1/182
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Coronary Artery Disease effects
Perfusion
Coronary Artery Disease Perfusion results in
O2 demand higher than supply
CAD defined
blood vessel disorder, generalized as atherosclerosis
atherosclerosis
hardening of the arteries
atheroma
fatty deposits in the coronary arteries (CAD)
CAD patho
caused by atherscleosis mostly
characterized by lipid deposits within intima of artery
endothelial injury and inflammation
Stages of Atherosclerosis
chronic endothelial injury
fatty streak
fibrious plaque
complicated lesion
C reactive Protein
marker of inflammation
increased in CAD patients
chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholestrol
Collateral Circulation
arterial anastomoses within coronary circulation
non modifiable risk factors for CAD
age
gender
ethnicity
family history
genetic predisposition
Modifiable risk factors
elevated serum lipids
cholestrol, triglycerdes, HDL, LDL
Hypertension
tobacco use
physical inactivity
diabetes
Obesity
substance use
homocystine
Nursing care of CAD
identify high risk people and manage modifiable risk factors
lifestyle changes with realistic goals
physical fitness
nutritional therapy
Lipid lowering drug therapy- CAD
fibric acid derivatives - lopid
bile acid sequestrates - welchol
eztemibe- zetia
Fibric Acid Derivatives ( Lopid )
decrease triglycerides and increase HDLS
gi side effects
Bile Acid Sequestrates (welchol )
increase conversion of cholestrol to bile acids
gi side effects- bind with other drugs
Ezetimibe ( Zetia)
Decrease absorption of dietary and biliary cholesterol
Antiplatelet therapy for CAD
ASA- reduce risk of blood clots
Clopidogrel- reduce risk of blood clots
gerontologic considerations for CAD
more older adults have CAD
treat hypertension and lipids
smoking cessation
Guidelines for Geratric with CAD
longer warmup
longer periods of low level activity
longer rest periods
avoid extreme temperatures
30 minutes a day
Chronic Stable Angina
a progressive disease where O2 demand is greater than supply leading to myocardial ischemia
occurs when arteries are blocked 70% or more
patho of CAD Angina
lack of oxygen and glucose leads to anaerobic metabolism
lactic acid- irrirates nerve fibers- leading to pain in cardiac nerves
refered pain from transmission to the upper thoracic posterior nerve roots
Anaerobic metabolism
creates energy by burning carbs in absence of oxygen. occurs when lungs cant put enough oxygen in bloodstream to keep up with demands of muscles for energy
Clinical Manifestations of CAD angina Pain
pressure/ ache
squeezing, heavy, choking, or suffocating sensation
rarely sharp
indigestion or burning
Clinical manifestations of Chronic stable Angina
5-15 minute duration
ST segment depression / T wave inversion
subsides when precipitating factor resolved
Predictable and controlled with meds
silent Ischemia
occurs in absence of any subjective symptoms
assocatied with diabetic neuropathy
confirmed by ECG changes
nocturnal angina
occurs at night
angina Decubitus
chest pain when lying down
relived by sitting or standing
Prinzmetals variant angina
occurs at rest in response to a spasm of a major coronary artery
seen in patients with history of migranes or raynauds
spasms cause
increased levels of certain substances, narrowed blood vessels from medications, or exposure to cold weather
Prinzmetals variant angina treatment
moderate exercise
SL NTG
CCB
stop coke use
Microvascular Angina
chest pain occurs in absence of significant coronary atherosclerosis or coronary spasms
Myocardial ischemia associated with abnormalities of the coronary microcirculation
coronary Microvascular Disease affects small distal coronary arteries
Chronic Stable Angina care
goal is to lower O2 demand and/ or higher O2 supply
short acting nitrates
Short Acting Nitrates education
