Exam 1 Flashcards
what ventricular wall of the heart is how much thicker
left, 2-3x
cardiac valves connected by what
chordae tendineae
QRS
depolarization from AV node through ventricles (heartbeat)
heart block in ECG
long time between isoelectric and QRS (PR interval >0.20)
effective and relative refractory period
nothing happens, cells let 3 major electrolytes in and out
normal CO
4-8 L/min
cardiac index and normal number
CO / body surface area
normal is 2.8-4.2 L/min/m^2)
3 factors that affect cardiac output
preload
contractility
afterload
afterload
the amount of pressure that the heart needs to eject blood during ventricular contraction
THINK OF BP
A patient is receiving a drug that decreases afterload. To evaluate the patient’s response to this drug, what is most important for the nurse to assess?
HR, lung sounds, BP, JVD
BP
HR influenced by what 3 things
acidosis
certain meds
hypoxemia
frank-starling law
r/t preload
cardiac and muscle cells can only stretch so far
afterload affected by
systemic and pulmonary vascular resistance
HR and adrenal gland
tumor can cause secretion of hormones like cortisol, epinephrine, and adrenaline
common symptoms of MI
chest pain/discomfort (neck and shoulder in women)
SOB/dyspnea
peripheral edema, weight gain, abd distention
palpitations
unusual fatigue, dizziness, syncope, change in LOC
peripheral edema upon waking
NOT NORMAL
except with ACE or calcium channel blockers
can actually be present in abdomen
C-reactive protein
elevated in heart problems, viral infection, lupus, RA
troponin and drawn how often?
cardiac muscle damage
drawn in series of 3 q8h
lab tests for cardiac
Cardiac biomarkers
Blood chemistry, hematology, coagulation
Lipid profile
Brain (B-type) natriuretic peptide
C-reactive protein
Homocysteine
TROPONIN
point of maximal impulse
at the apex
midclav, 5th intercostal space
pharm stress test
vasodilators given
echocardiography
measures EF
examine size, shape, and motion of cardiac structures
transthoracic
like an ultrasound
transesophageal
like an endoscopy
nuclear cardiology 2 tests
MUGA
stress perfusion imaging
CT angiography
calcium screening
looks for HARD calcium not soft
right heart cath
pulmonary artery pressure, O2 sats, and myocardial tissue biopsy may be obtained
left heart cath
uses contrast agent unless kidney failure
bed rest after cardiac cath
2-6 hours
some blocked arteries, what procedure?
coronary artery bypass
major blockage, what procedure
stent
what to know about insertion site
lots of pressure
can leak under skin and form hematoma (pt c/o pressure)
check pulse below insertion site
hemodynamic monitoring
central venous pressure
pulmonary artery pressure
intra-arterial BP monitoring
minimally invasive CO monitoring devices
5 factors of normal sinus rhythm
regular
60-100 BPM
P waves normal and precede QRS complex
PR 0.12-0.20
QRS <0.12
sinus tachy
100-160 BPM
sinus arrythmia
irregular rate
normal or brady
associated w respirations, NORMAL! tell pt to relax
premature atrial contractions causes and where is the focus
alcohol, drugs, stress
SA node
atrial flutter
reg or irreg
atrial rate 250-400
ventricular varies on # of impulses to AV node (less than atrial)
SAW TOOTH PATTERN
normal QRS but PR not measurable
afib
rapid irregular
atrial rate >400 (not measurable)
ventricular rate varies on # of impulses to AV node
P waves waving deflections entire baseline
PR and QRS not measurable
3 vfib causes
accident, drowning, electrocution
blood pathway (right side)
Blood enters the heart through two large veins, the inferior and superior vena cava, emptying the oxygen-poor blood from the body into the right atrium.
As the atrium contracts, blood flows from the right atrium into the right ventricle through the open tricuspid valve
When the right ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the atria while the ventricle contracts.
As the right ventricle contracts, blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs where it is oxygenated.
blood pathway (left)
The pulmonary vein empties oxygen-rich blood from the lungs into the left atrium of the heart.
As the left atrium contracts, blood flows from the left atrium into the left ventricle through the open mitral valve.
