Week 1 lecture 1 - Systolic Dysfunction Flashcards
Ischemia defn
what is reversible ischemia?
ischemia = imbalance between myocardial oxygen supply and demand
reversible ischemia only occurs during high oxygen demands (during exercise)
SOB vs SOBOE
SOB = all the time
SOBOE = at exercise only (SOB on exertion)
3 things (physiological) that cause ischemia
Ischemia is caused by
1. Decr oxygen supply to heart
2. Incr oxygen demand
3. Decr contractility
What causes decreased oxygen supply to heart (and therefore, ischemia)? (5)
- CAD - cholesterol build up in artery
- SCAD = sudden coronary artery dissection - tear inside artery causes a split in the layers; flap problem and/or blood gets trapped inside and clots
- Decr perfusion pressure (bc hypotension or AI..) so less flow to coronary arteries during diastole
- External factors - concentric LVH causes muscle to push into sulci and squeezes CA
- Decr oxygen carrying capacity of blood (anemia, asthma, COPD..)
What causes increase oxygen demand in heart (and therefore ischemia)? (2)
- Increased number of cardiomyocytes (heart size) - bc concentric or eccentric LVH
- Increased HR - bc exercise
What causes decreased contractility of cardiomyocytes (and therefore ischemia)? (4)
- DCM = Dilated Cardiomyopathy - damage to cardiomyocytes for no known reason (chemo?)
- Incr Preload - too much blood in LV and cardiomyocytes stretched beyond their ideal length (Frank-Starling law)
- Drugs - barbiturates and opioids
- HR > 200 bpm - heart doesn’t have time to fill
Law of LaPlace
what does it tell us?
Laplace’s tells us the oxygen demand of EACH CARDIOMYOCYTE
(must multiply by number of cardiomyocytes and HR to get oxygen demand of heart)
LaPlace’s ~ Wall stress
Law of LaPlace / Wall stress formula
Wall stress (H) = (LVSPr)/(2PW)
Wall stress (H) is the oxygen demand of a cardiomyocyte
LVSP is ~same as BP from cuff (increased if HT or Ao stenosis)
r is radius - LVID/2 - if r is too big cardiomyocytes are in non optimal position and have to pull as awkward angle
PW is wall thickness - thicker wall means more cardiomyocytes to share the load
*LaPlace’s law is based on a sphere
What is Angina
(Angina = Angina pectoris)
Angina is chest pain
squeezing and tightening in chest bc decr blood flow to heart
common symptom in ischemic heart disease (CAD)
What are the 4 classifications of Angina?
- Stable angina - only occurs with incr oxygen demand (exercise)
- Unstable angina = ACS (Acute Coronary Syndrome) - unexpected chest pain, often at rest, bc sudden blockage in CA = emergency
- Variant (Prinzmetal’s) angina - occurs at rest between midnight and early morning in young ppl (rare), bc spasm in CA
- Atypical angina -vague pain (possible not related to heart), more common in women
What is an MI
MI = Myocardial Infarct = heart attack
- complete blockage of CA
- damages heart muscle
What are the 3 types of MIs?
how are they diagnosed?
- UA / ACS - chest pain at rest
- Non-STEMI - partial blockage of CA
- STEMI - complete blockage of CA
type diagnosed by ECG and blood test for biomarkers
ECG for 3 types of MI: UA vs NSTEMI vs STEMI
Which one also has elevation of biomarkers (blood test)
UA - normal ECG with flat ST segment
NSTEMI - ST segment depression or T wave inversion
STEMI - ST elevation; elevation of biomarkers
What are the biomarkers of MI?
What do they indicate and how do we test for them?
- Troponin
- Creatine (phospho) kinase = CK
biomarkers are enzymes that are released into blood upon myocardial ischemia and indicate cardiac muscle death
check for biomarkers with blood test
heart attack (MI) vs cardiac arrest
MI - heart still pumps but not well
cardiac arrest - heart stops completely
Why are heart attack patients sent to Cath lab (and not US)?
Cath lab is an xray with fluoroscopy. Catheter goes through leg and into heart and releases dye into CAs so you can see which CA is affected. Can diagnose (find blockage) and treat (put in stent) on the spot
vs US - can’t see CAs
Causes of cardiac arrest?
