Most common ischemic location on the heart

A

On the left ventricle anteriorly running down the anterior descending artery causing infarct to the anterior heart and IV septum

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27
Q

If we see infarction on the posterior wall of the Left ventricle and the posterior aspect of the IV septum, what artery is affected?

A

Right coronary artery

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28
Q

Lateral LV infarction indicates what artery being affected?

A

Left circumflex artery

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29
Q

During the initial phase of MI, what damage do we see? EKG?

A

Subendocardial at first with ST depression and accounting for only about 50% of damage

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30
Q

How does the MI progress?

A

With time, we see full thickness necrosis (transmural) so we’ll see ST elevation

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31
Q

Lab tests for MI

A
  • Troponin I

- CKMB

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32
Q

Best marker for MI and what does it show?

A

Troponin I is the most sensitive and specific marker

Occurs 2-4 hours after an infarction and peaks at 24 hours. Returns to normal by 7 - 10 days

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33
Q

Besides Troponin I, what can we use? How does it work?

A

CKMB

  • Rises 4 - 6 hours after infarction
  • Peaks at 24 hours
  • Returns to normal by 72 hours
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34
Q

Best treatment for MI and why

A
  • ASA and Heparin to eliminate additional thrombosis
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35
Q

Besides ASA and Heparin what else can we treat MIs with?

A

Oxygen due to ischemia
Nitrates to vasodilate arteries and veins, veins in particular in order to decrease preload on the heart
Beta blockers to slow HR and decrease demand for oxygen and possibility of arrhythmia
ACE inhibitor to decrease left ventricular dilation.

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36
Q

ACE inhibitors are good for MIs. What do they do and why is it so great

A

ACE blocks angiotensin I to Angiotensin II.

Angio II constricts arterioles and also causes fluid retention after stimulating the adrenal glands to make aldosterone

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37
Q

More definitive treatments for MI

A
  1. Fibrinolysis

2. Angioplasty

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38
Q

Action of fibrinolysis

A

Destroy the thrombus

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39
Q

When blood is restored, it hits now dead heart tissue in MI. What complications does this cause?

A
  1. Contraction Band Necrosis - Calcium returns to dead cell and causes creation of band lines as it causes portions of it to contract.
  2. Reperfusion injury - returning oxygen to dead tissue can cause the creation of free radicals which can further injure the myocardium
40
Q

You help your patient who suffered from a MI but noticed that his enzymes were still present beyond the normal time. What happened?

A

Reperfusion injury!

41
Q

When and what microscopic changes occur after an MI?

A

<4 hours = nothing

4 - 24 hours = Coagulative Necrosis

1 - 3 days = Neutrophils

4 - 7 days = Macrophages

1 - 3 weeks = Granulation tissue with plump fibroblasts, collagen and blood vessels

Months - Fibrosis

42
Q

When do we see a yellow pallor on the heart?

A

1 - 7 days s/p an MI

43
Q

When do we see a Dark discoloration on the heart?

A

4 - 24 hours s/p MI

44
Q

When do we see a white scar on the heart?

A

Months s/p MI

45
Q

When, s/p and MI, do we see a red border emerge as granulation tissue enters the edge of an infarct?

A

1 - 3 weeks s/p MI

46
Q

When do MI affected cells lose their nuclei?

A

4 - 24 hours, during coag necrosis

47
Q

Complications within the first four hours of an MI (3)

A

Cardiogenic shock (massive infarction) where the heart fails and lack of blood flow to major organs.

You can also get CHF due to a decrease ejection fraction

arrhythmia

48
Q

Complication in the coagulative necrosis stage?

A

4 - 24 hours

Arrhythmias

49
Q

When the neutrophils arrive s/p an MI, what complications do we face? Why?

A

Fibrinous pericarditis - presents as chest pain with friction rub.
During these first few days when we are inflamming with neutrophils, some of that inflammation goes to the pericardium and causes pericarditis.

50
Q

When the macrophages arrive s/p an MI, what complications do we face?

A

Ruptures due to marcophages eating all that bad stuff

  1. Rupture of ventricular free wall (could lead to cardiac tamponade)
  2. Rupture of IV septum causing shock as blood gets shunted from LV to RV
  3. Rupture of papillary muscle, causing the valves to become messed up, causing systolic backflow into the atria
51
Q

If we have papillary muscle issues, what do we know about the MI?

A

It was caused by a blockage to the right coronary artery (which feeds the papillary muscles)

52
Q

Why does a red border form during granulation?

A

Blood vessels come from the outside in to heal

53
Q

When the scar formation occurs s/p an MI, what complications are we worried about?

A

Aneurysm due to a weakened wall

Also a mural thrombus due to a weakened wall.

Dressler Syndrome also possible. MI can cause the pericardium to release antibodies and your immune system to attack the pericardium causing pericarditis 6-8 weeks s/p MI.

54
Q

Moving on to heart failure, what can cause left sided heart failure?

A 
Ischemia
HTN
Dilated cardiomyopathy
MI
Restrictive cardiomyopathy
55
Q

Clinical signs of left sided heart failure will be indicated by what?

A

Pulmonary congestion - Can’t pump the blood forward, its gonna pump back towards the lung

56
Q

Symptoms of left sided heart failure

A
  1. Pulmonary edema with dyspnea
  2. PND
  3. Orthopnea
  4. Crackles
  5. Heart failure cells
57
Q

What are heart failure cells?

A

Hemosiderin laiden macrophages

58
Q

Decreased forward perfusion caused by left sided heart failure leads to what?

