Transcript 3.Angina and Acute Coronary Syndrome # 3 GDE revised 2015 (LC).

Angina Pectoris and
Acute Coronary Syndrome (ACS)
Jenny Huri 2015
PATHOPHYSIOLOGY
 CAD refers to the development and progression
of plaque accumulation in the coronary arteries.
 It is a continuum that starts with:
stable angina-> unstable angina-> MI
Smeltzer and Bare (2004) Management of Patients with Coronary Vascular Disorders – pg723-730
Angina Pectoris
 Angina Pectoris is
the result of
myocardial ischaemia
caused by an
imbalance between
myocardial blood
supply and oxygen
demand.
 Angina or chest pain
is the common
symptom of this
imbalance.
What is happening?
 Coronary blood flow becomes inadequate to
meet myocardial oxygen demands
 Myocardial ischaemia develops
 Contractility decreased , CO decreased
 Myocardial cells switch from aerobic to
anaerobic metabolism due to cellular hypoxia
(10 seconds)
 Lactic acid produced – irritates sensory
afferent nerve fibres in coronary arteries,
myocardium and upper thoracic posterior nerve
roots.
Types of Angina
 Stable –chest pain
precipitated by
exertion or stress.
Myocardial oxygen
demands increased.
 Unstable (preinfarction)
chest pain occurring at
rest.
 Intractable - severe
 Silent ischaemia diabetics
 Prinzmetal Angina
(varient) - vasospasm
http://www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/18054.jpg
Angina
 http://www.bing.com/videos/search?q=stable+angina&qs=n&form=QBVR
&pq=stable+angina&sc=6-13&sp=1&sk=#view=detail&mid=B777293AD5EAE34D41EDB777293AD5EAE34D
41ED
Clinical manifestations
 Pain – varying in severity
 Pain often felt deep in




chest (retrosternal)
may radiate to neck,jaw,
shoulders and inner aspects
of upper arms (left)
numbness with pain
SOB, diaphoresis, nausea
and vomiting, dizziness
light-headedness,syncope
subsides with rest or GTN
(glyceryl trinitrate
Common sites of Anginal pain
Diagnosis and Management
Management
Diagnosis
 clinical picture
 12 lead ECG
 bloods
 stress exercise
 echocardiogram
 nuclear scan
 angiography
 objectives are to
decrease oxygen
demand & increase
supply & prevent MI
 oxygen
 pharmacological
 revascularisation
 reduce anxiety
 self care and lifestyle
changes
SDL – Teaching Plan
Acute Coronary Syndrome
 Unstable angina and acute MI
 Same disease process on different points
along a continuum
Pathophysiology of chest pain

Lewis Pg 868
narrowing of coronary arteries
insufficient blood flow
myocardial oxygen demands exceed supply
anaerobic metabolism with lactic acid accumulation
Myocardial nerve fibres irritated
pain message transmitted to cardiac nerves and upper posterior
nerve roots
Myocardial Infarction (MI)
Exterior views of the heart
Anterior view
Posterior view
http://heart.healthcentersonline.com/angiogram/coronaryangiogram.cfm acquired 24-04-06
Myocardial Infarction
Occlusion of coronary
artery for >4-6hrs
Cell death -irreversible
necrosis of
myocardium
Cause of over 40% of
all deaths in NZ
“Time is muscle”
What happens in a MI ?
 http://www.youtube.com/watch?v=H_VsHmoRQKk&feat
ure=related
Myocardial Infarction
What has happened ?
 myocardial cells are
permanently destroyed
 reduced blood flow in
coronary artery
 cell injury and necrosis
 Pain usually longer than
30mins
 characteristic ECG
changes
Phases of an MI
Phases of an MI
MI Locations
 Right coronary artery supplies R atrium, R ventricle,
and part of posterior and inferior surface of L
ventricle as well as part of AV & SA node and bundle
of His
 Circumflex mainly supplies parts of the left atrium
and left ventricle
 Left anterior descending (LAD) coronary artery
supplies portions of the R & L ventricular myocardium
and most of the interventricular septum
 Circumflex and LAD branches of left main
CLINICAL MANIFESTATIONS
 Severe chest pain not relieved by rest and/or GTN
Pain may radiate to arms, neck , back and jaw
 Hypertension/hypotension brady/ tachycardia
 Anxiety, fear , feeling of doom
 Lightheadedness and syncope
 Neuro changes – disorientation, restlessness
 Dyspnea, rales, cough (could be productive )
 Diaphoresis with clammy skin and facial pallor
 Nausea and vomiting and /or hiccups
 ECG: ST elevation/ depression, Q waves, T wave
abnormal
 May present with fever
Smeltzer and Bare (2004) Management of Patients with Coronary Vascular Disorders – pg723-729
Class assignment
Discuss the clinical manifestations of an acute
Myocardial infarction with reference to
pathophysiology, under the following headings.
 cardiovascular
 respiratory
 genitourinary
 skin
 GI
 neurological
 psychological
Divide into 4 groups and pick a spokesperson
DIAGNOSTIC TESTS
 Blood tests (Troponin T&I, CPK-MB )
 Electrocardiograph (ECG): ST
elevation/depression Q waves and new
LBBB
 Imaging tests
 Echocardiography – evaluates ventricular
function
WHO markers = History of severe prolonged
chest pain , abnormal persistent Q waves
and changes in serial enzymes that indicate
injury and infarction
 Lewis page 706-710 (821 -824)
Smeltzer and Bare (2004) Management of Patients with Coronary Vascular Disorders – pg723-729
NSTEMI (non ST elevation MI)
 No ST elevation …. If
Troponin is Pos. the diagnosis
is Acute MI.
 Neg. Troponin the DX is
Unstable Angina.
S T Elevation M. I.
Evolution of an acute MI
http://www.frca.co.uk/images_main/resources/ECG/ECGresource44.jpg
Effects on ECG
Farrell, M. (2005).Textbook of Medical Surgical Nursing,
Philadelphia: Lippincott. p.730
STEMI - InvasiveTreatment
http://www.youtube.com/watch?v=36_qHWLFzI0
Differential diagnosis -MI
Anxiety
 Aortic stenosis
 Asthma
 Billary colic
 Indigestion
 CORD
 Chest infection
 Aortic dissection
 Myocarditis
 Pericarditis
Emergency Care for MI
FIRST:
 MONA
Morphine,Oxygen,Nitrate,Aspiri
n
PROCEDURES:
 IV access
 ECG
 Cardiac Monitoring
 SpO2
 CXR
 Bloods -Troponin I & T & CK-MB
 Invasive therapy
MEDICATIONS:
ß-blockade
ACE inhibitor
Thrombolysis
Heparin - IV
LMWH (low molecular weight
heparin)- Sub cut
 Platelet aggregation inhibitors
(IIb/IIIa)
 Anxiolytic (anti-anxiety drugs)





Management of MI
Goal is to minimize damage, preserve function and
prevent complications
 Reduce and eliminate Chest pain
Morphine IV
Oxygen ( Myocardial oxygen demands exceed supply )
Nitroglycerin spray
Aspirin
 Monitor for decreased systemic and Myocardial
tissue perfusion.
Monitor abnormal heart rate,rhythm,BP, Resp,cyanosis,
decreased urinary output and confusion
Prepare for Reperfusion Therapy –Thrombolysis if candidate
 Pharmacological management
 Reduce anxiety
Nursing Management Plan
 Chest discomfort related to imbalance between
myocardial oxygen demands and supply
Goals detection
reduce or eliminate
prevention
 Decreased myocardial tissue perfusion related to
imbalance between myocardial O2 supply and
demand
 Decreased systemic perfusion related to decrease in
cardiac output
 Fear or anxiety from patient and family related to Dx , Tx
and prognosis
 Knowledge deficit about disease, plan, risk factors, normal
ADL’s
PROGNOSIS for MI
Better
 Early reperfusion
 Inferior wall intact
 Preserved LV function
 Short and long term - ß-blockade, ACE +
Aspirin
Poor
 Delay in reperfusion
 LV dysfunction
Chest Pain group activity
Chest Pain flow chart and documentation
COMPLICATIONS of CAD/MI
Tachyarrhythmia
 Brady arrhythmia
 Cardiogenic shock
 Valvular insufficiency
 CHF
 Ventricular aneurysms
 Peri, endo and
myocarditis
 Pericardial effusion
 CardiacTamponade
Ventricular Aneurysm