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
2
Q
Cause of over 90% ischemic heart disease:
A
Atherosclerosis + coronary arterial obstruction (stenosis)
3
Q
What is the #1 cause of death in men and women over 50yoa?
A
ischemic heart disease
4
Q
Ischemic heart disease results from a complex, dynamic interaction between the following 4 factors:
A
- fixed coronary obstruction
- acute plaque change/ platelet aggregation
- coronary thrombus
- vasospasm
5
Q
What % of a coronary artery must be occluded in order to cause angina with exercise?
A
More than 70%
6
Q
What % of a coronary artery must be occluded in order to cause angina at rest?
A
More than 90%
7
Q
What is one way distal myocardium may be protected from ischemia in the event of coronary obstruction?
A
collateral circulation
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
9
Q
Which plaques are the most dangerous/ vulnerable?
A
moderately stenotic because they are asymptomatic most of the time
10
Q
3 possible roles for a coronary thrombus to play in ischemic heart disease:
A
- make partial occlusion–> total occlusion (most common)
- mural thrombus–> embolize and cause partial occlusion
- Activate SMCs–> ^ size of atherosclerotic lesions
11
Q
What role does vasoconstriction play in ischemic heart disease?
What two factors stimulate vasoconstriction?
A
Adrenergic agonists + platelet contents–> ^ vasocnstrxn–> ^ ischemia
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
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
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
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
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
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
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.
19
Q
Describe the 6 steps in pathogenesis of 90% of Transmural MIs:
A
- Acute plaque change (rupture, erode, hemorrhage)–>
- Platelet adhesion to sub endothelial collagen + necrotic material–>
- Platelets release aggregators–>
- Vasospasm + Extrinsic pathway –> Thrombus size& Occlusion
20
Q
How long must ischemia endure in order to cause irreparable injury to cardiac myocytes?
A
20 minutes
21
Q
How quickly do coronary thrombi heal?
A
30% clear within 12-24 hours via lysis/ relaxation of vasospasm
22
Q
4 alternative pathogenesis mechanisms for transmural MI (10% of cases):
A
- vasospasm +/- coronary atherosclerosis
- emboli from lt. atrium
(a fib., LV mural thrombus, paradoxical embolus) - vasculitis
- HypoTN (esp in cases of preexisting stenosis)
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
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
25
Most MIs are transmural or sub endothelial?
Transmural
26
3 common causes of transmural MI + typical EKG finding:
1. coronary atherosclerosis
2. acute plaque change
3. obstructive thrombus
ST Elevation on EKG
27
Define sub endocardial infarct.
Typical EKG finding?
What two features do they LACK?
- Infarct of inner 1/3-1/2 ventricular wall (watershed)
- NO ST on EKG (NON STEMI)
NO plaque disruption
NO superimposed thrombi
28
Causes of subendocaridal infarct (3)
1. diffuse stenosising coronary atherosclerosis
2. lysed thrombus
3. severe prolonged HypoTN (shock) + coronary stenosis
(NOT acute plaque change and subsequent thrombus)
29
By what time is necrosis of an ischemic myocardial segment complete?
6 hrs
30
The LCA branches into what two arteries?
Lt circumflex, LAD
31
The LAD supplies which regions of the heart?
1. anterior 2/3 vent. septum
2. anterior wall of LV
3. apex
32
The LCX supplies which regions of the heart?
| What does it branch into in the Lt dominant heart?
1. lateral wall LV
Lt Dominant Heart--> PDA
2. post 1/3 vent septum (20%)
3. posteriobasal LV wall (20%)
33
The RCA supplies which regions of the heart?
| What does it branch into in the Rt dominant heart?
1. RV
Rt Dominant Heart-->PDA
2. posterior 1/3 vent septum
3. posteriobasal LV wall
34
What percent of infarct occur in the LAD?
| Typical deficits?
50%
| - knock out entire supply's of anteroseptal region/apex
35
What percent of infarct occur in the RCA?
| Typical deficits?
30-40%
- posteriobasal LV wall
- posterior 1/3 septum
* occasionally the posterior RV wall
* isolated RV infarcts are rare
36
What percent of infarcts occur in the LCX?
| Typical deficits?
