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Study Guide=Cardiac

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

A. Acute Coronary Syndrome:


Stable Angina: no serum markers (like CPK or Troponin), no EKG changes
Unstable Angina: no serum marker, may have ST elevation, injury (more likely MI)
Myocardial Infarction (MI) Without ST segment elevation (NSTEMI or nonSTEMI):
+ for serum markers, no ST segment changes, with or without Q wave changes
MI with ST segment elevation (STEMI): + serum markers, ST segment elevation, with or
without Q wave changes

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)

Following acute phase (after 1st 24 to 36 hours)-


Assessment Findings- See letter W
Prevention- Normal ones
Treatments-
Risk Factors for cardiovascular disease- See letter W
Lifestyle changes/Cardiac Rehabilitation: (smoking cessation, dietary modification,
weight reduction, physical activity, control of diabetes, reducing hyperlipidemia, etc)

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)

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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

Variant (Prinzmetal’s or vasospastic, intractable, postinfaraction, Wellen’s syndrome)


Angina –
*Usually occurs at rest without other precipitating factors
*Caused by coronary spasm (coronary is clean, but the spasm closes off lumen,
restricting blood flow, causing possible ischemia), ECG may show ST-segment elevation
during pain
*MI may result from prolonged coronary artery spasm
Txmt: Ca+ channel blocker

Chronic Exertional Angina aka Stable Angina:


*May occur after large meal
*Digestion requires increased cardiac output resulting in increase myocardial oxygen
demands

Management and Implications: **Look over this below!!


Diagnostic studies for Angina: cardiac enzymes, cholesterol and triglyceride
levels, hemoglobin and hematocrit values, ECG studies at rest and during
exercise, exercise tolerance or stress testing, and coronary angiography
Complications from untreated or unstable angina: MI, CHF, dysrhythmias,
psychological depression
Medical Interventions: Nitrates, beta blockers (decrease HR and afterload, and
increase preload), Ca+ channel blocker
Patient Education: Use moderation in all ADLs, participate in all activities of
daily living which do not result in chest discomfort, dyspnea, or undue fatigue,
and avoid sudden exertional and all isometric exercise, avoid overeating, etc

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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

D. Coronary Artery Reperfusion/Revascularization:


Precutaneous Transluminal Coronary Angioplasty (PTCA): Revascularization of
coronary arteries by insertion of balloon tipped cath into a coronary artery and rapidly
inflating – deflating balloon to compress atheroma into intimal lining of artery resulting
in increased internal diameter and blood flow.
Patient Eligibility: Single vessel disease, uncompromised collateral flow, non-calcified
lesions in proximal 2/3s of coronary circulation, lesions accessible for dilatation, lesion
not present at vessel bifurcations, absence of left mainstem artery stenosis, must be
candidate for CABG surgery.
Procedure: balloon tipped cath inserted in manner of coronary arteriography, cath
threaded into occluded coronary and advanced with use of guide wire across the lesion,
balloon is inflated under pressure one or several times to compress lesion
Complications: MI, dissection of coronary artery, coronary artery occlusion, bleeding,
coronary artery spasm, embolization, decreased pulses distal to procedure site, intimal
trauma, adverse dye reaction, death
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”
Arthrectomy: device in which can either excise and retrieve plaque or emulsify it
Intra-coronary artery stents: revascularization of coronary arteries by insertion of balloon
tipped cath with attached stent (15 mm long tightly wrapped spring, slotted, or mesh tube
which becomes expanded with balloon inflation and is used to keep lumen open while
providing structural support)
Procedure: similar to PTCA with addition of stent placement
Complications: similar to PTCA with increased risk for coagulation
Nursing Interventions: similar to cardiac cath and PTCA including monitoring and
interventions r/t symptoms of re-occlusion (chest pain, SOB, diaphoresis, nausea, ECG
changes), stent re-occlusion may occur within 3 to 9 days after placement.