When the left ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts
As the left ventricle contracts, oxygen-enriched blood leaves the heart through the aortic valve, into the aorta and to the arteries and eventually into veins to complete blood circulation in your body.
tertiary pacemaker of heart
his-purkinje fibers (20-40)
lead 1
right side, 5th intercostal space
lead 2
left sternum, 4th intercostal space
lead 4
midclavicular, 5th intercostal space
costochondritis
mimics pain of MI, inflammation of cartilage that joins ribs to sternum
what 3 things can mimic cardiac disease
GERD
hiatal hernia
pregnancy
PR interval
time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)
QT interval
duration of ventricular depolarization and repolarization
manifestations of sinus brady (7)
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
SOB
Can be normal during sleep!
sinus tachy caused by vagal __________ or sympathetic ________
INHIBITION!!! STIMULATION!!!
valsalva maneuver (bearing down) stimulates vagus nerve, fixes sinus tach
4 manifestations of sinus tachy
dizziness (not getting enough oxygenated blood whether brady or tachy)
dyspnea
hypotension
angina in pts with CAD
PAC
-Contraction originating from ectopic focus in atrium in location other than SA node
-Travels across atria by abnormal pathway, creating distorted P wave
-May be stopped, delayed, or conducted normally at the AV node
8 causes of PAC
Stress
Fatigue
Caffeine
Tobacco
Alcohol (depletes electrolytes)
Hypoxia
Electrolyte imbalance
Disease states
2 manifestations of PAC
palpitations
heart skips a beat
3 treatments for PAC
monitor for more serious dysrhythmias
withhold sources of stimulation
beta blockers
aflutter
associated with disease
symptoms from high ventricular rate and loss of atrial “kick” (decreased CO –> risk of HF)
increases risk of CVA
3 treatments for aflutter
-Pharmacologic agent
-Electrical cardioversion
-Radiofrequency ablation (if someone has ectopic focus, wire gets threaded thru right atrium and gives meds to stimulate dysrhythmia so they can see it [can cause new dysrhythmia]. Ablated with high frequency or freezing)
afib
paroxysmal or persistent
most common in people over 65
in pts with underlying heart dx
can occur in other disease states
5 treatments for afib
-Drugs to convert ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most common)
-Electrical cardioversion
-Anticoagulation (work on platelet aggregation, careful with ppl with high or low platelets)
-Radiofrequency ablation
-Maze procedure (also done thru angiogram, different technique) with cryoablation
PSVT causes
Overexertion
stress
deep inspiration
stimulants
disease
digitalis toxicity (N/V, loss of appetite)
digoxin toxicity
N/V, loss of appetite
reentrant phenomenon
PAC triggers a run of repeated premature beats
manifestations of PSVT
HR 150-220
HR >180 leads to decreased CO and SV
hypotension
dyspnea
angina
6 treatments for PSVT
Vagal stimulation
IV adenosine
IV beta blockers
Calcium channel blockers
Amiodarone
DC cardioversion
vtach
-SA node nonfunctional
-Ectopic foci take over as pacemaker
-Monomorphic (all same shape), polymorphic (many), sustained, and nonsustained
-Considered life-threatening because of decreased cardiac output and the possibility of deterioration to v-fib
vtach- torsades de pointes associated with what
Associated with heart disease, electrolyte imbalances, drugs, CNS disorder (GBS, parkinsons, spinal cord injury)
manifestations of vtach
Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest
treatment for STABLE vtach
antidysrhythmics or cardioversion
treatment for UNSTABLE vtach
CPR and rapid defibrillation
vfib associated with?
