NUR 120 (UNIT 4) CAD, CABG and CHF 5.1- 6.1

Coronary Artery Disease is:
an umbrella disorder that includes:
– athereosclerosis
– angina pectoris
– acute coronary sndrome (can lead to MI if not resolved)
– myocardial infarction
– heart failure
– pulmonary edema
atherosclerosis is:
abnormal accumulation of fat in the arteries and arteries walls lipid deposit and fibrous tissue build up in the wall which leads to plaques which cause a decrease in blood flow
atherosclerosis is significant because:
it is the most common caused of CAD
atherosclerosis pathophysiology
foam cells (macrophages that have become distended with lipid) begin to form fatty streaks,
– fatty streaks build up to become fibrous atheromatous plaque
– these lead to damage to artery walls which causes an inflammatory response in the artery
– fibrous atheromatous plaque build up to become complicated plaques
– the inflamm response then leads to plaque build up
– the plaque build up slows blood flow
– the plaque can dislodge and becomes an emboli and may move to the brain or lung and cause stroke or death
Atherosclerosis clinical manifestations
– Acute Coronary Syndrome
– coronary ischemia
– coronary infarction
Angina and Coronary Artery Disease
– clinical syndrome with episodes of pressure and pain in the chest as a result of lack of O2 in the heart muscles due to insufficient blood flow to the myocardial tissues
– angina is progressive
How does activity effect Angina?
– it increases metabolic demands and O2 requirements which leads to exacerbation and angina caused by atherosclerotic disease
What may lead to an exacerbation of angina?
– significant obstrucution of major coronary artery
– high BP (increases O2 demand)
– cold weather (causes vasoconstriction)
– heavy dinner: blood shunt to the GI and increase in O2 demand, decrease peristalsis
Coronary Arteries and Angina
– right coronary artery becomes –> posterior descending artery
– left main coronary artery becomes –> circumflex and anterior descending arteries
– coronary arteries are filled during diastole
– if the coronary arteries are clogged and blood perfusion is decreased (along with diminished O2 supply) ischemia occurs and angina pain presents
clinical management and tx of angina
– decrease their O2 demand – REST (supine position)
– increase their O2 supply – NTG (sublingual, 3 doses every 5 mins, no more then go to ER)
– PCI/CABG
– Surgery to reduce plaque formation

**rest will resolve early angina, usually**

pharmacological tx of angina
– usually done in hospital
– O2 administration (increases O2 sat)
– Nitroglycerin admin (dilates coronary arteries and increases blood/O2)
– Beta Blocker admin (decreases sympathetic stimulation of the heart)
– Ca+ Channel Blocker admin (dilates blood vessels)
– Antiplatelet/anticoag admin (ASA) (thins blood/reduces viscosity)
Nursing Interventions for a pt with Angina
– start with assessment of pain (usu COLD AAA acronym)
– tx and prevent pain
– reduce anxiety
– teach self care
Myocardial Infarction and CAD
the left anterior descending (LAD) coronary artery is blocked with a blood clot causing damage to the heart muscle and reads with an irregular ECG/EKG
MI’s may also be called
– Acute Coronary Syndrome
– Heart Attack
– coronary infarction
Myocardial Infarction (diagram)
MI pathophysiology
– the coronary vessel is clogged by plaque and clotting factors
– the part of the muscle distal to blockage doesnt get blood or O2
– then the BP raises (sympathetic/parasym kicks in) increasing O2 demand
– heart rate and respiratory rate increases
– causes anaerobic environment which is ischemia
– ischemia causes pain
– no blood and no O2 causes infarction and necrosis of the tissue

**not all MI are the same**
**ask how bad was it?**

Where do MI’s mostly occur?
– anterior, inferior, lateral aspects of the heart –> right ventricle (ventricles)

**ask where was the MI occurred**

Typical causes of MI
– vasoconstriction that is persistent
– plaque
– clot
MI Chest pain is described as:
Severe, crushing, constrictive, heavy pain

