Cardiovascular Disease (exam 1) Flashcards
what is the leading cause of death in US
CVD
CAD
obstruction that doesn’t affect heart function
S&S of CAD
ppl may have no symptoms, depends on level of progression and number of AA involved
what is the #1 site of occlusion in CAD
LAD- left anterior descending, off L coronary A.
- then right coronary A
- then L circumflex (also off L coronary)
4 determinants of myocardial blood flow?
1) resistance- needs to be low
2) diastolic BP- driving push of blood back to system and back to heart
3) vasomotor tone- driven by autonomic control which is triggered by NO relesased by shear forces(but message can’t get accrossed if there are plaque buildups blocking the endothelial cells from being shorn
4) LV end-diastolic pressure- pressure on LV right before it contracts, pressure needs to be good to inc. stretch to inc. force of contraction to get enough blood into coronary AA when it recoils…
An active process involving molecular signals that produce altered cellular behavior as well as endothelial dysfunction and subsequent inflammatory response
translation: injury to vessel wall due to shear stress from lack of stretch, turbulent flow at bifurcations, etc. causes inflamm. response, releases cytokines, macrophages, forms scar tissue in your vessels)
atherosclerosis
atherosis
fatty streak
sclerosis
fibrotic
•Atherogenesis chain of effect
- Endothelial injury with increased infiltration of atherogenic lipoprotein(LDL, VLDL)
- Sub endothelial retention and modification of LDL,VLDL leads to intimal entry of monocytes and T lymphocytes
- Subintimal diffusion of monocytes to macrophage which internalize LDL ,transform into foam cells (First stage of fatty streak development)
- Hemodynamic stress or inflammatory process activate PDGF (platelet derived growth factor – angiogenisis) which will stimulate SMCs ending by having atherosclerotic plaque separated from blood by fibrous cap
- Death of foam cells by necrosis or apoptosis lead to necrotic core formation
- Rupture of fibrous cap, exposure of thrombogenic substrate, subsequent arterial thrombosis
HTN
chronic elevation in BP
what is prehypertension?
120-139/80-89
what is HTN stage 1
140-159/90-99
what is HTN stage 2?
160-179/100-109
what is HTN stage 3?
180-199/110-119
what is HTN stage 4?
> 210/>120
differentiate between primary, secondary and labile HTN?
primary= occurs in absence of disease, arteriole resistance secondary= presence of disease (silent killer) labile= fluctuates
when taking someone’s BP before exercise, when should u get medical clearance first?
when its >200 systolic or >105 diastolic
at what BP should u terminate exercise?
> 250 systolic or >115 diastolic
OR
anytime there is a drop of 20 mmHG of systolic or an increase of 10mmHG of diastolic during exercise.
exercise script for HTN pt
4-7x/week for 30-45 mins at 60-85% max HR (use RPE)
Ischemic heart disease: S&S for men
radiating pain (jaw or L side) crushing pain elephant on chest difficulty breathing sweating skin color changes
IHD: S&S for women
indigestion LV dysfunciton arrythmia (Vtach or Vflutter) syncope silent, no symps
precipitating factors of IHD
cold, exertion, anxiety, heavy meal, tachycardia, hypoglycemia
relief of IHD symps
rest, nitroglycerin
stable angina
inadequate blood supply to myocardium based on increased demand: chest pain, managed with ceasing the aggrivating activity and taking nitroglycerin
how long does it take for NTG to kick in?
