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Cardio Exam 2 > lecture 5b > Flashcards

lecture 5b Flashcards

1
Q

UA/NSTEMI definition

A
  • angina with at least 1/3:
  • occurs at rest, usually last >10 minutes
  • it is severe and new onset (w/in the last 4-6 weeks)
  • occurs with a crescendo pattern
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2
Q

NSTEMI=

A

UA + myocardial necrosis

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3
Q

UA/NSTEMI pathophys

A
  • atherosclerotic plaque rupture or erosion with a superimposed nonocclusive thrombus
  • dynamic obstruction
  • progressive mechanical obstruction
  • secondary to increased myocardial oxygen demand &/or decreased supply
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4
Q

UA/NSTEMI manifestatins

A
  • chest pain
  • usually severe enough to be described as frank pain
  • dyspnea & epigastric discomfort may also occur
  • large ischemia or NSTEMI: diaphoresis; pale, cool skin; sinus tachycardia; a 3rd &/or 4th heart sound; basilar rales and sometimes hypotension, resembling STEMI
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5
Q

UA/NSTEMI cardiac biomarkers

A
  • CKMB& troponin- distinguish pts w/ NSTEMI from UA
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6
Q

there is a direct relationship between the degree of troponin elevation and

A

mortality

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7
Q

minor troponin elevations can be caused by

A

congestive heart failure
myocarditis
PE
or can be false +

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8
Q

prinzmetal’s variant angina

A
  • syndrome of severe ischemia paint that occurs at reast but NOT usually with exertion and is associated with transient ST elevation
  • due to focal spasm of an epicardial coronary artery
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9
Q

STEMI definition

A
  • myocardial cell death due to prolonged & severe ischemia

- ST elevation

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10
Q

STEMI pathophys

A
  • thrombotic occlusion of a coronary artery prevsiously affected by atherosclerosis
  • thrombus develops rapidly at site of vascular injury
  • surface of plaque becomes disrupted ->thrombogensis
  • in rare cases can also be caused by coronary emboli, congenital abnormalities, coronary spasm, inflammation, etc
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11
Q

coronary plaque prone to disruption are those with

A

a rich lipid core and thin fibrous cap

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12
Q

extent of myocardial damage depends on

A
  • territory supplied by the affected vessel
  • extent of occlusions
  • duration
  • quantity of collateral vessels
  • demand for oxygen
  • endogenous factors that can produce early spontaneous lysis of the occlusive thrombus
  • adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery
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13
Q

STEMI risk factors

A
  • multiple coronary risk factors
  • UA
  • hypercoagulability
  • collagen vascular disease
  • cocaine abuse
  • intracardiac thrombi
  • coronary emboli
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14
Q

STEMI clinical manifestations

A
  • pain is deep and visceral; heavy, squeezing & crushing & sometimes stabbing or burning
  • similar to angina pectoris but occurs at REST, more severe and lasts longer
  • weakness, sweating, N/V, anxiety
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15
Q

what are considered in differential diagnosis of STEMI?

A

acute pericarditis, PE, acute aortic dissection, costochondritis & GI disorders

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16
Q

STEMI diagnosis

A

ECG
biomarkers
imaging
non-specific indicators or tissue necrosis & inflammation

17
Q

STEMI physical findings

A
  • angina >30 min & diaphoresis strongly suggests STEMI
  • tachycardia &/or hypertension (anterior MI)
  • bradycardia &/or hypotension (inferior MI)
  • a pericardial friction rub is heard in many pts w/ transmural STEMI
  • temp elevation up to 38*C
  • arterial pressure is variable; systolic BP declines 10-15mmHg from preinfarction rate
18
Q

STEMI ECG

A

ST elevation

Q wave

19
Q

STEMI biomarkers

A
  • cardiac specific troponin
    & toponin-1
  • CK
  • CKMB
20
Q

myocardial infaction

A

death of cardiac muscle due to prolonged severe ischemia

21
Q

MI pathology

A
  • in most cases of acute MI, PERMANENT DAMAGE to the heart occurs when the perfusion of the myocardium is severely reduced (usually at least 2-4 hours)
22
Q

longer occlusion->

A

larger area of tissue damage

23
Q

STEMI

A
  • transmural infarction
  • full thickness
  • ST elevation
24
Q

NSTEMI

A
  • subendocardial infarction
  • partial thickness
  • ST depression
25
Q

histology prior to 24 hours post MI

A
  • very minimal
26
Q

histology after 24 hours post MI

A
  • first changes involve the mycoytes
  • wavy appearance
  • still have nuclei
27
Q

histology 3-4 days post MI

A
  • neutrophils are recruited
  • lack of nuclei
  • can only see the remnants of nuclei
28
Q

histology 7-10 days post MI

A
  • macrophages come
  • process of healing starts
  • elongated cells=fibroblasts
  • tiny capillaries formed
  • granulation of tissue
29
Q

histology of day 10-14 post MI

A
  • collagen

- repair process leads to formation of scar

30
Q

histology weeks post MI

A
  • complete healing

- damaged tissue replaced by collagen

31
Q

reperfusion

A
  • RESCUE!

- restore circulation

32
Q

complications

A
  • acute LVF, PE, shock
  • arrhythmias
  • myocardial rupture, hemopericardium, cardiac tamponade
  • pericarditis (Dressler syndrome)
  • RV infarction
  • infarct extention (new necrosis)
    infarct expansion (stretching, thinning, & dilation)
  • mural thrombus
  • ventricular aneurysm
  • papillary muscle dysfunction->mitral regurgitation
  • progressive late HF
33
Q

cerebrovascular disease- stroke

A

thrombosis
emolism
hemorrhage

34
Q

cerebrovascular disease

A
  1. hypoxia, ischemia & infarction due to impairment of blood supply & oxygen to CNS tissue
  2. hemorrhage resulting from rupture of CNS vessels
35
Q

acute ischemic injury

A

global cerebral ischemia

focal cerebral ischemia

36
Q

global cerebral ischemia

A
  • (ischemic/hypoxic encephalopathy)
  • cardiac arrest
  • shock
  • severe hypotension
  • affects entire brain
  • mild cases: transient post-iscehmic confusional stat followed by complete recovery
  • severe case- brain death or a persistent vegitative state
37
Q

focal cerebral ischemia

A
  • (reduction/cessation of blood flow to localized area of the brain)
  • embolic occlusion
  • thrombotic occlusion
  • vasculitis: infections
  • atherosclerosis
  • only a portion of the brain is affected
  • if sustained, leads to infarction
38
Q

brain infarction

A
  • hemorrhagic: multiple, sometimes confluent petichial hemorrhages, typically associated with emboli
  • nonhemorrhagic: thrmbosis

Cardio Exam 2 (12 decks)

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