**does not go away with rest or NTG**

SNS Response during MI
– GI distress, nausea, vomiting
– Tachycardia (HR increases) and peripheral blood vessels will vasoconstrict (shunts blood to the heart)
– Anxiety, restlessness (may be caused by hypoxia)
MI may lead to:
– following the SNS response, hypotension and possibly shock
– if not treated can lead to cardiac arrest

**the SNS response is a compensatory state and hypotension is a decompensatory state**

MI Hx and Phys findings
– take VS
– take ekg (tells where, if and how bad MI is)
– get CK, ISO and troponins from blood (these help to dx.)
– do phys exam and take hx
MI pt Tx goals
– promote tissue perfussion (give O2 to treat hypoxia, ntg, ASA, beta blocker admin, thrombolytic therapy: clot busting tx = all of these are to reduce the size of the infarction)
– relieve pain
– reduce anxiety
– prevent complications
What are some complications of an MI
– dysrhythmias (like complete heart block, tachy, brady)
– cardiogenic shock
– acute pulmonary embolism (potential)
– cardiac failure
– thrombo-embolytic episodes
Nursing Responsibility for pt with MI
– assessment dx (head to toe for cardiac signs)
– Planning: tx and prevent pain
– reduce anxiety
– teach self care
– probably in CCU

**when writing pathophys of MI you had better mention how the inflamm process, edema, WBC, etc are involved**

Acute MI Medical Treatment
– Drugs
– Percutaneous Coronary Intervention (PCI)
– Coronary Artery Bypass Graft (CABG)
Acute MI Thombolytic Tx:
– if patient is Dx by symptoms and EKG, begin this therapy.
– ideally begins within 3-6 hrs of infarction.
– must get informed consent from pt.
– contraindicated in pt with bleeding abnormalities or recent surgery.
– tx is systemic, usu pressure dressings, sml needles, hold pressure (5-10mins) when inserting IV.
Thrombolytic Tx is used to
– increase blood flow
– decrease size of infarction
– cause re-perfusion

**thrombolytic tx is called door to needle time. once throm tx occurs the patient must have access to PCI usu at cath lab.**

Nursing Care for Pts with MI’s
– ongoing assessment
– dx
– planning: (independent interventions and dependent interventions and collaborative interventions)
Immediate tx of an MI
M- orphine
O- O2 (standing orders)
N- NTG
A- ASA