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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

Drugs that Enhance Contractility - Beta blockers and…


Digoxin: Inotropic/Cardiac glycoside which increases myocardial contractibility
and increased diastolic filling because augments vagal tone. Decrease rate of
electrical conduction, so prolong the refractory period in the conduction system.
0.5 to 2 ng/mL; digibind is antidote

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:

Antihypertensives: these consist of: diuretics, adrenergic agents, vasodilators, ACE


inhibitors, ARBs, and CCBs. They lower BP, CO, and peripheral vascular resistance,
uses: control HTN, antianginal, and HTN emergencies; contra-I is severe bradycardia;
never abruptly d/c
ACE Inhibitors: Ends in Pril like the month April
Beta-Blockers: Ends in OLOL
Meds for antihypertensive emergencies:
Norvasc/amlodipine, Calan/Verapamil, Procardia/Nifedipine, Cardizem (diltazem) are
the Ca+ Channel team [and Very Nice Drugs] and the Beta Blocker team is
Lopressor/metoprolol, Tenormin/atenolol, Inderal/propranolol, Corgard/nadolol [PLAN,
propranolol lopressor atenolol nadolol]

Antihypotensives (sympathomimetics): drugs to treat bradycardia and decrease BP


I = isoproterenol
D = dopamine
E = epinephrine
A = atropine

Prevention of V-tach = Mexiletine

Emergency cardiovascular care meds =


Drugs used with cardiac arrest:
Epinephrine: rtn of rhythm and pulse is the expected response 1 mg IV
bolus to start
Aminodarone: aka Cordarone anti dysrhy for vent dysrhy or atrial dysrhy
150 mg over 10 min
Dobutamine: aka Dobutrex 0.5 mcg/min IV infusion; increased BP is the
expected response

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Levophed
Vasopressin: 40 units IV bolus one time

Drug Therapy for Dysrhythmics:


Lidocaine: aka Xylocaine used for vent dysrhy bolus 1mg/kg
Amiodarone; Cardizem; Digoxin; atropine
Adenosine: aka Adenocard antidysrh 6 mg supravent tachycardia and
conversion to normal sinus rhythm

Drug Therapy for Vasodilation:


Nitroglycerine: Nitrate which is used as an antianginal and vasodilates,
relaxes vascular (arterial and venous) with more prominent effects on
veins, which decreases preload. Arteriolar relaxation reduces systemic
vascular resistance, which decreases afterload. In conjunction with beta-
blockers or Ca+ channel blockers to suppress tachycardia
Nipride: AKA Sodium nitroprusside/Nitropress a vasodilator and used for
HTN
Also, Beta blockers, Ca+ channel blockers, Anti platelet angents

Ca+ channel blockers: decrease O2 demand by causing peripheral arterial


vasodilation and by reducing myocardial contractibility and for the treatment of
coronary artery spasms (contra-I drug allergy, AMI, 2nd or 3rd degree AV block
[unless pacemaker present] and HoTN); diltiazem/Cardizem supravent dysrhy
0.25 mg/kg over 2 mins
Beta blockers: benefical because they help treat angina by slowing the heart rate
and decrease myocardial contractility (negative inotropic effect) and decrease rate
of AV conduction; basically they make you brady; atenanolol/Tenormin acute MI;
Coreg/carvedilol PO 3.125 to 25 mg bid used for HTN and heart failure;
metoprolol/Lopressor early MI
ACE inhibitors: decrease peripheral vascular resistance WITHOUT increase CO,
increase cardiac rate, and increase cardiac contractility
With Beta Blockers and Ca+ Channel blockers **watch for orthostatic HoTN!!!**

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:

Left Main Art: also known as the widow-maker


Left Circumflex Branch (Circ, LCX): supplies left atrium; posterior left ventricle
Left Anterior Descending: passes behind pulmonary artery and supplies anterior 2/3 of
intraventricular septum; anterior and lateral sections of left ventricle
Right Coronary Artery: supplies most of right atrium and right ventricle; SA node; AV
node; posterior portion of left ventricle
Indications of blockages according to artery:
Role of collateral arteries: between smaller arteries; helpful when larger arteries become
occluded

G. Diagnostic Tests and Procedures:


Cardiac cath with angiography: consent, labs, kidney function, coags, meds, diabetic, no
food, type and cross, chest x-ray, 12 lead, teaching, get weight and height too; Complex
procedure involving insertion of a catheter into heart and surrounding vessels to obtain
detailed information regarding structure and performance of heart, valves and circulatory
system.
Purpose: Confirm diagnosis of heart disease and determine extent to which disease has
affected structure and function of heart, establish existence of congenital abnormalities,
obtain clear picture of cardiac anatomy prior to heart surgery, obtain pressures within
heart chambers and great vessels, measure blood oxygen concentration, tension, and
saturation within heart chambers, determine CO, and perform angiography for
visualization of coronary arteries
Procedure: Dye injected thru a cath into coronary arteries. Radiographic pictures
recorded as dye progresses or fails to progress thru coronary circulation. Dye injected
into heart chamber and amount of dye ejected with next systole is measured to determine
ejection fraction or fraction of total end diastolic volume ejected during systole.
Right heart cath: placement of cath in femoral or brachial vein, advancement of cath into
right atrium, right ventricle and pulmonary artery [complications- cardiac dsyrhy,
venous spasm, infection at entrance cut down site, cardiac perforation, cardiac
arrest]

