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DT3- EXAM 1 > Ischemic & Hypertensive Heart Disease- Melissa (6)* > Flashcards

Ischemic & Hypertensive Heart Disease- Melissa (6)* Flashcards

1
Q

Another name for ischemic heart disease?
Definition:
What four conditions does it include?

A 
Coronary artery disease 
Heart's demand for nutrients, O2, waste removal >>> Blood supply 
1. Angina 
2.Chronic IHD 
3.MI 
4. Sudden Cardiac Death
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2
Q

Cause of over 90% ischemic heart disease:

A

Atherosclerosis + coronary arterial obstruction (stenosis)

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3
Q

What is the #1 cause of death in men and women over 50yoa?

A

ischemic heart disease

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4
Q

Ischemic heart disease results from a complex, dynamic interaction between the following 4 factors:

A
  1. fixed coronary obstruction
  2. acute plaque change/ platelet aggregation
  3. coronary thrombus
  4. vasospasm
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5
Q

What % of a coronary artery must be occluded in order to cause angina with exercise?

A

More than 70%

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6
Q

What % of a coronary artery must be occluded in order to cause angina at rest?

A

More than 90%

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7
Q

What is one way distal myocardium may be protected from ischemia in the event of coronary obstruction?

A

collateral circulation

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8
Q

2 Possible triggers for acute plaque change in atherosclerotic coronary arteries:

A
  • Adrenergic activity (emotions, circadian rhythm)

- Dynamic changes make plaques more vulnerable

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9
Q

Which plaques are the most dangerous/ vulnerable?

A

moderately stenotic because they are asymptomatic most of the time

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10
Q

3 possible roles for a coronary thrombus to play in ischemic heart disease:

A
  1. make partial occlusion–> total occlusion (most common)
  2. mural thrombus–> embolize and cause partial occlusion
  3. Activate SMCs–> ^ size of atherosclerotic lesions
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11
Q

What role does vasoconstriction play in ischemic heart disease?
What two factors stimulate vasoconstriction?

A

Adrenergic agonists + platelet contents–> ^ vasocnstrxn–> ^ ischemia

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12
Q

Define angina pectoris including:

  • how long does it last?
  • what causes it?
  • when might it be asymptomatic?
A

Paroxysmal, recurrent substernal/ precordial chest discomfort (constrict, squeeze, choke, stab)

  • 15s-15 min
  • incomplete occlusion of a coronary artery usually by an atherosclerotic plaque
  • Asymptomatic in DM/ neuropathic ppl
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13
Q

Stable angina:

  • defintion?
  • prevalence?
  • cause?
  • triggers?
A
  • Predictable angina relived by NG or rest
  • Most common angina pectoris
  • Fixed obstruction–> decrease coronary perfusion
  • Triggers: excitement, exercise, ^ cardiac workload
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14
Q

Unstable angina:

  • prevalence?
  • definition
  • of what might this be a warning?
  • cause?
A 
#1 Acute Coronary Syndrome! 
Unpredictable chest pain occurring with progressively less effort, lasting progressively longer duration 
*POSSIBLE MI WARNING*
  • Disruption of atherosclerotic plaque + superimposed partially occluding thrombus
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15
Q

What is Prinzmetal angina? Prevalence? Tx?

A

Angina caused by coronary spasms w/ possible underlaying IHD
- rare
- episodic and may occur at rest
Tx: NG, Ca++ channel blockers

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16
Q

What are the #1, #2, #3 Acute coronary syndromes?

What is their common pathological link?

A 
#1: Unstable angina
#2: MI
#3: Sudden cardiac death

All have atherosclerotic plaque disruption w. intra-luminal platelet-fibrin thrombus formation

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17
Q

What separates MI from angina in terms of pathology?

A

MI has IRREVERSIBLE cardiac cell death due to ischemia
–> necrosis

Angina causes REVERSIBLE damage due to ischemia/ cellular swelling

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18
Q

What are the risk factors for MI?

How do African American prevalence rates compare to Caucasian?

A

same as atherosclerosis
-black and white prevalence are equal.
(I thought Black > White for some reason.) * I must remember.

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19
Q

Describe the 6 steps in pathogenesis of 90% of Transmural MIs:

A
  1. Acute plaque change (rupture, erode, hemorrhage)–>
  2. Platelet adhesion to sub endothelial collagen + necrotic material–>
  3. Platelets release aggregators–>
  4. Vasospasm + Extrinsic pathway –> Thrombus size& Occlusion
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20
Q

How long must ischemia endure in order to cause irreparable injury to cardiac myocytes?

A

20 minutes

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21
Q

How quickly do coronary thrombi heal?

