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Myocardial Deficiency -
Inadequate Contractibility: MI, CAD, cardiomyopathy, infection
Inadequate Filling: A-fib, Infection, tamponade, ischemia
Increase workload –
Pressure Overload: HTN, outflow obstruction
Volume overload: Hypervolemia, congenital abnorm, anemia, thyroid disease
Implementation:
Acute phase-MONA or One Arm Nasty Man
Oxygen 2-4 L/min via NC titrated to SaO2 > 96%, ASA 160 to 325 mg (2 to 4 baby ASA
chewed), Nitro SubL, spray, or IV titrated until relief of CP, keep systolic BP > 90 mm
Hg, Morphine IV 2-4 mg for pain not relieved by Nitro
VS, O2 sats, IV access, 12-lead ECG, targeted H & P, determine eligibility for
fibrinolytic therapy (absolute contrai: prior intracranial hemorrhage, cerebral vascular lesion, ischemic
stroke within 3 months, aortic dissection, active bleeding, significant closed head trauma within 3 months;
relative contrai: hx of chronic, severe HTN, ischemic stroke, traumatic CPR >3 mos, allergy to
streptokinase, pregnant, active peptic ulcer, current anti-coag use), serum marker levels, electrolyte
and coag studies, and type and cross (<30 mins)
B. Chest Pain
Angina [like generic brand at grocery store, it is an umbrella term]-
*chest pain or discomfort caused by myocardial ischemia due to imbalance between
myocardial oxygen supply and demand
*myocardial oxygen requirements are related to – heart rate, force of contraction,
myocardial wall tension (determined by after-load, preload and wall thickness)
1
Precipitating factors- emotional stress, exercise, exposure to temperature
extremes, ingestion of heavy meal (especially high in sat fat), smoking
Etiology-CAD, coronary artery spasm, HTN, anemia, dysrhythmias, congestive
heart failure
S/S-pain frequently retrosternal, left pectoral, or epigastric and may radiate to jaw
left shoulder or left arm (elderly gets confused)
Described as-burning, squeezing, heavy, or smothering and last 1 to 4 mins
-***Classic placing of clenched fist against sternum
-Sx may be confused with indigestion
-Usually begins with exertion and subsides with rest
Angina Types:
Unstable Angina (Pre-infaract) -
*Demonstrated by definite change in quality, severity, frequency and duration, unusually
over 3 month period
*Pain may precipitate at rest and can last as long as 20-30 mins
*Nitro tablets are no sufficient to relieve pain
*During episode of pain ECG may show ST-segment depression
*Pt is at increased risk for MI within 18 months of angina onset
2
Management: Carry Nitro at all times, keep tightly capped in dark colored glass
bottle, discard cotton filler, avoid opening bottle unnecessarily, discard unused
tablets after 3 months, fresh tablet will cause burning sensation when placed
under tongue, place Nitro under tongue at first sign of chest discomfort, allow tab
to dissolve, sit upright, stop activity until pain subsides, Nitro taken every 3 to 5
mins X 3-if sx cont, go to hospital, Nitro may be taken prophylatically, s/e: H/A,
flushing, dizziness,
Differentiate chest pain origin: pain could be from acid reflux, hernia, gallbladder,
stomach, esophagitis, pancreatitis, etc
C. Lab Tests
Cardiac Enzymes:**Know the levels, onset, peak and normalizations!!
CK (creatine kinase) 26–174 U/L: enzyme found in muscles; increase from damaged
muscle (according to Baird: elevates 2-6 hr; peaks 18hrs; normalizes – unknown)
CK-MB (cardiac muscle specific) < 4-6% of total CK: level begins to elevate within 4
to 6 hours (3-12 hr according to Baird) of myo damage; peaks in 18 to 24 hours; rtns to
normal within 72 hours and used to evaluate success of reperfusion interventions
Troponin I (most specific) < 0.6 ng/mL: contractile protein and increases 2 to 6 hours
after MI; biphasic peak at 15 to 24 hours then 60 to 80 hrs, rtn to normal after 7 days
(according to Baird: elevation starts – 3-12 hrs, peaks 24 hrs; normalizes 5-10 days)
Troponin T < 0.2 ng/mL: rises 2 to 6 hrs after MI and remains elevated; rtns to normal
level in 7 days (according to Baird: elevation starts – 3-12 hrs, peaks 12 hrs to 2 days;
normalizes 5-14 days)
Myoglobin (not heart specific) 5-7 mcg/dL: O2 binding skeletal and cardiac muscle
protein and elevates within 1 to 2 hours of cell death; peaks 6-7 hr; normalizes 24 hrs
RBC 4.2 – 5.14: increases in response to inadequate tissue oxygenation
WBC 4.5 – 11: # increase in response to inflammation from damaged myocardium
Coagulation factors VIII, IX, and XII: may increase during and after MI and increase
risk of Thrombophlebitis
Coagulation studies: PT, PTT, INR obtained as part of screening for thrombolytic
therapy in acute MI patients, wherein a question exists about potential for bleeding and if
there is an increased risk for thrombosis formation.