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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

Cardiac cath (Coronary angiocardiograhpy or cardiac catherization) from Baird: must


have client consent and client preparation; possible complications: myocardial infarction,
stroke, Thromboembolism, arterial bleeding, lethal dysrhy and death; follow up care –
restricted bed rest, insertion site extremity kept straight to prevent hemorrhage, monitor
vs to prevent another MI, and assess for complications
to determine presence and extent of CAD or Valvular disease as the cause of the chest
pain or myocardial infarction. Reliably determines the status of coronary perfusion to the
left and right sides of the heart. A radiopaque catheter is inserted thru a peripheral vessel
and advanced to the heart, where measurements are done of ejection fraction, degree of
stenosis of vessels and valves, status of pressures in the major vessels and chambers
(atrial and vent), and wall motion. Characteristics of lesions can be described for
prescription of most appropriate treatment. Cardiac cath also allows for direct injection of
thrombolytics into the coronary system during acute MI.

Angiography or arteriography: [Angiography aka cardiac cath] measure heart chamber


pressures, determine blood oxygen saturation, assess patency of coronary arteries, may be
followed with PTCA or CABG; Diagnostic radiography of the heart and blood vessels
using a radiopaque contrast medium. Types include magnetic resonance angiography,
interventional radiology, and CT. It can determine any pathological obstructions to blood
flow to the heart muscles.

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.

TEE (Transesophageal Echocardiography): Ultrasound technique done via a high


frequency transducer attached to an endoscope inserted into the esophagus as the patient
swallows. Provides clearer ultrasonic images of the heart.

Stress Testing: Treadmill: pt to avoid stimulants or depressants night before test


(coffee, ETOH, caffeine); Pt instructed to notify doctor of symptoms during test
(CP, dizziness, SOB)
Patient exercises while being monitored by electrocardiography. It’s purpose is to elicit
chest pain and document any associated ECG changes. Positive stress test results elicit at
least a 1-mm horizontal depression or down sloping ST segment in one or more leads that
last 0.08 sec. In addition, frequent premature ventricular complexes (PVCs) or runs of
ventricular tachycardia are suggestive of ischemia. Not indicated if acute MI is suspected.
Thallium treadmill stress test: normal myocardial tissue will accumulate thallium,
whereas infracted or ischemic areas will have decreased uptake, appearing as “cold
spots” on the scan. To identify areas of decreased uptake, the patient exercises after an
injection of thallium. A scan is obtained both immediately after exercise and 4 hours later
to determine if areas with decreased uptake fill in after 4 hrs. Ischemic areas that fill are
considered to have viable tissue and reversible damage, whereas areas that remain as
“cold spots” are diagnosed as infracted. For MI pts, generally used after the acute phase
of the MI.

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.

MUGA scan (Multiple-gated acquisition scanning): (MUGA, elevates LV function); IV


injection of the isotope technetium pertechnetate to evaluate left vent function and detect
aneurysms, wall motion abnormalities, and intracardiac shunting. In the stress MUGA
test, the same test is performed at rest and after exercise.

Radionuclide Imaging: technetiumpyrophosphate, thallium imaging (detects ischemic or


necrotic tissue), multigated cardiac blood pool imaging

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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.