A

30% clear within 12-24 hours via lysis/ relaxation of vasospasm

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22
Q

4 alternative pathogenesis mechanisms for transmural MI (10% of cases):

A
  1. vasospasm +/- coronary atherosclerosis
  2. emboli from lt. atrium
    (a fib., LV mural thrombus, paradoxical embolus)
  3. vasculitis
  4. HypoTN (esp in cases of preexisting stenosis)
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23
Q

What should you suspect in young patient that has transmural MI as a result of vasospasm? No vasospasm?

A

COCAINE

Kawasaki, Congenital defect

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24
Q

Describe the timeline of myocardial response to ischemia:

A

Seconds:
Stop glycolysis–> LOW ATP, ^ Lactic acid

2 min:
LOW Contractility, Acute HF, reversible myocyte injury

20-40 min:
Irreversible myocyte injury, hemorrhage

1 hr:
Microvascular Injury, arrhythmia due to ischemia

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25
Q

Most MIs are transmural or sub endothelial?

A

Transmural

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26
Q

3 common causes of transmural MI + typical EKG finding:

A
  1. coronary atherosclerosis
  2. acute plaque change
  3. obstructive thrombus

ST Elevation on EKG

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27
Q

Define sub endocardial infarct.
Typical EKG finding?
What two features do they LACK?

A
  • Infarct of inner 1/3-1/2 ventricular wall (watershed)
  • NO ST on EKG (NON STEMI)

NO plaque disruption
NO superimposed thrombi

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28
Q

Causes of subendocaridal infarct (3)

A
  1. diffuse stenosising coronary atherosclerosis
  2. lysed thrombus
  3. severe prolonged HypoTN (shock) + coronary stenosis

(NOT acute plaque change and subsequent thrombus)

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29
Q

By what time is necrosis of an ischemic myocardial segment complete?

A

6 hrs

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30
Q

The LCA branches into what two arteries?

A

Lt circumflex, LAD

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31
Q

The LAD supplies which regions of the heart?

A
  1. anterior 2/3 vent. septum
  2. anterior wall of LV
  3. apex
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32
Q

The LCX supplies which regions of the heart?

What does it branch into in the Lt dominant heart?

A
  1. lateral wall LV

Lt Dominant Heart–> PDA

  1. post 1/3 vent septum (20%)
  2. posteriobasal LV wall (20%)
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33
Q

The RCA supplies which regions of the heart?

What does it branch into in the Rt dominant heart?

A
  1. RV

Rt Dominant Heart–>PDA

  1. posterior 1/3 vent septum
  2. posteriobasal LV wall
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34
Q

What percent of infarct occur in the LAD?

Typical deficits?

A

50%

- knock out entire supply’s of anteroseptal region/apex

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35
Q

What percent of infarct occur in the RCA?

Typical deficits?

A

30-40%

  • posteriobasal LV wall
  • posterior 1/3 septum
  • occasionally the posterior RV wall
  • isolated RV infarcts are rare
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36
Q

What percent of infarcts occur in the LCX?

Typical deficits?

A

15-20%

- lateral wall LV sparing apex

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37
Q

Describe the gross pathological changes w/ timing for MI:

A

12 hrs: asymptomatic
24 hrs: reddish blue (trapped blood)
2-10 days: sharply defined soft, yellow infarct
2 weeks: pink granulation tissue surrounds yellow infarct
6 weeks: prominent scar
8 weeks: complete scar, can’t tell age of infarct

38
Q

Describe microscopic pathological changes w/ timing for MI:

A

4*-12hrs: wavy fibers, coag. necrosis, hemorrhage, edema

24hrs: PMN infiltrate

1-3 days: NEUTROPHILS, loss of nuclei and striations

3-7 days: MQs eat dead neutros and myocytes

7-10 days: granulation tissue + necrosis cleared up

1 mos: GRANULATION TISSUE most prominent

+ 6 weeks: scar formation replaces necrotic myocytes

8 weeks: completion of scar formation

39
Q

At what point post MI is does the myocardium become vulnerable to rupture?

A

3-7 days: due to complete removal of necrotic myocytes without replacement (only soft granulation tissue, and no scar yet)

40
Q

At what point post MI is granulation tissue most prominent?

A

2-4 weeks

41
Q

At what point post MI is necrotic myocardium replaced by fibrosis (scar)?

A

6 weeks, total scar formation by week 8

42
Q

List 3 ways to modify infarct by reperfusion and identify which two are immediate therapies:

A
  1. TPA (immediate)
  2. Angioplasty (immediate)
  3. Coronary artery bypass graft (CABG)
43
Q

List two vessels normally harvested to perform CABG; which is preferred?

