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SAV NUR 406 exam 1 > week 1 content > Flashcards

week 1 content Flashcards

1
Q

__________ angina: coronary artery spasms

Caused by -
endothelial dysfunction = spasms of the coronary arteries = decreased blood flow to heart = leading to intermittent chest pain even at rest

A

Prinzmetal/variant/vasospastic

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2
Q

Prinzmetal/variant/vasospastic angina
T/F

  1. Issue = Supply ischemia
  2. r/t to atherosclerotic plaque build up
  3. CAD (atherosclerotic plaque) may or may not be present
  4. onset can be both at rest or with minimal exertion
  5. onset is not at night
  6. EKG changes – elevated ST segment (during spasm)
  7. treatment – nitrates to relax spasms
  8. can range from benign or cause serious dysrhythmias
A
  1. T
  2. F - NOT r/t atherscletosis. is r/t spasms
  3. T
  4. T
  5. F - can be
  6. T
  7. T
  8. T
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3
Q

Issue = type of chest pain that occurs when the heart muscle does not receive enough blood and oxygen.

cause = (Fixed stenosis) a narrowing of the coronary arteries, which supply blood to the heart. This narrowing is often due to atherosclerosis, a buildup of plaque in the arteries (demand ischemia)

A

Chronic Stable angina

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4
Q

Issue= thrombus can form in a coronary artery, which supplies blood to the heart muscle. This can block blood flow and lead to ischemia. (Supply ischemia)

often associated with the rupture of a vulnerable/unstable atherosclerotic plaque and results in formation of a thrombus.

A

Unstable angina:

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5
Q

type of chest pain that:
- occurs at rest or with minimal exertion
- may be more severe or frequent than usual
- is occurring for the first time (myocardial ischemia occurring)
- different in any way (new regions of the heart are undergoing myocardial ischemia)

A

Unstable angina:

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6
Q
  1. Does Myocardial infarction (blood flow to a section of the heart muscle is blocked) occur with unstable angina? why?
    - The thrombus occlusion/blockage is ___________
    - Thrombus ________
  2. EKG changes show:
    - Ischemia or infarction changes?
    - Transient, temporary, or both abnormalities
  3. are troponin or other cardiac enzymes elevated? why?
A
  1. NO b/c
    - The thrombus occlusion/blockage is only partial (so some blood flow is getting through)
    - Thrombus dissolves
  2. ischemia, both
    • No – troponin is and indicator of heart muscle damage, and that doesn’t happen with UA
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7
Q

An umbrella term that includes a range of conditions that occur when blood flow to the heart muscle is suddenly reduced or blocked.
- similar patho
-similar presentation and early management rules
- _______ would require eval for acute reperfusion intervention

A

Acute coronary syndrome

STEMI

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8
Q

s/s of MI or ACS?
- chest pain lasts a long time
- no relief with nitrates
- tightness
- elephant on chest
- diaphoresis
- SOA
-n/v
- anxiety
- discomfort or tingling in arms, back, neck, shoulder, jaw
- remember men and women can present different
- GI symptoms (heartburn, n/v) – women
- suddenly dizzy – women
- cold sweat – women
- unusual tiredness – women

A

ACS

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9
Q

when stable angina changes or gets worse that’s when we consider ______

A

ACS

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10
Q

ACS s/s
remember men and women can present different. what are (4) unique women s/s?

A
  • GI symptoms (heartburn, n/v) – women
  • suddenly dizzy – women
  • cold sweat – women
  • unusual tiredness – women
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11
Q

_______ plaque: This type of plaque is less likely to rupture or break off. It often has a fibrous cap that helps to stabilize it.

________ plaque: This type of plaque is more likely to rupture, leading to a blood clot that can block blood flow to the heart or brain. It often has a thinner, more fragile cap.

A

Stable

Unstable

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12
Q

Chest pain that:
- occurs at rest or with minimal exertion
- often indicating a more severe underlying condition.
- plaque disruption and platelet aggregation
- Unstable plaque
- clot is small
- blood supply is maintained
- New or changing chest pain caused by ischemia (insufficient blood flow to an organ or tissue,)

A

unstable angina

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12
Q

unstable angina
- _______ disruption and _______ aggregation
- Unstable or stable plaque?
- clot is big or small?
- blood supply is maintained or blocked?
- New or changing chest pain caused by ischemia or infarction?

