Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CardioPulmoaryPT1 > CV Conditions: Ischemic Cond's: Exam 1 > Flashcards

CV Conditions: Ischemic Cond's: Exam 1 Flashcards

1
Q

Ischemic cond’s or

A

lack of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Leading cause of death====

A

Heart Disease!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Myocardial perfusion involves which aa’s

A

CA’s

L and R branch off of aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Basic rules of hemodynamics

2

same is true for CAs!!!

A
  • Fluid flows from an area of HIGH pressure to LOW pressure
  • Fluid follows the path of LEAST resist.

NOTE: more blood flow during Diastole=== HIGHER press in aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Determinants of CA blood flow:

Myocardial perfusion occurs primarily during pds of _______________

A

myocardial relaxation

Diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Determinants of CA blood flow:

Vasomotor tone (ability to vasodilate) of CAs allows for what?

A

vol. of blood to enter CAs during Diastole

when they are relaxed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Determinants of CA blood flow:

O2 attaches to myoglobin to be released as needed during _________

A

Systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Determinants of CA blood flow:

CA perfusion and O2 cont’s to be delivered during __________

A

Systole

as long as pressure is LOW enough

remember HIGH pressure during Diastole and goes to LOW pressure (systole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2 Factors that DECREASE myocardial perfusion

A
  • Elevated DBP—-bigger issue vs. SBP
  • CA atherosclerosis OR resist. to CA blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

If the R CA gives NO blood flow to heart=====

A

Dysrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

If L CA no blood flow to heart====

A

Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rt. CA supplies:

A

SA node

R atrium

Post and Inf surf vents

AV node in 80% pop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

L CA supplies:

A

Sternocostal surf (ant myocardium) BOTH vents

L atrium

L vent

Septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anatomy of CA’s

Inner layer

whats here?

A

Intima

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

These are MOST likely to accumulate in the Intima (inner layer of CAs)

A

Lipopro’s and fibrinogen

*this creates hardening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MODIFIABLE RISK FACTORS CARDIAC DIS.

A
  • smoking
  • high BP (>140/90)
  • High CHO lvls ​
  • phys inactivity
  • obesity
    • BMI >/= 30 kg/m2
    • normal== <25
  • stress/Type A
  • metabolic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MODIFIABLE RISK FACTORS CARDIAC DIS.

Talk more about High blood CHO lvls ….

A
  • BEST predictor is ratio of tot. CHO to HDL CHO/HDL >4.5
    • ​norm== 3.3
    • Tot. CHO
      • ​<200 = norm
    • HDL <35
      • ​>60= norm
    • Triglycerides >150​
      • ​<150= norm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NON MODIFIABLE RISK FACTORS CARDIAC DIS.

A

Heredity

sex

female post menopause

age

T2D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Risk factors Cardiac Disease

Emerging risk factors

A
  • LipoPRO A
  • LDL subclasses
  • Oxidized LDL
  • Homocysteine
  • Hematological factors
  • Inflamm markers
    • C-reactive PRO=== high stress
  • infective agents
    • C. pneumoniae
  • alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical Dx from Worse to WORST

A
  1. CAD
  2. angina
  3. acute coronary syndrome (ACS) or MI
  4. cardiac mm dysf
  5. Sudden cardiac death
  6. Other atherosclerotic dis’s
    1. ​PAD
    2. Renal athero –> renal HTN
    3. Aortic athero–> aortic aneurysms
    4. Ischemic and Hemorrhagic CVA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  1. CAD or
A

Atherosclerosis

  • progress. hardening/narrow of coronary, cerebral, renal, aortic and periph aa’s

***atherosclerotic plaques composed of lipid, fibrin and thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

CAD

2 step process:

remember this is CHRONIC athero=== long term buildup, slow w/ sx’s

A
  1. Atherosis
    1. ​fatty streak of lipid laden macrophages causes endothel damage/exposure of endothelium
  2. Sclerosis
    1. ​“fibrous cap” of thrombi and platelets over advanced plaques dev. on endothelial lining
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When CAD progresses enough

Total occlusion of aa by thrombus

MI from tot. occlusion

ACUTE— blockage BUT clot lodges

A

MI

Full occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CAD Medical mgmt

Dx testss

A

ECHO

Cornoary angio

Ex/pharma stress test

CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CAD medical mgmt

Meds

A

Statins

Antithrombotic/Antiplatelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CAD

PT intervents

A
  • ASCM:
    • Aerobic end training @ least 2d/wk @ >/= 50% VO2max for >= 10mins
      • decs athero build up
  • EX has been proven more effective than ANY med @ preventing and slowing progress of CAD****
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Angina