MI, ischemia, disease states, procedures
unresponsive, pulseless, and apneic
vfib treatment
CPR and ACLS (defibrillation and drug therapy including epinephrine, vasopressin [-pressors bring BP up], anything to restore blood flow
asystole is a result of what
advanced cardiac disease, severe conduction disturbance, or end-stage HF
treatment for asystole
immediate CPR and ACLS measures
Epinephrine and/or vasopressin
Intubation
PEA
weak electrical activity shown in ECG, no pulse
NONSHOCKABLE
6 Hs of PEA
HYPOvolemia
HYPOxia
Hydrogen ion (acidosis)
HYPER/HYPOkalemia
HYPOglycemia
HYPOthermia
5 Ts of PEA
Toxins
Tamponade
Thrombosis (MI and pulmonary)
Tension pneumothorax
trauma
treatment of PEA
CPR followed by intubation and IV epinephrine
Correct the underlying cause
SCD (sudden cardiac death)
death from cardiac cause
majority from ventricular dysrhythmias (vtach and vfib)
prolonged QT
defibrillation
treatment of choice for vfib and pulseless VT
most effective within 2 mins of dysrhythmia
passage of shock through heart to depolarize myocardial cells
allows SA node to become pacemaker
output in joules/watts per second
monophasic and biphasic defibrillators
mono: deliver energy in one direction
bi: 2 directions, lower energies, fewer post-shock abnormalities
recommended energy for initial shocks in defibrillation
bi: 120-200 joules
mono: 360
START CPR AFTER FIRST SHOCK
8 steps to defibrillation
-start CPR and set up defibrillator
-turn on and select energy
-turn off sync button
-gel pads
-charge
-position paddles firmly on chest
-all clear!
-deliver charge
steps to synchronized cardioversion and initial energies
same but make sure sync is ON
initial energy 70-75 (bi) or 100 (mono)
if pt stable, sedate prior
if pt pulseless, turn sync button off and defib
synchronized cardioversion rhythms
VT with a pulse or supraventricular tachydysrhythmias
how does synchronized cardioversion work
delivers a countershock on the R wave of the QRS complex of the ECG
ICDs (who are they for and how do they work)
for pts who:
-have survived SCD
-have spontaneous sustained VT
-syncope w inducible vtach/fib during EPS
-high risk for LT dysrhythmias
lead system in subclavian vein to endocardium
delivers 25 joules when dysrhythmia detected
CHECK FOR BLEEDING AND HEMATOMA
includes antitachy/antibrady pacemakers
-overdrive for tachy
-backup for brady
pre and postop care for ICDs
same as pacemaker
fear of body image change and recurrent dysrhythmias
expectation of pain w discharge
anxiety about going home
SUPPORT GROUP
pt teaching for ICD
-Follow-up appointments
-Incision care (check site for drainage, heat, redness, swelling)
-Arm restrictions (don’t lift that arm above head for 6 weeks and don’t lift anything above 5 lbs on that side)
-Sexual activity (not that forbidden unless symptoms)
-Driving
-Avoid direct blows
-Avoid large magnets, MRI (newer ones [2 years] are usually compatible)
-Air travel (don’t use wand over site)
-Avoid anti theft devices (can disarm mechanics)
-What to do if ICD fires
-Medic alert ID
-ICD identification card (defibrillator brand, serial number, etc)
-Caregivers to learn CPR
pacing circuit consists of
-Programmable pulse generator (power source)
-One or more conducting (pacing) leads to myocardium
goes in the same way as ICD but 2 wires
3 temporary pacemakers
outside of the body:
transvenous
epicardial
transcutaneous
epicardial pacing
-leads placed on epicardium during heart surgery
-passed through chest wall and attached to external power source
transcutaneous pacing
-For emergent pacing needs
-Noninvasive
-Bridge until transvenous pacer can be inserted
-Use lowest current that will “capture”
-Pt may need analgesia/sedation
fail to sense and capture in pacemaker
fail to sense causes inappropriate firing
failure to capture causes lack of pacing when needed (leading to brady or asystole)
5 complications of pacemaker placement
infection
hematoma
pneumothorax
atrial or ventricular septum perforation
lead misplacement
postop care for pacemaker
OOB once stable
limit arm and shoulder activity
monitor insertion site
pacemaker pt teaching
Follow-up appointments for pacemaker function checks
Incision care
Arm restrictions
Avoid direct blows
Avoid high-output generator
No MRIs unless pacer approved
Microwaves OK
Avoid anti theft devices
Air travel
Monitor pulse
Pacemaker ID card
Medic Alert ID
ECG changes with ACS
ischemia
-ST depression (1 mm below isoelectric line) or T wave inversion
-changes reverse once adequate blood flow is restored
injury (cell death) in ECG
ST elevation (1 mm above isoelectric)
QUICK treatment to prevent infarction
absence of serum markers shows no infarction
infarction in ECG
pathologic Q wave (deep and >0.03 seconds in duration)
5 noncardiovascular causes for syncope
Stress
Hypoglycemia
Dehydration
Stroke
Seizure
5 cardiovascular causes for syncope
Cardiogenic or “vasovagal” syncope (Carotid sinus sensitivity)
Dysrhythmias (tachy/brady)
Prosthetic valve malfunction
Pulmonary emboli
HF
4 diagnostic tests for syncope
Echocardiography
Stress test
EPS (internal rhythm of heart)
Head-up, tilt test
C-reactive protein
Nonspecific marker of inflammation
Increased in many patients with CAD
Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol (like a pt with a viral problem that doesn’t go away, autoimmune)
manifestations of CAD
symptoms caused by MI
symptoms and complications related to location and degree of obstruction
angina pectoris!!