15-20%
| - lateral wall LV sparing apex
37
Describe the gross pathological changes w/ timing for MI:
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
Describe microscopic pathological changes w/ timing for MI:
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
At what point post MI is does the myocardium become vulnerable to rupture?
3-7 days: due to complete removal of necrotic myocytes without replacement (only soft granulation tissue, and no scar yet)
40
At what point post MI is granulation tissue most prominent?
2-4 weeks
41
At what point post MI is necrotic myocardium replaced by fibrosis (scar)?
6 weeks, total scar formation by week 8
42
List 3 ways to modify infarct by reperfusion and identify which two are immediate therapies:
1. TPA (immediate)
2. Angioplasty (immediate)
3. Coronary artery bypass graft (CABG)
43
List two vessels normally harvested to perform CABG; which is preferred?
Internal mammary artery>>>>> Great Saphenous vein
44
TPA: list two therapeutic functions
salvage (not necrotic) ischemic myocytes;
| no effect on atherosclerotic plaque
45
Angioplasty: list two therapeutic functions
- improves stenosis/ salvage ischemic myocytes
| - stabilizes atherosclerotic plaque
46
Coronary artery bypass graft (CABG): list one therapeutic function
- facilitates flow around plaque
47
By what time do doctors try to reperfuse MI?
3-4 hrs (usually within 1)
48
Describe the gross morphology of reperfused myocardium:
hemorrhagic due to leaky, injured vessels
49
Describe microscopic morphology of reperfused myocardium:
eosinophilic *contraction bands* (due to fresh Ca++ from plasma)
50
3 mechanisms of injury by reperfusion of infarcted myocardium:
1. O2 free radical cell damage
2. Apoptosis
3. Microvascular injury--> hemorrhage, swelling, capillary occlusion
51
What is is stunned myocardium?
What do we measure to determine whether this is happening?
What do we do clinically for these patients?
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
How does a cardiac assist device work and what is it used to treat?
Decreases afterload to maintain good SV & EF in pts. with stunned myocardium post MI
53
When do you see contraction banding associated with MI? What causes this phenomenon?
See with reperfusion of infarcted myocardium
| Caused by Ca++ in fresh plasma
54
How many patients with MI are asymptomatic?
| Which patients are likely to be asymptomatic?
10-15%, DM
55
Which patients typically present with atypical signs/ sx of MI?
WOMEN!
56
List 4 signs/ sx of MI caused by adrenergic response:
1. rapid weak pulse
2. diaphoresis
3. nausea
4. Dizziness/ light headedness
57
List two intracellular enzymes measured to dx MI.
| When do they begin to rise/ peak/ fall to normal?
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
Which intracellular enzyme test is more specific?
- TnI, TnT are specific to heart
| - CKMB is sensitive but not specific because it is found in skeletal m.
59
How many isoenzymes of CK are there and where is the enzyme found?
3 isoenzymes
MM- skeletal mm, heart
MB- skeletal mm, heart>>>
BB- brain, lung
60
How often should you check cardiac enzymes to rule in or out an MI?
every 8 to 6 hrs in sets of 3 or 4
61
4 Factors associated with poor prognosis of MI:
1. Age
2. Female
3. DM
4. Previous MI
62
Describe how contractile dysfunction post-MI can cause complications.
How severe is this?
What type of MI causes this?
Contractile dysfunction--> HypoTN + Pulm congestion-->
*CARDIOGENIC SHOCK* (failure to perfuse vital organs)
70% mortality
- Large LV MI
63
How can MI cause arrhythmia/ dysrhythmia?
What are 2 fatal arrhythmias?
When would arrhythmia with MI occur?
- 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
When does a myocardial rupture typically occur post MI?
Where are they most likely to occur?
List 3 possible outcomes pending location of rupture.
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
Which side of the heart fails first during cardiac tamponade; why?
What are two clinical signs of this type of heart failure?
- right heart bc thinner wall
| - look for JVD + distant heart sounds
66
When/ how does pericarditis ensue after MI?
