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CABS2: Cardiology > Cardiac ischemia > Flashcards

Cardiac ischemia Flashcards

1
Q

what is hyperlipidemia associated with

A

genetic and acquired causes

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2
Q

what is total cholesterol

A

maintains cell membranes
requires building block for some nutritional absorption and hormone synthesis

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3
Q

what is LDL

A

low density lipoprotein
increases risk of cardiovascular disease - atherosclerotic plaque formation
helps to move cholesterol within the circulation
BAD

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4
Q

what is HDL

A

high-density lipoproteins
this is the “good” cholesterol, is considered bad if it is too low
brings cholesterols back to the liver

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5
Q

what are triglycerides

A

stored energy
breaks down for cellular metabolism, stored in adipose, liver

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6
Q

what is primary hyperlipidemia

A

familial
typically polygenetic source
types I-IV
can lead to xanthomas, pancreatitis, hepatosplenomegaly, atherosclerosis

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7
Q

what is secondary hyperlipidemia

A

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…)

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8
Q

what is the tunica intima

A

inner layer of simple squamous endothelium
contains properties discussed in heme (nitric oxide, PGI, heparin sulfate, TPA)
allows for immune system activation and diapedesis

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9
Q

what is the tunica media

A

smooth muscle layer, under autonomic control

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10
Q

what is the tunica externa (adventitia)

A

connective tissue layer
contains vasa vasorum

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11
Q

what is the vasa vasorum

A

vessels that feed the layers of the thichker/larger vesssels

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12
Q

what is smooth muscle

A

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

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13
Q

where within the artery does atherosclerosis occur

A

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

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14
Q

what are the stages and development of atherosclerosis

A

initial lesion- normal
fatty streak
intermediate lesion
atheroma
fibroatheroma
complicated lesion

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15
Q

what is the fatty streak

A

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

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16
Q

what can cause the development of the fatty streak

A

associated with stressors, increased lipid deposition in the subendothelial space

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17
Q

What are foam cells

A

accumulation of monocytes (macrophages) that are engorged with cholesterol and create atherosclerotic plaques

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18
Q

what is a fibrous plaque

A

lipid rich core that will necrose and calcify = atheroma

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19
Q

what does atheroma lead to

A

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

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20
Q

what are risk factors of CAD

A

hypercholesterolemia- elevated LDL
diabetets
hypertensions
smoking
inflammatory disorders

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21
Q

what are non-modifiable risks for CAD

A

age, gender, FH, ethnicity, genetic evidence, previous history of CVD

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22
Q

what are modifiable risks for CAD

A

BP
total cholesterol
HDL cholesterol
smoking
blood sugar/diabetes
BMI
markers of chronic inflammation

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23
Q

what are female-specific or predominant risk factors for CAD

A

pregnancy induced HTN
preeclampsia/eclampsia
gestational diabetes
PCOS
Menopause
systemic inflammatory rheumatologic diseases
mental stress/depression

24
Q

when do the coronary vessels fill

A

during diastolic relaxation

25
Q

what determines coronary vascular resistance

A

hormones
neural stimulation
metabolic demand
peripheral vascular resistance

26
Q

what is a STEMI characterized by

A

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

27
Q

what are ischemia symptoms

A

classic: chest pain, +/- radiation
anginal equivalent: dyspnea, Nausea, diaphroesis and fatigue

28
Q

what is levines sign

A

gripping the chest

29
Q

what is angina

A

chest discomfort typically substernal or slightly to the left

30
Q

what is myocardial ischemia

A

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

31
Q

what is chronic coronary syndrome

A

stable angina
(reproducible)

32
Q

what is stable angina

A

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

33
Q

what are the symptoms of stable angina

A

angina with increased cardiac demand
non-anginal symptoms: dyspnea, pain away from substernal area, nausea, diaphrosesis, fatigue

34
Q

what occurs during stable angina

A

acidosis, decreased ATP K+/Na+ pumps, increased lactate, release of serotonin, bradykinin, histamine, adenosine, increase thromboxane A2

35
Q

what is stimulated with stable angia

A

stimulates sympathetic afferent pathways - syumpathetic ganglia
discomfort can spread along corresponding dermatomes, neck, shoulder, jaw discomfort

36
Q

What is acute coronary syndrome (ACS)

A

ST segment elevation - STEMI
Non ST segment elevation - NSTEMI and Unstable angina

37
Q

what are typical ACS descriptors

A

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

38
Q

how many types of acute myocardial infarctions are there

A

Type 1-type 5

39
Q

what is type 1 MI due to

A

coronary atherothrombosis

40
Q

what is the cause of type 2 MI

A

supply-demand mistmatch

41
Q

how long does it take without blood supply does it take to cause tissue pallow and decreased contractility with AMI

A

one minute without blood supply

42
Q

how long does it take for AMI to lose contraction

A

3-5 minutes
ATP depletes, glycogen stores used up, lactate accumulates

43
Q

what is unstable angina

A

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

44
Q

what is a NSTEMI

A

acute coronary syndrome (ACS)
m/c d/t disrupted atherosclerotic plaque
- partial or intermittent blockage
- ischemic disease
- apoptosis/necrosis of myocytes
- release of troponin

45
Q

What is STEMI

A

event typically begins with atherosclerotic plaque rupture
TRANSMURAL MI (complete obstruction of blood flow)

46
Q

What is the J point

A

transition point into the ST portion

47
Q

what is seen on a STEMI ECG

A

J point elevation > 1mm in 2+ contiguous leads

48
Q

what is right ventricular infarction

A

associated with right coronary artery occlusion
hypotensive - preload dependent
decrease CO d/t decrease LV filling
- shock
DO NOT give nitroglycerine

49
Q

What are STEMI mimics

A

Acute pericarditis
myopericarditis (typically viral or autoimmune)
left ventricular hypertrophy
aortic dissection
severe hypercalcemia

50
Q

what is coronary vasospasm

A

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

51
Q

what causes coronary vasospasm

A

hyper-reactivity of smooth muscle

52
Q

what are the triggers of coronary vasospasm

A

Drugs: COCAINE
smoking (major risk)
vagal response
PCI
Botulism
low magnesium
Kounis syndrome

53
Q

what is the presentation of coronary vasospasm

A

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

54
Q

what are complications of ischemia

A

arrhythmias
blocks
cardiogenic shock
ventricular free wall rupture
ventricular septal defect
decrease CO
acute mitral regurgitation

55
Q

what is papillary muscle dysfunction

A

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

56
Q

what is ventricular aneurysm

A

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

57
Q

what is a mural thrombi

A

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

CABS2: Cardiology (11 decks)

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