A
  • “strangling”
  • sub-sternal pressure
  • Some imbalance in supply and demand of myocardial O2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

NOTE: Angina and Myocardial O2 consumption

A

supply/demand problem

Rate Pressure Product RPP== HR*SBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Typical Cardiac Pain Referrals

visceral or somatic pain referrals bc heart has NO pain receptors—-so that’s why “referred” pain

A

see pics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Atypical Cardiac Pain Referrals

More likely Female

A
  • Can also include:
    • breathlessness
    • R bicep pain
    • acid reflux
    • tongue pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Angina== imbalance in Supply and Demand

what does that mean?

A

Demand > Supply of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Stages of Stable Angina

A

see pics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Stable Angina

stage 1

A

initial percept of discomfort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

stable angina

stage 2

A

INC in int. of lvl 1 OR radiation of pain to other areas (jaw, throat, shoulders, arms, other)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Stable angina

stage 3

A

Relief only obtained through cessation of activity

***when demand is relieved**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

stable angina

Stage 4

A

Infarction pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

6 types of Angina

A
  1. Chronic/Stable or Classic or Exertional
  2. Prinzmental or Vasospastic or Variant
  3. Nocturnal
  4. *Post-Infarction
  5. Metabolic or Diabetic or Macrovascular
  6. Unstable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Chronic Stable/Classic/Exertional Angina

A

onset @ specific MET lvl when supply no longer meets demand

when you cease activity===GONE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Prinzmental or Vasospastic or Variant Angina

A

CA vasospasms

same time everyday

restricts supply O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Nocturnal Angina

A

during sleep

supply does NOT meet new INCd demand due to INC SNS activation or INCd Preload in Supine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Post-Infarction Angina

A

angina pain exp’d AFTER MI that has been med./sx managed

NOT NORMAL TO HAVE THIS!!!

42
Q

Metabolic or Diabetic or Macrovascular Angina

A

exp’d by persons w/ met. syndrome or DM

43
Q

Unstable Angina

A

acute onset

accels in freq & severity

indicative of MI—> CALL 911*****

44
Q

Angina: Med mgmt

Pharmaceutical

A
  • NITRATES @ onset of event
    • short-acting nitrates
  • Nitrates prophylactically
    • ​Long-lasting
45
Q

Dx test to det. cause of Angina

A

CA angio

Ex/pharm stress test

EKG

46
Q

Other angina med. mgmt

A

Treat HTN OR underlying cardiac issues

47
Q

Angina:

PT imps

A
  • FULL cardiac assess***
  • until angina controlled AND CA bloodflow reestablishing or meets myocardial demands…..
    • ​Pt @ risk of myocardial ischemia
  • VITALS!!!

**If yesterday angina===> cardiac screen

**if treated selves w/ nitrates—-> get med. clear

48
Q

Acute Coronary Syndrome (ACS) or MI

2 types:

A
  • ST-segment elevation MI
    • STEMI
  • Non-STEMI
49
Q

Acute Coronary Syndrome/MI

or…

A
  • Acute coronary syndrome
  • MI
  • “Coronary”
  • Acute MI

NOTE: 90% MI==> atherosclerosis (CAD), 10% vasospasms (cocaine, vasoconstrict, aortic stenosis, vasculitis)

50
Q

Acute Coronary Syndrome or MI:

2 types

A

STEMI and Non-STEMI

51
Q

Alterations in Myocardial Perfusion

Acute:

A

NO PRIOR SX’S

  • Dislodged embolus
    • ends up in CA
52
Q

Alterations in Myocardial perfusion:

Chronic

A

PRIOR SX’S

  • prolonged progress. of athero. over time
53
Q

Progression of Myocardial Necrosis

A
  • NOTE:
    • LAD== widow maker
    • Zone of Perfusion
      • ​area @ risk
      • where MI occurs
    • Zone of Ischemia
      • ​NO O2
    • Zone of necrosis
      • ​perm, irrev dead tissue
54
Q

Acute Coronary Syndrome/MI

Labs

“Biomarkers of Cardiac Injury”

