Acute Coronary Syndrome

Nancy Stone PhD ACNP ANP CCRN

&
Linda Ethier MSN RN
After completing the assigned readings and attending lecture the student will:
Describe the patho-physiology of acute coronary syndrome and myocardial infarction.
Describe the clinical manifestations, collaborative care and nursing management for the patient with acute
coronary syndrome and myocardial infarction.
Identify major coronary arteries and the area of heart muscle supplied by each.

Interpret diagnostic data and differentiate between unstable angina, NSTEMI and STEMI by location.
Identify commonly used drug therapy in treating patients with acute coronary syndrome and myocardial
infarction.
Compare and contrast left heart catheterization and right heart catheterization and nursing care post procedure.
Describe percutaneous coronary interventional and coronary artery revascularization procedures.
Describe the nursing care of a patient who has had a percutaneous coronary intervention.
Identify major complications following a myocardial infarction.
Describe the patho-physiology, clinical manifestations, collaborative care and nursing management of the
patient with pericarditis, pericardial tamponade and cardiogenic shock.
Describe the patho-physiology, clinical manifestations, collaborative care and nursing management of the
patient with thoracic aorta dissection.
Acute Coronary Syndrome
Characterized by prolonged (> 10 minutes) of repetitive cardiac symptoms indicating ischemia; occurring @ rest
or with minimal exertion
Associated with either ST/T wave changes on EKG; or elevated cardiac enzymes, including Unstable Angina ,
and Non Q wave MI (NSTEMI), Q wave or ST elevation MI
However, treatment differs for STEMI
Angina & MI Interventions
All interventions relate to oxygen supply & demand
There is a decreased O2 supply in hypoxemia, such as anemia
An increased O2 demand in tachycardia, increased preload, increased afterload
The goal is to increase O2 supply (increase coronary blood flow) & decease O2 demand (decrease ht rate,
decrease preload & afterload)
Cardiovascular Assessment
Subjective Data:Personal/Fam HX, CP, Dyspnea, weight changes etc.
Physical Assessment: Skin, extremities, BP, JVP, Lungs, Precordium
Objective Data: Labs: CPK/ troponin
Hypo/ Hyperkalemia
Hypocalcemia
Serum NA
Normal electrical excitation of the heart
EKG: Einthovens Triangle
I, II, III measure differences in activity between the limb leads
AVR, AVL, AVF measure activity between the heart & the limbs
V1-V6 measure activity of heart on horizontal plane
12 Lead EKG
Testing: Non invasive
Holter monitor
Echocardiogram: TTE and TEE
Exercise stress test
Nuclear cardiography: Thallium Muga (multiple gated acquisition scan)
Echocardiogram Images
Cardiac Catheterization: Coronary Angiogram
Most definitive: most invasive
Purpose: To define clinically suspected lesion, assess pathophysiology of cardiac dx, information R/T LV function
CO= SVxHR
Right Ht Cath: venous access ; brachial or femoral: measures pressures: RA-RV-PA-PCWP Note: does not involve
injection of dye; measures pressure in heart chambers and pulmonary artery
Left Ht cath: arterial access; radial, brachial, or femoral : checks patency of coronary arteries
Left Heart Catheterization
Cardiac Cath : Followup Care
Bedrest 4-24 hours (Dependent on site closure method; and if PCI (percutaneous transluminal intervention)
was done post cath. Bedrest limited with radial site.
Supine; unless radial site access utilized
Insertion site nonflexed: check pulse, color skin temp with each VS check
Different closure devices: ex. Angioseal
Check ACT prior to sheath pull; usually can pull sheath when ~ 150
Complications: Bleeding/ hematoma, R/P Bleed
CAD Treatments
Medications
PTCA (percutaneous transluminal coronary angioplasty)
PTCA/ Stents (vessel must be considered @ about 80% blocked)
Rotoblade
Radiation therapy
CABG
CAD Treatment
Other Measurements
Pulmonary artery catheter: PAP: left ventricular function, norm:25/9 mean=15 (same as right heart
catheterization)
PCWP= approx. left atrial pressure & LVEDP
CVP: right atrial pressure
CO=4-8L/min
Electrophysiology Studies (EPS): To evaluate dysrhythmias
CPK/ MB/ Index & Troponin
Pulmonary Artery Catheter
Prinzmetal Angina
CP @ rest or sleep
Coronary artery spasm
May or may not have coronary atherosclerosis
Rx: calcium channel blockers
Myocardial Infarction
Life Threatening: formation of dead tissue
Coronary artery occlusion: may be spasm
Types: Anterior, Lateral, Inferior, Posterior
All three layers: Transmural
Through one or two layers: Nontransmural (nonQ wave MI; non STEMI)
Phys. Exam: pale, anxious, clammy, diaphoretic, SOB, nausea
Tests:Enzymes, CBC, BMP, CXR, BNP
Myocardial Infarction
Anterior: I, AVL, V1- V4
Lateral: I, AVL, V5- V6
Inferior: II, III, AVF
Posterior: V1, V2 (Tall R wave with ST depression)
All 3 layers: Transmural infarct
Not all 3 layers: Non Transmural infarct
Acute MI
Infarction Zones
Ischemia: ST depression, T wave inversion, Both changes above are seen in both leads
Injury: (1)subendocardial: still reversible, ST down 1 mm, transient, returns to baseline when pain subsides
(2)subepicardial: ST/T elevated, usually with Prinzmetal angina; often precedes an MI
MI: Q wave, ST elevated in affected leads, T wave changes for weeks or rest of life
Subendocardial MI: (no Q waves)
Infarction Zones
MI: Complications
Dysrhythmias: Ventricular
CHF/ Pulmonary Edema
Cardiogenic Shock
Papillary muscle dysfunction: follows impaired blood flow to coronary arteries
Papillary muscle rupture: 1st week post MI; floppy & inefficient valves
MI: Complications
Dresslers Syndrome: pericarditis post MI; fever, cp, dyspnea; EKG changes. CP intensifies with thoracic
movement & deep inspiration
Ventricular aneurysm: Occurs in weeks to years later
Ventricular wall rupture: death from cardiac tamponade
MI Complications
Cardiac cripple syndrome: patient resists resuming ADLs due to anxiety, fear of death, & disability
Thromboemboli: thrombus formation in the left ventricle; leads to systemic circulation, pulmonic emboli can
arise from deep leg veins. Early ambulation Important!!