A

Activation of Renin angiotensin system

59
Q

Most common cause of right sided heart failure?

A

Left sided failure.

60
Q

Other important causes of right sided heart failure besides left sided heart failure

A

Left to right shunt and chronic lung disease

61
Q

Cor Polmonale

A

When your heart fails due to chronic lung disease

62
Q

Clinical features of right cardiac failure

A

Due to congestion

  1. JVD
  2. Painful Hepato Splenomegaly that may lead to cardiac cirrhosis
  3. Dependent pitting edema
63
Q

Ventricular Septal Defect

A

Defect in the septum dividing the ventricles

64
Q

VSD associated with what?

A

Fetal Alcohol syndrome

65
Q

What is the most common congenital heart defect?

A

VSD

66
Q

Key problem in VSD? Explain timeline.

A

Blood chooses lower pressure and will go from LV to RV leading into Left Right shunt.

This leads to lung back up as more fluid is coming from the Right side. Eventually the pulmonic pathway will have the highest pressure, and the RV willchoose the lower pressure pathway, the LV, which will send deoxygenated blood back around systemically

This leads to Cyanosis

67
Q

Small vs. large defects from VSD

A

Small - Asymptomatic

Large - Eisenmenger - RV hypertrophy due to larger pressure gradients, clubbing, etc

68
Q

ASD?

A

Defect in atrial septa

69
Q

Most common type of ASD?

A

Ostium secundum

70
Q

What is ostium primum type associated with?

A

Down Syndrome

71
Q

Heart sound associated with ASD? How?

A

Split S2

Blood in LA travels to RA, causing it to have more blood, leading to a delay in pulmonic valve closure

72
Q

Paradoxical Embolus

A

Normally emboli from DVT goes into the RA then RV and into the lungs to cause a Pulmonary Embolus but inASD, it can go from the RA to LA to LV and then anywhere in the body, even the brain.

73
Q

What is Patent Ductus Arteriosus? What is it associated with?

A

Failure of Ductus Arteriosus to close.This is associated with congenital Rubella

74
Q

Problem with Ductus Arteriosus being active in an adult?

A

Blood will go from the Aorta back to the pulmonary artery and cause pulmonary HTN, increasing pressure and causing blood to go from the RV to the pulomary artery and then straight to the Aorta which is now a lower pressure.

This will cause deoxygenated blood to circulate, causing cyanosis in the LE only (the DA occurs after the upper extremity pathways, so those are unaffected)

75
Q

Results of Left to Right Shunt between aorta and PA?

A
  • Asymptomatic t birth

- Eisenmerger Syndrome results in lower extremity cyanosis

76
Q

Treatment of Patent DA?

A

Indomethacin which decreases PGE, which results in PDA closure

77
Q

Problems with Tetralogy of Fallot

A
  1. Stenosis of RV outflow tract
  2. Right ventricular hypertrophy
  3. VSD
  4. Aorta that overrides the VSD
78
Q

Explain what is happening with Tetralogy of Fallot

A

Stenosis of RV outflow and an enlarged Right Ventricle cause the ventricle to be less efficient. Since these patients also have a VAD with the Aorta taking over, the blood from the RV will go through the Aorta immediately and cause cyanosis

79
Q

Patients learn to ____ in response to cyanotic changes caused by Tetralogy of Fallot

A

Squat

80
Q

Film study for Tetralogy of Fallot

A

CXR with heart looking like a boot

81
Q

In transposition of great vessels what happens?

A

Aorta and Pulmonary Artery switch, but not their end goals, so they just feed their own sided chmbers

Ex. Blood to RA to RV to aorta back to RA

82
Q

How do we treat transposition of great vessels?

A

Keep the Ductus Arteriosus open with PGE and make a shunt

83
Q

___ ___ is associated with Transposition of Great vessels

A

Maternal diabetes

84
Q

Presentation of transposition of great vessels

A

Early cyanosis due to no oxygenated blood in circulation

85
Q

What is happening with Truncus Arteriosus?

A

Single large vessel arising from both ventricles due to the trunk failing to divide

86
Q

How does Truncus Arteriosus also show signs of early cyanosis?

A

Deox and ox blood are mixed together and then sent through Aorta or pulmonary.

87
Q

Tricuspid Atresia

A

Tricuspid valve orifice fails to develop, so blood cannot enter the RV.
- Causes opening to occur between atria (ASD) and causes the right ventricle to become hypoplastic

88
Q

Sign of Tricuspid Atresia?

A

Early cyanosis

89
Q

What is Coarctation of the Aorta?

A

Narrowing of the Aorta

90
Q

Child Coarctation of the Aorta

A

Associated with PDA. Narrowing occurs between the aortic arches and the DA. Blood will flow from the RA to the RV to the pulmonary, through DA and through the rest of the body, giving you LE cyanosis since the DA is after the arches.

91
Q

Infantile Coarctation is associated with ____ ____.

A

Turner syndrome

92
Q

Adult Coarctation

A

Not associated with a PDA
Get coarctation after the aortic arch. Causes buildup of blood (HTN) in the upper extremities with lower blood pressure in the LE since the blood cannot get to the LE.

93
Q

Presentation of adult coarctation

A

HTN in UE and hypotension in LE with weak pulses in LE

94
Q

Adult coarctation associated with ___ ___ ___.

A

Bicuspid Aortic valve

95
Q

____ ____ develops across intercostal arteries due to Adult coarctation

A

Collateral circulation

96
Q

Chest x ray of someone with adult coarctation

A

Engorged arteries cause notching of ribs in xray due to collateral circulation

CPR Week 3 (16 decks)

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