CAD; heart attack (eg. as LV dies, cells become pacemakers which causes VT)
Congenital abnormalities in electrical sys
Enlarged heart
PEA
Tamponade (excess fluid around heart)
Hyperkalemia (high K)
Resp failure
Toxins
Pulmonary embolism
PEA Arrest
PEA = pulseless electrical activity - get cardiac electrical activity (ECG) without palpable pulse
- heart is unable to contract and create enough CO for life
- usually caused by respiratory failure (stop breathing so no oxygen)
-poor prognosis: patient usually falls asleep and never wakes up
Cardiogenic shock
Cardiogenic shock - inadequate tissue perfusion due to damaged heart
go into organ failure
Role of echo: CAD (yearly exam)
Look for
- evidence of old, infarcted muscle (thin, bright, lack of movement, is wall contracting and getting thicker or just getting dragged along?)
- paradoxical septal motion - IVS moving away from PW is systole (timing of IVS contraction is wrong)
- LV aneurysm
- RWMAs (lack of RWMAs does NOT mean lack of CAD)
- MR …
if dilated LV, maybe MV leaflets can’t close right? or wall damage pulls walls and tethered leaflets? not emerg
if damage to pap muscles? emerg bc can cause sudden severe MR
- Thrombus - usually months post MI; low EF so blood gets stuck in heart
Role of echo: immediately post MI
Look for
- RWMAs - areas at/past damaged CA?
- Ventricular Aneurysm
- LV Pseudoaneurysm
- Ruptured myocardium
- Arrhythmias
- Pericarditis (or Dressler’s syndrome - if later)
- MR - damage to pap muscles can cause sudden severe MR which is life threatening (emergency)
Ventricular aneurysm vs LV pseudoaneurysm
Ventricular Aneurysm - dead myocardium stretches out; usually at LV apex
- has no neck, entire apex is wide, looks like light bulb
- common, not an emergency, permanent
LV Pseudoaneurysm - rupture of LV free wall but blood contained by thin outer layer
- has neck
- emergency, may rupture fully
Pericarditis vs Dressler’s syndrome
Pericarditis - inflammation response to dying tissue (24-96 hrs) - happens immediately
Dressler’s syndrome is pericarditis that forms 2-8 weeks post MI (happens later bc autoimmune response to inflammation)
Non-Ischemic (non CAD) causes of chest pain?
Many including
- panic attack
- indigestion
- heart burn
- AR or Ao stenosis
- Ao dissection
- Acute pulmonary embolism
- pericarditis
- pericardial effusion
- CA spasms
- Takotsubo cardiomyopathy
- Kawasaki’s disease
-PEA arrest
Takotsubo cardiomyopathy
Takotsubo cardiomyopathy = “broken heart syndrome” - sudden surge in stress hormone causes LV dysfunction and LV apical ballooning
goes away on its own
Kawasaki’s disease
Kawasaki’s disease - in children under 5, damage to CA, symptoms include rash, fever, swollen lips, tongue, hands/feet, glands
more likely to have heart attack as adult
Treatment for Angina
- manage risk factors - lifestyle
- Meds
- Balloon angioplasty or stents (Cath lab)
- CABG (open heart surgery); CABG can be single, double, triple, or quadruple
Treatment for MI
- ambulance
- Hospital
- triage: diagnosis, 12 lead ECG within 10 min, type of MI
- pain med
for STEMI
- door to balloon time <90 min
- if PCI not avail, transfer to another hospital with 120 min or Fibrinolysis therapy (meds that break down clots but high risk of stroke)
- if PCI and Fibrinolysis unsuccessful, CABG
time is muscle
for NSTEMI
- stable? estimate risks and determine treatment plan (same as STEMI but more time)
PCI
Percutaneous Coronary Intervention (i.e. cath lab)
Treatment for cardiac arrest
- CPR
- attach defibrillator
- if patient survives, treat the cause
What can cause paradoxical septal motion?
paradoxical septal motion - IVS is moving away from PW in systole
caused by
- Pericardial disease (pericarditis - L and R sides compete for space)
- Disease of IVS (CAD?)
- LBBB
- post open heart surgery (damage)