ICU Psychosis: confused, personality changes, fear of death, sleep deprivation, death. Adverse effects from
drugs, hypotension, with impaired cerebral blood flow; isolation from family
MI Complications
Hiccups (Inferior wall MI)
N&V: Dysrhythmias
Abdominal distention: constipation
Curlings stress ulcer: GI prophylaxsis
Cardiac Rehabilitation
Phase I: CCU & medical Unit: Disease management, pt. & family education, activity progression, low level
exercise
Phase II: Discharge to Home & Community: Begin supervised exercise program or walk program @ home.
Education, vocational counseling, multiple evaluations & testing
Cardiac Rehabilitation
Phase III: Maintenance: Emphasis on resuming normal lifestyle, continued evaluation & assessment, individual &
prescriptive exercise program
Goals: risk stratification, limitation of potential adverse psychological consequences of CVD
Modification of lifestyle, alleviation of symptoms, reduction of morbidity & mortality, improvement of function,
decreasing probabiltiy of future clinical S&S of CAD
Dietary Issues
400 mg: Na = 1 Gm salt
4 Gm Na diet: no added salt
2 Gm Na diet: all salt eliminated from cooking
Salt is 40% sodium
All foods contain some sodium
Salt substitutes contain potassium
Teach patients to read labels
Beware of processed foods
Pericarditis
Acute
Chronic
Differentiate between pericardial effusion and pericardial (cardiac) tamponade
Pericarditis
Pericardium: The pericardial sac is a fixed fibrous structure normally containing approximately 20-30 ml serous
fluid. Can accommodate larger amounts of fluid without the patient becoming symptomatic if the accumulation
is done gradually
Pericarditis
Pericardial Effusion: Collection of fluid or blood in the pericardium. Acute & chronic forms. As the fluid or blood
increases in the pericardial sac, the sac fills to a point & then can no longer expand.
Pericarditis
Perciardial (cardiac) Tamponade:
As this increase in fluid/blood continues, the pressure within the sac compresses the heart. Attempts to correct
this deficiency by increasing the HR & contractility are often effective but temporary since fluid/blood within the
pericardial sac will further depress ventricular filling.
Eventually the right atrial pressure increases, enlarging the pressure gradient between the right atrium & right
ventricle and is termed Pulsus Paradoxsus
Pericarditis
Pericarditis
During initial healing period
Develops from pericardial irritation due to cellular debris & exudates in infarct area
May last up to 3 months
S & S: Atypical, long lasting chest pain, low grade fever, chills, diaphoresis, dyspnea, pericardial friction rub,
persistent ST segment elevation, dysrhythmias & atrial fibrillation
Pericarditis
Diagnosis: CXR, Echocardiogram (may show pericardial effusion); CT Scan, Cardiac MRI, CK/ MB elevated,
elevated Sed rate, & elevated WBC
Pain: sharp, stabbing, localizes to the left or right, shoulder, arm, elbow or neck. Aggravated by inspiration,
coughing swallowing, coughing. Relieved by sitting up & leaning forward
Pericarditis
Friction Rub: Grating, scratchy, scraping sound
Dyspnea is from compression of bronchi by distended pericardium
Treatment: Bedrest, NSAIDS, ASA, Motrin, sometimes steroids, antibiotics if bacterial
Pericardectomy: surgical removal of pericardium for recurrent disabling pericarditis; may do pericardial window
Chronic
Pericarditis
Chronic pericardial effusion occurs after pericardial inflammation
Atrial fibrillation is common
Constrictive pericardium leads to the pericardium being scarred & rigid
Effusive Pericarditis: constrictive pericarditis; thickened visceral pericardium leading to cardiac constriction
Adhesive Pericarditis: Involves entire pericardium & adjoining mediastinal structures
Complications of Acute & Chronic Pericarditis
Pericardial Effusion: excess pericardial fluid accumulates. If it builds up slowly, the pericardium stretches &
accomodates up to 2 Liters.However, Rapid accumulation bars pericardial stretch; as little as 80- 200 ml
can cause cardiac compression
Complications
Cardiac Compression: Muffled heart sounds, paradoxical pulse, decreased CO, decreased BP, increased CVP,
tachycardia & distended neck veins
Diagnosis: Echocardiogram, CXR, EKG, CT Scan, Cardiac MRI
Pericardial Tamponade
Increased CVPIncreased venous pressure/ neck vein distention. Reflects increase in right atrial pressure.