H. Hemodynamics and hemodynamic monitoring:


Stroke Volume (SV): amount of blood ejected with each ventricular contraction; 60-100
mL
Ejection fraction: (EF) percent of blood ejected from the ventricle with each stroke; 60-
80% (usually from the left ventricle unless otherwise specified)
Cardiac Output (CO): volume of blood ejected by heart in L/min; CO=HRxSV; 4-7
L/min, affected by preload, afterload, contractility, muscle synchrony, and HR
Cardiac Index (CI): cardiac output adjusted by body size
Preload: volume of blood used to stretch resting ventricular muscle at end diastole
Afterload: resistance to blood ejected from ventricle; pressure ventricles must contract
against; determines amount of time cardiac muscles shorten and contract (increase
afterload, increase work-load, increase O2 consumption)
**High afterload increases cardiac workload and myocardial oxygen consumption
(decrease in stroke volume) [affected by outflow obstructions: aortic stenosis,
pulmonic stenosis, coarctation of aorta, HTN, vascular resistance)
PVR: Pulmonary Vascular Resistance –Right Ventricular Afterload
SVR: Systemic Vascular Resistance –Left Ventricular Afterload (stuff after the left side)
PAP (pulmonary artery pressure):
Starling’s Law: the GREATER the end-diastolic ventricular filling volume (the greater
the amount of stretch on myocardial muscle fibers) the greater the force of the next
contraction and therefore the greater the stroke volume
Mean Arterial Pressure needed to perfuse coronary arteries: >60 mm Hg required
Low Vascular Resistance: vasodilation, sepsis, elevated temperature, lactic acidosis
High Vascular Resistance: vasoconstriction, HTN, vasopressors

Hemodynamic monitoring – may reveal increased pulmonary artery pressure (PAP,


pulmonary wedge pressure (PAWP), decreased cardiac output (CO), and increased
systemic vascular resistance (SVR); invasive system used in CCare areas to provide
quantitative information about vascular capacity, blood volume, pump effectiveness and
tissue perfusion e.g. Swan Gantz and these are also used to double check usefulness of
cardiac meds
Pulmonary artery cath; systemic intra-arterial monitoring [fancy term for arterial line]

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Impedance cardiography: external monitoring

I. Acute and Chronic:


Congestive Heart Failure (CHF): may be acute or chronic; low output failure: not enough
CO to meet tissue oxygen needs; high output failure: secondary to excess demand on the
heart; systolic failure: poor contraction and ejection; diastolic failure: relaxation and over
filling with blood
Etiology: ventricle/s become enlarged, over filled stretched out and loose contractile
strength which diminishes CO; diastolic filling increases; volume increases leading to
increased pressure in the ventricle/s
Differentiating between types –
Right [for Rest of body] Ventricular: {dependent edema, hepatamegaly, JVD}
Left [for Lung] Ventricular: backward flow occurs in L atrium then pulmonary
veins; increased pulmonary congestion leads to impaired gas exchange, dyspnea,
and adventitious lung sounds, increased risk for contracting resp
infections{orthopnea, etc}
Txmt: treat existing sxs, prevent further complications, treat underlying cause
1. improve pump function, + inotropics (dig (better), dobutamine, /& dopamine),
decrease work load and O2 consumption, avoid stress/anxiety, elevate HOB to increase
ventilation by keeping abdominal contents off of diaphragm thus decrease preload,
alternate rest periods with periods of activity, vasodilators (NTG, morphine, captopril)
2. Intra-aortic balloon pump for severe cases of CHF which deteriorates into cardiogenic
shock, augments diastolic filling of coronary arteries, decreases afterload
3. Optimize gas exchange, supplemental O2, diuresis, monitor arterial blood gases,
decrease sodium intake, decrease fluid intake, cautious IV fluid admin
4. Promote adequate nutrition thru small low calorie, low residue meals
5. Monitor hemodynamics including CO, pulmonary pressures, and Central Venous
Pressure (normally 3-12 cm/h2o or 4-6 mmHg read with manometer or transducer zeroed
at mid-axillary line)

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

J. Complication of CAD, ACS and other disorders affecting the cardio


system:
Pulmonary edema: Flash ARDs, occurs secondary to CHF, acute life threatening for of
CHF, contractility and CO severely compromised, pulmonary vascular system becomes
engorged with fluid, can occur during AMI, decreases amt of pulmonary tissue available
for gas exchange; s/s: extreme dyspnea, cyanosis, severe anxiety, diaphoresis, pallor,
blood-tinged frothy sputum, arterial blood gases – severe acidosis and hypoxemia; 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.