5-15 mins
when is angina considered “stable”
well controlled and unchanged for 60 days
unstable angina
inadequate blood supply to myocardium regardless of demand. angina at rest, change in “stable angina” (occurs at lower exertion), drop in HR or BP with usual exercise
Prinzmental Angina
smooth mm spasms and occluded coronary AA causing ischemia and chest pain
when does Prinzmental angina occur?
exculsively AT REST
what causes Prinzmental angina?
inc. coronary vasomotor tone
tx for Prinzmental angina?
nitrates, Ca Channel Blockers,
what meds are AVOIDED with Prinzmental angina?
beta blockers- alpha andrenergic activty causes worsening vasoconstriction
what street drugs causes Prinzmental angina ?
cocaine
what is required for a diagnosis of MI?
evidence of myocyte death as consequence of prolonged ishechemia
types of MI
transmural
non-transmural
transmural- full thickness MI
non-transmural (subendocardial)- partial thickness
MI classification: STEMI
ST elevation MI:
>2mm in leads V1,V2,V3
>1 mm in all other leads
the more leads with ST elevation the greater the MI
indicated occulsion of large vessel and large area at risk
tx of STEMI
EMERGENCY- immediate clot busters and or cardiac cath!
NSTEMI
S&S but no findings on EKG
may be smaller vessel or w/o total occlusion
what therapeutic intervention has the most potency for cardioprotective effects?
aerobic exercise
Name the occluded Artery:
inferior heart
EKG shows leads II, III, and AVf
Right coronary
Name the occluded Artery:
anterioseptal heart
EKG shows leads V1-V3
LAD
Name the occluded Artery:
anterior heart
EKG shows V2-V4
LAD some more
Name the occluded Artery:
lateral heart
EKG shows: I, aVL, V5,V6
LAD or circuflex
Name the occluded Artery:
posterior heart
EKG shows: V1-V2, tall broad initial R wave, ST depression, tall upright T wave
posterior descending
what leads detect LAD only
, V1-V3 or V2-V4
what leads detect a posterior descending MI?
V1-V2, and will have tall broad R wave (like tall broad robert burone who’s always standing in the posterior) will have ST depression (bc he’s always depressed) and will have a tall upright T wave, like how he stands when he finally marries Amy.
What leads detect LAD or circumflex?
LL 1, aVL, V5,V6
What leads detect R coronary A. MI?
aVF, II,III
Cardiac markers:
when does Ck-total MB come onset?
3-4 hours
when does CK-total MB peak
33 hours
when does CK-total MB leave?
3 days
when do troponins show up?
3-12 hours (1/2 day)
when do troponins peak?
18-24 hours (1 day)
when do troponins leave?
up to 10 days
when does myoglobin (kristin) show up?
1-4 hours (comes early, leaves earliest)
when does myoglobin peak?
3-15 hours
when does LDH show up?
12-24 hours (like LVH, always latest) (1 day)
when does LDH peak?
72 hours (at the conference, she was at her peak for 3 days! ) (3 days)
when does LDH leave?
5-14 days (like our trip with LVH) (2 weeks)
what 2 things determine oxygen consumption?
cardiac output
AVO2 difference
what are the rate limiting factors for o2 consumption?
periphery in healthy ppl
CV system for diseased ppl
how does exercise training affect o2 consumption?
increase in SV and in relaxation recoil gives more blood to cardiac mm tissue, improving perfusion
VO2= (HR*SV)(AO2-VO2)
peak VO2 in healthy vs. CAD pts
healthy= 35-70 ml/kg/min CAD= < 20 ml/kg/min
what causes the difference in VO2s for diseased pts?
O2 delivery, usually uptake at the tissues is still unaffected and not the problem. (O2 delivery impaired bc of damage to the heart by MI resulting in dec. EF,SV and diastolic filling)
what is abnormal HR recovery after exercise?
<22 bpm at 2 mins of SUPINE recovery
what do beta blockers do?
inhibit sympathetic stimulation
when do u use Ca channel blockers?
when beta blockers are not affective
what do Ca channel blockers do?
block Ca from being able to bind to its receptors and stopping the mm contraction from occuring so that the heart rate has to stay lower or the blood vessels have to stay dilated.
what medication improves LV fxn?