Cholesterol, HDL, LDL: HDL > 65 mg/dL is cardio-protective; HDL < 40 mg/dL is
associated with increased risk of CAD; optimal level LDL is <100 mg/dL; LDL is
considered high above 160 mg/dL and very high when > 190 mg/dL
Potassium 3.5 – 5.3 mEq/L: most abundant intracellular cation; decreased levels
contribute to dig toxicity, vent dys, small T waves (small tits), sagging (boobs) ST
segments, u (FU) waves, increased amt causes vent dys and asystole (aka flat boobs)…
hopefully that help to remember what K+ does…
Sodium 135-145 mEq/L: most abundant in extracellular [SEX – sodium extracellular]
and levels decrease with diuretics and with water excess associated with heart failure
Calcium 8.2-9.6 mg/dL: most abundant cation in the body!! [ABC-abundant Ca+
cation!] Increased levels lead to shortened QT intervals, AV block, tachy or bradycardia,
dig hypersensitivity, cardiac arrest, decrease amt may result in vent dys, prolonged QT
interval, cardiac arrest
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Magnesium 1.6-2.6: required for numerous enzymatic processes inc muscle contraction;
may cause V-tach, V-fib, Torsades de point, muscle weakness, HoTN, respers dep,
prolonged PR interval and widened QRS complexes are related to increased levels
BNP (B-type “brain” natriuretic peptide: differentiates heart failure from pulmonary
issues; a cardiac neurohormone secreted in response to ventricular volume expansion and
pressure overload. Levels may be obtained in pts with MI to assess for presence/degree of
ventricular dysfunction. If elevated, vent dysfunction is present.
C-Reactive Protein: marker for inflammation (more plaque); if elevated (normal range
0.003-1.11mg/dl), indicate coronary artery plaques are inflammatory, placing the patient
at higher probability of an imminent acute coronary event
Homocysteine (give B vitamins): by-product of protein breakdown; a toxic highly
reactive amino acid synthesized during protein catabolism. Pt’s lacking folate and
vitamins B6 and B12 have been shown to have elevated levels (>15mmol/L in critically
ill patients), which can lead to accelerated arterial plaque formation
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Directional coronary atherectomy (DCA): revascularization of coronary arteries by
insertion of a balloon tipped cath with attached cutter or rotoblator into coronary artery
and rapidly inflating – deflating balloon, as well and cutting or stripping away
compressed plaque and part of intimal layer followed by suction removal of debris.
Excimar Laser Angioplasty: revascularization of distal/& torturous coronary arteries
using a very flexible cath which contains a multi-fiber optical or glass material which
directs ultraviolet energy resulting in photochemical tissue vaporization. This procedure
allows precise cuts to atheroma, collagen, or calcium without injuring surrounding tissue.
Cardiovascular surgery –
Open heart surgery: treatment for CAD with coronary arteries that are at least 70%
occluded, Valvular dysfunction, and congenital heart defects
Grafts: Internal mammary artery and saphenous leg vein
Valvular Surgery: surgical txmt including valvuloplasty and replacement
Precutaneous balloon Valvuloplasty: procedure parallels technique for PTCA. A balloon
valvuloplasty cath is placed in a diseased cardiac valve and inflated three times for 12-30
seconds leading to decreased resistance to blood flow across the valve
Patient Eligibility: High risk for surgical complications, refuse surgery, > 80 yo, chose
this txmt over others
Complications: similar to cardiac cath and PTCA; embolization to brian, disruption of
valve ring, acute valve regurgation, Valvular re-stenosis
Nursing Implications: see cardiac cath
CABG (coronary artery by-pass grafting): surgical management for clients who do not
respond to less invasive txtments for acute or chronic cardiac ischemia. The internal
mammary artery and or a spahenous vein from a leg are used to bypass an occlusion or
lesion in one or more coronary arteries. A vein or artery is anastomosed (sutured)
proximally and distally to the diseased coronary artery to bypass blood flow around the
occlusion.
There are two methods of CABG. Saphenous vein revascularization is more common, but
results appear to be longer lasting with internal mammary artery revascularization. The
procedure used depends on the nature of the CAD and the condition of the vessels
available for grafting.