Decreased BP; narrowing pulse pressure Difference in systolic & diastolic pressure readings: normally
40mmHg ; will be less than 30mmHg in pericardial tamponade
Muffled Heart SoundsResults from increased pericardial fluid
Pericardial Tamponade
Pulsus Paradoxsus: Decrease in pulse volume & systolic BP greater than 10 mmHg during normal inspiration
related to changes in the left ventricular filling; produced by pericardial restriction and accentuated by
inspiration.
Sinus tachycardia resulting from decreased stroke volume
Weakened or absent peripheral pulses from decreased circulating blood volume
Pericardiac Tamponade
Rapid accumulation of fluid; decreased CO from pressure, decreased ventricular filling therefore, the
pericardium compresses the ventricles
BECKS TRIAD: decreased BP, increased CVP, & muffled heart sounds
Distended neck veins, tachycardia, dyspnea, pulsus paradoxsus
Treatment: Percardiocentesis: Pt in ICU with drain
Pericardial Tamponade
Nursing Care:
Ensure equipment for pericardiocentesis is available
Maintain IV line; monitor VS Q 15-30 minutes; changes in mental status; administer IV meds as ordered
Low Fowlers position; EKG; monitor telemetry strips
Assist with pericardiocentesis: removal of 100-200 ml dramatic improvement in pt.
Check for presence of Kussmauls sign resulting from restriction to diastolic filling (absence of normal fall in
pressure during inspiration)
Cardiogenic Shock
Definition: Impaired ability of the heart to function as a pump. Decrease in systemic blood flow resulting in
inadequate tissue perfusion. Often associated with Anterior Wall MI. Results from severe left ventricular failure
Causes: MI (lose 40-45% of myocardium), acute dysrhythmia, severe CHF, cardiac tamponade, cardiomyopathy,
spontaneous damage to heart valves
Pathophysiology
The cardiac output is severely affected.inadequate tissue oxygenation & severe hypoperfusion of the
tissueswhich will lead to metabolic acidosis
Cardiogenic Shock
Marked Depressed Cardiac Output.hypotension.inadequate tissue perfusion
Clinical Presentation:
Increased CVP
Decreased CO
Decreased CI
Hypotension (sys<80)
PCWP (> 18 mm Hg)= pulmonary congestion & peripheral edema
Increased HR
Cold, clammy skin, oliguria (< 20 ml/HR)
Cardiogenic Shock: Management
Vasopressors: Dopamine & Dobutamine
Alpha adrenergic stimulators: Norepinephrine
Afterload increases & deleteriously affects cardiac muscle
Vasodilators: Nipride & NTG IV
IABP
Other measures to improve cardiac function: improve O2, decrease workload, improve LV function, decrease pt.
stress
Thoracic Aorta Dissection
Acute and life threatening
Mortality rate 90% if not surgically treated
Tear in intimal lining allows blood to track between intima and media
Creates a false lumen of blood flow
Thoracic Aorta Dissection
As heart contracts, each systolic pulsation pressure on damaged area
Further dissection
May occlude major branches of aorta
Cutting off blood supply to brain, abdominal organs, kidneys, spinal cord, and extremities
Thoracic Aorta Dissection
Clinical Manifestations:
Sudden, severe pain in anterior part of chest or intrascapular pain radiating down spine to abdomen or
legs
Described as tearing or ripping
May mimic that of MI
Cardiovascular, neurologic, and respiratory signs may be present
Complications
Cardiac tamponade
Occurs when blood escapes from dissection into pericardial sac
Aorta rupture
Results in exsanguination and death
Diagnostic Studies
Chest x-ray
Trans-esophageal echocardiography-(TEE)
CT/MRI
Angiography
Collaborative Care
BP-maintain SBP 100-120 mm Hg
IV beta blocker
Esmolol (Brevibloc)
Metoprolol (Lopressor)
Calcium channel blocker
Sodium nitroprusside (Nipride)
Agiotensin-converting enzyme inhibitors
Collaborative Care
Surgical Intervention:
Resection of aortic segment and replacement with synthetic graft material
Endovascular grafts implanted percutaneously
Post-operative care:
Requires intense monitoring of pulmonary, cardiovascular, renal, and neurologic status