**must watch respiratory rate, heart rate, LOC, etc**
**MONA**
**dependent and collaborative interventions**

MONA (memory)
MONA (memory)
Invasive Med Interventions for MI
– Percutaneous Transluminal Coronary Angioplasty (PTCA)
– Coronary artery stent
– CABG
– Heart Transplant
Percutaneous Transluminal Coronary Angioplasty (PTCA) (diagram)
Percutaneous Transluminal Coronary Angioplasty (PTCA) (diagram)
PTCA: Percutaneous Transluminal Coronary Angioplasty
– used for pts who have had acute MI, helps reperfuse,
– can use for angina and recurrent chest pains
– done in cath lab
– use angiography to locate of plaque
– surgeon uses fem artery and inserts balloon cath
– uses flouroscopy to place
– balloon inflates to compress plaque against wall
– insert stents to hold wall lumen open.
– can have angioplasty without stent placement
PTCA Nursing Considerations
– may cause coronary artery rupture
– may cause emboli from dislodged plaque to move to the brain
– may cause bleeding
– may cause hematoma formation
– do 5 P assessment
– with CABG you need to worry about clot, shock, impaired tissue perfusion
– keep leg straight and secure (sandbag, restraints)
Coronary Artery Stinting Pts Teaching
– not permanent solution
– must have lifestyle change to prolong lifetime of stent
– stent is coated with anticoag drugs to prevent coag
– risk of thrombus with stint
– wire mesh
Percutaneous Coronary Intervention (PCI)
an invasive procedure in which a catheter is placed in a coronary artery, and one of several methods is employed to remove or reduce a blockage within the artery
Complications of PCI’s
– dissection
– perforation
– abrupt closure
– or vasospasm of the coronary artery
– acute MI
– acute dysrhythmias (eg, ventricular tachycardia), and cardiac arrest.
Post operative Complications of PCI’s
– abrupt closure of the coronary artery
– bleeding at the insertion site
– retroperitoneal bleeding
– hematoma
– arterial occlusion
– acute renal failure
Periprocedure care for Pt’s receiving PCI
– Patients who are not already hospitalized are admitted the day of the PCI.
– Those with no complications go home the next day.
– During the PCI, patients receive IV heparin or a thrombin inhibitor
– are monitored closely for signs of bleeding
– pt may receive medication tx for several hours following the PCI to prevent platelet aggregation and thrombus formation in
the coronary artery.
– sheaths where PCI was inserted will be replaced after blood studies confirm that heparin is inactive and clotting times are normal
– The patient must remain flat in bed and keep the affected leg straight until the sheaths are removed and then for a few hours afterward to maintain hemostasis.
– Because immobility and bed rest may cause discomfort, treatment may include analgesics and sedation.
– Sheath removal and the application of pressure on the vessel insertion site may cause the heart rate to slow and the blood pressure to decrease (vasovagal response).
– An IV bolus of atropine is usually given to treat this response
– a pressure dressing is applied to the site
Coronary Artery Bypass Graft (CABG) (diagram)
Coronary Artery Bypass Graft (CABG) (diagram)
– A.K.A Coronary Artery Revascularization
CABG procedure (diagram)
CABG procedure (diagram)
CABG uses:
– can be used to prevent MI
– viable option pts with CAD
– variant angina (prinzmetal angina) happens at rest
– unstable angina
– positive exercise stress test
– pts not responding to NTG
– pts that have blockages that arent treatable by angioplasty
CABG Nursing Considerations
– need to preped for OR: clean skin, prep for gen anesthesia
– will use coronary artery bypass machine due to stopping heart
– blood vessels taken from another part of body and used for the heart (leg, mammary artery)
– pts will be on heparin – anticoagulated
– will be hypothermic 82-89 degrees (slow body processes like metabolic rate to reduce O2 demand)
– not permanent
Complications of CABG
– potential for death
– when veins are used they don’t last as long, not as muscular, not as many layers as arteries, will fail due to arterial pressure
– possible infection r/t long incision
– possible edema from removal of vein in leg
What veins are commonly used for CABG?
– greater and lesser saphenous veins
– mammary artery
CABG preop care
– preop teaching: IV meds – PCA – morphine, inc spiro, cough and deep breathe, splinting incision,
– phys and psych assessment
– pts who are less anxious do better postop
– health hx
– informed consent
– nursing process
Nursing Dx for CABG
– impaired tissue perfusion
– pain
– risk for infection
– impaired gas exchange r/t ineffective airway clearance
– altered breathing pattern
– anxiety
– decreased cardiac output
– activity intolerance
– risk for injury
CABG intraoperative care:
– Holding: Assess, prepare for OR & PACU
– IV lines are inserted
– Anesthesia –> ETT –> Mechanical Ventilator
– Periop RN: Assist with procedure and Ensure pt comfort and safety
CABG Postoperative care
– Hemodynamic stability (assess for pressures in and around the heart)
– Recover from general anesthesia
– Wound care (slow healing, dehiscence)
– Fluid and Electrolytes
– Progressive activity
– Diet
– D/C home in 3-5 days
CABG Complications
– MI
– Dysrhythmias
– Hemorrhage
– Stroke
– Infection
“Congestive” Heart Failure is
** r/t Inadequate Tissue Perfusion**

– Evaluate cardiac, pulmonary and systemic congestion
– when you have heart failure the heart is not able to provide sufficient O2 to meet tissue needs which results in inadequate tissue perfusion
– is contributed to by coronary artery disease
– can be acute or chronic (insidious-gradually occurring and moves from stage A to B to C to D)
– can be left or right sided
– A form of cardiac failure
– A syndrome – not a disease

CHF is usually a:
lifelong issue (chronic) some symptoms may be able to be resolved.
CHF Pathophysiology:
– systolic or diastolic overloading & myocardial weakness –>
– then as this physiological stress reaches critical level, contractility is reduced (pain is a late symptom) –>
– Cardiac Output declines –>
– Venous input to ventricles remains the same
CHF Acute vs Chronic Patho
– Acute – short term response (Ventricular muscle dilatation and increased force of contraction)
– Chronic – ventricular hypertrophy
CHF Etiology
– damage to the heart muscle (affects afterload)

