Cardiac Flashcards
Stable Angina
predictable and consistent
pain with exertion
relieved by rest/Nitro/both
Unstable Angina
“preinfarction”
episodes increase in frequency and severity, happens for no reason, may not be relieved by rest and Nitro
Intractable/Refractory Angina
severe and incapacitating, nothing relieves it
Variant (Prinzmetal) Angina
pain at rest due to coronary artery vasospasm
Silent ischemia
objective EKG evidence of ischemia with no CP or other s/s
s/s may accompany angina
anxiety, dyspnea/SOB, dizziness, n/v
leads to collateral development
chronic ischemia, genetics
atypical s/s of myocardial ischemia in these groups
elderly (maybe only dyspnea and fatigue d/t decreased SNS response)
Women (get more GI s/s)
DM (neuropathy)
Three effects of smoking that make it a RF for CAD
increased CO2 decreases oxygenation
Nicotine stimulates catecholamines, which increase HR, BP, and demand on heart
Increased plt aggregation increases risk of thrombus
elevated lipids are a well establish RF of
CAD
cholesterol over 200
TGA over 200
Metabolic syndrome
cluster of metabolic abnormalities that are a major RF for CVD (3 more more) DM obestiy dyslipidemia HTN increased fibrinogen level
4 things that increase injury to arterial endothelium
smoking
HTN
DM
genetics
Coronary arteries are perfused at this time, so…
During diastole when resistance is low
So, and increased HR shortens diastole, which can decrease myocardial perfusion
Need diastolic BP of at least 60 for good perfusion
Coronary arteries
Right CA
Left Main CA-branches into LAD and Circumflex
leading COD in US, all ages and races
CVD
leading cause of CVD
CAD
HR is determined in the heart by
myocardial cells with fastest firing rate
SA node : 60-100
AV node: 40-60 some ppl will show s/s, some not
Ventricular pacemaker sites: 30-40 too slow
PNS influences HR
via vagus nerve
slows HR by affecting SA node
SNS influences HR
increases HR by increasing circulating catecholamines from adrenal gland
HR is controlled by (4)
ANS
CNS
baroreceptors
pacemakers
Specialized nerve cells in aortic and carotid arches that are sensitive to increased BP
Baroreceptors
when stimulated by increased BP they signal the medulla to increase PNS stimulation of heart, which inhibits SA node and inhibits SNS influence, lowering HR and BP
Three factors that affect Stroke Volume
Preload
Afterload
Contractility
Preload
Degree of stretch in ventricular muscle fibers at the end of filling (diastole)
Determined by volume of blood in LV
Frank-Starling Law
As volume of blood returning to heart increases, muscle stretch increases, resulting in a stronger contraction and greater SV
increased stretch=increased degree of shortening
As preload increases, SV increases
UNTIL physiologic limit is reached
Base of heart is at the
top
Apex of heart is at the
bottom
normal SV
70 ml/beat
normal CO
5L/min
atrial and ventricular systole are not simultaneous because
this allows ventricles time to fill passively and receive “atrial kick” prior to ejecting blood
the only veins that carry oxygenated blood
pulmonary veins
apical impulse (PMI) is located
5th intercostal space and left midclavicular line
These valves are open during diastole and close in response to contraction
AV valves:
Tricuspid (Rt)
Mitral (Lft)
These valves open during systole
Pulmonic and Aortic valves
Heart uses the % of O2 delivered
80%, most organs use 25%
If HR rises above this level, increase risk MI due to shortened diastole
100, especially in CAD pt
Two cell types in heart
Electrical–initiate and conduct impulse
Mechanical–contract in response to stimulation
Job of AV node
coordinates incoming impulse from atria and after a slight delay relays impulse to ventricles
Impulse relayed to ventricles from AV node to
Bundle of His (AV bundle) to
Right and Left Bundle Branches, to
Purkinje fibers
Purkinje fibers are specialized to
rapidly conduct impulse through thick wall of ventricles
In Resting state of myocytes, ions distribution
K higher inside cell (— charge)
Na higher outside cell (+++)
Repeated cycle of depolarization and repolarization of cardiac myocytes
Cardiac Action Potential
Depolarization
Na and Ca enter cell, make inside cell more +++
K goes out of cell, makes outside more —
Repolarization
Ions revert to resting state
must be complete before cell can depolarize again correctly (refractory period)
Effective refractory period