A
  • plaque disruption and platelet aggregation
  • Unstable plaque
  • clot is small
  • blood supply is maintained
  • New or changing chest pain caused by ischemia
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13
Q

A type of acute Myocardial Infarction
-thrombus is present
- vessel is more narrowed (b/c of unstable plaque and plaque disruption and platelet aggregation that turned into a thrombus)
- some blood is still able to get through

A

NSTEMI

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14
Q

A type of acute Myocardial Infarction
- thrombus is present
- vessel is completed occluded (b/c of the thrombus)
- blood flow is completely blocked

A

STEMI

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15
Q

s/s of MI or unstable angina?
- diaphoresis
- dyspnea
- extreme anxiety
- levine’s sign – fist to chest
- pallor
- retrosternal crushing chest pain that radiates to shoulder, arm, jaw, back
- weak pulses

A

MI

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16
Q
  1. ST segment = depression or normal
    ST segment = elevation “tombstone”
  2. QRS complex = wide, develops over hours
    QRS complex = normal “narrow”
  3. T wave = peaked, then inverted
    T wave = inverted
  4. Troponin = elevated, goes back to normal
    Troponin = sudden elevation, continues
  5. Size of infarct/necrosis = smaller area
    Size of infarct/necrosis = larger area

6.
Outcomes = poorer
Outcomes = better

A
  1. NSTEMI
    STEMI
  2. STEMI
    NSTEMI
  3. STEMI
    NSTEMI
  4. NSTEMI
    STEMI
  5. NSTEMI
    STEMI
  6. STEMI
    NSTEMI
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17
Q

stable vs unstable plaque:

  1. Size of lipid core
    - ______ plaque = small lipid core
    - ______ plaque = large lipid core
  2. Size of fibrous cap
    - _______ plaque = large
    - _______ plaque = small
  3. Inflammation (CRP levels)
    - ________ plaque = not as active
    - ________ plaque = active
A
  1. stable - small core is good
    unstable - large core is bad (if the core is big it means the fibrous cap is small, the cap is what stabilizes it, so plaque is unstable and could break off)
  2. cap stabilizes lipid core
    stable = large cap is good
    unstable = small cap is bad
  3. stable
    unstable
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18
Q

stable vs unstable plaque

  1. Smooth muscle cell
    -_______ plaque = more smooth muscle
    - ______ plaque = fewer smooth muscle cells
  2. Proliferation of smooth muscle cells
    - _______ plaque = less proliferation of smooth muscle cells
    - ______ plaque = Smooth muscle cells often proliferate
  3. Intima - innermost layer of a blood vessel
    - ______ plaque = intima is often covered by a thick, fibrous cap
    - _______ plaque = intima may be thinner
A
    • stable plaque = smooth muscle cells often migrate to the surface and form a thick, fibrous cap. This fibrous cap helps to stabilize the plaque and reduce the risk of rupture.
    • unstable plaque = fewer smooth muscle cells, This can lead to a thinner, more fragile fibrous cap, making the plaque more likely to rupture.
    • unstable plaque = less proliferation of smooth muscle cells or the proliferating cells may be dysfunctional. This can lead to a thinner, more fragile fibrous cap and increase the risk of plaque rupture.
    • stable plaque = Smooth muscle cells often proliferate in stable plaque, contributing to the formation of a thick, fibrous cap that helps to stabilize the plaque.
    • stable plaque = intima is often covered by a thick, fibrous cap that helps to stabilize the plaque. This fibrous cap is formed by the proliferation of smooth muscle cells and the deposition of extracellular matrix proteins.
    • unstable plaque = intima may be thinner and more vulnerable to rupture.
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19
Q

Theory of plaque rupture

  1. Factors such as
    - ________ stress
    - _______
    - _________
    Cause
  2. ___CREASED SNS ACTIVITY =
  3. ___creased BP, HR and force of contraction =
  4. ___creased force of coronary artery blood flow =
  5. ___creased force exerted against injured endothelium =
  6. _________ RUPTURE =
  7. _________ adhere to ruptured plaque
  8. substances are released that:
    - attract more _________
    - contribute to vaso______
  9. __________ FORMATION
A

Theory of plaque rupture

  1. Factors such as
    - psychological stress
    - exercise
    - circadian rhythms
    Cause
  2. INCREASED SNS ACTIVITY =
  3. increased BP, HR and force of contraction =
  4. increased force of coronary artery blood flow =
  5. increased force exerted against injured endothelium =
  6. PLAQUE RUPTURE =
  7. platelets adhere to ruptured plaque
  8. substances are released that:
    - attract more platelets
    - contribute to vasospasm
  9. THROMBUS FORMATION
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20
Q

ACS vs stable angina

  1. which lasts longer?
  2. which one is relieved by Nitrates?
  3. which one has additional pain descriptors that include tightness, elephant on chest?
  4. Which one has Accompanying symptoms that include diaphoresis, SOA, n/v, anxiety?
A
  1. ACS
  2. SA
  3. ACS
  4. ACS
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21
Q

Acute myocardial infarctions (STEMI and NSTEMI)

  • AMI is associated with the rupture of a _____________ and results in formation of a ___________
  • The thrombus can cause ______ or _________ disruption in blood flow
  • We classify AMI as STEMI or NSTEMI based on _____________
  • myocardial cells suffer irreversible ischemic _________

AMI is ACS with:
- temporary or prolonged ischemia?
- without recovery or with recovery?