E. Pharmacology:
Anticoagulants: drugs that prevent the formation of a clot by affecting clotting cascade
(contra-i bleeding). Drugs like: warfarin, coumadin, lovenox (LMWH) is what is used.
Watch coag studies for effectiveness. Antidote is Vit K
Antiplatelets agents: also coag modifier, but works on initial step of the coag process,
preventing platelet adhesion (contra-i known drug allergy and bleeding)
Ex: ASA 81-325 mg; Plavix/clopidogrel 75 mg/300-375 loading dose [reduction of
atheroscherotic events; acute coronary syndrome without ST segment elevation]
Thrombolytics/fibrinolytics: break down or lyse clots (contra-i drug allergy and use with
other drugs that alter clotting); streptokinase 1.5 million IU infused over an hour
(indication- AMI and DVT); alteplase (Activase, tissue plasminogen activator) 100 mg
over 90 min (indication- AMI, PE, acute ischemic stroke)
Nursing Considerations: monitor for bleeding and watch coag studies
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Antidote: for thrombolytics – packed RBCs, fresh plasma, whole blood, or
Amicar/aminocaproic acid
Medications to lower blood cholesterol: Statins- Lipitor/atorvastatin 10-80 mg/day (HMG
– CoA reductase inhibitors; Zocor/simvastatin used to treat hyperlipidemia; Niacin the
vitamin can also be used to decrease lipids; and last class is fibric acid derivatives
Diuretics: Manage edema associate with heart failure and to control HTN, and heart
failure from diastolyic dysfunction; Lasix/furosemide 20-40 mg; K+sparing – Aldactone
for edema, HTN, heart failure 25-200 mg/day
Potassium Supplements:
6
Levophed
Vasopressin: 40 units IV bolus one time
Meds/Considerations:
With Bradycardia: check K+ and BP
Sinus Tachycardia: check pt-is it from pain? Hypovolemia? Stimulants? Exercise?
Atrial Tachycardia: chech pt- Vagal maneuver, Adenosine, Ca+ channel blocker
(diltazem), Beta blocker (atenanolol)
Sinus with 1 PVC: check pt- check electrolytes, stimulants?, monitor
V-tach: pulse or no pulse? Stable or unstable? See ACLS algorithm
V-fib: check pt and verify rhythm, follow ACLS algorithm
A-fib or A-flutter: 12 lead and determine if fib or flutter then Rx accordingly
1st degree heart block: check pt- observe, RCA blockage? AV or other ischemia? Drug
effect?
Iggy charts: 37-3, 37-6, and 39-3
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F. Coronary Arteries:
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Left heart cath: cannulation of femoral or brachial artery, advancement of cath thru aorta
into left atrium and left ventricle [complications- cardiac dsyrhy, MI, cardiac and
great vessel perforation, systemic embolization, infection at cath enterance cut down
site]
Nursing Interventions:
Pre-cath teaching
“A cath will be placed in a femoral or brachial artery using local anesthesia”
“You may feel a warm or flushing sensation when the dye is injected”
“You may feel a flutter with movement of the cath”
Post-cath procedure-really know these!!
Monitoring (chest pain, neuro changes, resp difficulties, VS, ECG, labs) and bed rest for
at least 8 hours, extremity used for cath insertion kept immobile, cath insertion site
observed for hematoma and or sheath care, venous and arterial if present, HOB NOT
raised more than 15 degrees (because don’t want hip flexion, almost a reverse
Trendelenberg), peripheral pulses, color and sensation of extremities checked (instruct
pt to immediately report changes), fluid intake encourage to get rid of dye, I & O
monitored, observation for adverse reaction to dye (if allergy to banana, avocado, really
watch!), monitoring and interventions associated with pharmacological, as well as
anticoagulation therapies
Echocardiogram (ECHO): Ultrasound technique used on the chest wall above the heart to
detect abnormalities of the left ventricular wall motion, measure ejection fraction
evaluate valve function, and estimate left ventricular end-diastole pressure (LVEDP).
Normal ejection fraction is >60%. Wall motion abnormalities or reduced ejection fraction
may indicate an MI and will help define any risk of heart failure.
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Intravascular Ultrasound:
ECG leads 12, 15, 18: 12 lead is designed for evaluation of the anterior, inferior, and
lateral walls of the left ventricle. Infarcts that extend to the right ventricle and/or the
posterior wall of the LV can’t be clearly detected by the 12 lead. Indications for 15 or 18
leads include: ST segment elevation suggestive of an inferior wall MI and T wave
changes. ECGs are performed approx every 30 mins for 2 hrs to determine if the pt is
having MI initially, and after done every 8-24 hours.