cell is completely unresponsive, cannot depolarize early
Relative refractory period
if impulse is stronger than normal, cell may depolarize prematurely
early depolarization of atria cause premature contractions and dysrhythmias
Why is Vfib or Vtach dangerous
not enough time for ventricles to fill properly or eject, blood pools, clots form, decreased perfusion, can lead to asystole
PVC + myocardial ischemia can trigger
Vtach or Vfib
P wave signifies
atrial depolarization
QRS complex signifies
Ventricular depolarization (atrial repolarization is hidden under wave)
T wave signifies
Ventricular repolarization (relaxation and filling)
chamber pressures are measured in
hemodynamic monitoring
Cardiac Output
Volume of blood pumped out of heart in L/min
=SV x HR
to increase preload, you need to
increase blood return to the heart
Afterload
resistance of ejection of blood from the ventricle
As afterload increases, SV
decreases
Contractility
force generated by contracting myocardium; ability of muscle fibers to shorten in response to electrical impulse; related to number and state of myocardial cells
Contractility is increased by
circulating catecholamines
SNS influence
certain meds
Contractility is decreased by
hypoxemia acidosis certain meds (Beta Blockers)
Percentage of End Diastolic Volume ejected with each beat; used as a measure of myocardial contractility and LV function
Ejection Fraction
normal LV: 55%-65%
decreased LV function, heart failure are signified by EF of
less than 40%
s/s of CAD
CP n/v cool extremities diaphoresis xanthelasma
Cholesterol deposits around eyes often seen in CAD patients
xanthelasma
CP is caused by
myocardial ischemia
s/s fo myocardial ischemia besides CP
Dyspnea, exertional dyspnea, PND
weight gain and dependent edema
syncope
fatigue
Goal of angina treatment
Decrease demand on heart and increase O2 supply to heart, reduce other complications
myocardial injury
Reversible–increasing O2 and nutrients can save area, no intervention, area will become necrotic
ST segment elevation on EKG
myocardial ischemia
Still Reversible
ST segment depression on EKG
Myocardial necrosis
Irreversible, dead heart tissue in area of infarct
begins 20-30 min from time of occlusion
Nitroglycerin serves to
vasodilate coronary arteries
decrease O2 consumption by myocardium
store nitro
in dark glass bottle, away from light and moisture
good for 6 months from opening
touching nitro to skin can cause
HA and decreased BP
MI results from
reduced blood flow in a coronary artery, usually d/t both a plaque and a thrombus
Acute Coronary Syndrome includes
Unstable angina and MI (same process at different points on a continuum)
check thyroid tests with CP because
hyperthyroidism can cause CP
CK-MB
Creatine kinase
Enzyme in cardiac cells that is released when they die
no longer evident after 3-4 days
false + by exercise from skeletal muscle
Myoglobin
protein in cardiac cells, short lived and not always elevated
Troponin 1
protein in cardiac cells
Top marker for acute MI, no longer evident after 7 days
Troponin T
protein in cardiac cells
evident for up to 21 days
Beta Blockers overall function
reduce workload of heart
decrease HR and BP, and contractility
improved LV diastolic function
give morphine for acute MI because
helps relax heart and decrease CP
AE of nitroglycerin
HA, decreased BP, decreased HR
Acute MI treatment (
EKG in 10 minutes O2 aspirin nitroglycerin morphine beta blockers ACE inhibitor in 24h blood thinners bed rest stool softeners
These meds decrease risk of re-infarction after MI and increase survival rate after MI
Beta Blockers
why stool softeners after MI
avoid straining, increased pressure can signal baroreceptors to lower BP, cause syncope
Prevent a clot from becoming larger
antiplatelet meds
aspirin, plavix
Inhibit new clot formation
Anticoagulants
Coumadin, heparin
Angioplasty aka
Percutaneous Coronary Intervention
balloon, place stents
After Cardiac Cath care
Watch bleeding at site, pressure dsg
Contrast dye can be lethal to kidneys, Mucomyst can protect kidneys from dye
Watch for dysrhythmias (from cardiac manipulation)
these veins often used for bypass graft procedures
Greater and lesser saphenous veins of leg
Triple vessel disease requires
open heart surgery, CABG
lipitor is best cholesterol reduction med but
can damage liver, need to watch liver function
What raises HDL?