epigastric distress, pain that radiates to jaw or left arm, SOB, atypical symptoms in women
HF
sudden cardiac death
risk factors for CAD
cholesterol abnormalities, tobacco use, HTN, and diabetes**
LDLs are primary target in meds
framingham risk calculator
metabolic syndrome
hs-CRP (high sensitivity CRP)
6 lipid lowering agents
HMG-CoA (statins, NO GRAPEFRUIT AND RHABDO)
nicotinic acids (facial flushing and hot flashes)
fibric acids
bile acid sequestrants (resins, cause diarrhea)
cholesterol absorption inhibitors
omega-3 acid ethyl esters (some benefit but dose causes increased bleeding)
Gerontologic considerations for CAD
Diminished pain transition that occurs with aging may affect presentation of symptoms
“Silent” CAD
Teach older adults to recognize their “chest pain–like” symptoms (i.e., weakness or heaviness, may miss symptoms because they take so many meds)
Pharmacologic stress testing; cardiac catheterization
Medications should be used cautiously!
Start low and go slow
Liver or kidney dysfunction
treatment for CAD
decrease oxygen demand and increase supply
meds for CAD
-Nitroglycerin (potent vasodilator, may give migraines bc they dilate temporal vessels)
-Beta blockers (watch HR and blood sugar, may go up from some beta blockers)
-Calcium channel blockers (may cause tachycardia and pedal edema)
-Aspirin (antiplatelet)
-Clopidogrel and ticlopidine
-Anticoags like heparin
-Glycoprotein IIb/IIIa agents
Angina pectoris
A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow
Physical exertion or emotional stress increases myocardial oxygen demand, and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand
intractable or refractory angina
severe incapacitating pain
variant (prinzmetal’s) angina
pain at rest w reversible ST elevation, caused by coronary artery vasospasm
assessment of angina
May be described as tightness, choking, or a heavy sensation
Frequently retrosternal (behind sternum, deep pain) and may radiate to neck, jaw, shoulders, back or arms (usually left)
Anxiety frequently accompanies the pain
Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and vomiting
NTG and angina
Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG.
requires medical intervention!
7 collaborative problems of angina
ACS
MI
both of the above
dysrhythmias
cardiac arrest
HF
cardiogenic shock (collapse of CV system, BP plummets, pulse pressure widens)
nursing priorities for treating angina
pt should stop activity and rest in semi fowlers
assess
with VS, assess for resp distress and pain assessment
ECG
oxygen 2L/min nasal cannula
pt teaching for angina
avoid OTC meds that increase HR or BP
low fat high fiber diet
NTG AWAY FROM SUN AND KIDS
maintain normal BP and glucose
treatment for stable angina
medication and interventional treatment (procedures to open or bypass narrowed coronary arteries)
3 forms of ACS
unstable angina
STEMI
NSTEMI
unstable angina diagnostics
manifestations of coronary ischemia, ECG & biomarkers show no evidence of acute MI
STEMI diagnostics
ECG evidence of acute MI, characteristic changes in two contiguous leads on a 12-lead ECG. There is significant damage to the myocardium
NSTEMI diagnostics
Elevated cardiac biomarkers (e.g., troponin, no definite ECG evidence of acute MI. There may be less damage to the myocardium
myocardial infarction treatment MONA
morphine
oxygen
nitrates
aspirin
myocardial infarction priorities VOMIT
vitals
oxygen
monitor
IV access
time to decision (when did this happen? clot busters if within a few hours)
assessment of ACS
chest pain: sudden, SOB, C/O indigestion, nausea, anxiety, cool pale skin, increased HR and RR
ECG changes: ST elevation in 2 contiguous leads
lab studies: troponin, creatinine kinase (muscle damage), myoglobin, BNP
collaborative problems with ACS
Acute pulmonary edema
HF
Cardiogenic shock
Dysrhythmias and cardiac arrest
Pericardial effusion and cardiac tamponade
7 symptoms of MI in women
sweating (like stress sweat, not exercise)
SOB
fatigue
chest pain (not limited to left)
pain in arms, back, neck, or jaw (gradual or sudden)
nausea (flu-like, days before MI)
stomach pain (heartburn to severe abd pressure)
5 risk factors women and heart
anemia
metabolic syndrome
sleep apnea
BC
preeclampsia
nursing management ACS/MI
Oxygen and medication therapy
Frequent VS assessment
Physical rest in bed with head of bed elevated
Relief of pain helps decrease workload of heart
Monitor I&O and tissue perfusion
Frequent position changes to prevent respiratory complications
Report changes in patient’s condition
Evaluate interventions!