A
  • AMI is associated with the rupture of a vulnerable/unstable atherosclerotic plaque and results in formation of a thrombus.
  • The thrombus can cause partial or total disruption in blood flow
  • We classify AMI as STEMI or NSTEMI based on EKG findings
  • myocardial cells suffer irreversible ischemic necrosis
  • AMI is ACS with:
    prolonged ischemia
    without recovery (permanent)
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22
Q

AMI

  1. does Myocardial infarction (blood flow to a section of the heart muscle is blocked) occur with AMI? why?
    - The thrombus occlusion/blockage is causing _______ or ________ to blood flow
  2. EKG changes:
    ______ – normal or depressed ST segment
    ______ – elevated ST segment
  3. troponin or other cardiac enzymes elevated?
A
  1. yes
    - The thrombus occlusion/blockage is causing prolonged disruption in blood flow (none or very little blood flow is getting through for a prolonged time)
    OR
    - The thrombus occlusion/blockage is causing total blood flow disruption in blood flow (no blood flow is getting through)
  2. NSTEMI
    STEMI
    • Yes – troponin is and indicator of heart muscle damage, heart damage occurs with both STEMI and NSTEMI acute MI. - Should be back to normal after occlusion is fixed
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23
Q

The extend of damage occurred during AMI depends on 3 factors

A
  • location or level of occlusion in the coronary artery – small or large artery occluded, total or partial occlusion?
  • length of time that the coronary artery has been occluded – time is tissue!
  • hearts availability of
    collateral circulation - body naturally builds other vessels around the occlusion to keep blood flow, like a compensatory mechanism, can be a good thing
24
Q

ischemia vs infarction

insufficient blood flow to an organ or tissue, leading to a lack of oxygen and nutrients.
- This can cause tissue damage, but the tissue may still be viable if blood flow is restored quickly (reversible)

A

ischemia

25
Q

insufficient blood flow to an organ or tissue, leading to a lack of oxygen and nutrients, is prolonged and severe, leading to tissue death.
- it cannot be revived (irreversible)
- this can occur within 30 min – 4 hour

A

infarction

26
Q

Infarction - ischemia is prolonged and severe, leading to tissue death.
- Once tissue has infarcted, it cannot be ___________
- this can occur within ___ min – ___ hours
- at 4 hours – tissue _______ begins
- in 1-2 weeks – ____ tissue is cleared away
- in 6 weeks – _________ tissue replaces the necrotic tissue

A
  • Once tissue has infarcted, it cannot be revived (irreversible)
  • this can occur within 30 min – 4 hour
  • at 4 hours – tissue necrosis begins
  • in 1-2 weeks – necrotic tissue is cleared away
  • in 6 weeks – tough fibrous scar tissue replaces the necrotic tissue
27
Q

AMI
3 zones of damage

1st – __________ zone (reversible)
- full recovery is possible

2nd – ________ (reversible)
- not dead yet
- some recovery is possible – so we can perfuse it and restore it to become viable

3rd – _________ = necrosis (irreversible)
- MI
- dead cells
- cant recover dead cells
- can stop it from increasing
- Increase oxygen
- Decrease the demand on the heart

A

ischemic
injury
infarction

28
Q

infarction
1. can we recover dead cells?
2. can we stop necrosis from increasing?
- ___crease oxygen
- ___crease the demand on the heart

A
  1. no
  2. yes
    - Increase oxygen
    - Decrease the demand on the heart
29
Q

____________ artery
- supplies the left ventricle (worst one to occlude b/c without LV heart can’t pump blood out to body)
- most commonly involved in MI
- “widomaker”

A

Left anterior descending (LAD) artery

30
Q

AMI treatment
(6)

A

morphine
oxygen
nitroglycerin
ASA
beta blockers
thrombolytic agent - maybe

31
Q

AMI pharm
Acute MI/STEMI treatment
__________
- Increases o2 delivery to ischemic myocardium
___________
- Suppresses platelet aggregation
- Decreases mortality
- Chew first dose
___________
- Decrease pain
- Reduce preload and afterload
- Helps preserve ischemic tissue
__________ (if no contraindications)
- Reduce HR and contractility = reduces oxygen demand
- Reduces pain, infarct size, and mortality
___________
- Reduces preload and afterload
- Limits infarct size
- Doesn’t reduce mortality
_________ (if pt is eligible)
- ideally used within 4-6 hours of onset of MI