– ventricular overload rt increased *preload*: 2° MI, IV fluid volume overload & kidney failure –> increased venous return

– ventricular overload rt increased *aferload*: 2° uncontrolled chronic HTN, valve problems
– constriction of the ventricles: r/t cardiac temponade

Cardiac Reserve is:
– the ability of the heart to compensate under stress
Cardiac reserve is affected by:
– increased sympathetic activity (fight or flight)
– Na and water retention (ALD, RAAS can increase preload)
– anaerobic metabolism of affected cells
– increased uptake of O2 by peripheral cells

**when these fail or overwork, cardiac reserve is affected negatively**

CHF Compensatory Mechanisms include:
– Tachycardia
– Ventricular dilation
– Cardiac Hypertrophy
– Changes in Vasculature, Kidneys, and Liver
CHF Compensatory Mechanisms (diagram)
CHF Compensatory Mechanisms (diagram)
Right and Left Hear Failure (diagram)
Left Sided Heart Failure (memory)
– notice he is in tripod position to facilitate breathing
Left Sided Heart Failure
– decreased cardiac output and pulmonary congestion
– from decreased Cardiac Output you see activity intolerance and signs of decreased tissue perfusion.
– if left ventricle is congested –> blood backs up into the pulmonary vein –> then into the lungs –> then into the pulmonary artery causing pulmonary congestion
– from pulmonary congestion you can have impaired gas exchange (alveoli and caps) which means the blood that moves through will have *less O2* which causes *decreased tissue perfusion*
– decreased tissue perfusion leads to cyanosis and signs of hypoxia.
– because of congestion in the lungs, capillary pressure in the lungs begins to change
– protein rich fluids begin to seep out of the caps into the alveoli which presents as *crackles* –> which leads to pulmonary edema
– pulmonary edema can show as a cough with frothy sputum (can be pinkish due to blood)
– orthopnea (pop up in bed to breathe)
– paroxysmal nocturnal dyspnea
– dont worry about elevated pulmonary capillary wedge pressure

**most of these symptoms are heart and lung related –> symptoms close to the heart**

With left ventricular failure there is
– a stroke volume problem
– compromised stroke volume and decreased cardiac output
Right Sided Heart Failure (memory)
Right Sided Heart Failure (memory)
Right Sided Heart Failure
– congestion is in the right ventricle
– blood will back up into the right atria –> & then the superior and inferior vena cava –>
which leads to congestion of peripheral tissue –> which leads to dependent edema and ascites (r/t portal HTN) and JVD
– can cause liver congestion
– from liver congestion may see signs r/t to impaired liver funx
– can caused GI tract congestion
– from GI you may see anorexia, GI disress and weight loss

**Most of these symptoms extend to more peripheral systems –> away from heart and lungs**

What is Systolic Heart failure?
– the most common type
– is when there is *alteration in ventricular contraction*

remember *systolic* = *contraction*

What is diastolic heart failure?
– is char by stiff and non compliant heart muscle
– wont relax enough to fill correctly
– *doesnt relax and fill properly* (Preload problem in ventricle)

remember *diastolic* = *relax*

What is Ejection Fraction?
– % of blood volume in the ventricle at end of diastole that is ejected during systole
– measure of contractility
– an indicator of severity of CHF

**% of blood volume in the ventricles that can be squeezed from the ventricles at the end of systole.**

What is normal ejection fraction
– we want it to be greater than 55%
CHF signs and symptoms:
– fatigue and tiredness
– hypertrophy (XRAY)
– lower ejection fraction (ECHO)
– SOB
CHF Dx studies
**help evaluate cardiac, pulmonary and systemic congestion**

– CXR
– Echocardiogram: shows = ejection fraction which is an indicator for severity of disease
– pulse ox (not diagnostic but indicator)
– hemodynamic monitoring