4 invasive coronary artery surgeries
percutaneous transluminal coronary angioplasty (PTCA) (opening vessels and putting stent or CABG
coronary artery stent
coronary artery bypass graft (CABG)
cardiac surgery
vasovagal response is an overstimulation of _______
parasympathetic nervous system (vagus nerve)
3 types of bypass grafts
internal thoracic arteries
radial artery
saphenous veins
internal thoracic artery bypass
under the left and right sides of the breast bone. They are not fully removed from their original position.
Least invasive and little scar, often collapse and stent is needed later
radial artery bypass graft
Radial arteries are taken from the inner forearm. Long-term outcome is almost equivalent to that of the internal thoracic artery.
Good!
saphenous vein bypass graft
taken from the leg (calf or thigh). Narrowing (stenosis) of the vein graft due to changes that are similar to those of a coronary artery is a major problem with saphenous vein grafts.
Great except for pt with diminished circulation, they are at risk for infection so watch donor and incision site
10 potential complications from CABG
Bleeding during or after the surgery
Blood clots
Infection at incision site
Pneumonia
Breathing problems
Pancreatitis
Kidney failure
Abnormal heart rhythms
Failure of the graft
Death
rheumatic endocarditis can be from what infection
unresolved strep-A
adhesive vs malignant pericarditis
adhesive: forming scar tissue and sticking to other parts of the body
malignant: leads to more complicated problems
causes of pericarditis
connective tissue disorders (SLE, arthritis, scleroderma)
hypersensitivity
disorders of adjacent structures
neoplastic (cancer)
trauma
nursing management of pericarditis
pain management w analgesics
positioning
psych support
gradual increase of activity
enhance immune system
be alert for cardiac tamponade and HF
nursing assessment of pericarditis
Substernal (underneath breast bone), precordial pain (in front of heart, hurts w deep breathing, coughing, and swallowing), can radiate to left neck, shoulder, and back
Increases with breathing, coughing, swallowing
Pericardial friction rub
Distinguish between acute and chronic restrictive pericarditis
Treatment depends on type
acute pericarditis
elevated WBC
St-T wave elevation (looks like MI)
fever
treatment for acute pericarditis
NSAIDS (GI effects, not for cardiac pts)
corticosteroids (glucose!)
abx (blood culture bc systemic)
rest
chronic restrictive pericarditis
right sided HF
pericardial thickening on echo and CT
inverted or flat T wave
chronic afib
chronic restrictive pericarditis treatment
Surgical excision of the pericardium (pericardiectomy or pericardial window)
complications of pericarditis
Pericardial effusion
Cardiac tamponade
Failure to identify and treat can lead to death
endocarditis
Can start with valve disease
Can become incompetent
Can happen as a result of many illnesses, including viral
endocarditis treatment
Spironolactone can cause gynecomastia (large boobs) in men and women
Use eplerenone instead
Empagliflozin is best bc less hospital revisits
class 1 HF
The patient does not display symptoms (fatigue or shortness of breath) with regular activity; no limitation of physical activity is needed
class 2 HF
The patient may display some symptoms with activity but is comfortable when resting; slight limitation of physical activity is required.