A

oxygen
ASA
morphine
beta blockers
nitroglycerin
thrombolytic agent

32
Q

fibrinolytic therapy/thrombolytic agent

MOA
Dissolves existing clot by converting plasminogen into plasma

Adv - Most effective
Disadv – works best within ___-___ mins, ideally used within ___-___ hours of onset of MI

s/e
________

contraindicated with hx of brain bleed

always give with heparin and antiplatelet therapy (prevents new clot from forming)

A

alteplase (tPa)
30-70 min
4-6 hours

bleeding

33
Q

s/e
hypotension
h/a
flushing
severe hypotension especially when given with nitrates

do not give with sildenafil (Viagra) – risk of severe hypotension

A

nitroglycerine

34
Q

__________ - medical procedures aimed at restoring blood flow to an organ or tissue that has been deprived of oxygen due to ischemia
ex: balloon catheter or stent

_____________ - rapid restoration (surge) of blood flow to the myocardium also contributes to injury b/c of myocardial stunning

A

reperfusion

reperfusion injury

35
Q

reperfusion injury

caused by
- oxidized free radicals generated by _______
- ________ response to restored blood flow

Monitor for
- reperfusion ________ - esp. _____ and _____

A

caused by
- oxidized free radicals generated by WBCs
- cellular response to restored blood flow

Monitor for
- reperfusion dysrhythmias
– esp. VTACH and VFIB

36
Q

Long term drug therapy after MI:
_______
– inhibit platelet aggregation
________
– reduce HR and BP
- lowers risk of death when continued long-term after MI
________
– stimulate dilation of blood vessels by inhibiting angiotensin II
- improves ventricular remodeling after MI
________
– addresses the CV disease

A

Aspirin
Beta blockers
ACE inhibitors
statin

37
Q

localized dilation or outpouching of a vessel wall
- cause turbulent blood flow
- are susceptible to rupture
- bruits may be heard over it

A

aneurysms

38
Q

aneurysms
localized dilation or outpouching of a vessel wall
- cause ________ blood flow
- are susceptible to _______
- _______ may be heard over aneurysm

A

aneurysms
localized dilation or outpouching of a vessel wall
- cause turbulent blood flow
- are susceptible to rupture
- bruits may be heard over aneurysm

39
Q

aneurysms patho
1. ______ weakens the artery walls
2. increases development of ______ in artery walls “aneurysms”

A
  1. HTN weakens the artery walls
  2. increases development of bulges in artery walls “aneurysms”
40
Q

Risk factors for _______ are Anything that causes damage to blood vessels:
- atherosclerosis
- HTN
- disease of blood vessels
- trauma
- tobacco use
- age >65 years
- hereditary

s/s
- depend on location
- may be asymptomatic

A

aneurysms

41
Q

most common aneurysms:
1. veins or arteries?
2. which 3 arteries?
3. whats the “triple A”
4. variation: ______ ________

A
  1. aortic
  2. aortic, thoracic, and cerebral
  3. abdominal aortic aneurysm
  4. aortic dissection
42
Q
  1. auscultation of a bruit over the abdominal aorta suggests the presence of an ___________
  2. if a pulsatile mass is evident in the abdomen during inspection or light palpation: ________ should not be performed until the possibility of AAA is ruled out
    - complications of AAA: __________ – will bleed out quickly
A
  1. abdominal aortic aneurysms (AAA)
  2. deep palpation
  3. rupture
43
Q

bulging in all 3 layers of the vessel wall =

tear in the artery wall that causes separation of the vessle, and blood is getting in between vessel layers, only single outside layer is still intact =

localized tear in 1-2 layers of the artery wall =

A

aneurysm

dissecting aneurysm

pseudo aneurysm

44
Q

variation: aortic dissection/dissecting aneurysm:
1. ______ of the artery wall are separated and blood enters the region
2. having an ________ can increase your risk of having an aortic dissection
3. dx with a ____ or ______
4. surgical emergency – minutes counts (most important intervention is _______)
5. emergency pharm – ______ (lower HR and BP) and _______

