Standard GXT
- research or rx
- theraputic indications
- no EKG monitoring
- Ventilatory gasses
Diagnostic GXT
- EKG monitoring
- BP/HR monitoring
- used for diagnostic/prognostic
- ventilatory gasses in presence of HF
magnitude of ischemia due to lesion directly proportional to
- st segment depression
- # of EKG leads associated w st segment depression
- duration of st segment depression
magnitude of ischemia due to lesion is indirectly proportional to
- st slope
- RPP at which st segment depression occurs
- HR max, SBP, METs achieved
GXT post MI
- prognostic
- ex rx
- evaluation of medical therapy or surgical interventions
- submax testing rec after discharge
- 4-6d after acute MI
- cant do it w/o revascularization
- fx capacity <5Mets
Functional Testing
- PA counceling
- EXrx
- Disability assessmet
- estimate prognosis
- return to work eval
MET increase VS all cause mortality
1 MET increase = 1.3% decrease in all cause mortality
how much weight do treadmills hold
350
which protocol is more accurate in estimation of ex capacity and ventilator threshold
ramp
proper ECG monitoring
- skin prep
- LEAD PLACEMENT
- continuous monitoring
Echo is good for
- aortic stenosis
- low cardiac output
- milld mitral stenosis resulting symptoms
- severe aortic insuffieciency or mitral regurgitation
Risk of complication hospital admission, acute mi, sudden cardiac death
-hospital admission <0.01 %
CVD meds that don’t really affect ex
- ARBs
- ACE inhibitors
- Dieuretics
- Anticoagulants
- antiplatelet
- lipid lowering meds
CVD meds that will affect ex
- Beta blockers
- Calcium channel blockers
Beta blocker response w ex
-Blunted HR and BP response to ex
-faulty HR and BP
-OLOL
(selective or non selective)
Calcium channel blockers
- lower HR
- used when changing electrical
- DIPINE
ACE Inhibitors
- work through kidneys not heart
- PRIL
ARBs
- do NOT get ACE cough
- block all actions of angiotensin 2
- SARTAN
Dieuretics
- lasix is most common
- usually first med prescribed
Anticoagulants
-heparin used in hospital
Antiplatelet
- dont effect ex rx
- less sticky
- easier for blood to flow
Lipid lowering drugs
- statins
- anyone at risk or might be at risk should be on one
- might feel sore/cramps
Know table a1
put in here
common CVD
- HTN
- CAD
- PAD
- atherosclerotic arterial disease
- acute coronary syndromes
- cerebrovascular disease/stroke
- MI
- myocardial ischemia
where does CAD occur
tunica intima
how many deaths per year bc of HTN
9.4 mil
how many deaths per year cvd
17.3 million
howm many deaths expected bc of cvd by 2030
23.3 million
plaque progression has to deal with…
lipoproteins
CVD risk factors
- dislipedemia
- smoking
- HTN
- DM
- sedentary
- age
- male
- family hx
Common cholesterol meds
- bile acid sequestriants
- fibric acid sequestriants
- statins
- nicotinic acid
- cholesterol absorption inhibitor
Acute coronary syndomes
- > 90% due to plaque rupture and thrombus formation
- thrombus leads to severe or complete occlusion
Table 7.3
put in first 2
Diagnosis of ACS
- presenting symptoms
- acute EKg abnormalities
- serum marker of necrosis
Treatment of ACS
- rapid initiation is critical
- therapy targets initiating intracoronary thrombus
- reverse ischemia and restore coronary supply and demand to normal
- treatment of STEMI is different than treatment of NSTEMI
- acute treatment may include oxygen therapy morphine and EKG monitoring
Acute medical management of NSTEMI
- anti ischemic therapy
- antithrombotic therapy
Put in basics of table 9.6
put in
how many people suffer from HTN
- 1 bio worldwide
- 60 mil americans
how many people w HTN are unaware
-2/3
HTN risk factors
- age
- gender
- obesity
- diabetes
- race/heredity/genetics
- lifestyle
Classifications of HTN
-normal 160 >100
Consequesnes of HTN
- nosebleeds/headache/dizziness
- flushin
- sweating
- blurred vision
- most are asymptomatic
Organ damage from HTN
- vaasculature
- heart
- cerebrovascular
non medical treatment for HTN
- dec weight
- ex
- diet
- sodium
- potassium
- alcohol
- smoke cess
- relaxation therapy
medical treatment for HTN
- dieuretics
- sympatholytic agents
- peripheral vasodialators
- ACE inhibitors
- ARBs
- antithrombotic/platelet/coagul
- lipid lowering
components of outpatient CR program
- ex rx
- aeorbic
- resistance
- flex
- nm training
FITT for cardiac patient
F- 3 d/wk pref all days
I- RPE 11-16 40-80% VO2
T- warm up/cool down 5-10 Ex 20-60
T- large musc rythmic, resistance
what we use to determine progression for cardiac patients
- px levels
- hr response (remember beta blockers)
- BP response
- RPE
- Err on side of safety
chemicals affecting HR
- epinephrine
- norepinephrine
- acetylcholine
- dopamine
chemicals affectng BP
- caffeine
- norepenipherine
- renin
- aldosterone
- adh
- epinepherine
- acetylcholine
what is HTN
> 140 >90
vo2 factors that negatively affect
- mi
- meds
- asthsma
- chronic kidney disease
- cancer
- hiv/aids
- osteopenia
- obesity
- any disease pathology
measurements we take in GXT
- hr
- rpe
- bp
- dyspnea
- gas measurement
- blood lactate
- ekg
hypokinesis
-low movement
akinetic
no movement
diskenisis
moves wrong way
what is a calcium channel blocker
- impedes calcium to cell
- dec HR
- dec contractility
what is an ACE inhibitor
- controls the bv
- bp dec b.c blocks angiotensin 2 which would have inc bp with symp ns
how does beta blocker work
-no adronergic affect
what does arg do
- block angiotensin 2
- bp will be lower
most important factor to resistance of blood flow
- diameter
- by 1/2 ing resistance increase rest by 16 timesi
positive inotropic affect
affect contractility of heart by increasing
negative chronotropic response
hr decreased (neg affected)
why don’t we like beta blockers
-major effect of ex (difficult to prescribe)
rt sided heart failure
-lung disease
risks of untreated HTN
- mi
- copd
- stroke
- cad
- kidney disease
- retinopathy
- heart failure
how can we tell if angina is result of ischemia
-12 lead ekg st segment
with damage to endothelium what gets into arteries
LDL
risk factors for atherosclerosis
- dislipidemia
- htn
- obesity
- diet
- sedentary lifestyle
- age
- heredity
- smoking