ACE inhibitors
what do statins do?
decrease production of cholesterol in the liver and have anti-inflammatory effects.
phases of cardiac rehab
I- ambulation for ADLS and home mobility only
II- exercise and risk reduction
III- maintence
Cardiac Muscle dysfunction results from what?
from abnormality of structure or function, not from atherosclerosis
what is the number one cause of CMD?
MI–>scar tissue decreases the heart’s ability to stretch and so SV and EF decrease
also caused by coronary atery spasm and thrombotic occlusion
CMD is the number one cause of what?
CHF
S&S of CMD as it leads to CHF
angina-worse with exercise
arrhythmias and conduction problems
EF= 30-40%, (norm is 60-70%)
inc. HR to maintain Q
MI
HTN
Myocardium stiffens
LV weakens and dilates (valves too=regurgitation)
pulmonary edema–>R vent has to work harder so it hypertrophies
renal insufficiency as inc. fluid overwhelms kidneys
what causes ischemic and nonischemic cardiomyopathies?
ischemic= from MI non-ischemic= from probs with the actual heart mm
hypertrophic cardiomyopathy
inherited gene mutations
autosomal dominant
onset at ages 10-25
LV hypertrophy and dec. cavity size= dec. SV
poor heart relaxation= poor myocardial profusion
restrictive cardiomyopathy
stiffening of cardiac walls due to infiltration by abnormal tissues
worst prognosis
diastolic dysfunction
types of restrictive cardiomyopathy
amyloidosis- abnormal protein fibers (amyloids)
sarcoidosis: inflammatory disease that causes abnormal lumps to form in organs (usually lungs)
heochomatosis: iron overload, usually genetic
S&S of CHF
cardiac silhouette fluid in lungs EF >30% cold, pale, cyanotic extremities increased symp. activity in attempt to compensate for poor perfusion S3 heart sound peripheral edema ( gaining >3lbs/day) quick shallow breathing and dyspnea ascites crackles/rales (heard with inspiration) Jugular Vein Distention paroxysmal nocturnal dyspnea and orthopnea
what is the hallmark sign of CHF?
S3 heart sound
New York Heart Association Classifications
Class I: cardiac disease dx w/o limitation
Class 2: cardiac disease dx w/ slight limitation
-PA results in fatigue, dyspnea, palpatation, angina
Class 3: cardiac disease dx with marked limitation
-ok at rest but less than ordinary activities cause symps
Class 4:cardiac disease dx with inability to perform any PA w/o discomfort
- symps felt at rest, PA intensifies symps
what happens to your renal system with CHF?
water retention due to decreased Q= oligouria (low output of urine) - treat with diuretics
what is the MAX amount of nitroglycerin a person can take before u have to call 911?
3 tablets, each= 5 min apart, if that doesn’t work u can’t take another and u should call 911!
ppl with CHF cannot have what meds?
NSAIDS- periph. vasoconstriction, inc. Na retention
Ca channel blockers- inc. risk of CV event
antiarrhythmics- will have proarrhythmic effects
devices for CHF
ICD for EF <35%
LVAD= bridge to transplant
intraaortic balloon pump- inflates during diastole, improves myocardial blood flow
PT program for inpts with CHF
30 mins, 3-5x/week, 2-4 weeks, 50-70% MHR
walking, ADLS, breathing exercises
assess thoroughly: auscultate lungs, 6MWT, RR, breathing patterns, O2 sat.
home health CHF program
walking, cycle ergometry
20-60 mins, 3-7 days/week, 2-6 mo. 50-80% MHR
rehab center CHF pt
20-60 mins, 3-7 days/week, months to years, 40-90% MHR
strength: 10 reps, 2-4 mo. 60-80% 1RM
what does RR get to in order to stop exercise
> 40 breaths/min
what do blocked or incompetent valves lead to?
ventricular hypertrophy
What is pericardial effusion?
fluid in the pericardial sac, does not allow heart mm to stretch and fill as much as it needs to= diastolic dysfunction
SCI and CV function
disconnect between CV system and SNS control