Lab Tests for CHF
– BNP – shows LVH (normals are 100 and under-usually)
– CK-MB – shows cardiac muscle stress
Stage A of Heart Failure
– Stage A Patients at high risk for developing left ventricular dysfunction but without
structural heart disease or symptoms of heart failure
– pts can usu have pretty normal lives with limited symptoms
Stage B of Heart Failure
– Stage B Patients with left ventricular dysfunction or structural heart disease who have
not developed symptoms of heart failure
– pts have slight limitations with ADL, symptoms with activity
Stage C of Heart Failure
– Stage C Patients with left ventricular dysfunction or structural heart disease with current or prior symptoms of heart failure
– pts have marked limitiation in ADL, comortable at rest
Stage D of Heart Failure
– Stage D Patients with refractory end-stage heart failure requiring specialized interventions
– pts can’t breath or manage themselves at rest (usu tx is heart transplant)
UNLOAD FAST for CHF
U – pts will be in *upright position* to help breathing – tripod
N – give *Nitrates* to vasodilate and increase tissue perfusion
L – give *lasix* (loop diuretic) to loose fluids (will loose K too)
O – give *O2*
A – give *ACE-Inhibitors* (chronic cough and angioedema can become hypotensive)
D – admin *digoxin*

F -* fluid restriction* (caution c IV fluids, 1500-2000ml of H2O or less)
A – decrease *AFTERLOAD*
S – *Sodium restriction* (less than 2g)
T – *Test* (ABG’s, digoxin level, potassium levels)

**will need to give potassium supplement due to lasix**

Treating Congestive Heart Failure (memory)
Clinical Mgt of CHF
– Decrease preload
– Decrease afterload
– Improve contractility
Conditions that decrease preload
– tachycardia (ventricles cant fill properly- effects stroke volume)
– venous stasis
– dehydration (either cellular or vascular): high temp, diarrhea, diuretics, heat
Things that affect Afterload:
– vascular tone (constricted vessels increase afterload and dilated vessels decrease afterload) –> System Vascular Resistance –> vasodilators and vasoconstrictors

**after load is is the pressure that the ventricles must overcome to eject the blood during systole**

Things that affect contractility:
– think Starling’s Law: the greater the stretch the greater the force of ejection until the muscle is overstretched then there is hypertrophy and weakened force of contraction

** it is the force generated by the heart muscles**

Nursing Care for CHF
– Nursing Process
– Assessment
– Promote Activity Tolerance
– Manage Fluid Volume
– Control Anxiety
– Be aware of conditions that affect preload/afterload
– Interventions that increase venous return which increase preload (foot pumps, massage – distal to proximal, elevate the lower extremities)
– fluid retention is a big deal (1500-2000 fluid per day or less)
– weight daily
– teach to weigh daily at home
– pt call md if more than 3 lbs of weight gain in one day
– need occup therapist to check to see if home is okay for activity level
– teach about diet
– may be on home health care
– may be on transplant list
– may have pacemeaker
Nursing Interventions for CHF
– Promote Activity Tolerance
– Reduce Fatigue
– Manage Fluid Volume
– Control Anxiety
– Minimize Powerlessness
– Promote Home and
– Community Based Care
Digoxin and CHF
– cardiac glycoside, PO, 0.25 – 0.125 mg, once daily
– decreases heart rate and increase contractility to decrease blood pressure
– Therapeutic serum digoxin levels range from 0.5-2 ng/mL
– be aware for Digoxin overdose
– antidote = digifab
– check apical and must be 60 or above
– pts are “digitalized” = at therapeutic level of drug
Digoxin overdose S/S:
EENT: Blurred vision, Halos around objects (yellow, green, white) *
Skin: Allergic reaction (see: Stevens-Johnson syndrome), Hives, Rash
GI: Diarrhea, Loss of appetite*, N/V, Stomach pain,
CV: Irregular heartbeat (or slow), Weakness
CNS: Confusion, Depression*, Disorientation, Drowsiness
Fainting, Hallucinations*, Headache, Lethargy
Psychological: Apathy (not caring what happens)

*are usu only seen in chronic toxicity

Dopamine drip and CHF
– vasodilator to increase tissue perfusion

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