What are the two types of pericarditis?
What are 3 clinical signs of pericarditis?
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
How do you diagnose isolated RV failure?
What type of patients can get this?
How common is this?
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
When do MIs cause a mural thrombus?
| How do we treat these patients; what are we trying to prevent?
When there are locations of hemostasis, as in during AFIB.
| Treat with anticoagulants to prevent brain embolus
69
When/ where does MI cause a ventricular aneurysm?
Late complication of transmural anterioseptal infarct
| - Occurs while heart is healing (weekS post MI)
70
What are 3 complications caused by ventricular aneurysm?
| Do they commonly rupture?
- mural thrombus (hemostasis; aneurysm doesn't contract)
- arrhythmia
- heart failure
* Rupture = rare due to strength of scar tissue
71
Describe 2 problems caused when an MI results in papillary muscle dysfunction.
1. mitral regurg>>>
| 2. progressive heart failure
72
3 common outcomes of large transmural infarcts:
cariogenic shock; arrhythmia; late CHF
73
3 common outcomes of anterior transmural infarcts:
Free wall rupture/ expansion; mural thrombus; aneurysm
| *worse clinical course*
74
2 common outcomes of inferior/ posterior infarcts:
conduction block; RV involvement
75
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?
Hypertrophy!
- ^ O2 demand without w/ DECREASED capillary supply
- Precedes HF!
* Prevent with ACEi's and prophylactic meds
- Termed Ventricular dilation
76
Two most important prognostic factors of MI:
1. Quality of LV function (ejection fraction)
| 2. Degree of IHD (vascular obstruction perfusing viable myocardium)
77
Describe briefly the differences in primary and secondary prevention of MI:
Primary: modify risk--> smoking cessation, HTN, LDL, DM
Secondary: prevent reinfarction
78
Which age group typically gets chronic IHD?
When do we usually see this (2)?
What can chronic IHD lead to?
Elderly
- Post MI>>> or with severe CAD--> cardiac decompensation
- Leads to HF
79
Describe morphological changes to the heart and coronary aa's in response to chronic IHD:
Heart: hypertrophy, dilation--> enlarged and heavy
| CA's: stenosis (moderate to severe)
80
What can chronic IHD progress to?
CHF
81
What is sudden cardiac death?
| Most common cause + 4 others?
```
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
How does sudden cardiac death kill you?!
Ischemic + Electrically unstable myocardium distal to conduction system--> LETHAL ARRHYTHMIA
(A systole, v fib)
83
What will improve prognosis in survivors of sudden cardiac death?
Implantation of automatic cardioverter-defibrillator
84
Minimal criteria for dx. of Lt HTN Heart Disease
| + 3 complications:
1. LV Hypertrophy
2. Hx./ pathological evidence HTN
Complicaitons:
- Myocardial dysfunction
- Cardiac dilation --> CHF
- Sudden death
85
How does Lt. HTN Heart failure lead to CHF?
```
DIASTOLIC dysfunction (issue with ventricular filling)--> DECREASED SV with maintained EF
BECAUSE the ventricle is too thick to stretch/ fill up.
```
86
Describe 2 gross morphological changes that occur with Lt. HTN heart disease:
1. Circumferential hypertrophy (2cm) of LV w/o dilation
- -> poor compliance--> poor diastolic function
2. LA enlargement
87
How do we detect/ dx. HTN L Heart disease (3)?
- EKG (good for asymptomatic patients)
- Afib.
- CHF w/ atrial dilation
(And exclude other causes, duh.)
88
3 Possible outcomes of Lt HTN Heart disease:
Progressive IHD or CHF; Renal disease or stroke (poor perfusion); Sudden cardiac death
89
Describe the acute (2) and chronic (3) changes in heart morphology associated with Rt HTN Heart disease (Cor Pulmonale):
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
What causes Rt. HTN Heart failure: Acute (1) Chronic (5)
*Pulm HTN due to disorders of lungs or pulm vasculature*
Acute:
- Massive PE
Chronic:
- prolonged pressure overload
- chronic pulm HTN
- emphysema
- cystic fibrosis
- Obesity