A

Internal mammary artery»»> Great Saphenous vein

44
Q

TPA: list two therapeutic functions

A

salvage (not necrotic) ischemic myocytes;

no effect on atherosclerotic plaque

45
Q

Angioplasty: list two therapeutic functions

A
  • improves stenosis/ salvage ischemic myocytes

- stabilizes atherosclerotic plaque

46
Q

Coronary artery bypass graft (CABG): list one therapeutic function

A
  • facilitates flow around plaque
47
Q

By what time do doctors try to reperfuse MI?

A

3-4 hrs (usually within 1)

48
Q

Describe the gross morphology of reperfused myocardium:

A

hemorrhagic due to leaky, injured vessels

49
Q

Describe microscopic morphology of reperfused myocardium:

A

eosinophilic contraction bands (due to fresh Ca++ from plasma)

50
Q

3 mechanisms of injury by reperfusion of infarcted myocardium:

A
  1. O2 free radical cell damage
  2. Apoptosis
  3. Microvascular injury–> hemorrhage, swelling, capillary occlusion
51
Q

What is is stunned myocardium?
What do we measure to determine whether this is happening?
What do we do clinically for these patients?

A

Prolonged post-ischemic ventricular dysfunction lasting several days after reperfusion

Measure EF immediately post MI and again weeks after injury–may ^30% due to healing of ischemic myocytes

Use cardiac assist device in interim

52
Q

How does a cardiac assist device work and what is it used to treat?

A

Decreases afterload to maintain good SV & EF in pts. with stunned myocardium post MI

53
Q

When do you see contraction banding associated with MI? What causes this phenomenon?

A

See with reperfusion of infarcted myocardium

Caused by Ca++ in fresh plasma

54
Q

How many patients with MI are asymptomatic?

Which patients are likely to be asymptomatic?

A

10-15%, DM

55
Q

Which patients typically present with atypical signs/ sx of MI?

A

WOMEN!

56
Q

List 4 signs/ sx of MI caused by adrenergic response:

A
  1. rapid weak pulse
  2. diaphoresis
  3. nausea
  4. Dizziness/ light headedness
57
Q

List two intracellular enzymes measured to dx MI.

When do they begin to rise/ peak/ fall to normal?

A
  1. CKMB (falls in 72 hrs)
  2. Troponin I, T (falls by 10 days)

Both rise within 2-4 hrs
Both peak @ 24 hrs

58
Q

Which intracellular enzyme test is more specific?

A
  • TnI, TnT are specific to heart

- CKMB is sensitive but not specific because it is found in skeletal m.

59
Q

How many isoenzymes of CK are there and where is the enzyme found?

A

3 isoenzymes
MM- skeletal mm, heart
MB- skeletal mm, heart»>
BB- brain, lung

60
Q

How often should you check cardiac enzymes to rule in or out an MI?

A

every 8 to 6 hrs in sets of 3 or 4

61
Q

4 Factors associated with poor prognosis of MI:

A
  1. Age
  2. Female
  3. DM
  4. Previous MI
62
Q

Describe how contractile dysfunction post-MI can cause complications.
How severe is this?
What type of MI causes this?

A

Contractile dysfunction–> HypoTN + Pulm congestion–>
CARDIOGENIC SHOCK (failure to perfuse vital organs)
70% mortality
- Large LV MI

63
Q

How can MI cause arrhythmia/ dysrhythmia?
What are 2 fatal arrhythmias?
When would arrhythmia with MI occur?

A
  • Ischemia in area involving conduction
  • New arrhythmia in area of ischemic myocytes
    1. asystole
    2. V-fib
  • early complication occurring on the same day as MI.
64
Q

When does a myocardial rupture typically occur post MI?
Where are they most likely to occur?
List 3 possible outcomes pending location of rupture.

A

Within 1 week (removal of necrotic tissue w/o replacement)
#1: ventricular free wall–> cardiac tamponade
2. intraventricular septum–> (Lt–>Rt shunt)
3. papillary muscle (usually mitral valve)–> severe regurg.

65
Q

Which side of the heart fails first during cardiac tamponade; why?
What are two clinical signs of this type of heart failure?

A
  • right heart bc thinner wall

- look for JVD + distant heart sounds

66
Q

When/ how does pericarditis ensue after MI?
What are the two types of pericarditis?
What are 3 clinical signs of pericarditis?

A

Within 2-3 days due to ^ neutros in myocardium–> pericardium

  1. Fibrinous
  2. Fibrinohemorrhagic

Clinical signs:

  1. friction rub
  2. chest pain alleviated by leaning forward*
  3. EKG changes (ST^)
67
Q

How do you diagnose isolated RV failure?
What type of patients can get this?
How common is this?

A

EKG–check RV with precordial leads
Left dominant patients can get this
Rare: 1-3 % all MIs
(Because most patients are right dominant, most RCA MIs would result in damage to the posterior LV as well.)

68
Q

When do MIs cause a mural thrombus?

How do we treat these patients; what are we trying to prevent?

A

When there are locations of hemostasis, as in during AFIB.