Thallium stress test with medications: used when exercise is not possible because of
physical disabilities or exercise intolerance. Either dypyridamole (Persantine),
dobutamine, or adenosine has been used to “stress” the pt. Not generally used for pts at
high risk of infarction or those who are experiencing acute MI, because the test can
prompt MI.
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Holter or ambulatory ECG monitoring: records ECG for 24 hrs or more and pt needs
to keep time log of when symptoms occur (palps, syncope, angina)
Electrophysiology studies (EPS):
Toxicology screens:
CXR: may demonstrate cardiomeagly, possible interstitial pulmonary edema secondary to
left vent failure
Magnetic Resonance Imagining (MRI): used to assess ventricular size, morphology,
function, and status of cardiac valves and coronary circulation. MRI generally provides
more detail than does computed tomography (CT).
CBC: may provide useful information regarding possible anemia or
infection/inflammation and can assist in differential diagnosis of chest discomfort.
Serum Electrolytes: May provide information regarding potential for development of
dysrhythmias or the cause of dysrhythmias occurring with chest discomfort.
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Impedance cardiography: external monitoring
Pulmonary Edema: left vent failure causing crackles, dyspnea at rest, disorientation, and
confusion especially in the elderly; can get air hunger, anxiety; severe-hemoptysis
Myocardial Infarction (MI): caused by imbalance between myocardial oxygen supply and
demand r/t decreased coronary artery perfusion; normal function is disrupted as ischemia
and injury lead to cellular death, MI necrosis evolves over 3 hours, scar tissue is formed,
ultimate size of infarct depends on txmt
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improve gas exchange with supplemental O2, ventilator, diuretics, high Fowlers position,
IV morphine to decrease O2 consumption
Cardiogenic shock: most acute and ominous form of pump failure, inability of heart to act
as a pump, occurs after severe MI, dysrh, CFH, PE, cardiac tamponade, or abdominal
aortic aneurysm, low survival rate; s/s: increase pulmonary artery pressures, decreased
CO, decreased BP in the absence of hypovolemia, cyanosis, decreased urine output,
decreased or absent pulses, anxiety, confusion; aggressive txmt: vasopressors –
dopamine, norepi (Levophed), dobutamine to increase contracitility, intra-aortic balloon
pump until surgical intervention available
Thrombophlebitis: refers to a thrombus that is associated with inflammation and can
occur in superficial veins, however, it usually occurs in the deep veins of the lower
extremities aka DVT
Pericarditis: inflammation of the pericardium; s/s: pericardial pain (leaning forward will
relieve pain)- chest, shoulder, arms, neck, back and increased with movement and
coughing, dyspnea, fatigue, increased temperature, increased WBCs, pericardial friction
rub (most definitive part of assessment); txmt: pain relief, antibiotics, anti-inflammatory
agents, can lead to pericardial effusion, cardiac tamponade, chronic/& constrictive
pericarditis
Ineffective endocarditis: Infection of circulatory micro-organisms that attach to an
endocardial surface, frequently involves heart valves; caused by streptococcus,
staphylococci, and fungi; infectious lesions, or vegations form on the heart; ports of
entry-oral, cutaneous, invasive or surgical procedures; Hx of IVDA, valve replacements,
MVP, or structural defects; s/s: fever, chills, night sweats, cough, weight loss,
musculoskeletal complaints, CHF, friction rub, MI, petechial splinter, hemorrhages,
Osler’s nodes, Janeway’s lesions, finger clubbing, and emboli; Rx: specific to infective
organism, valve replacement
Cardiac Tamponade: (muffled heart sounds) JVD, low BP, clear lungs; txmt: fluids,
dopa/epi, vasopressors, pericardial centesis
Myocarditis: Inflammation of myocardium secondary to pericarditis, systemic infection,
or allergic response; s/s: fever, pericardial friction rub, gallop murmur, pulsus alternans,
heart failure, fatigue, dyspnea, tachycardia, chest pain; Rx: analgesics, limit oxygen
consumption, cardiac glycosides, antibiotics, antidysrhythmics; complications: thrombus
formation, heart failure, cardiomyopathy
Rheumatic carditis aka rheumatic endocarditis: sensitivity response that develops after an
upper respiratory tract infection which occurs in about 40% of clients with rheumatic
fever; is characterized by the formation of Aschoff’s bodies, small nodules in the
myocardium that are replaced by scar tissue, but the most serious damage occurs to the
endocardium, with inflammation of the valve leaflets developing. Hemorrhagic and
fibrous lesions form along the inflamed surface resulting in stenosis or regurg primarly in
the mitral and aortic valves.
