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CVS-Alaa > chest pain & ACS > Flashcards

chest pain & ACS Flashcards

1
Q

what r the risk factors of atherosclerosis/IHD ? and why

catagorize them as modifiable and non-modifiable

A

Non-modifiable:

1) AGE 40-60
2) Family history
3) Males

Modifiable:

  • Hyperlipidemia- high LDL
  • Smoking-activates Sympathetic nervous sys, making platelets very sticky
  • Hypertension-increase in Bp, damages epithelium.
  • Diabetes- flunctuations in glucose levels damages BV endothelium and increases hypercholestremia
  • Obesity
  • hypercholestremia
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2
Q

a young 16 yr boy comes to ur clinic w/ MI.

what 2 things should u take into account?

A
  • Familial hypercholestremia

- Cocaine abuse-can produce INTENSE coronary Spasm!

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3
Q

what is acute coronory syndrome?

A

Its is due to acute plaque rupture! (thats why Stable angina is NOT part of it)

group of diseases that includes:

Unstable angina
Myocardial infarction
Non-ST elevation myocardial infarction (NSTEMI)
ST elevation myocardial infarction (STEMI)

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4
Q

Most pateints of Angina do NOT ususally complain of chest pain…so what complaint would they present with

A 
CHEST DISCOMFORT
-chest is heavy
-burning sensation in chest
-squeezing pain 
"an elephant sitting on my chest"

if u ask them to localise the discomfort in chest they cannot exactly localize it, “hal na7ya” hal 9ob»this is called DIFFUSED SENSATION >bc its coming from the viscera

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5
Q

why can angina be present when u r walking against cold wind?

A

when u walk against cold wind, ur heart is working harder, and its o2 damad is high.

cold constricts arterioles> blood flow is difficult > TPR is increased> harder for heart to push blood through these naroow vessle> heaet works harder> o2 demand goes up>

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6
Q

when tachycardia occurs… what changes diastolic time or systolic and how?

A

Diastolic time decreases from 0.5->0.15 bc the heart doesnt have time to fill

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7
Q

when does the heart get most its blood supply and why?

A

heart get most its blood supply during DIASTOLE (relaxation) , bc during systole, the heart is contracting therefore squeezing on its own blood supply!

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8
Q

why does Tachycardia cause angina?

A

1) heart is working more> oxygen demanding is increased

2) heart rate goes up> less time for diastole> means heart is less perfused> oxygen supply is low

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9
Q

if patient develops Angina pain, describe how he will describe it

A

-Dull
-diffused ( cannot localise it)
may radiate to arm, jaw, nack

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10
Q

women said she using spinning machine on her right arm, but felt the pain on her opposite arm, u ask her do u feel chest pain she says NO
what could u diagnose her with?

A

ANGINA,
bc she is exerting.

it was a case of angina only felt in the area of RADIATON

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11
Q

Explain some symtoms of Stable/typial/classical Angina,
how r they usually releived?
who is at higher risk of getting it?

A
  • pain on physical exertion (excerise)
  • emotional stress
  • heavy meal
  • walking against cold wind

RELIVED:

  • By taking REST
  • sublingual Nitrates (may feel burning sensation)

MEN-bc instable angina is due to athosclerosis

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12
Q

when does heart ischemia tissue occur?

A

ONLY when metabolic demands of the cardiac Muscle is higher than what can be delivered to the tissue.

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13
Q

HISTORY TAKING POINTS TO CONSIDER:

A

S ite: location of the pain and if it radiates
Q uality: how pain feels (e.g. sharp, dull)
I ntensity: effect on patient, severity score
T iming: when it started; sudden or gradual onset
A ggravating factors: what makes pain worse
R elieving factors: what makes pain better
S econdary symptoms: other symptoms

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14
Q

difference in pain sympotms in Stable angina and unstable angina. how can u relieve the pain

A 
Stable:
triggered by exertion
Pain goes AWAY in rest
dull, restrosternal pain 
GTN spray

Unstable:
Pain is more INTENSE
Pain is LONGER
Pain occurs at REST

extra: Glyceryl trinitrate (GTN) belongs to a group of medication called nitrates. Nitrates work by relaxing and widening the blood vessels that increase the blood supply to the heart.