class 3 HF
The patient displays symptoms with minor activity but is comfortable when at rest; increased limitation of activity is required
class 4 HF
The patient displays symptoms with any activity and also while at rest; severe limitation of activity is required
Causes of sinus brady
in response to carotid sinus massage, valsalva maneuver, hypothermia, increased ICP, vagal stimulation, certain drugs (beta-adrenergic blockers, ca+ channel blockers)
Hypothyroidism, hypoglycemia, inferior MI
ventricular heart rate classifications
sinus tachy: 100-160
160+: SVT
180+: beats no longer productive
sinus tachy pharm causes
Drugs like epinephrine, norepinephrine, atropine, caffeine, theophylline, hydralazine. albuterol, pseudoephedrine
PAC ECG
distorted P waves
normal PR, QRS
atrial rate with aflutter
200-350
atrial rate in afib
350-600
afib with a rapid or uncontrolled ventricular response
afib with ventricular rate above 100
PVC
unifocal or multifocal
bigeminy
trigeminy
quadrigeminy
vtach and PVCs
3+ PVCs means vtach
insurance and hospital admission with HF
need an IV, diuretics, and echo (IN FIRST 2 DAYS OR ELSE INSURANCE DOESN’T COVER)
INSURANCE CAN CONTEST PAYING IF PT COMES BACK IN 30 DAYS
right sided HF
Viscera (near abdominal area, ASCITES) and peripheral congestion
JVD
Dependent edema
Hepatomegaly
Weight gain
left sided HF
Pulmonary congestion, crackles
S3 or ventricular gallop (happens with HTN, right after S2, S4 is right before S1)
Dyspnea on exertion (DOE)
Activity level before you feel out of breath, diet, how many pillows
Low O2 sat
Dry, nonproductive cough initially (Ace inhibitors, arbs taken instead)
Oliguria
patho of SYSTOLIC HF
caused by:
-impaired contraction (like scar tissue from MI)
-increased afterload
-cardiomyopathy (hypertrophic and dilated)
-mechanical abnormalities
-DECREASED EF (<45%, 5-10%=transplant)
patho of DIASTOLIC HF
can’t relax and fill causing decreased SV and CO
normal EF
result of left ventricular hypertrophy from HTN, MI, valve disease, or cardiomyopathy
patho of MIXED HF
seen in disease states like cardiomyopathy
poor EF (<35%)
high pulmonary pressure
biventricular failure (both dilated and poor emptying/filling)
patho of general HF
ventricular failure leads to:
-Low BP
-Low CO
-poor renal perfusion
abrupt or subtle
end of viral infection
compensatory (adrenal) mechanisms to maintain adequate CO
5 compensatory mechanisms for HF
-SNS activation (epi and norepi, increases HR, myocardial contractility, peripheral vasoconstriction, helps then hurts)
-neurohormonal responses (kidneys release renin and initiate RAAS, pos pituitary releases ADH, endothelin released, proinflammatory cytokines (CRP, homocysteine like MI)
-ventricular remodeling (hypertrophy of ventricular myocytes, larger but less effective, can cause dysrhythmias and SCD (get implantable defib)
-dilation (enlargement of chambers when pressure in left ventricle is elevated, later inadequate and CO drops)
-hypertrophy (increases muscle mass and wall thickness, effective but then leads to poor contractility, increased O2 needs, poor coronary artery circulation, and risk for ventricular dysrhythmias)
pulmonary edema clini manifestations
Anxious, pale, cyanotic
Cool and clammy skin
Dyspnea
Orthopnea
Tachypnea
Use of accessory muscles
Cough with frothy, blood-tinged sputum (small capillaries in the lungs are breaking, red specks)
Crackles, wheezes, rhonchi
Tachycardia
Hypotension or hypertension
chronic HF clini manifestations
depends on age, underlying type and extent of heart disease, and affected ventricle
FACES clini manifestations chronic HF
Fatigue
Activity intolerance
Chest congestion/cough
Edema
Shortness of breath
also syncope
anasarca
seen in chronic HF
entire body having a pitting edema, skin is weeping (fluid comes from pores of skin, soaking bed thru skin, end stage 🙁)
Pt can’t be comfy, given morphine
acute decompensated HF
meds work and then suddenly don’t work
sudden weight gain 3lbs in 2 days
exacerbation of chronic HF
chronic HF nursing assessment
frothy, blood tinged sputum, electrolytes, NT-proBNP or BNP
chest xray for displacement of the heart
echo
HF complications
pleural effusion
dysrhythmias
left ventricular thrombus
hepatomegaly
renal failure (bad)
meds for HF
-ACE inhibitors (vasodilation, diuresis, decreases afterload, monitor for hypotension, hyperkalemia, and altered renal function; COUGH
-angiotensin II receptors (alternative for ACE)
-hydralazine and isosorbide (alternative for ACE)
-BB (in addition to ACE, takes weeks to see effects, careful in asthmatic pts)
-diuretics (decreases fluid volume, watch electrolytes)
-digitalis (improves contractility, TOXIC ESP IF HYPOKALEMIC)
-IV meds (for hospitalized pts with ADHF [milrinone and dobutamine])
milrinone
for ADHF
decreases pre/afterload
causes hypotension and increased risk for dysrhythmias
dobutamine
for ADHF
used for pts with left ventricular dysfunction
increases contractility and renal perfusion
what electrolyte to check for in chronic HF
potassium!