Exercise, moderate alcohol consumption, estrogen (in women, cholesterol can begin to rise at menopause)
81 mg ASA
protective from MI, same as 325 mg
minimum effective dose bc ASA can be hard on stomach lining
Fastest to slowest absorption for injections
IV, IM, SC
Omega 3
Provides essential fatty acids, decreases inflammation
Angles and gauge for typical SC
45, 3/8-5-8 inch
SC sites
Upper arms, abd, ant and lat thighs
Complication of sc injection
Sterile abcess
SC insulin
Insulin syringe
90 deg
28 gauge
To mix insulin
Draw up clear, then cloudy
Hold for 10 sec after insulin SC injection
To prevent hematoma and ensure absorption of viscous med
Lovenox dose is based on
Weight
Before giving heparin or lovenox you should know
Platelet count
Gauge and Needle length for IM injections
1 to 1 1-2 inches
20-23 gauge
Gauge selection depends on
Viscosity of medication
Larger number, smaller bore
Tuberculin syringe used to
Measure doses less than 1 mL
Filter needle used when
Withdrawing fluid from and ampule
Change before injecting
Main fluid will hang
Lower than minibag
Secondary solution set tubing is connected
At the Y port ABOVE the pump
Aortic area
Right side of sternum
2nd ICS
Pulmonic area
Left side of sternum
2nd ICS
Erb’s Point
Left 3rd ICS
Hear S1 and S2
Tricuspid area
Lower left sternal border
4th ICS
Mitral area
Left 5th ICS, medial to MC line
S1 “Lub”
Sound of AV valves closing
Beginning of systole
S2 “Dub”
Sound of aortic and pulmonic valves closing
Beginning of diastole
Murmurs caused by
Turbulent blood flow due to narrowed valves or other defect; or normal process (pregnancy, fever, hyperthyroid)
Difference between apical and radial pulses
Pulse deficit, signifies arrhythmia
CIWA
Clinical Intoxication Withdrawal Assessment
MD may have SO for benzodiazepines based on positive findings
Death can occur from abruptly stopping use of these drugs
Alcohol
Benzodiazepines
Barbiturates
Different drugs have a specific syndrome that results from their withdrawal, and the s/s are due to
Effect of the substance on the CNS
Alcohol absorbed by the
Mouth, stomach, and SI
Normal alcohol metabolism is 10 mL in
90 minutes
Metabolic tolerance
Increased drug-metabolizing enzyme in the liver
Sign of drug dependence
Tolerance/withdrawal
BA of .05% to .15
Disinhibition and impaired judgement, euphoria
1-2 drinks
Slurred speech, staggering gait, and double vision occur at BA of
.15 to .25
Severe respiratory depression and coma (alcohol poisoning) can result from BA of
.40-.50%
Why does alcohol affect Brain before spinal column? (Disinhibition before unsteady gait)
Alcohol rapidly crosses BBB
Women are more easily intoxicated than men, Asians more easily than other races, because?
They have less alcohol dehydrogenase
A person who fails to fulfill role due to Substance use, has legal problems and yet continues to use, and uses dangerously and yet has not met criteria for dependence, their problem is defined as
Substance abuse
Criteria for drug dependence
Tolerance and withdrawal
Drug tolerance
Need to use more to get same effect
Physical tolerance
Tissue adaptation
Changes in cells of NS so more drug is needed
Cross tolerance
Need more of drugs like the drug you depend on also ex-alcohol dependence and benzodiazepines
Behavioral tolerance
Ability to mask behavioral effects of intoxication
Tolerance is never developed to
Effects of respiratory depression ( can stop breathi g I. Sleep)
Substance withdrawal
Substance specific syndrome due to cessation or reduction in use
Minor alcohol withdrawal
Hangover (6-12 hours after last drink)
Irritable, agitated
Alcohol withdrawal
24 hours after last drink
Tachycardia, increased BP–can go very hi, needs treatment
Diaphoresis , n/v, hallucinations
Major alcohol withdrawal
48-72 hours after last drink
Seizures
Delerium tremens
Deletion tremens
Hallucinations from major alcohol withdrawal- bugs crawling over you, pt can be terrified
Nsg care during alcohol withdrawal
Monitor VS closely
Safety
Management of alcohol withdrawal
Early detection Safety Fluids Benzodiazepines MgSO4 and Dilantin for seizures B vitamin replacements
Why B vitamin supplements for alcohol withdrawal
Alcohol decreases B vitamins and PTA often don’t eat we’ll. needed for nerve conduction.
Wernicke-Korsakoff Syndrome
Irreversible alcohol encephalopathy
Amnesia, confabulation, peripheral neuropathy
more likely to develop in women
Wernicke Korsakoff syndrome results from
Poor nutrition, especially inadequate thiamin and niacin and from neurotoxicity of alcohol
physical effects of alcohol
CNS selective anesthetic and depressant, cytotoxic and toxic to organs (cirrhosis, cardiomyopathy, pancreatitis, gastritis, psoriasis, increased cancer risk)
kills brain cells, blackouts auditory hallucinations dementia peripheral neuritis, muscle weakness, ataxia delirium tremens
Delerium tremens
extreme motor agitation, visual and tactile hallucinations, and seizures
very dangerous to combine alcohol with
other CNS depressants (benzos, opiates)
FAS
Fetal Alcohol Syndrome: alcohol inhibits fetal development in first trimester.