K. Cardiac Murmurs, normal and abnormal heart sounds, gallops (S1,


S2, S3, S3):
Precordial landmarks [All People Enjoy Time Magazine]: Aortic area (2nd intercostals,
right), pulmonic area (left 2nd intercostals), Erb’s point (left 3rd intercostals), Tricuspid
area (left, lower 4-5th), and mitral (apical) area (left, mid-clavicle, 4-5th intercostals)
PMI (Papillary muscle infarct):
S3: Ventricular gallop (have pt lay on left side to hear better), mitral focused resp
assessment dyspnea, parasosimal crackles, JVD, oliguria
Murmur: Where do you hear the murmur the loudest? Loudness, timing, pitch,
configuration/shape, quality (blowing), grade (VI-loudest), location, radiation, duration,
and ausculatory sites:
Insufficiency = blowing Stenosis/stiff = harsh sound
Timing = systole or diastole?
AV – live open except during systole; stenosis – diastolic & insufficiency –
systolic
Semi lunar – live closed; insufficiency – diastolic & stenosis – systolic
Pericardial Friction Rub: distinct sound when two dry surfaces are rubbed together;
present in pericarditis; particularly when the disease process first starts.

L. IABP:
Indications for:
Potential Complications:
Contraindications:

M. ECG monitoring and interpretation:


Electrocardiographic paper:
1 (small) box on paper = 0.04 sec; 5 (small) boxes = 0.20 sec; 5 (large) boxes = 1 sec
Determination of heart rate:
6 second method aka Rule of 10s [ you count the number of P-waves to determine atrial
rate and QRS complex to determine vent rate; count the number of these complexes in a 6
second strip {or every 30th large box} and multiply by 10 [ex. 6 complex per strip is 6 X
10 = 60 is the estimated HR
Rule of 300 [memorize 300, 150, 100, 75, 60, 50; start at a complex near the beginning of
a large box and count down – 300…150…100…etc until you reach the next similar
complex and that will determine the estimated HR
Normal and Abnormal waves:

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Peaked T wave – from increase K+ (insulin D50 to tx)

Flattened T wave – decrease K+


Inverted T wave - ischemia
Junctional – there is no P waves

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

Precipitating factors: MI, vagal stimulation, stimulants, anxiety, depressants, trauma,


acid-base disturbances, electrolyte disturbance, myocardial ischemia, medications,
congenital defects

6 H’s: Hypovolemia (trauma, dehydration), Hypoxia, Hypo/Hyper K+, Hypoglycemia,


Hypothermia, H+ ion (acidosis)

6 T’s: Thrombosis (heart), Trauma, Tamponade, Tension pneumo, Toxins, Thrombosis


pulmonary

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]

Pulseless or Unstable Ventricular Tachycardia (VT) or Ventricular fibrillation


(VF): Can defib with these rhythms!!!
(CPR, O2, defib with 1 shock, CPR, defib with 1 shock, CPR, ETT, IV, epi if still no
pulse, vasopressin may replace 1st or 2nd dose of epi, CPR, shock, CPR, aminodarone
(dysrhythmia) or lidocaine, consider magnesium (if hypo-mag), CPR)

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V-tach aka V Flutter = **The R is flutter stands for regular and so is this strip…

**Just think the “I” in fib is irregular 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

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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

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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

Atrial Tachycardia, PAT, SVT


Stable: vagel maneuvers, adenosine (may make them flat line), Ca+ Channel blocker,
beta blockers
Unstable: Ativan or Versed, IV, conscious sedation, synchronized cardioversion (low
energy level then what you use to shock)

Irregular narrow-complex tachycardia (timing of QRS) (atrial fib, atrial flutter, or


multifocal atrial tachycardia {MAT}:
Stable: Ca+ channel blockers, beta blockers

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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

ECG Changes: Pathologic Q wave, ST segment elevation or depression, changes in QRS


complex (Q wave or LBBB) consistent with ischemia, infarction, injury, hypo-
hyperkalemia, hypomagnesemia (torsades de point) (Homag is not one of the H’s)

Sinus Bradycardia – if symptomatic – O2, atropine, TCP, permanent pacer

Sinus Tachycardia - treat cause

N. Pacemakers and other electrical therapies:


Temporary (transvenous, epicardial, TCP)
AICDs: Class I Know this!! *cardiac arrest due to VF and VT, not due to transient or
reversible cause; spontaneous sustained VT; syncope of undetermined origin with

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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