gerontologic considerations HF
atypical signs like fatigue and somnolence
resistance to diuretics and more sensitive to volume changes
watch for bladder distention caused by enlarged prostate gland
chronic HF management
oxygen therapy
rest
structured exercise program
chronic HF nursing intervention
treatment plans and quality of life
restrict salt and water
conserve energy
maintain support systems
chronic HF activity intolerance
bed rest for acute exacerbations
30-45 mins regular activity
2 hrs after eating for activity
avoid activities in hot and cold
elevate HOB and support arms
pulmonary edema and LV failure
acute event results in LV failure
when LV fails, blood backs up in pulmonary circulation, causing pulmonary interstitial edema
hypoxemia!!
manifestations of pulmonary edema
restlessness, anxiety, dyspnea, cool and clammy skin, cyanosis, weak and rapid pulse, cough, lung congestion (moist, noisy respirations), increased sputum production (sputum may be frothy and blood tinged), decreased LOC
management of pulmonary edema
easier to prevent than treat
monitor lung sounds and signs of decreased activity tolerance and increased fluid retention
minimize exertion and stress
nonrebreather
diuretics and vasodilators
nursing management of pulmonary edema
upright w legs dangling
fowler’s or semi
psychological support
I&O
cardiogenic shock
decreased CO leads to inadequate tissue perfusion and initiation of shock syndrome
cardiogenic shock clini manifestations
symprtoms of HF, shock state, and hypoxia
cardiogenic shock treatment
reduce preload and afterload to decrease cardiac workload
improve oxygenation and restore perfusion
monitor hemodynamic parameters
fluid status, and adjust meds
diuretics, positive inotropic agents, and vasopressors
intra-aortic balloon pump does work for the heart (temporary)
thromboembolism S&S
dyspnea, pleuritic chest pain, tachypnea, cough
thromboembolism treatment
anticoag therapy
unfractionated heparin (low weight)
fondaparinux (arixtra) or rivaroxaban (xarelto)
FALL RISK!!!
clini manifestations of pericardial effusion
ill-defined chest pain or fullness, pulsus paradoxus, engorged neck veins, labile or low BP, shortness of breath
4 cardinal signs of cardiac tamponade
falling systolic BP, narrowing pulse pressure, rising venous pressure, distant heart sounds (bc behind fluid)
medical management of pericardial effusion and cardiac tamponade
Pericardiocentesis: Puncture of the pericardial sac to aspirate pericardial fluid
Pericardiotomy: Under general anesthesia, a portion of the pericardium is excised to permit the exudative pericardial fluid to drain into the lymphatic system
emergency management: cardiopulmonary resuscitation (ABCD of priority)
airway
breathing
circulation
defib for VT and VF
cardiac transplantation
for pts with refractory end-stage HF, inoperable CAD, and cardiomyopathy
candidate goes under physical, diagnostic, and psychological eval
stable pts wait at home
unstable pts stay in hospital for intensive therapy
steps of cardiac transplantation
retrieve heart
remove recipient heart except portions of atria and venous connections
implant donor heart
anticoags for rate control
paroxysmal, persistent, long-standing persistent, and permanent afib
paroxysmal: terminates with no intervention within 7 dats
persistent: 7+ days
long-standing: 12+ months
permanent: persists beside all efforts, no further attempts made
management of afib (8) mostly lifestyle
-obesity (BMI >30), reduce weight by 10%, 150 min mod exercise or 75 vigorous
-HTN (BP >140/90) reg physical activity 2-3 days/week
-obstructive sleep apnea (use CPAP)
-diabetes (reg testing, activity, quit smoking, nutrition)
-smoking (vasoconstriction and workload)
-alcohol (decreases effectiveness of meds, 2 drinks per day for men, 1.5 for women)
-caffeine (moderate!)