Cardiomyopathy: disorder of the heart muscle; txmt: palliative only for relief of Sx,
diuretics, cardiac glycosides, vasodilators, antidysrhythmics, beta-blkr, calcium
antagonist, avoid ETOH; goal of txmt: to optimize cardiac output
Dilated Cardiomyopathy (DCM): most common form, EF <40%, decreased CO,
progresses to heart failure; s/s: left heart failure, eventually sx of right failure
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Hypertropic Cardiomyopathy (HCM): Massive left vent hypertrophy leads to
hypercontration and rigid vent walls resulting in obstruction of vent outflow; s/s:
dyspnea, syncope, CP, dysrhy; Rx: ventriculomyotomy or muscle resection, MVR
Restrictive Cardiomyopathy (RCM): Restricting vent filling
Mitral valve insufficiency:
Post infarction angina:
Ventricular rupture:
Dressler’s syndrome: complication of MI, it is a group of syndromes together consisting
of pericardial effusion, pleural effusion, and pericarditis.
L. IABP:
Indications for:
Potential Complications:
Contraindications:
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Peaked T wave – from increase K+ (insulin D50 to tx)
Complex/Intervals:
P wave – atrial repolarization ~ firing of the SA node
PR interval – 0.12 – 0.20 sec (No more than [3] - 5 small boxes!) {Represents the period
from atrial repolarization to atrioventricular holding and is measured from the beginning
of the P wave to the beginning of the QRS complex} ~ from AV to bundle of His
QRS complex – < 0.12 sec (or fewer than 3 small boxes) depolarization of vent and is
measured from the beginning of the Q wave to the end of the S wave ~ Right and Left
bundle branch and Purkinje’s fibers
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T wave – represents vent repolarization
QT interval: 0.32 to 0.44 sec and represents from depolarization to repolarization of the
ventricles and is measured from the beginning of the Q to the end of the T wave
Asystole (confirm in 2 leads, CPR {x 5 30:2 cycles}, O2, ETT (endo trach tube), IV,
epinephrine, Vasopressin (ADH) may replace 1st or 2nd dose of epinephrine, atropine,
reversal cause {6H’s and 6 T’s}, consider pacing
NOT shockable!! Start with BLS ABC’s
Pulseless Electrical Activity (PEA): (CPR {x 5 30:2 cycles}, O2, ETT, IV, epi,
Vasopressin (ADH) may replace 1st or 2nd dose of epinephrine, atropine,
reversal cause {6H’s and 6 T’s}, consider pacing for bradycardias [ABCs/CPR]
16
V-tach aka V Flutter = **The R is flutter stands for regular and so is this strip…
Fairly stable VT with a pulse: (IV, 12 lead ECG, aminodarone [or lidocaine], for
torsades de pointes give magnesium, elective synchronized cardioversion)
Blocks – 1st degree, 2nd degree (type I {Mobitz I or Wenchebach}, and type II
{Morbitz II, pacemaker}), 3rd degree (pacemarker). For high degree blocks (type II or
3rd degree, the higher concern) consider atropine (to speed up “p”s, epinephrine and
dopamine (both for vasoconstriction)
1st degree: AV block >0.2 sec
17
2nd degree Type 1 or Mobitz I or Wenchebach(think old, sleepy man-watching
jeopardy, so his P wave gets farther and farther apart, until he snorts awake.) It is
transient and curious, self corrects and goes away.