A
  1. layers of the artery wall are separated and blood enters the region
  2. having an aneurysm can increase your risk of having an aortic dissection
  3. dx with a CT scan or MRA (Magnetic Resonance Angiography - type of MRI scan that specifically looks at blood vessels and blood flow)
  4. surgical emergency – minutes counts (most important intervention)
  5. emergency pharm – beta blockers (lower HR and BP) and nitrates
45
Q

high vs very high risk for rupture:

  • Aneurysm: A bulging of the aorta.
  • Dissection aneurysm: A tear in the inner layers of the aorta. only outer layer is still intact.
A
  • Aneurysm: A bulging of the aorta. High rupture risk!
  • Dissection: A tear in the inner layer of the aorta. outer layer is still intact… but for how long? Very high rupture risk!!
46
Q

which type of aneurysm?
s/s
- sudden severe, tearing pain in chest, neck, back, jaw or abdomen

early sign
- BP rises

late sign
- BP is so low it may be unobtainable
- syncope
- hemiplegia – paralysis/weakness on one side of the body
- paralysis of LE
- CV collapse = shock = death

A

variation: aortic dissection/dissecting aneurysm

  • sudden severe, tearing pain in chest, neck, back, jaw or abdomen (indicates dissection)
47
Q

Types of aneurysms:
___________
- Balloon shaped
- Involves only one part of circumference of vessel
- wide neck

A

saccular

48
Q

Types of aneurysms:
_________
- entire circumference of vessel
- gradual/progressive dilation
- potentially extensive involvement
- usually r/t diffuse anterior sclerotic changes
- treatment - may be monitored for growth, intervention not required until it gets to a certain size

A

fusiform

49
Q

__________ aneurysm
- localized dissection/tear in 1-2 layers of inner artery wall
- type of hematoma
- complication of vascular interventional procedures
- treatment – may heal on own or require intervention

A

pseudo/false

50
Q

Pericardial disease
any condition that affects the __________, the sac-like membrane that encases the heart

A

pericardium

51
Q

pericardial layers listed superficial to deep
1. __________ - thin, fibrous sac that surrounds the heart.
Contains 2 layers:
- _________ pericardium: The outer layer, which is tough and inelastic.
- ________ pericardium: The inner layer, which is divided into two parts: the parietal pericardium and the visceral pericardium.
__________ : This is the thickest layer of the heart and is made up of cardiac muscle tissue. It is responsible for the heart’s pumping action.
____________ : This is the innermost layer of the heart, lining the chambers and valves. It is composed of endothelial cells, which help to prevent blood clots from forming.

A

pericardium
- Fibrous
- Serous
Myocardium
Endocardium

52
Q

pericardium is inflamed and fluid (pericardial effusion) accumulates in the pericardial space surrounding the heart

A

pericarditis

53
Q
  • some fluid in the pericardial space surrounding the heart is =
  • if fluid accumulates to >200 mL = __________ the heart = “_________ _________”
  • cardiac tamponade – ______ ______ are restricted by the surrounding pericardial fluid so they can’t stretch and fill with blood
  • medical emergency
  • drain fluid STAT or pt will die
A

ok, it serves as lubrication

compresses
cardiac tamponade

heart chambers

54
Q

s/s of acute _________
- chest pain – sharp and worsens with deep breathing
- fever – inflammatory response
- dyspnea
- pericardial friction rub – scratching sounds
- EKG findings – ST segment can be elevated or depressed
- pulsus paradoxus – decrease of 10 or more systolic blood pressure during inspiration
- “Beck triad”:
- hypotension
- jugular vein distension
- muffled heart sounds

which (2) are associated with cardiac tamponade?

A

pericarditis

  • pulsus paradoxus
  • “Beck triad”:
  • hypotension
  • jugular vein distension
  • muffled heart sounds
55
Q

treatment for _______
- NSAIDS
- ASA
- corticosteroids – pros and cons
- colchicine – indicated when not responding to ________

A

pericarditis

NSAIDS

56
Q

Inflammatory disease of the myocardium (muscle layer of heart) with degeneration and necrosis of cardiac myocytes (muscle cells)
- can range from a mild disorder (pain) to a lethal condition (HF, needs transplant to survive)
- dysrhythmias/conduction disruption is common

A

myocarditis

57
Q

Etiology
- virus most common – coxsackie viruses A and B

A

myocarditis

58
Q

________ aneurysm
- subtype of saccular
- small neck
- dx by angiography
- get hx of clinical manifestations
- located at bifurcation of arteries
- common location – circle of Willis (at base of brain - provides connection between the anterior and posterior circulation systems, arteries that stem off from the COW supply a lot of blood to the brain)
- treatment – medical control of HTN and vasospasms OR surgical drain, clipping, coiling

A

Berry

SAV NUR 406 exam 1 (3 decks)

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