CV Conditions: Ischemic Cond's: Exam 1 Flashcards
Ischemic cond’s or
lack of O2
Leading cause of death====
Heart Disease!!!
Myocardial perfusion involves which aa’s
CA’s
L and R branch off of aorta
Basic rules of hemodynamics
2
same is true for CAs!!!
- 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
Determinants of CA blood flow:
Myocardial perfusion occurs primarily during pds of _______________
myocardial relaxation
Diastole
Determinants of CA blood flow:
Vasomotor tone (ability to vasodilate) of CAs allows for what?
vol. of blood to enter CAs during Diastole
when they are relaxed
Determinants of CA blood flow:
O2 attaches to myoglobin to be released as needed during _________
Systole
Determinants of CA blood flow:
CA perfusion and O2 cont’s to be delivered during __________
Systole
as long as pressure is LOW enough
remember HIGH pressure during Diastole and goes to LOW pressure (systole)
2 Factors that DECREASE myocardial perfusion
- Elevated DBP—-bigger issue vs. SBP
- CA atherosclerosis OR resist. to CA blood flow
If the R CA gives NO blood flow to heart=====
Dysrhythmias
If L CA no blood flow to heart====
Heart failure
Rt. CA supplies:
SA node
R atrium
Post and Inf surf vents
AV node in 80% pop.
L CA supplies:
Sternocostal surf (ant myocardium) BOTH vents
L atrium
L vent
Septum
Anatomy of CA’s
Inner layer
whats here?
Intima
These are MOST likely to accumulate in the Intima (inner layer of CAs)
Lipopro’s and fibrinogen
*this creates hardening
MODIFIABLE RISK FACTORS CARDIAC DIS.
- smoking
- high BP (>140/90)
- High CHO lvls
- phys inactivity
- obesity
- BMI >/= 30 kg/m2
- normal== <25
- stress/Type A
- metabolic syndrome
MODIFIABLE RISK FACTORS CARDIAC DIS.
Talk more about High blood CHO lvls ….
- 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
NON MODIFIABLE RISK FACTORS CARDIAC DIS.
Heredity
sex
female post menopause
age
T2D
Risk factors Cardiac Disease
Emerging risk factors
- LipoPRO A
- LDL subclasses
- Oxidized LDL
- Homocysteine
- Hematological factors
- Inflamm markers
- C-reactive PRO=== high stress
- infective agents
- C. pneumoniae
- alcohol
Clinical Dx from Worse to WORST
- CAD
- angina
- acute coronary syndrome (ACS) or MI
- cardiac mm dysf
- Sudden cardiac death
- Other atherosclerotic dis’s
- PAD
- Renal athero –> renal HTN
- Aortic athero–> aortic aneurysms
- Ischemic and Hemorrhagic CVA
- CAD or
Atherosclerosis
- progress. hardening/narrow of coronary, cerebral, renal, aortic and periph aa’s
***atherosclerotic plaques composed of lipid, fibrin and thrombus
CAD
2 step process:
remember this is CHRONIC athero=== long term buildup, slow w/ sx’s
-
Atherosis
- fatty streak of lipid laden macrophages causes endothel damage/exposure of endothelium
-
Sclerosis
- “fibrous cap” of thrombi and platelets over advanced plaques dev. on endothelial lining
When CAD progresses enough
Total occlusion of aa by thrombus
MI from tot. occlusion
ACUTE— blockage BUT clot lodges
MI
Full occlusion
CAD Medical mgmt
Dx testss
ECHO
Cornoary angio
Ex/pharma stress test
CT
CAD medical mgmt
Meds
Statins
Antithrombotic/Antiplatelets
CAD
PT intervents
- ASCM:
- Aerobic end training @ least 2d/wk @ >/= 50% VO2max for >= 10mins
- decs athero build up
- Aerobic end training @ least 2d/wk @ >/= 50% VO2max for >= 10mins
- EX has been proven more effective than ANY med @ preventing and slowing progress of CAD****
Angina
- “strangling”
- sub-sternal pressure
- Some imbalance in supply and demand of myocardial O2
NOTE: Angina and Myocardial O2 consumption
supply/demand problem
Rate Pressure Product RPP== HR*SBP
Typical Cardiac Pain Referrals
visceral or somatic pain referrals bc heart has NO pain receptors—-so that’s why “referred” pain
see pics
Atypical Cardiac Pain Referrals
More likely Female
- Can also include:
- breathlessness
- R bicep pain
- acid reflux
- tongue pain
Angina== imbalance in Supply and Demand
what does that mean?
Demand > Supply of O2
Stages of Stable Angina
see pics
Stable Angina
stage 1
initial percept of discomfort
stable angina
stage 2
INC in int. of lvl 1 OR radiation of pain to other areas (jaw, throat, shoulders, arms, other)
Stable angina
stage 3
Relief only obtained through cessation of activity
***when demand is relieved**
stable angina
Stage 4
Infarction pain
6 types of Angina
- Chronic/Stable or Classic or Exertional
- Prinzmental or Vasospastic or Variant
- Nocturnal
- *Post-Infarction
- Metabolic or Diabetic or Macrovascular
- Unstable
Chronic Stable/Classic/Exertional Angina
onset @ specific MET lvl when supply no longer meets demand
when you cease activity===GONE
Prinzmental or Vasospastic or Variant Angina
CA vasospasms
same time everyday
restricts supply O2
Nocturnal Angina
during sleep
supply does NOT meet new INCd demand due to INC SNS activation or INCd Preload in Supine