2nd degree Type II: more Ps than QRS (2 to 1 “p”s) and pacemarker
18
L
BBB and 2nd degree AV Block, Mobitz Type II
3rd degree: “p” is the same and QRS is regular, but there is no rhyme or reason and will
have to do pacemarker
19
Unstable: IV, conscious sedation, synchronized cardioversion
Atrial Fib: Controlled response if ventricular rate < 100 bpm, uncontrolled ventricular
response > 100 bpm, oxygen, anticoagulants, cardioversion, dig (increase SV, preload,
stronger contractions), Ca+ channel blockers
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induced sustained VT at electrophysiological study when drug therapy is ineffective, not
tolerated, or not preferred; nonsustained VT with coronary artery disease, prior MI, LV
dysfunction, and inducible VF or sustained VT at electrophysiology study that is not
suppressible by class I antidysrhythmic drug
Considerations for at home with and ICD: carry an id card, wear medical alert bracelet,
carry list of meds and dosage, keep emergency # available, call physician after receiving
shock and don’t feel completely recovered, inform family members and friends, inform
airline security, and encourage family to take CPR class
Spikes: energy from the pacemaker (spike before p wave, targeted toward atrium)
Capture: Myocardium needs to capture energy or take the energy to depolarize the heart
Indications of pacing: High degree block (2nd type II or 3rd degree)
Indication for permanent cardiac pacing:
Atrioventicular block – class 1: symptomatic second-degree AV block,
symptomatic complete heart block; asymptomatic complete heart block with a
heart rate <40 beats/min or asystolic pause >/= 3.0 seconds while awake or after
AV node ablation
Chronic bifascular or trifascicular block – class 1: bifascicular block with
intermittent complete heart block; bifascular or trifascicular block with type II 2nd
degree AV block
Sinus Node Dysfunction – class 1: Sinus node dysfunction with documented
symptomatic bradycardia and symptomatic chronotropic incompetence
Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic syncope – class 1:
recurrent syncope associated with clear, spontaneous events provoked by carotid
sinus stimulation; asystole of > 3 seconds induced by minimal carotid sinus
pressure in the absence of any medication that depresses sinus and AV node
conduction
Tachydysrhythmias – class 1: symptomatic recurrent supraventricular tachycardia
refractory or intolerant to drugs and failing ablation
Pacemarker syndrome: when the pacemaker is not firing the correct way, they will have
CHF symptoms like fatigue
Prevention of complications: be sure that the pacemaker is firing correctly, check
battery/generator often
AED: automated external defib
Defibrillation: Not sure what type of defib, do 200 joules
Monophasic: 360 joules and Biphasic: 120 joules (One – I am clear, two – you are clear,
and three – we are all clear)
Indications for: De-fib: Pulseless V-tach and V-fib
O. Aortic Aneurysms:
Dilation or sac formation on wall of aorta which may involve one or all layers of arterial
wall. Generally classified as thoracic aortic aneurysm, or abdominal aortic aneurysm
(AAA).
Etiology: atherosclerosis, HTN, trauma, infection, or congenital defects of arterial wall
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Pathophy: damage to medial arterial layer causes loss of elasticity, vessel increases in
size d/t continuous pulsation of blood, eventually vessel ruptures and if untreated leads to
death
Fusiform – diffuse dilation, involves entire circumference of artery
Saccular – localized outpouching of arterial wall
Dissecting – blood separates layers of artery wall and forms cavity
False (pseudoaneurysm) – clot and connective tissue outside arterial wall, may be formed
after complete rupture and scar sac formation
Diagnostic Tests: ECG, X ray, sonogram of aorta, (transthoracic echocardiogram – TTE,
transesophageal echocardiogram – TEE), MRI, aortagram, CT scan, 80% of AAAs are
palpable
Desired Treatment Outcomes: control disease progression, modify risk factors, control
BP to prevent strain on tissues, early recognition of symptoms, prevention of rupture
Assessment -
Thoracic: pain, neck, shoulders, lower back, abdomen. Syncope, dyspnea, increased
pulse, cyanosis, weakness
Abdominal: pulsating mass in abdomen, systolic bruit heard over aorta, tenderness to
palpation, abdominal or back pain
****Rupturing – severe abdominal pain or back pain, lumbar, flank, and or groin pain,
HoTN, increase pulse rate, changes in LOC, cardiac tamponade
Surgical Management: removal of aneurysm and restoration of vascular continuity using
a vascular graft
Abdominal aneurysm resection: aneurysm excised and replaced with graft sewn
end to end
Thoracic aneurysm repair: thoracotomy or sternotomy approach, aneurysm
excised and graft sewn onto aorta, requires cardiopulmonary bypass for clients
with descending aortic aneurysm
Post op care: monitor for signs of graft occlusion or rupture; monitor for signs of
hemorrhage; assess for bowel or spinal cord ischemia; evaluate for distal embolization;
maintain chest tubes; instruct client not to lift more than 15 lbs for 6 to 12 weeks
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Precutaneous balloon Valvuloplasty: procedure parallels technique for PTCA. A balloon
valvuloplasty cath is placed in a diseased cardiac valve and inflated three times for 12-30
seconds leading to decreased resistance to blood flow across the valve
Patient Eligibility: High risk for surgical complications, refuse surgery, > 80 yo, chose
this txmt over others
Complications: similar to cardiac cath and PTCA; embolization to brian, disruption of
valve ring, acute valve regurgation, Valvular re-stenosis
Nursing Implications: see cardiac cath
Annuloplasty:
Commissurotomy or valvotomy:
Heart Valve replacement: Incompetent heart valves
Bioprostetic or heterografts (pig valves)
Mechanical
Homografts (human valves) from cadavers
Patient Eligibility: moderate to severe Valvular calcification, mixed stenosis and
insufficiency, pure insufficiency
Procedure: excision of old valve and placement of new valve during open heart surgery
Complications: similar to patients under going CABG surgery, with increased risk for
clot formation especially r/t artificial valves and Valvular endocarditis.
