Cardiac ischemia Flashcards
what is hyperlipidemia associated with
genetic and acquired causes
what is total cholesterol
maintains cell membranes
requires building block for some nutritional absorption and hormone synthesis
what is LDL
low density lipoprotein
increases risk of cardiovascular disease - atherosclerotic plaque formation
helps to move cholesterol within the circulation
BAD
what is HDL
high-density lipoproteins
this is the “good” cholesterol, is considered bad if it is too low
brings cholesterols back to the liver
what are triglycerides
stored energy
breaks down for cellular metabolism, stored in adipose, liver
what is primary hyperlipidemia
familial
typically polygenetic source
types I-IV
can lead to xanthomas, pancreatitis, hepatosplenomegaly, atherosclerosis
what is secondary hyperlipidemia
acquired:
dietary (M/C assoicated with meat/animal fats)
medication SE
hypothyroidism,
DM
CKD
sedentary lifestyle
inflammatory disease states (psoriasis, crohn’s, IBD, COPD, smoking…)
what is the tunica intima
inner layer of simple squamous endothelium
contains properties discussed in heme (nitric oxide, PGI, heparin sulfate, TPA)
allows for immune system activation and diapedesis
what is the tunica media
smooth muscle layer, under autonomic control
what is the tunica externa (adventitia)
connective tissue layer
contains vasa vasorum
what is the vasa vasorum
vessels that feed the layers of the thichker/larger vesssels
what is smooth muscle
non-striated (thick and thin filaments but less organized)
lack sarcomere
involuntary
uninucleated fusiform cell
more elastic
spread of depolarization allow for spiral corkscrew pattern
where within the artery does atherosclerosis occur
within the intima of the arteries
foam cells (lipid filled macrophages) will accumulate in this layer
typically form in areas where there is repetitive injury to vessel wall
what are the stages and development of atherosclerosis
initial lesion- normal
fatty streak
intermediate lesion
atheroma
fibroatheroma
complicated lesion
what is the fatty streak
first stage in development of atherosclerosis
seen on the inner layer of the vessels (may be seen in earlier parts of life (by 20))
clinically silent as there is no luminal narrowing
what can cause the development of the fatty streak
associated with stressors, increased lipid deposition in the subendothelial space
What are foam cells
accumulation of monocytes (macrophages) that are engorged with cholesterol and create atherosclerotic plaques
what is a fibrous plaque
lipid rich core that will necrose and calcify = atheroma
what does atheroma lead to
remodeling with vascular expansion
allows for lumen size to stay intact
puts the patient at increased risk for unstable plaques - unstable angina
if no remodeling, have have shrinking of the atheroma included vessel - closure of the lumen - obstructive symptoms - stable angina
what are risk factors of CAD
hypercholesterolemia- elevated LDL
diabetets
hypertensions
smoking
inflammatory disorders
what are non-modifiable risks for CAD
age, gender, FH, ethnicity, genetic evidence, previous history of CVD
what are modifiable risks for CAD
BP
total cholesterol
HDL cholesterol
smoking
blood sugar/diabetes
BMI
markers of chronic inflammation
what are female-specific or predominant risk factors for CAD
pregnancy induced HTN
preeclampsia/eclampsia
gestational diabetes
PCOS
Menopause
systemic inflammatory rheumatologic diseases
mental stress/depression
when do the coronary vessels fill
during diastolic relaxation
what determines coronary vascular resistance
hormones
neural stimulation
metabolic demand
peripheral vascular resistance
what is a STEMI characterized by
complete occlusion of blood vessel lumen, resulting in trasmural injury and infarct to the myocardium, which is reflected by ECG changes and rise in troponin
what are ischemia symptoms
classic: chest pain, +/- radiation
anginal equivalent: dyspnea, Nausea, diaphroesis and fatigue
what is levines sign
gripping the chest
what is angina
chest discomfort typically substernal or slightly to the left
what is myocardial ischemia
oxygen demand of the cardiac muscle outweight the oxygen being delivered
when O2 demand increases, so do the symptoms: elevated HR, BP, wall tension/stress, increased contractility