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15
Q

common causes of stable and unstable angina

A

stable

-atherosclerosis

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16
Q

how do nitrates releif Angina pain? and which type of angia do we administer it in? and what is the mode of administration?

A

Nitrates will convert into NO.

VENODILATION > sublingualy

less VR to heart, less blood goes to heart, less heart filling,> the heart will contract LESS (LESS wall tension) due to shwayat preload available > less work needed so oxygen demand to heart is LESS> (frank starling) heart mu m7taj wayid oxygen to work.

ARTERIOLAR DILATION
Dialte arteries (low TPR)  therefore reducing afterload on heart, so heart only now has to work against a LESS resisance > less work again. less oxygen needs

SO NITRATES R RELEVING PAIN BY REDCUING WORK OF HEART VIA VENODIALTION AND ARTERIOLAR DILATION.

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17
Q

what is the differenc in the plaques in stable and unstable angina?

A

stable> the plaque is Stable

Unstable> plaque is unstable, very vunerable to rupture! if it ruptures it calls in platelet (clotting shit) andu get formation of THROMBIS that can COMPLETELY OCCLUDE the coronory vessel!

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18
Q

where on the heart layers does ischemia usually occur incase of angina?

A

subendocardial layer, bc it is the furthest away frok the coronory arteries.

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19
Q

why is unstable angina called unstable?

A

it is so dangerously unstable due to UNSTBALE characteristics of the plaque that can fall into the catagory of MI

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20
Q

SOME DR’S SAY U SHOULD TREAT UNSTABLE ANGINA AS IF IT WAS MYOCARDIAL INFARCTION!

A

cool.

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21
Q

difference btw stable and vunerable/ unstable plaque

A

Stable plaque> has a fixed obstruction. no ischemia, only if their is increased o2 demand.

Unstble plaque> more vunerbale to rupture bc it has
-more foam cells, lipids, macrophages
-macrphages can secret metalloprotienases which digest fibrous material to make the plaque MORE WEAK & susceptible to rupture!
this can lead to formstion of thrombus

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22
Q

At what point can u say that Unstable angina has converted into MI?

A

when the ischemia becomes IRREVERSIBLE and death of myocardiam had occured (NECROSIS) itll release its shit like Troponin

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23
Q

If a pateint has severe, prolonged chest pain but biomarkers r not present in the blood, what is the mostly diagnosis and why?

A

it is NOT MI, bc necrosis is not there! myocardiam hasnt died yet> so it hasnt release biomakrer from it tissue , it only releases its contentts when it dies (necrosis)

–so it is unstable angina

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24
Q

what converts a severly ischemic area into a necrotic area?

A

its depends on the severity and duration of ischemia!

if ischemia is prolongled for more than 20-3- mins> area will undergo Necrosis !

But if u treated the patient f

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25
Q

why is it important that u treat unstable angina fast! ( preferably before 30 mins!)

A

bc with in 20-3- mins in unstable angina, the ischemic cardia tissue and undergo necrosis! and patient develops MI!

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26
Q

which type of angina occurs at rest?

A

Unstable

27
Q

which type of angina occurs at physcial exertion?

A

stable

28
Q

most MI r asymptomatic 25% this is most common is what ppl? what do u call this type of MI

A

SILENT MI&raquo_space; Diabetic, bc their nerves in the heart may have undergone diabetic neuropathy» so they fell no pain
also in those with transplanted heart.

29
Q

what r acute coronory syndromes?

A

acute Myocardial Ischemia caused by atherosclerotic coronory A. disease.

30
Q

difference btw Heart tissue Ishcemia and heart tissue death (infarction) ?

A
  • heart tissue Ischemia» no cardiac enzymes leak

- Heart tissue death» cardiac enzymes will leak from necrotic cardiac muscle cells.