Nursing Interventions: see preop assessment and intervention, as well as post op
intervention for open heart surgery
Open Heart Surgery:
Pre op nursing assessment –
Patient History: cardiac/cardiovascular hx: HTN, CAD, current – past interventions &/
procedures
Pulmonary Hx: conditions which predispose pt to postop resp complications
including: pulmonary HTN, pulmonary congestion or edema, pre-existing lung
disease, pulmonary infections, advanced age or debilitation
Emotional disorders: anxiety disorders, depression
Social Hx: life style aspects which may affect recovery and future health
Labs: collaborative assessment and correction of abnormalities; collaborative assessment
and alleviation of infectious process (may postpone surgery)
Pharmacological Therapy: include current prescribed (dig, diuretics, beta-blockers,
psychotropic drugs, antihypertensives, anticoagulants, corticosteroids, and antibiotics)
OTC meds, supplemental, herbal therapies, &/ “recreational” chemicals
Anxiety reduction: Listen, support, encourage verbalization and ventilation, provide and
clarify information: videos, written materials, rehab guides
Prepare pt for and explain procedure: cardiac cath and angiography, pulmonary function
tests, ECHO, exercise stress test, ECGs, and CXR
Pre-op teaching: ICU tour, inclusion of family members, pulmonary hygiene teaching,
prepare pt for numerous tubes and machines, explain surgical prep and monitoring,
explain pain management, encourage smoking cessation, document teaching and pt
response
Intra op: general anesthesia, hypothermia: decreased metabolic need resulting in
decreased oxygen consumption
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Cardiopulmonary Bypass (CPB): (aka Extracorporeal circulation, heart-lung machine,
pump-oxygenator, extracorporeal membrane oxygenator) pump performs all perfusion
and gas exchange functions. CPB is accomplished by cannulation of inferior and superior
vena cava. Blood is diverted from heart to bypass machine, which oxygenates blood and
returns it thru a cannula placed in ascending aortic arch.
Procedure: CABG, valve replacement, congenital abnormality repair, other
Complications: shock, hemorrhage, hemolysis, kidney damage, lung damage,
embolization, CVA, inability to wean from CPB
Txmt: drugs, intra-aortic balloon pump (IABP)
Intra-aortic balloon pump (IABP): Counter pulsation device which supports a failing
heart by increasing coronary artery perfusion and reducing afterload, balloon inflates
during diastole forcing blood back into aorta and thru coronary arteries, balloon deflates
during systole causing decrease pressure or resistance in aorta and assisting forward flow
of blood thru the arterial system
Indications: Cardiogenic shock, pre or post infarction angina resistant to medical therapy;
AMI with or without mechanical defects (papillary muscle rupture, VSD, vent aneurysm)
or failed thrombolytic therapy; high risk or unstable clients waiting for cardiac
intervention (PCI), intra post and pre op CV surgery clients; low output syndrome; bridge
to cardiac transplantation
Contrai: Irreversible brain damage; thoracic or abdominal aortic aneurysm with or
without dissection; severe PVD; end stage heart disease without expectation of heart
transplant; aortic insufficiency
Complications: helium embolism (helium is the air used with the pump), leg ischemia,
renal artery occlusion (monitor urine output)
Rheumatic heart disease:
Requires review of atrioventricular and semilunar valves:
R. Cardiac Transplantation:
Heart Transplantation:
Indications: end stage cardiomyopathy, ischemic heart dz, valvular dz, or rejection of
previously transplanted heart
*Usually reserved for clients younger than 55 yo with other organs still functional
*Requires a donor heart from a person with comparable body weight and ABO
compatibility transplanted within 6 hours of procurement
Procedure: removal of diseased heart leaving posterior walls of atria followed by
anastomosis of atria, aorta, and pulmonary arteries
*Two unrelated P waves are noted on ECG (because of 2 SA nodes)
*Transplanted heart unresponsive to vagal stimulation (nerves are not attached)
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*Client does not experience angina
*HR approx 100 bpm, responds slowly to exercise or stress
Complications: rejection, HoTN, dysrh, weakness, fatigue, dizziness, endomyocardial
biopsies to rule out rejection, arterisclerosis or coronary arteries, HTN, HoTN, alterations
in CNS, GI, respiratory, and or renal function, psychological stresses, medication s/e
Client teaching: medication regimen, avoidance of crowds and individuals with
infections
Post-op cardiac innervation (lack of and implications):
Potential for additional p waves of ECG:
Prevention of infection of infection and rejection:
T. Hypertension:
Causes – generally defined as systolic BP > or = to 135 mmHg and or diastolic > = 85
mmHg; high BP
Primary or Essential HTN: No Known Cause, but has risk factors like: over 60, family
history, excessive calorie consumption, physical inactivity, excessive ETOH,
hyperlipidemia, smoking, stress, obesity, etc
Secondary: renal vascular disease, pheochromocytoma, Cushings, brain tumor, etc
Prevention of complication: decrease causative factors
Management: drug, decrease risk factors
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Blood pressure = cardiac output x peripheral vascular resistance
Systemic intra-arterial monitoring:
S1 (systole) is caused by the closure of the AV valves and semilunar valves open and
depolarization of the ventricles!!
