Ischemic & Hypertensive Heart Disease- Melissa (6)* Flashcards
Another name for ischemic heart disease?
Definition:
What four conditions does it include?
Coronary artery disease Heart's demand for nutrients, O2, waste removal >>> Blood supply 1. Angina 2.Chronic IHD 3.MI 4. Sudden Cardiac Death
Cause of over 90% ischemic heart disease:
Atherosclerosis + coronary arterial obstruction (stenosis)
What is the #1 cause of death in men and women over 50yoa?
ischemic heart disease
Ischemic heart disease results from a complex, dynamic interaction between the following 4 factors:
- fixed coronary obstruction
- acute plaque change/ platelet aggregation
- coronary thrombus
- vasospasm
What % of a coronary artery must be occluded in order to cause angina with exercise?
More than 70%
What % of a coronary artery must be occluded in order to cause angina at rest?
More than 90%
What is one way distal myocardium may be protected from ischemia in the event of coronary obstruction?
collateral circulation
2 Possible triggers for acute plaque change in atherosclerotic coronary arteries:
- Adrenergic activity (emotions, circadian rhythm)
- Dynamic changes make plaques more vulnerable
Which plaques are the most dangerous/ vulnerable?
moderately stenotic because they are asymptomatic most of the time
3 possible roles for a coronary thrombus to play in ischemic heart disease:
- make partial occlusion–> total occlusion (most common)
- mural thrombus–> embolize and cause partial occlusion
- Activate SMCs–> ^ size of atherosclerotic lesions
What role does vasoconstriction play in ischemic heart disease?
What two factors stimulate vasoconstriction?
Adrenergic agonists + platelet contents–> ^ vasocnstrxn–> ^ ischemia
Define angina pectoris including:
- how long does it last?
- what causes it?
- when might it be asymptomatic?
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
Stable angina:
- defintion?
- prevalence?
- cause?
- triggers?
- Predictable angina relived by NG or rest
- Most common angina pectoris
- Fixed obstruction–> decrease coronary perfusion
- Triggers: excitement, exercise, ^ cardiac workload
Unstable angina:
- prevalence?
- definition
- of what might this be a warning?
- cause?
#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
What is Prinzmetal angina? Prevalence? Tx?
Angina caused by coronary spasms w/ possible underlaying IHD
- rare
- episodic and may occur at rest
Tx: NG, Ca++ channel blockers
What are the #1, #2, #3 Acute coronary syndromes?
What is their common pathological link?
#1: Unstable angina #2: MI #3: Sudden cardiac death
All have atherosclerotic plaque disruption w. intra-luminal platelet-fibrin thrombus formation
What separates MI from angina in terms of pathology?
MI has IRREVERSIBLE cardiac cell death due to ischemia
–> necrosis
Angina causes REVERSIBLE damage due to ischemia/ cellular swelling
What are the risk factors for MI?
How do African American prevalence rates compare to Caucasian?
same as atherosclerosis
-black and white prevalence are equal.
(I thought Black > White for some reason.) * I must remember.
Describe the 6 steps in pathogenesis of 90% of Transmural MIs:
- Acute plaque change (rupture, erode, hemorrhage)–>
- Platelet adhesion to sub endothelial collagen + necrotic material–>
- Platelets release aggregators–>
- Vasospasm + Extrinsic pathway –> Thrombus size& Occlusion
How long must ischemia endure in order to cause irreparable injury to cardiac myocytes?
20 minutes
How quickly do coronary thrombi heal?
30% clear within 12-24 hours via lysis/ relaxation of vasospasm
4 alternative pathogenesis mechanisms for transmural MI (10% of cases):
- vasospasm +/- coronary atherosclerosis
- emboli from lt. atrium
(a fib., LV mural thrombus, paradoxical embolus) - vasculitis
- HypoTN (esp in cases of preexisting stenosis)
What should you suspect in young patient that has transmural MI as a result of vasospasm? No vasospasm?
COCAINE
Kawasaki, Congenital defect
Describe the timeline of myocardial response to ischemia:
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
Most MIs are transmural or sub endothelial?
Transmural
3 common causes of transmural MI + typical EKG finding:
- coronary atherosclerosis
- acute plaque change
- obstructive thrombus
ST Elevation on EKG
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
Causes of subendocaridal infarct (3)
- diffuse stenosising coronary atherosclerosis
- lysed thrombus
- severe prolonged HypoTN (shock) + coronary stenosis
(NOT acute plaque change and subsequent thrombus)
By what time is necrosis of an ischemic myocardial segment complete?
6 hrs
The LCA branches into what two arteries?
Lt circumflex, LAD
The LAD supplies which regions of the heart?
- anterior 2/3 vent. septum
- anterior wall of LV
- apex
The LCX supplies which regions of the heart?