31
Q

20 mins is a criritcl time, before it theres no NECROSIS after it u get MI

A

ok

32
Q

describe symptoms of MI

A

-Substernal, severe prolonges pain
-sudden onset…but NOT instantaneous why?
-diffuse pain (cannot localise)
-gripping pain
-may radiate to arm, jaw, neck, epigastric
-dyspneo, pulmonary edema
-sweating (diaphoresis
-Nausea
-vomitting
-

33
Q

describe the changes in ECG in stable, unstable, and MI

A

stable: ST - depression
Unstable: ST - depression
MI (subendocardial): ST- depression

MI (transmural): ST - Elevation

34
Q

If unstable Angina and MI both show on ECG ST depression, then how can we differentiate btw the both?

A

by the Biomarkers

which is only present in MI bc of necrosis that occurred to cardiac myscle.

35
Q

what diagnostic tests do u perform if u suspect Acute coronory syndrome? what r u looking for in each test?

A

ASAP!»-ECG–>look at ST segments, T waves, Pathalogical Q waves

  • Blood Tests–>Troponin (it indicates myoctye death)
  • Other
36
Q

what change in ECG do u find in Unstable angina?

A

NSTEMI

ST-segement depression

37
Q

other than MI what else can cause chest pain? how would u describe their chest pain?

A 
Respiratory
Pneumonia
Pulmonary embolism
-sharp
-well localised
-worse when coughs
CARDIAC >> pericardiam or cardiac muscle
IHD
-dull
-retrosternal (behind sternum)
-radiating Jaw neck shoulder
-eased when sitting up and leaning forward

Pericarditis

  • sharp
  • retrosternal
  • eased when sitting up and leaning forward

Gastrointestinal

  • reflux
  • peptic ulcer disease
  • BURNING pain
  • worse after food
  • worse when lying flat

Musculoskeletal

  • rib fracture
  • costochondritis
  • Sharp
  • well localised
38
Q

how does a patient with pericarditis sit to ease the pain?

how would they describe their pain?

A

eased when sitting up and leaning forward

  • sharp
  • retrosternal
  • worse after food, worse when lying flat
39
Q

what is costochondritis?

A

inflammation of costal cartilages

40
Q

what is the difference btw pleural/pericardial pain vs cardiac ischaemic chest pain?

A

SOMATIC PAIN>
if u have pneumonia for ex, the area of the lung affected is gunna rub on the pleural sac!
if pericardium is also effected the samee pain will happen

VISCERAL PAIN> associated with the organ
-dull, poorly localised. ex cardiac ischemic pain.

41
Q 
what is pericarditis? 
who is more prone?
causes?
how would they describe their pain? when does it get worse?
what do u hear upon auscultation?
what changes do u see in a ECG?
A
  • inflammation of pericardium
  • MEN more prone than women
  • ADULTS

secondary to VIRAL illness

  • central restrosternal
  • sharp pain,
  • worse with inspiration, coughing, and lying down
  • Pericardial rub is what u hear!

ST segment elevation!-saddle shaped

42
Q

describe the Clinical Examination Findings u see in stable angina and Acute coronary syndromes (UA, NSTEMI, STEMI)

A

stable
– Clinical examination often normal
– chest pain free at rest

Acute coronary syndromes (UA, NSTEMI, STEMI)
– Clinical examination is often normal!
– But may appear sweaty, anxious, pale
– +/- clinical signs secondary to complications of cardiac tissue death (NSTEMI/STEMI) e.g. acute heart failure, heart murmur

43
Q

why r those w/ MI, have a high tendacy to develop tachyarrythmia?

A

bc ischemic or myocytes r overloaded with cations, this will cause the RMP to fluctuate slightly (move to + side) and hit threshold and the cel will AUTOFIRE! and produce ventricular fibrillation, electrical activity in the hear will go up and the mechanical activity cannot follow! leaving us with NO PULSE on patient!

44
Q

which ventricle is more prone to MI? which coronory arteries

A

LV

L.anterior descending>RCA>circumflux

45
Q

when is MI more likely to occur? (time of day) and why?

A

Morning, bc ur adregernic levels go up,

Adreniniline shoots> activate simp, heart beats faster, increase in BP, platelets adhesively increase!

46
Q

which vein is mostly used during CABG?

A

saphenous vein

47
Q

why would a person with MI, pallor, sweat, vomits?

A

due to activation of sympathetic nervous sys.