Only preventable mental retardation
most addictive drug
cigarettes, then heroin
endorphin agonists that relieve pain and reduce anxiety
opioids: Morphine, oxycodone, heroin, Fentanyl, methadone, Demerol, diluadid, codeine
Heroin has highly addictive because
readily crosses BBB
death from opioid abuse is caused by
respiratory depression
AE of opioid use
resp depression constipation decreased GI secretions reduced pupil size Hypotension
opioid antidote
naloxone (Narcan) Blocks neuroreceptors affected by opioids. Give for suspected OD, wont hurt pt if its not an OD
Examples of stimulants
Cocaine, amphetamines (Meth), crack
Withdrawal from stimulants
physical withdrawal mild, not life threatening; psychological withdrawal is severe, with intense cravings
Mode of action of stimulants
deplete monoamine NTs associated with depression, are highly pleasurable
Due to difficult psych withdrawal from cocaine, pts are
high suicide risk
presentation and withdrawal very similar to alcohol
benzodiazepines
Examples of benzodiazepines
Versed, Ativan, valium, Xanax, Rohypnol
HIghes risk of inhalant abuse
kids and poor
Inhalant abuse causes
CNS depression
hilarity, asphyxiation
some lipid soluble, can have prolonged effect on brain
Examples of hallucinogens
marijuana, mescaline, mushrooms, LSD, PCP. Ecstacy
Effect of hallucinogens
altered sense of reality, hallucinations, panic, confusion, paranoia
No withdrawal but effects can last a long time
Effects of marijuana
sense of well being
altered perception
increase hunger, antiemetic (THC)
impaired balance
impaired short term memory and concentration
harms lungs, weakens heart contraction, immunosuppression, reduces sperm count
depression increases risk of poor outcomes in
cardiac disease due to decreased compliance
2 most prevalent causes of death and disability worldwide
CV disease and depression
To be a depressive illness, s/s have to last for at least
2 weeks
anhedonia
Hallmark of depression: loss of interest in things you used to enjoy
Depression-decrease in NTs
serotonin and NE
with physical illness, risk for MDD increases
50%
medications associated with depression
Beta Blockers and other anti-HTN meds
steroids
CNS depressants: benzodiazepines, alcohol, opioids
amphetamines, when coming down
depression in elderly probably arises from
multiple losses
this group is high risk for substance abuse and underreported depression
elderly
to asses a client with depression use
Mental Status Exam: Appearance (Hygeine? eye contact? affect?) Behavior (slowed?) Mood (subjective-ask) Thoughts (psychomotor retardation?) Interactions (Isolative?) Hx
Most common med for depression
SSRIs
Celexa, Lexapro, Paxil, Zoloft, Prozac, Luvox
Tricyclic antidepressants-try to avoid due to
anticholinergic AEs
Danger of MAOI use
dietary restrictions (could cause Hypertensive crisis if eat aged cheese)
Bipolar Affective Disorder is characterized by
pathological mood swings from mania to depression
NT imbalance in Bipolar
decreased serotonin
increased NE
Bipolar 1 disorder
alternate MDD to mania (at least one episode of each)
Bipolar II disorder
alternate MDD to hypomania
Mirror image of depression
mania
s/s of mania
intrusive, restless, frenzied, rapic speech, loose associations, irritable to hostile, delusional, graindiose, no fear, engages in risky behavior
drug of choice for bipolar
lithium
manic pt high risk for suicide due to
impulsivity and lows experienced after
Therapeutic zone for lithium
0.6-1.2 mEq/L
s/s of lithium OD
Diarrhea Ataxia Blurred vision BAD Higher--coma and death
Do not use lithium with these pts
cardiac diseases
renal diseases
pregnancy
hypothyroid
Anticonvulsant mood stabilizers
Tegretol, Depakote
Drugs for bipolar
Mood stabilizers:
- Lithium
- Anticonvulsants
- Atypical antipsychotics
low lethality, low intent/planning, little physical damage
suicide gesture
Best place to hear s1 and s2
.
SAD PERSONAS
Sex Age Depression History Past Attempts Etoh Rational Thinking Loss Social supports lacking Organized plan No spouse Availability of means Sickness
CAP-color and agent
Strep Pneumoniae
Rust colored sputum
HAP-color and agent
yellow-green sputum
Staph, Klebsiella, Pseudomonas
latent TB infection
test positive by ppd but do not have active tb disease because immune system fights it off
bronchiectasis often results from
chronic repeated respiratory infections, pneumonias, and CF
lung abcess often secondary to
aspirations
occupation lung disease r/t dust particle inhalation
pneumoconiosis
lung cancer with poor prognosis, linked to smoking, occurs centrally in lungs
small cell
oat cell
fluid in pleural space
pleural effusion
inflmn of both layers of pleura
pleurisy
alveolar collapse due to sticky secretions and mucus plugs
atelectasis
dx of chronic bronchitis
productive cough for 3 months each year for two consecutive years
flattened diaphragem and barrel chest
emphysema
often first sign of emphysema
DOE
often first sign of asthma
chest tightness