A
  • Cardiac Troponin I (cTnI)== BEST INDICATOR OF MI
    • ​
    • whenever trending UP —> hold pt
    • trending DOWN—> pt OK
      • ​Must obtain “trending down lab value” to initiate PT
  • Cardiac Troponin T (cTnT)
  • Creatine Kinase (CK-MB)

cTnT and CK-MB take LONGER to peak

55
Q

Anatomy and Loc. of Infarct

A
  • Right CA
    • ​Loc= inf
    • Comps
      • risk of AV block and/or arrhythmias
      • 50%
  • Left Main
    • ​Loc= Ant and Lat
    • Comps
      • pump dysf/failure
  • LAD (widow maker)
    • ​Loc= Ant
    • Comps
      • pump dysf/failure
  • Circumflex
    • ​Loc= Lat
    • Comps
      • NONE SPECIFIC
56
Q

MI: MED mgmt

Medical mgmt ACS

A
  • Cardiac angio (how occluded aa’s are) and cardiac angioplasty (PTCA) or stent
  • antithrombotics/antiplatelets
  • anticoagulants
  • tPA
    • <12 hr pd–> minimize Zone of Necrosis
  • prophylaxis for arrhythmias
  • nitrates, morphine, beta blocks
    • last 2 to dec SNS, relax heart
57
Q

MI: med mgmt

GOALS

A

IMPROVE oxygenation

LIMIT infarct size

58
Q

MI

Prognosis

A
  • Related to comps, infarction size (zone of necrosis), presence of dis on other CAs, LV function (EF, SV)
59
Q

MI:

Ventricular Remodeling

A
  • w/ STEMI
    • changes in size, shape and thick. of myocardium
  • areas of vent dilation and vent hypertrophy
  • Factors that affect remodeling:
    • ​Size infarct
    • Vent load
    • Patency of the aa infarcted
60
Q

Cardiac mm dysf or

A

Zone of Necrosis

Transmural= thru whole depth

61
Q

Cardiac MM Dysf can include the following

A
  • Dyssynchrony
  • Hypokinesis
  • Akinesis
  • Dyskinesis
  • CHF
62
Q

Dyssynchrony

A

timing off

diff timing of contracts

63
Q

Hypokinesis

A

LESS mvmt myocardium

64
Q

Akinesis

65
Q

Dyskinesis

A

w/in area: contraction NOT coord’d properly

area dilated

66
Q

CHF

A

Pump failure

EF diminished

67
Q

Sudden Cardiac Death or

A

WORST

Myocardial Ischemia

68
Q

Sudden Cardiac Death

there are NO______

A

electrical impulses

69
Q

Sudden Cardiac Death

Myocard ischemia leats to ________ and ________ ===> cessation of CO

A

leads to arrhythmias (Vtach) and vent fibrillation (Vfib) leads to cessation of CO

70
Q

sudden cardiac death

when a person has MI…

A

PROMPT delivery of CPR w/ AED and entry to ER are necessary to prevent sudden cardiac death

71
Q

Risk factors assoc’d w/ Sudden Cardiac Death

Undiagnosed CHD pop.

A

age

SBP (elevated)

LV hypertrophy

Intravent block on ECG

Nonspecific ECG abnorms

Serum CHO (elevated)

HR (elevated RHR)

VC (low, esp factor in females)

smoking

rel. wt.

72
Q

Risk Factors Assoc’d w/ Cardiac Sudden Death

Diagnosed CHD Pop.

A
  • DECd LVEF
    • ​<35%
73
Q

ALL of these involve Coronary Atherosclerosis

A
  • CAD
  • Angina
  • ACS/MI
  • Cardiac MM Dysf.
  • Sudden Cardiac Death
74
Q

OTHER dis’s of Athero

A
  • PAD
  • Renal HTN
  • Aortic HTN—-aortic aneurysms
  • Ischemic/Hemorrhagic CVAs
75
Q

Vascular Dis’s think…

A

Arterie***

76
Q

PAD or

A

Atherosclerotic occlusive disease (AOD)

Atherosclerosis Obliterans

77
Q

PAD

explain

A

SAME process as CAs:

atheromatous plaque obstruction of lg or md sized aa’s that supply blood to extremities

ACUTE== plaque build up

CHRONIC== slow, progressive

78
Q

PAD can also cause what?

A

Aneurysm dilation of aa wall

79
Q

PAD

when will pt be symptomatic?