48
Q

what is normal function of troponin in skeletal or cardiac muscle cells?

A

is a complex of three regulatory proteins (troponin C, troponin I, and troponin T).
Troponin is attached to the protein tropomyosin.
When calcium binds to TnC of troponin, a conformational change moves tropomyosin away from actin’s binding sites.

This displacement allows myosin heads to bind actin, and contraction begins.

49
Q

What is the name of the clinical syndrome of cardiac pain brought on by exertion and relieved by rest?

A

Stable angina

50
Q

What are the advantages of CT coronary angiogram compared to
catheter based angiography in assessing whether a patient has a
blockage of a coronary artery?

A

Non inavasive more detailed

51
Q

define Angina pectoris? what causes it?

A

Chest pain due to ischemic myocardium, secondary to coronory artery narrowing or spasm.

no myocyte necrosis!

cause by any condition that incresaes myocardium oxygen demand (ex: tachycardia, wall stress, contractility)

52
Q

Angina ALWAYS lasts more than a phew seconds!

A

this helps to differentiate from sharper and BRIEf musculoskeletal pain

53
Q

what can cause incresaes myocardium oxygen demand?

A

Physical exertion
anger
emotional exciteemtn

54
Q

What is a bruit sound?

A

or vascular murmur,[1] is the abnormal sound generated by turbulent flow of blood in an artery due to either an area of partial obstruction; or a localized high rate of blood flow through an unobstructed artery.

55
Q

If angina is suspected, what diagnostic procedures may help in confirming myocardial schemia as the cause?

A
  • Electrocardiogram
  • stress testing
  • standard excersize testing
  • nuclear imaging studies
  • Exersize echocardiography
  • coronory angiography
56
Q

If angina is suspected, what diagnostic procedures may help in confirming myocardial ischemia as the cause?

A
  • Electrocardiogram
  • stress testing
  • standard excersize testing
  • nuclear imaging studies
  • Exersize echocardiography
  • coronory angiography
57
Q

pharmacological treatment, is the first line defense in the prevention of ANGINAL ATTACKS

what would u administer for ‘acute attacks”
what about for longer acting prevention?

what is your main goal in giving this drug (what do u want to achieve)

A

ORGANIC NITRATES

relieve ischemia mainly through venodilation.

Acute attacks: Sublingual Nitroglycerin or spray>rapid onset of action

Longer acting: Oral tablets of isosorbide denigrate or mononitrate
or
a transdermal nitrogylerin patch ( applied once a day)

Our goal is:

  • decrease cardiac workload (less o2 demand on heart)
  • increase myocardial perfusion
58
Q

Stable angina, UA, NSTEMI and STEMI are all manifestations of

A

IHD

59
Q

Acute coronary syndromes include:

A

UA, NSTEMIs and STEMIS

60
Q

why is unstable plaque more vulnerable to rupture?

A

more vunerbale to rupture bc it has
-more foam cells, lipids, macrophages
-macrphages can secret metalloprotienases which digest fibrous material to make the plaque MORE WEAK & susceptible to rupture!
this can lead to formstion of thrombus

61
Q

What is Creatine Kinase (CK), which cases can it be elevated? What does it indicate?

A

CK is an important enzyme in metabolically active tissues like muscle.

CK used to be measured to diagnose heart attacks , but has been largely superseded by troponin assay.

CK is an enzyme that is also released into the blood by damaged skeletal muscle and brain.

A rise in plasma CK can result from: 
• intramuscular injection, 
• vigorous physical exercise, 
• a fall (especially in the elderly), 
• rhabdomyolysis (severe muscle breakdown), 
• muscular dystrophy,
• acute kidney injury.
62
Q

Beta blockers are sometimes prescribed in cases of stable angina.
How would a beta blocker help?

A

Slow down heart rate

63
Q

Beta blockers are sometimes prescribed in cases of stable angina.
How would a beta blocker help?

A

Slow down heart rate

64
Q

what is the relationship between the
radius of a tube and the resistance it offers to (laminar) blood
flow? What impact will narrowing of a coronary artery have on
blood flow?

A

Causes turnulence due to increased resistence

CVS-Alaa (21 decks)

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