what is chronic coronary syndrome
stable angina
(reproducible)
what is stable angina
chronic ischemic heart disease
history of reproducible angina (exercise induced myocardia ischemia) PLUS known risk factors for atherosclerotic disease
symptoms last < 20 minutes once provocative activity has stopped
has for atleast 2 months
what are the symptoms of stable angina
angina with increased cardiac demand
non-anginal symptoms: dyspnea, pain away from substernal area, nausea, diaphrosesis, fatigue
what occurs during stable angina
acidosis, decreased ATP K+/Na+ pumps, increased lactate, release of serotonin, bradykinin, histamine, adenosine, increase thromboxane A2
what is stimulated with stable angia
stimulates sympathetic afferent pathways - syumpathetic ganglia
discomfort can spread along corresponding dermatomes, neck, shoulder, jaw discomfort
What is acute coronary syndrome (ACS)
ST segment elevation - STEMI
Non ST segment elevation - NSTEMI and Unstable angina
what are typical ACS descriptors
onset: gradual, varies based on activity
provocation: exertional increase in symptoms
Quality: discomfort, pressure, aching, tightness
Radiation: arms and neck
Site: can be diffuse
Time: typically lasts < 30 minutes
how many types of acute myocardial infarctions are there
Type 1-type 5
what is type 1 MI due to
coronary atherothrombosis
what is the cause of type 2 MI
supply-demand mistmatch
how long does it take without blood supply does it take to cause tissue pallow and decreased contractility with AMI
one minute without blood supply
how long does it take for AMI to lose contraction
3-5 minutes
ATP depletes, glycogen stores used up, lactate accumulates
what is unstable angina
new-onset angina or change in precipitating factors
- takes less exertion/stress to induce symptoms than previous
- may occur at rest
- length of symptoms may last longer
- increases severity or frequency
increase risk of AMI
no necrosis
what is a NSTEMI
acute coronary syndrome (ACS)
m/c d/t disrupted atherosclerotic plaque
- partial or intermittent blockage
- ischemic disease
- apoptosis/necrosis of myocytes
- release of troponin
What is STEMI
event typically begins with atherosclerotic plaque rupture
TRANSMURAL MI (complete obstruction of blood flow)
What is the J point
transition point into the ST portion
what is seen on a STEMI ECG
J point elevation > 1mm in 2+ contiguous leads
what is right ventricular infarction
associated with right coronary artery occlusion
hypotensive - preload dependent
decrease CO d/t decrease LV filling
- shock
DO NOT give nitroglycerine
What are STEMI mimics
Acute pericarditis
myopericarditis (typically viral or autoimmune)
left ventricular hypertrophy
aortic dissection
severe hypercalcemia
what is coronary vasospasm
presents like a STEMI
diffuse or focal spasm of the coronary arteries
defined as nitrate responsive angina with transient ECG findings
may occur when at rest
what causes coronary vasospasm
hyper-reactivity of smooth muscle
what are the triggers of coronary vasospasm
Drugs: COCAINE
smoking (major risk)
vagal response
PCI
Botulism
low magnesium
Kounis syndrome
what is the presentation of coronary vasospasm
chronic, recurrent episodes of CP
present like typical ACS from atherosclerotic disease
gradual onset/offset
may have radiation of discomfort
Nausea, sweating, dizziness, dyspnea
often younger patients
GET A GOOD HISTORY
what are complications of ischemia
arrhythmias
blocks
cardiogenic shock
ventricular free wall rupture
ventricular septal defect
decrease CO
acute mitral regurgitation
what is papillary muscle dysfunction
rupture that may be due to ACS (STEMI or NSTEMI)
may be partial or complete rupture
most common at posteromedial papillary muscle - causes acute mitral regurgitation
what is ventricular aneurysm
complication of acute myocardial infarction
infarcted areas of ventricles weakens
chamber will enlarge
overtime will scar- calcification
increase risk for arrhythmias, HF
increased risk for clot formation within ballooned areas
what is a mural thrombi
M/c with anterior STEMI - left anterior descending artery (LAD)
associated with pts who have suffered apical aneurysm
poor contractility of the apex
relative blood stasis
thrombus formation
can lead to arterial embolic events