Treat with anticoagulants to prevent brain embolus

69
Q

When/ where does MI cause a ventricular aneurysm?

A

Late complication of transmural anterioseptal infarct

- Occurs while heart is healing (weekS post MI)

70
Q

What are 3 complications caused by ventricular aneurysm?

Do they commonly rupture?

A
  • mural thrombus (hemostasis; aneurysm doesn’t contract)
  • arrhythmia
  • heart failure
  • Rupture = rare due to strength of scar tissue
71
Q

Describe 2 problems caused when an MI results in papillary muscle dysfunction.

A
  1. mitral regurg»>

2. progressive heart failure

72
Q

3 common outcomes of large transmural infarcts:

A

cariogenic shock; arrhythmia; late CHF

73
Q

3 common outcomes of anterior transmural infarcts:

A

Free wall rupture/ expansion; mural thrombus; aneurysm

worse clinical course

74
Q

2 common outcomes of inferior/ posterior infarcts:

A

conduction block; RV involvement

75
Q

What happens to the non-infarcted myocytes in the area of an MI?
Why is this problematic?
What can we do to treat it?
What is this called?

A

Hypertrophy!

  • ^ O2 demand without w/ DECREASED capillary supply
  • Precedes HF!
  • Prevent with ACEi’s and prophylactic meds
  • Termed Ventricular dilation
76
Q

Two most important prognostic factors of MI:

A
  1. Quality of LV function (ejection fraction)

2. Degree of IHD (vascular obstruction perfusing viable myocardium)

77
Q

Describe briefly the differences in primary and secondary prevention of MI:

A

Primary: modify risk–> smoking cessation, HTN, LDL, DM
Secondary: prevent reinfarction

78
Q

Which age group typically gets chronic IHD?
When do we usually see this (2)?
What can chronic IHD lead to?

A

Elderly

  • Post MI»> or with severe CAD–> cardiac decompensation
  • Leads to HF
79
Q

Describe morphological changes to the heart and coronary aa’s in response to chronic IHD:

A

Heart: hypertrophy, dilation–> enlarged and heavy

CA’s: stenosis (moderate to severe)

80
Q

What can chronic IHD progress to?

A

CHF

81
Q

What is sudden cardiac death?

Most common cause + 4 others?

A 
Unexpected death from cardiac causes in asymptomatic patients or under 1 hr after symptom onset: 
#1: silent IHD
- congenital anomalies 
- valvular disease 
- myocarditis
- cardiomyopathy
82
Q

How does sudden cardiac death kill you?!

A

Ischemic + Electrically unstable myocardium distal to conduction system–> LETHAL ARRHYTHMIA
(A systole, v fib)

83
Q

What will improve prognosis in survivors of sudden cardiac death?

A

Implantation of automatic cardioverter-defibrillator

84
Q

Minimal criteria for dx. of Lt HTN Heart Disease

+ 3 complications:

A
  1. LV Hypertrophy
  2. Hx./ pathological evidence HTN

Complicaitons:

  • Myocardial dysfunction
  • Cardiac dilation –> CHF
  • Sudden death
85
Q

How does Lt. HTN Heart failure lead to CHF?

A 
DIASTOLIC dysfunction (issue with ventricular filling)--> DECREASED SV with maintained EF
BECAUSE the ventricle is too thick to stretch/ fill up.
86
Q

Describe 2 gross morphological changes that occur with Lt. HTN heart disease:

A
  1. Circumferential hypertrophy (2cm) of LV w/o dilation
    - -> poor compliance–> poor diastolic function
  2. LA enlargement
87
Q

How do we detect/ dx. HTN L Heart disease (3)?

A
  • EKG (good for asymptomatic patients)
  • Afib.
  • CHF w/ atrial dilation
    (And exclude other causes, duh.)
88
Q

3 Possible outcomes of Lt HTN Heart disease:

A

Progressive IHD or CHF; Renal disease or stroke (poor perfusion); Sudden cardiac death

89
Q

Describe the acute (2) and chronic (3) changes in heart morphology associated with Rt HTN Heart disease (Cor Pulmonale):

A

Acute: (as in caused by a pulmonary embolus)

  • RV dilation
  • NO ^ wall thickness (this event happens too quickly!, else thickening would take place)

Chronic:

  • ^ RV thickness (1 cm)
  • Compression of LV
  • Tricuspid regurg. (valve is fibrous and thickened)
90
Q

What causes Rt. HTN Heart failure: Acute (1) Chronic (5)

A

Pulm HTN due to disorders of lungs or pulm vasculature

Acute:
- Massive PE

Chronic:

  • prolonged pressure overload
  • chronic pulm HTN
  • emphysema
  • cystic fibrosis
  • Obesity

DT3- EXAM 1 (26 decks)

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