What does it branch into in the Lt dominant heart?
- lateral wall LV
Lt Dominant Heart–> PDA
- post 1/3 vent septum (20%)
- posteriobasal LV wall (20%)
The RCA supplies which regions of the heart?
What does it branch into in the Rt dominant heart?
- RV
Rt Dominant Heart–>PDA
- posterior 1/3 vent septum
- posteriobasal LV wall
What percent of infarct occur in the LAD?
Typical deficits?
50%
- knock out entire supply’s of anteroseptal region/apex
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
What percent of infarcts occur in the LCX?
Typical deficits?
15-20%
- lateral wall LV sparing apex
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
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
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)
At what point post MI is granulation tissue most prominent?
2-4 weeks
At what point post MI is necrotic myocardium replaced by fibrosis (scar)?
6 weeks, total scar formation by week 8
List 3 ways to modify infarct by reperfusion and identify which two are immediate therapies:
- TPA (immediate)
- Angioplasty (immediate)
- Coronary artery bypass graft (CABG)
List two vessels normally harvested to perform CABG; which is preferred?
Internal mammary artery»»> Great Saphenous vein
TPA: list two therapeutic functions
salvage (not necrotic) ischemic myocytes;
no effect on atherosclerotic plaque
Angioplasty: list two therapeutic functions
- improves stenosis/ salvage ischemic myocytes
- stabilizes atherosclerotic plaque
Coronary artery bypass graft (CABG): list one therapeutic function
- facilitates flow around plaque
By what time do doctors try to reperfuse MI?
3-4 hrs (usually within 1)
Describe the gross morphology of reperfused myocardium:
hemorrhagic due to leaky, injured vessels
Describe microscopic morphology of reperfused myocardium:
eosinophilic contraction bands (due to fresh Ca++ from plasma)
3 mechanisms of injury by reperfusion of infarcted myocardium:
- O2 free radical cell damage
- Apoptosis
- Microvascular injury–> hemorrhage, swelling, capillary occlusion
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
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
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
How many patients with MI are asymptomatic?
Which patients are likely to be asymptomatic?
10-15%, DM
Which patients typically present with atypical signs/ sx of MI?
WOMEN!
List 4 signs/ sx of MI caused by adrenergic response:
- rapid weak pulse
- diaphoresis
- nausea
- Dizziness/ light headedness
List two intracellular enzymes measured to dx MI.
When do they begin to rise/ peak/ fall to normal?
- CKMB (falls in 72 hrs)
- Troponin I, T (falls by 10 days)
Both rise within 2-4 hrs
Both peak @ 24 hrs
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.
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
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
4 Factors associated with poor prognosis of MI:
- Age
- Female
- DM
- Previous MI
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
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.
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.
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
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
- Fibrinous
- Fibrinohemorrhagic
Clinical signs:
- friction rub
- chest pain alleviated by leaning forward*
- EKG changes (ST^)
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.)
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
When/ where does MI cause a ventricular aneurysm?
Late complication of transmural anterioseptal infarct
- Occurs while heart is healing (weekS post MI)
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
Describe 2 problems caused when an MI results in papillary muscle dysfunction.
- mitral regurg»>
2. progressive heart failure
3 common outcomes of large transmural infarcts:
cariogenic shock; arrhythmia; late CHF
3 common outcomes of anterior transmural infarcts:
Free wall rupture/ expansion; mural thrombus; aneurysm
worse clinical course
2 common outcomes of inferior/ posterior infarcts:
conduction block; RV involvement
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
Two most important prognostic factors of MI:
- Quality of LV function (ejection fraction)
2. Degree of IHD (vascular obstruction perfusing viable myocardium)
Describe briefly the differences in primary and secondary prevention of MI:
Primary: modify risk–> smoking cessation, HTN, LDL, DM
Secondary: prevent reinfarction
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
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)
What can chronic IHD progress to?
CHF
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
How does sudden cardiac death kill you?!
Ischemic + Electrically unstable myocardium distal to conduction system–> LETHAL ARRHYTHMIA
(A systole, v fib)
What will improve prognosis in survivors of sudden cardiac death?
Implantation of automatic cardioverter-defibrillator
Minimal criteria for dx. of Lt HTN Heart Disease
+ 3 complications:
- LV Hypertrophy
- Hx./ pathological evidence HTN
Complicaitons:
- Myocardial dysfunction
- Cardiac dilation –> CHF
- Sudden death
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.
Describe 2 gross morphological changes that occur with Lt. HTN heart disease:
- Circumferential hypertrophy (2cm) of LV w/o dilation
- -> poor compliance–> poor diastolic function - LA enlargement
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.)
3 Possible outcomes of Lt HTN Heart disease:
Progressive IHD or CHF; Renal disease or stroke (poor perfusion); Sudden cardiac death
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)
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