P. Valvular Heart Disease:


Mitral stenosis: Increased left atrial volume and pressureatrial hypertrophy
acute/chronicacute: increased pulmonary pressurepulmonary congestion and edema;
chronic: increased pulmonary artery resistancepulmonary HTNdecrease lung
compliance
Mitral regurgitation: blood backs into left atrium during left vent systole [decrease
CO]increased left atrial pressureincreased pulmonary vascular pressurepotential
pulmonary edema
Tricuspid stenosis: decreased systemic venous return to the right ventincreased right
atrial volume and pressuresystemic venous congestionperipheral edema and liver
enlargementascities
Aortic regurgitation: blood leaks into left vent during diastoleincreased volume in left
ventleft vent dilationleft vent failure

Valvular Surgery: surgical txmt including valvuloplasty and replacement

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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:

Q. LVADs (Left Ventricular Assist Devices):


Mechanical device which assists a person with heart failure temporarily in order for heart
to recover or a temporary measure for a severely diseased heart while waiting for a donor
heart transplant
LVAD – inserted into abdomen and attached to client’s aorta and left vent
Artificial Hearts – designed to replace both ventricles and client’s heart has to be totally
removed

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:

S. Review Peripheral vascular disease:


Peripheral arterial disease (PAD):
Raynaud’s disease/phenomenon: occurs in people older than 30; etiology – unknown;
caused by vasospasm of the arterioles and arteries of the upper and lower extremities,
usually unilaterally. Txmt is relieving or preventing the vasoconstriction by drug therapy
like procardia, vasodilating agents may help relieve the symptoms, but lead to
uncomfortable s/e. For severe cases, lumbar sympathectomy can be performed. Physician
cuts sympathetic nerve that was causing vasoconstriction. Minimize cold exposure, stop
smoking, and decrease stress.
Buerger’s diease or thromboangitis obliterans: uncommon occlusive disease limited to
the medium and small arteries and veins. The distal upper and lower limbs are mostly
affected. Usually found in young men who smoke. Cause unknown, except possible
correlation between this disease and tobacco use, so txmt is to stop smoking!

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

U. Blood pressure regulation:


Autonomic nervous system – Vagel nerve  Vegas BABY!! What regulation happens in
Vegas stays BEER [there]!
Baroreceptors: located in the aorta, carotid and wired into the brain stem and senses bp
Chemoreceptors: located in the aorta, carotid and wired into the brain stem and senses bp
Renal (rennin-angiotensin-aldosterone mechanism): Renninangio I angio
IIvasoconstriction [like ACE inhibitor] which releases aldosterone from adrenal cortex
Endocrine system (aldosterone, ADH aka vasopressin): ald-adrenal; pit-ADH
External factors: pain, anger, physical activity, stress, cold/hot weather

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Blood pressure = cardiac output x peripheral vascular resistance
Systemic intra-arterial monitoring:

V. Review Anatomy and physiology of vascular system and heart:


Review of structure and function: Within mediastinum between lungs, apex rests on
diaphragm and purpose is to pump blood!
Three muscle layers – epicardium (outer layer), myocardium (middle, utilizes 70-80% of
delivered oxygen), endocardium (inner)
Mechanical and electrical cycles:
Electrical Conduction:
SA Node (60-80 intrensic rate)  AV Node (40-60 rate)  Bundle of HisAV
Junction Bundle Branches (left and right respectively) Purkinje Fibers
Myocardial cells

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}

Cardiac Muscle properties –


Conductivity: each heart cell’s ability to transmit electrical impulses rapidly and
efficiently to all areas of the heart; conduction velocity/speed
Rhythmicity: ability of the heart muscle to depolarize in an organized rhythmic
fashion (antidysrhythmics- aminodarone)
Automatcity: ability of each heart cell to beat spontaneously and generate an
impulse without external stimulation (problem-PVCs, cells beat wrong)
Excitibility: each cell’s ability to respond to electrochemical stimulation (epi and
nor-epi)
Contractility/Inotrophy: ability of muscle fibers to adjust force and speed of
muscular contraction (Dig-increase contractility; beta and Ca+ decreases it, CHF
and a-fib affect it)
Refractoriness: rest period, a time following effective stimulation, during which
the heart muscle fails to respond to a normal intensity stimulus

Link to medications that modify the various properties:

W. Review assessment of the vascular system and heart:


Gathering relevant historical: Familial hx of coronary artery disease (CAD), age >70 yo,
male (risk for females increases after menopause), cigarette smoking,
hypercholesterolemia, hyperlipidemia, HTN, diabetes, obesity, increased stress, sedentary
lifestyle
Familial/genetic: see above
Demographic Information: see above