dilate peripheral and coronary blood vessels
if no relief in 5 mins call EMS
repeat every 5 min max 3 dose
can use prophylactically
Chronic stable Angina meds
aspirin
SL NTG
causes headache and orthostatic hypotension
long acting nitrates
Chronic stable angina meds ( cont)
ACE inhibitors- lisinopril
Beta blockers- Metopolol
CCBS- Amlodipine
Sodium Current Inhibitor- Ranolazine
Chronic Stable Angina Diagnostic Studies
chest X ray
labs
12 lead ECG
calcium score screening heart scan
echocardiogram
exercise stress test
pharmacologic nuclear imaging
Blood pressure
pressure exerted by blood on arterial walls
Systolic BP
peak pressure against arteries during ventricular contraction
normal is less than 120 mm hg
Diastolic BP
residual pressure in arteries during ventricular relaxation
normal = less than 80 mm Hg
Systemic Vascular Resistance SVR
force opposing movement of blood
bp =
CO x SVR
Orthostatic Hypotension BP Measurement
BP and HR after laying for 5 minutes
measure BP and HR at 1 minute and 3 minutes of position change
abnormal orthostatic hypotension measurement
SBP decreased 20 mm Hg or more
DBP decreased 10 mm Hg or more
HR increased 20 bpm or more
Reportedly lightheaded or dizzy
Pulse Pressure
difference between SBP and DBP
1/3 of SBP
MAP - Mean Arterial Pressure
average pressure within arterial system that is felt by organs in body
greater than 60 mm hg needed to perfuse vital organs
Metabolic Syndrome
increase risk of heart disease, stroke, diabetes
increased BP
high blood sugar
Excess body fat around waist
abnormal cholestrol or triglycerides
apple or pear shape
hypertension complications
CAD
atherosclerosis
HF
Peripheral vascular disease
atherosclerosis leads to PVD
Kidney
nephrosclerosis leads to CKD
eyes
retinal damage
hypertensive emergency
over hours or days
bp over 180/110 with target organ disease
hypertensive urgency
occurs over days to weeks
bp over 180/110 with no evidence of target organ disease
Clinical Manifestations and Complications of Hypertensive crisis
stroke
retinopathy
hypertensive encephalopathy
renal insufficency
cardiac decomposition
aortic dissection
Hospitalization plan for HTN emergency
IV drug therapy to titrate to MAP
monitor cardiac and renal
neurological checks
education
Questions to ask for HPI of HTN emergency
neurologic symptoms
Headache
n/v
visual disturbances
dyspnea, orthopnea, cough, fatigue,
meds and social history
sudden onset of severe headache suggests
subarachnoid hemorrhage
rapid onset of radiating pain in chest or back may suggest
aortic dissection
dyspnea, orthopnea, cough, fatigue can suggest
cardiac decompensation ( pulmonary edema)
cardiac assessment for HTN emergency
assess for murmurs and gallops
assess for HF signs
chest pain
lung assessment for hypertensive emergency
assess for evidence of pulmonary edema
wheezes
crackles, rales
cough
dyspnea
abdominal assessment for HTN emergency
bruits
abdominal aortic aneurysm
auscultate for murmur - aortic dissection
bruits suggests
renal artery stenosis
neuro assessment for HTN emergency
A and O x4
BEFAST- stroke
unequal pulses suggest
aortic dissection
imaging and diagnostics for HTN emergency
chest x ray
chest ct or mri
tee
When would the Chest x ray be used
signs of left ventricular failure
when would chest ct or mri be indicated
patients with unequal pulses or widened mediastinum on Chest x ray
looking for dissecting aortic aneurysm
When would a TEE be indicated
patients presenting with pulmonary edema
Peripheral artery disease
thickened artery walls leading to degeneration of arteries, oxygen going to tissue
PAD risks
smoking
family history of premature MI or strokes
over 50
overweight
inactive
Dm
HTN
high cholesterol
PAD mainfestations
intermittent claudication
paresthesia
butt pain
pallor
skin temp changes
sores
PAD causes
reduced blood flow to limbs and pain at rest
PAD reduced blood flow to limb signs
thin, shiny, taut skin
loss of hair on LL
dimished pedal pulses
pallor with elevation
feel better putting legs down fter they were elevated
PAD pain at rest signs
occurs in the foot or toes
aggravated by limb elevation
occurs from insufficent blood flow
occurs more at night
often relieved by gravity
PAD complications
atrophy of skin and underlying muscles
delayed healing
wound infection
tissue necrosis
arterial ulcers
diagnosing PAD
ankle Brachial Index
ultrasound doppler test
angiogram
treatment of PAD
bp control - reduce sodium
tobacco cessation
lower HgbA1C
diet and statins
ace inhibitors
Invasive interventions for PAD
angioplasty and stents
atherectomy
Surgical interventions for PAD
peripheral artery bypass
PVD
inadequate return of venous blood from legs to heart
PVD symptoms
tired and heavy and achy leg cramps
pain worsens with standing
pain improves with leg elevation and activity
brown leathery skin
flaking and itching
skin is hard and thick
stasis ulcers
PVD education
exercise improves oxygen extraction in leg
walking is the best choice of exercise
lower bmi
decrease waist circumfrince
diet healthy
stop smoking
dont sit or stand too long
compression socks
PVD foot care education
daily feet inspection
comfortable shoes
show how to check skin temp, cap refill and palpate the pulses
PVD Cause
damage to valves letting blood lead backwards
due to age, extended sitting, standing, reduced movement
Diagnosis of PVD
vascular ultrasound
Cardiomyopathies
disease of heart muscle, not letting heart pump blood correctly, can cause someone to have HF
types of cardiomyopathies
hypertrophic
dilated
Restrictive
cardiomyopathy diagnosed through
TEE
Dilated Cardiomyopathy
pumping dysfunction- mostly left ventricle chamber enlargment
age 30-60 , most common in black male
Ischemic dilated cardiomyopathy
CAD
MI
non ischemic dilated cardiomyopathy
genetic disorder- autosomal dominant - duchenne muscular dystrophy
structural heart
alcohol
drugs
endocrine
immune issues
Evaluation of Dilated cardiomyopathy
echocardiogram
ecg
stress test
labs
cardiac biopsy
troponin and BNP
Treatment of Dilated Cardiomyopathy
ace or arbs
nitrates- preload
diuretics- preload
beta blockers
treat underlying issue
implantable cardioverter defibrillator
LVAD - no pulse or cardiac transplant
Hypertrophic Cardiomyopathy
commonly inherited and caused by mutations in genes
complications like syncope, HF, death
clinical manifestations of hypertrophic cardiomyopathy
Family history
asymptomatic
if any symptoms- chest pain, dyspnea, syncope, palpatiations
sx - systolic murmur
testing for hypertrophic myopathy
ekg
tee
cardiac mri
genetic testing
troponin and BNP
treatment of hypertrophic myopathy
improve ventricle filling
no hard sports
beta blockers, ccb if intolerant to BB
cardizem for those who cant tolerate CCB
implantable cardioverter device
permanent pacemaker
septal ablation
heart transplant
Restrictive cardiomyopathy
heart muscle characterized by impaired ventricular filling with typically persevered systolic function and normal increased ventricular wall thickness
evaluation of restrictive cardiomyopathy
s/s of adv HF
look for History of radiation tx, chemo
echo
cardiac cath
cardiac biopsy
genetic testing
Management of restrictive cardiomyopathy
improve diastolic filling
diuretics or aldosterone antagonisys
permanent pacer for AV blocks
Amyloidosis
cardiac transplant
implantable cardioverter- defibrillator
Takotsubo - broken heart syndrome
secondary to extreme stress and mimics heart attack
acts like acute coronary syndrome
left ventricular balloning
EF reduced, but can recover
symptoms of broken heart syndrome
acute chest pain with ST elevations
testing for broken heart syndrome
ekg
cardiac markers- troponin and bnp
coronary angiography
echocardiogram