Systole = “closing/contraction of the ventricle” {S = C}
S2 (diastole) is cause by the closure of the semilunar valves
Diastole = “draining of the atria into the vent” {D = F}
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Risk Factors: Smoking and pack-years, sedentary lifestyle, obesity, stress, chronic disease
like HTN and diabetes, hyperlipoproteinemia, socioeconomic status (like household
members, living environment, occupation, income-non modifiable, age, gender, race
4 Classess of cardiovascular disability:
Class I: cardiac disease – no limitations of physical activity
Class II: cardiac disease – slight activity; comfortable at rest and ordinary
activity results in fatigue, palps, dyspnea, or angina
Class III: cardiac disease – producing marked activity limitation; comfortable at
rest
Class IV: cardiac disease – resulting in inability to carry on physical activity
without discomfort; sxs may be present at rest
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Postural hypotension: drop in systolic pressure >15 mmHg and increase in HR > 15 to 20
beats/min when a person goes from lying down resting to 1 to 3 mins after going to a
sitting or standing position
Skin: Color - pallor, rubor, jaundiced, cyanosis; temperature, moisture, texture, tugor,
presence of lesions, cap refill, clubbing from chronic hypoxia
Pulses: rate, quality and rhythm, strength, equality between extremities, texture of vessels
palpated; soft, thickened, or tortuous, BP
Edema: local, dependent, generalized (anacrica), pitting, periorbital; Peripheral and
pulmonary edema and rapid unexplained increase of weight 10 lbs (1L=1 kg) in less than
a week (Urinary status – quantity, quality of urine and last time voided, Monitor I&Os!!)
Extracardiac causes of chest pain include: PE, pneumonia, bronchitis, pneumonthorax,
aortic arch or high thoracic aortic aneurysm, esophagitis, hiatal hernia, pleurisy, anxiety,
cholecystitis, choletithiasis, GERD, costochrondritis, musculoskeletal strain, anemia,
hypoglycemia, fractured rib or sternum, hyperthyroidism, obstipation, and bowel
obstruction.
Assessment of the precordium (area over the heart) involves:
Inspection and Auscultation [normal heart sounds- S1 S2, paradoxical splitting, gallops
S3 S4, quadruple, summation, murmurs, pericardical friction rub- high pitched scratchy
sound over tricuspid area with pt leaning forward
Palpation and Percussion: usually don’t do!!
X. Nursing Interventions:
Physical rest: keep back elevated while in bed or chair to promote oxygenation and
decrease chest discomfort, upright position increases tidal volume and decrease cardiac
work-load d/t decreased preload
Respiratory: encourage deep breathing to prevent secretion pooling, administer fluids
cautiously to prevent pulmonary edema
Promote Tissue Perfusion: by limiting activities which increase cardiac workload
Reduce Anxiety: provide therapeutic communication, encourage verbalization of post MI
expectations r/t lifestyle changes including activity level, encourage verbalization of
beliefs and fears r/t MI
Y. Patient Education:
*Mod activities to support myocardial tissue healing (about 6-8 weeks)
*Lifestyle mod: avoid activities which lead to chest pain, dyspnea, or undue fatigue
*Avoid extreme temperatures
*Maintain healthy body weight
*No smoking
*Alternate activity periods with rest periods
*Use strengths to compensate for limitations
*Avoid large/& hurried meals
*Restrict caffeine-containing beverages
*Modify calorie, fat and salt intake
*Take prescription medications and know names, dosages, as well as actions and side
effects
*Keep recommended medical appts
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*Pursue stress reducing activities
*Engage in physical conditioning with gradual increase in activity levels
*Manage occurrences of symptoms
*Report to emergency facility if chest pressure or pain not relieved by nitro
*Contact physician if the following occur: SOB, fainting, slow or rapid breathing,
swelling of feet /& ankles
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