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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

Subjective and Objective Information: n/v, dyspnea, orthopnea, anxiety, apprehension,


diaphorsis, unexplained weakness and fatigue, cyanosis, and denial, heartburn, syncope,
congestive heart failure.
General appearance: Presence or absence of distress; LOC, logical thinking indicates
cerebral perfusion, respiratory pattern, general health, self maintenance, weight, skin
S-Sx: palpations, syncope, cyanosis, n/v, assess for JVD (right side backin’ up!! –
normally distends no higher than 2 cm above sternal angle), may have temp due to
inflammatory response
LOC: may be decreased due to hypoxia
VS: Including pain: elevated bp – may be related to sympathetic response to the pt’s pain,
BP may also be decrease when pain is caused by ischemia or infarct. HR may increase in
response to hypoxia and enhanced sympathetic tone, or pt may have dysrhythmias such
as brady. Other chest sounds may include a pericardial friction rub, crackles in the lungs,
and new murmurs. The elderly may manifest sensorimotor and cognitive deficits if stroke
is also present.
Pain: discomfort, heaviness, pressure, indigestion, aching, choking, strangling, tingling,
squeezing, constricting, or vise-like are used to describe pain [women-don’t often
experience pain the chest, but rather feelings of discomfort or indigestion] {approx 20-
60% of MIs are silent occurring with no presenting s/sx, could even be up to 80%}
Pain Assessment: Onset, manner of onset, duration, frequency, precipitating factors,
location, radiation, quality, intensity (scale from 0-10)
Heart sounds: Increased HR, sinus brady, atrioventricular (AV) blocks, or vent ectopy. S4
heart sounds may be audible during ischemic and infarct episodes. Abnorm split of S1
and S2, as well as S3 if left sided-heart failure ensues. S3, S4, murmurs
ECG: first ECG done immediately to differentiate AMI from angina and other causes,
plus to help determine suitable antiplatelet meds (often given to pts with unstable angina
or NSTEMI) verses thrombolytic therapy or other reperfusion strategies (coronary
angioplasty) for MI.
Pulmonary status – (dyspnea on exertion (DOE), paroxysmal nocturnal dyspnea (PND)
after lying down for several hours, orthopnea when lying flat, crackles, wheezes,
hemoptysis, etc) possible clubbing; respirations – get rate, depth, effort, and adventitious
sounds (Note: you can get wheezes from non selective Beta Blockers)

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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

Z. Open Heart Surgery:


*NG tube to decompress stomach from ‘escaped air’
*ET tube for providing mechanical ventilation, ventilatory assistance, suctioning and use
for end-tidal CO2 monitor (within 4 hours of getting off vent, get up and sit in chair)
*Swan-Ganz cath for monitoring CVP, pulmonary artery and pulmonary artery wedge
pressures, temp, SaO2; can be used for determining CO, for venous and pulmonary artery
blood sampling, and for med admin. Venous lines can be used for fluid admin; fluid
intake is monitored.
*ECG electrodes for monitoring heart rate and rhythm continuously
*SaO2 monitor for measuring arterial oxygen saturation continuously
*Assess peripheral pulses: radial, popliteal, posterior tibial, dorsalis Pedis
*Neuro assessment: LOC, hand grasps, pupils, pain
*Assess skin color and temp, color of lips, and color and cap refill
*Epicardial pacing electrodes to temporarily pace the heart
*Mediastinal and pleural chest tubes attached to suction; drainage and wound healing are
monitored
*Radial arterial line with wrist armboard; used for monitoring arterial blood pressure and
blood sampling
*Indwelling cath to closed drainage system for accurate output monitoring, a temp probe
may be part of the indwelling cath.
*Complications: aspiration, pneumonia, oral care, hemorrhage, H&H, electrolytes,
kidney fx, dysrh, d/c, organ failure, cardiac tamponade, MI, heart failure, infection, post
cardiomyopathy syndrome, post perfusion syndrome (whole body gets involved with
inflammatory response), hepatitis
*ECG changes/changes assess of MI:
-ST segment elevation/depression
-wide/deep Qs
-STEMI, NSTEMI
-T inversion
-Bundle branch block

***GO OVER ALGORITHMS!!!!!

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