A

When blood flow is NOT adequate to meet demand of periph tissue

80
Q

PAD

what is the Supply

A

HgB

O2

size of aa’s

81
Q

PAD

what is the Demand

A

whatever pt is doing/activity

82
Q

When supply DOES meet demand===

83
Q

S/S of PAD

A
  • Trophic changes
    • hair loss
    • thin shiny dry skin
    • mm atrophy
    • hypERsensitive to palp
  • pain w/ elevation
  • claudication @ certain MET lvl
  • pallor
  • non-healing wounds
84
Q

PAD Med. Mgmt

Dx Tests

A

ABI

pulses (diminshed or absent)

Arterial dopplers (check for acute aa clots)

85
Q

PAD med. mgmt

Pharma. mgmt

A
  • Ca+ channel blocks
  • Alpha inhibitors
86
Q

PAD and PT evals

A
  • Vitals
    • ​HR/BP during PT eval
  • Rubor of Dependency test and Claud. test
    • check MET lvl and onset of PAD s/s
  • ABI or req. ABI
  • Doc. sx’s and trophic changes
  • check for Wounds
  • Check periph pulses
87
Q

PAD and PT

A
  • Ex and PAD
    • pts unable to prod norm inc’s in periph blood flow
    • @ a LOWER threshold:
      • ​pts switch to anaerobic ex
    • intermittent claud leads to mod-severe impair in ambulation and ADL
88
Q

PAD and PT

Research and Exercise

A

Reverses sx’s!!!

  • Ex. can improve pain-free and max walking tolerance on lvl ground and during intermitt-load TM
    • ​how???
      • ​inc’d walking eff.
      • incd periph blood flow (collateral circ)
        • compensates
      • reduced blood viscosity
        • less like tomato sauce
      • regress of atherosclerotic dis.
      • RAISES pain threshold
89
Q

Ex recco’s for indiv’s w/ PAD

A

see pics

NOTE: Inc DURATION and FREQ before Intensity***

90
Q

Renal AA dis

A

athero of renal aa (blood to kidneys)

inc’d CV dis and mortality

91
Q

Aortic Aneurysms

A
  • patho perm dilation of aortic wall (around athero) involving any # of segments of aorta (irrev)
  • described:
    • ​loc, size, appearance, origin
  • occurs from:
    • athero
    • idiopathic
    • HTN
  • RUPTURE IS A MAJOR RISK OF ABD AORTIC ANEURYSMS (aneurysm==bulging)
92
Q

Aortic Aneurysm

PT implications

A
  • Visceral pain:
    • “pressure” on surrounding parts such as low back
      • ​eval resp to ex
  • leg pain/claud pain
  • numbness in LEs
  • excess fatigue
  • poor distal pulses
  • ESSENTIAL
    • monitor vitals—specifically BP
93
Q

Cerebrovascular Disease

A
  • Ischemic is most likely due to atherosclerosis –85%
  • Hemorrhagic most likely due to HTN

***tPA w/in 6 hours!!!

94
Q

Surgical mgmt:

CAD

@ least 75% occluded

usually Radial or Femoral aa’s

A
  • Percutaneous Transluminal Coronary Angioplasty
    • PTCA
    • Stent
    • ​where?
      • RCA
      • RPD (r post descending)
      • LCA
      • LAD
      • Circumflex
95
Q

Surgical Mgmt CAD

Coronary Artery Bypass Graft

CABG

A

Bypass

“alternate route”

96
Q

Surgical Mgmt CAD:

Median Sternotomy

A
  • **Sternal Precautions***
    • they open the ribs
  • First month after sx:
    • ​cough w/ heart pillow
    • do NOT hold breath/NO valsalve
    • do NOT twist upper body
    • use arms as little as poss.
    • when using arms to lift, push, pull
      • ​use BOTH @ same time (B/L)
      • NO lifting more than 5-10lbs
      • NO reaching
    • do not sit in front of air bag in car
97
Q

Pacemakers

explain…

A
  • temp or perm
  • pacing location
  • programmability
  • Anti-bradycardia arrhythmic function
  • Anti-tachy arrhythmic function

can be Atrial== fake SA node

can be Ventricular== fake AV node

98
Q

Pacemaker and PT

A
  • facility/phys specific
    • No Precautions
    • ​Arm in sling 24-48hrs
    • IPSILAT. shoulder elevation restrict <90o
      • 1-14 days
    • no heavy lifting 14 days
99
Q

Implantable Cardioverter Defibrillator

AICD

A

detects life-threatening arrhythmias & defibrillates

100
Q

Pts w/ AICD and PT

A
  • Facil/phys specific same as post op pacemaker
  • **watch HR on EKG/telemetry if avail.
  • know settings
  • BE READY!!!
    • ​know WHEN/IF AICD fires***
101
Q

IF AICD fires…..

A
  • Stop and assess pt
  • if single shock and asymptomatic
    • ​call and notify MD/Cardiologist/referring phys.
  • if mult shocks or pt symptomatic
    • ​call 911 or start hosp emergency med system

CardioPulmoaryPT1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions