Cardiac Exam 1 Flashcards
Acute Coronary Syndrome
- stable angina
- unstable angina
- non-ST elevation (NSTEMI)
- ST elevation (STEMI)
ACS patho
begins with rupture / erosion of plaque
-thrombus progresses and occludes blood flow
stable angina
chest pain that occurs with physical activity but is RELIEVED WITH REST / MEDS (nitroglycerin)
unstable angina
chest pain that occurs at rest NOT RELIEVED WITH REST OR MEDS
-scary kind!! could mean MI
prinzmetal’s angina
type of unstable angina , due to coronary artery spasm
-occurs at night
ACS non-modifiable risk
male
postmenopausal female
family hx
ACS modifiable risk
smoking
obesity
high fat diet
sedentary lifestyle
HTN
type II DM
MI occurence
normally happen in the morning, BP is highest and blood most viscous
ACS meds
- OXYGEN!!!
- nitro
- beta blockers
- CCB
- antiplatelets
- antithrombins
- morphine
- ACE inhibitors
MI modifiable risk
smoking
high LDL
type II DM
obesity
HTN
MI nonmodifiable risk
male
postmenopausal female
family hx
MI s/s
ches pain
L shoulder / arm pain
tooth / jaw pain
n/v
sweating
fatigue
SOB
upper back pain
MI female s/s
achiness in arms (elbows)
fatigue
SOB
indigestion
n/v
stress level
MI questions
- how long have symptoms occurred
- chest pain , location , scale 1-10
- n/v
- surgical hx
- family hx
- smoking
- meds
MI assessment
neuro assessment
skin assessment
respiratory assessment
vitals
pulses
heart sounds
MI tests
- Oxygen !!
- 12 lead EKG
- CXR
- ABGs
- CBC
- CMP
- lipid panel
- cardiac enzymes
- coag studies
IV access
cardiac enzymes
- myoglobin
- creatinine kinase
- troponin I and T
coag studies
PT / PTT
international normalized ratio
STEMI
ST elevation indicating one or more vessels are blocked
NSTEMI
ST depression , only partial occlusion of vessel
MI MONA
morphine
oxygen
nitroglycerin
aspirin
MI meds
- O2
- MONA
- betal blockers
- heparin drip
MI cardiac enzymes
will show elevation
MI lipids
elevated , most MI are secondary to atherosclerosis
MI therapy
tPA (fibrinolytic therapy)
PCI
tPA
-symptoms must be present for < 12 hours
-not effective on NSTEMI
MI PCI
cardiac cath , uses balloon to open lumen of blocked artery
-radial artery preferred
-2-6 hours heal time
door to balloon time
90 MINUTES
MI coronary artery stent
wire mesh is placed to prevent blocked artery from renarrowing
MI home meds
aspirin
plavix
lisinopril
metoprolol
atorvastatin
nitroglygerin
stool softener
MI education
follow up w/ cardiologist
med education
cardiac rehab
MI s/s
low cholesterol diet
high fiber diet
healthy weight
CABG
alternative MI tx , major surgery
-bypass blockages of coronary arteries
-unsuccessful PCI or 3 vessel disease
CABG complication
bleeding
dysrhythmias
MI
stoke
nonunion of sternum
sternal infection
renal failure
HF
post CABG assessment
monitor HR and BP continuously
hemodynamic monitor
cardiac monitor
s/s of infection
assess heart tones
core temp hourly
intake / output
pulses, skin , cap refill
chest tube
H and H
electrolytes
BUN / creatinine
Valvular heart disease
- stenosis
- regurgitation
- prolapse
valvular stenosis
stiffening / thickening of valve , caused by calcium deposits or scarring
valvular regurgitation
blood flows or leaks backwards because of incomplete closing of valves
valvular prolapse
valves bulge backwards and do not close
-normally not tx unless needed
valvular disease risk
- infective endocarditis
- STREP INFECTIONS
- CAD
- MI
- HF
- congenital defect
- cardiomyopathy
- older age
- pregnancy
valvular disease s/s
- MURMUR (systolic or diastolic )
- dyspnea
- SOB
- orthopnea
- dizziness
- palpitations
- weight gain
- decrease physical activity ability
- palpitations
- crackles
- angina
valvular disease questions
- medical hx
- smoke / drink / illicit drugs
- meds
- family hx
- social hx
valvular disease drugs
most seen with COCAINE USE
valvular disease assessment
vitals
pain assessment
breath sounds
heart sounds
vascular assessment
activity tolerance
valvular disease test
EKG
CBC
CXR
CMP
cardiac enzymes
TEE
valvular disease meds
beta blockers
ACE inhibitors
ARBS
anticoagulants
nitroglycerin
valvular disease education
- medication
- low sodium / caffeine
- s/s of HF
- daily weights
- bleeding precautions
- follow up
-prophylactic ABX for dental procedures
daily weight education
use same scale and check at same time everyday
carotid artery disease
wall thickening , plaque formation , progressive narrowing of carotid artery
-no s/s until almost completely occluded
carotid artery disease modifiable risk
smoking
HTN
DM
dyslipidemia
sedentary lifestyle
obesity
ineffective stress management
carotid artery disease nonmodifiable risk
age
gender
ethnicity
family hx
coronary artery disease pts have high risk of developing ….
carotid artery disease
carotid artery disease s/s
symptoms resembling TIA
weakness
dizziness
loss of coordination
slurred speech
facial droop
vision problems
HA
carotid artery disease test
- carotid duplex ultrasonography
- computed tomography angiogram
- CTA / MRI / MRA
- carotid angiography
- cardiac echo
- heart cath
- EKG
- CBC
- lipid profile
- CMP
carotid artery disease med
- antiplatelets
- antihypertensive
- satins
carotid artery disease BP
needs to be below 140 / 90
carotid artery disease major sign
BRUIT when listening over side of neck
carotid artery disease education
s/s of stroke
medication
lifestyle change
limit alcohol
DASH diet
heart failure
inadequate pumping / filling of heart and cannot meet oxygenation needs of tissues
HF classifications
based off of ejection fraction
left sided HF
weakened contraction –> poor peripheral perfusion
-backflow of blood accumulating fluid in lungs
left sided HF s/s
SOB
orthopnea
fatigue
weight gain
poor color
tachypnea
blood tinged sputum
CRACKLES
S3 , S4 GALLOP
right sided HF
inability of R side of heart to pump blood to pulmonary vasculature
right sided HF s/s
JVD
generalized edema
hepatomegaly
ascites
loss of appetite
n/v
increased abdominal girth
HF primary test
- CXR!!!
- EKG
- CMP
- CBC
- cardiac enzymes
- ABGs
- BNP and NT-pro BNP
BNP
biomarkers elevated due to overstretching of ventricles
lactic acidosis
reduction of blood flow throughout the body
-formed as by-product of ANAEROBIC METABOLISM
-lead to cell death and organ failure
dysrhythmias and HF
these are and adverse effect of HF , a-fib is the MOST COMMON
ischemic cardiomyopathy
secondary to MI
nonischemic cardiomyopathy
dilated cardiomyopathy
hypertrophic cardiomyopathy
restrictive
rapid intubation
- induction agents
-ketamine
-fentanyl
-propofol
-etomidate
-midazolam - neuromuscular blockers
-vecuronium
-succinycholine
cardiomyopathy meds
beta blocker
diruetics
nitroglycerin
heparin drip
morphine
digoxin
digoxin consideration
DO NOT given when HR < 60
shocking joules
120 - 200
post shock meds
atropine
dopamine OR
norepinephrine OR
epinephrine
cardiogenic shock
happens from diminished CO , ventricular dysfunction initiates compensatory mechanisms
-initially stabilize pt but later cause deterioration as O2 demands increase
intra-aortic balloon pump
used to increase myocardial oxygen supply and demand
-used in major occlusion of coronary artery and low ejection fraction
AICD
recommended for pts with < 30% ejection fraction and high risk for lethal dysrhythmias
post cardiogenic shock meds
- beta blockers
- ACE inhibitors
- nitroglycerin
- digoxin
- ARBS
- ARNIs
- inodilators
- vasodilators
- diuretics
cardiomyopathy / HF education
- management
- oxygen use
- rest / pace activity
- fall precaution
- FACES
- daily weight
- no smoking
- reduce sodium
- cardiac rehab
- potassium rich foods
potassium rich foods
banana
orange juice
weight concerns
> 2.5 lbs in a day
5lbs in a week
FACES for HF
fatigue
activity limitation
cough / congestion
edema
SOB
shock
life threatening syndrome occurs when circulatory system is unable to supply O2
aneurysm dissection s/s
chest , back , flank pain
tearing or ripping feeling
sweating
n/v
faintness
tachycardia
pain gets progressively worse
BP can vary from one limb to another
aneurysm questions
- onset of pain
- description of pain
- severity of pain
- pain radiation
- medical hx
- family hx
- peripheral sensation
- smoking
- n/v
- trauma
aneurysm risks
SMOKING
family hx
male
atherosclerosis
HTN
high cholesterol
CAD
genetic disorders : Marfan’s syndrome
aortic dissection
sudden tear in aortic intima creating false lumen where blood can enter aortic wall
aneurysm labs
CBC
lipids
coagulation
cardiac enzymes
EKG
CT abd with contrast
abd US / TEE
aneurysm pre -surgery
blood type and crossmatch
two large IVs
O2
IV fluids
hypovolemic shock
rapid fluid loss resulting in poor circulation volume
-r/t ruptured AAA
hypovolemic shock intervention
prepare for ventilation
cardiac monitor
ABGs
rapid fluid / blood transfusion
hemodynamic monitor
foley
repeat CBC
lactate level
hypovolemic shock meds
dobutamine
dopamine
epinephrine / norepinephrine / phenylepinephrine
vasopressin
distributive shock
result of diseased state such as
-sepsis
-anaphylaxis
anaphylaxis
give EPINEPHRINE
then ANTIHISTAMINE
arterial line
transducer must be in line with midpoint of R atrium
-can give wrong reading if too high or low
obstructive shock
caused by mechanical barrier to ventricular filling / emptying
-tension pneumothorax
-cardiac tamponade
central venous catheter advantage
CVP and ScvO2 monitor
monitor preload
volume resuscitation
frequent blood draws
long term IV abx
parenteral nutrition
transvenous pacemaker insertion
what is done before an arterial line insertion
allen’s test
CVP reading
can indicate low volume states or high volume
hypovolemic shock values
- decreased CO
- decreased CVP
- decreased PCWP / PAOP
- decreased central venous oxygenation
- decreased mixed venous oxygenation
- increased systemic vascular resistance
- decrease MAP
- hypotension and tachycardia
shock interventions
- vitals
- hemodynamic reading
- neuro status
- monitor UO
- skin color and temp
- ABGs
- venous O2 sat
- H and H
- metabolic profile
- lactic acid
- IV fluids
anaerobic metabolism
cells use anaerobic (without O2) pathway to produce energy
-blood is more acidic
-leads to cell death
ARDS
leading cause of sepsis
sepsis
life-threatening organ dysfunction caused by a deregulated host response to infection
septic shock
occurs when circulatory and metabolic abnormalities are profound
sepsis and septic shock complications
MODS and DIC
DIC
widespread clotting
MODS
involves two or more organ systems not working
-initial organ is typically the lungs
-GI / hepatic / renal follow
sepsis tx
treat underlying cause ( IV abx)
maximize O2
IV fluids
blood products
DIC diagnosis
based off of clinical picture of cyanosis and ischemia plus labs
DIC tx
treat underlying cause
maximize O2
volume replacement
-NS
-blood
-plasma
-FFP
-replacement clotting factors
swan catheter
measures L heart preload or amount
-can also draw venous oxygen samples
CVP low
hypovolemia
peripheral vasodilation
CVP low tx
fluid bolus
vasopresser
CVP high
R heart failure
tension pneumothorax
HTN
pericardial tamponade
CVP high tx
inotropic or vasodilator therapy
PA high
pulmonary hypertension
R sided HF
PA high tx
inotropic and vasodilator
diuretics
Pulmonary capillary wedge pressure (PCWP)
high :
-HTN
-cardiogenic shock
-hypoxia
-ARDS
PCWP high tx
inotropic and vasodilator therapy
diuretics
low CO
MI , all shock forms
-except early septic shock
low CO tx
fluid bolus
inotropic therapy
treat MI cause
CO high
septic shock (early)
hypervolemia
hyperthermia
CO high tx
only if concerned
systemic vascular resistance (SVR) low
vasodilation
-distributive shock (anaphylaxis and sepsis)
SVR low tx
fluid bolus
vasopressors
tx underlying cause
SVR high
vasoconstriction
-hypovolemia
-hypotension
-cardiogenic shock
SVR high tx
vasodilators
pulmonary vascular resistance high
HTN
PVR high tx
vasodilators
mixed venous O2 low
increased oxygen needs of tissue
low CO
low hemoglobin
low O2
SvO2 low tx
increase CO
increase oxygenation
increase hemoglobin
lactate level
increased lactate and negative base are evidence of poor perfusion and cellular level
sepsis bundle of care
- measure lactate
- obtain blood culture
- administer abx
- administer NS
- administer vasopressors if BP unresponsive after fluids
v-tach
pulseless = shock
pulse = cardioversion
v-fib
always shock , start CPR without pads
cannot feel pulse in carotid
feel for femoral pulse
R heart cath
go into vein , looking at R heart pressure
-valve disorders, ejection fraction
L heart cath
femoral or radial entrance
-MI or angioplasty
cardiogenic shock
forms from high wedge pressure
ARDS cannot happen without….
acute respiratory failure because it creates scar tissue
pts with this HF are at high risk for blood clots
R sided HF
R and L sided HF
both create extra strain can go into v-fib
-VERY COMMON