-surgery (monitor pain, electrolytes, stressors, may need BB)
4 meds of choice to achieve target HR
target HR <110
-BB (rapid onset, better than digitalis, can be combined w amiodarone and digitalis, NOT FOR PTS WITH ACUTE HF OR BRONCHOSPASM)
-calcium channel blockers (verapamil, diltiazem, for COPD and asthma pts, HTN and HF with good EF)
-digitalis (lower dose or with BB and calcium channel)
-amiodarone (with BB and digoxin for reduced EF)
when is rhythm control indicated with afib
when pt has persistent symptoms and poor quality of life
how to assess for atrial thrombus
transesophageal echo
IF PRESENT, CARDIOVERSION CONTRAINDICATED
electrical cardioversion (npo for how long and what 2 meds given)
patient NPO for 6 hours
pt sedated with midazolam and propofol
pharmacologic cardioversion
antidysrhythmics (amiodarone, sotalol, flecainide) for pt with afib in past 7 days
monitor HR, BP, K+, 12-lead EKG for QT prolongation
contraindicated in digitalis toxicity, multifocal atrial tachy, and sub-optimal coag
catheter ablation
catheter in femoral vein into heart releasing radiofrequency energy targeting pulmonary vein in left atrium to ablate abnormal current
surgical ablation (maze proceure)
sternotomy or mini-thoracotomy to restore NSR by creating scar tissue w cryotherapy or radiofrequency. For pts with failed pharm or catheter ablation, or during mitral valve repair
what med preferred in pts w mechanical heart valves and what to watch
warfarin
fequent INR
watch vitamin K
anticoags for thromboembolism prevention
apixaban, dabigatran, edoxaban, and rivaroxaban
don’t require blood draws
what to do if pt can’t tolerate long-term anticoags
left atrial appendage obliteration for CVA prevention bc this is where thrombi form
complications of afib
risk of stroke, MI, and cognitive decline (from micro thrombi and hypoperfusion)
depression
KEEP PT AT CENTER OF CARE
education to adhere to plan and lifestyle mods
palliative care
philosophy of and system for delivering care that expands on traditional medical care for serious, progressive illness to include a focus on quality of life, function, decision making, and opportunities for personal growth
hospice and international considerations
a coordinated program of interdisciplinary care and services for terminally ill patients and their families that in the United States is provided primarily in the home
If person is not from the US, what is their perception of what should happen now?
grief
feelings
mourning
behaviors and expressions
assisted suicide
DOCTORS ONLY NOT NURSES
palliative vs hospice
All hospice care is palliative care; not all palliative care is hospice care
Palliative care can start the second the pt gets the diagnosis, hospice is once the pt has 6 months or less to live
Pts don’t have to stay in hospice!! They can come off it by choice or by medical reasons!
eligibility for hospice
Serious, progressive illness
Limited life expectancy
Informed choice of palliative care over cure-focused treatment
-Teach back method used so you know pt understands
last sense to disappear when dying
hearing
vision at EOL
blurry
no blinking
half open eyes
skin at EOL
waxy, looks wet
HR at EOL
fast then slow and weak
move to IV and transdermal drugs
how long does fentanyl patch last
72h
bereavement
time which grief is experienced and mourning occurs
dysfunctional grief
denial of loss for 6 months +
can we euthanize and what is it
hastening of death on purpose and NO
who decides to withhold nutrition and hydration
pts and healthcare team
Rule for mcg/kg/min
Dose ordered x mL/mg x conversion factor x 60 min x kg = ml/hr
