ABC Revised
Transcript of ABC Revised
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I. Definition of Terms
1. Stress is the consequence of the failure to adapt to change. Less simply: it is
the condition that results when person-environment transactions lead the
individual to perceive a discrepancy, whether real or not, between the demands
of a situation and the resources of the person's biological, psychological or
social systems.
In medical terms, stress is the disruption of homeostasis through physical or
psychologicalstimuli. Stressful stimuli can be mental,physiological, anatomical
or physical[1] .
2. Crisis (plural: crises) may occur on a personal or societal level. It may be atraumatic or stressful change in a person's life, or an unstable and dangeroussocial situation, in political, social, economic, military affairs, or a large-scale
environmental event, especially one involving an impending abrupt change.More loosely, it is a term meaning 'a testing time' or 'emergency event'.
3. Biologic Crisis- Biology, the science of life/ Changed in persons life which could
be traumatic or stressful but not extremely serious or severe.
4. Acute Biologic Crisis- extremely serious, severe, or painful.
5. Emergency- Emergency, serious situation or occurrence that happens
unexpectedly and requires an immediate response.
6. Nursing - Nursing, in general, the process of caring for, or nurturing, another
individual. More specifically, nursing refers to the functions and duties carried
out by persons who have had formal education and training in the art
and science of nursing. Professional nurses combine many different
disciplines, including aspects of biology and psychology, to promote the
restoration and maintenance of health in their clients.
7. Care- to be interested in, or concerned about something.
8. Nursing Assessment
Nursing assessment
The nursing assessment process for any clients entering the ED is
divided into primary and secondary assessments
The purposed of the primary assessment is to immediate identify
any client problem that poses a threat , immediate or potential, to life,
limb, or vision. If any abnormalities are found during the primary
assessment immediate interventions such as cardiopulmonary
resuscitation (CPR)and Advance Life Support (ALS) must be instituted to
aid in preserving the clients life, limb or vision.
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The primary assessment uses the ABC mnemonic:
A Airway
B Breathing effectiveness
C Circulation
The secondary assessment is performed to identify any othernon life- threatening problems the client may be experiencing. Both
subjective information and objective data are obtained.
9. The purposed of this triage process is to expediently determine the
severity of a clients problem or condition. The acuity level of the
presenting problem is rated according to the predetermined categories;
the most frequently used ratings are emergent, urgent, and non-urgent.
II.Review of the Anatomy of the Heart
a. Definition
A hollow muscular organ lying between the lungsresponsible for pumping blood to the bodys circulation.
b. Description
Weight: 300 gms
Shape: Cone- shaped
Location: Mediastinum; lies on the diaphragm; the apex(tip of the cone) is at its bottom and lies left of themidline; the base is at the top where the blood from thegreat vessels enter the heart and lies posterior to thesternum.
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c. Anatomy of the Heart
Pericardium two-layered sac that encases and protects the heart
Chambers of the Heart : 2 atrium, 2 ventricles
1. Atrium : Right Atrium receives deoxygenated bloodLeft Atrium receives oxygenated blood
2. Ventricles : Right Ventricle receives blood from atriumvia
tricuspid valve, pumps it to thepulmonary circulation
Left Ventricle receives blood from atriumvia the bicuspid
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valve, pumps it to the systemiccirculation
Cardiac Valves :1. Atrioventricular Valves: Tricuspid Valve and Bicuspid (Mitral) Valve
- prevents backflow of blood from RV to RAand from LV to LA respectively
2. Semilunar Valves: Pulmonic Valve and Aortic Valve- prevents backflow of blood from PA to RV
(Pul. Semilunar)and from Aorta to Left Vent. (Aortic
Semilunar)
Cardiac Blood Supply / Coronary Arteries supply blood to the heart1. Right Coronary Artery supplies RA, RV, inferior portion of the LV, posterior
septal wall, SA and AV node.2. Left Coronary Artery3. Left Anterior Descending Artery supplies to anterior wall of LV, anterior
ventricular septum and apex of left ventricle4. Circumflex Artery supplies to left atrium, lateral and posterior surface of LV,
occasionally the posterior intraventricular septum, sometimes to the SA and AV
d. Functions of the Heart
Excitability ability of cardiac muscles to depolarize inresponse to a stimulus
Automaticity (Rhythmicity) ability of cardiacpacemaker cells to initiate an impulse simultaneouslyand repetitively without neurohormonal control.
Contractility muscle contraction of the heart Refractoriness hearts inability to respond to a new
stimulus while still in a state of depolarization from anearlier stimulus.
Conductivity ability of heart muscle fibers topropagate electrical impulses along and across cellmembranes.
** ** Conduction System:
1. Sinoatrial (SA) Node initiates electrical impulses
2. AV Node - receives elec. Impulses from the SA node3. Bundle of His and Bundle Branches4. Purkinje Fibers
** The bundles give rise to thin filaments known as Purkinje fibers.
These fibers distribute the impulse to the ventricular muscle.
Collectively, the bundle branches and purkinje networkcomprises
the ventricular conduction system. It takes about 0.03-0.04s for the
impulse to travel from the bundle of His to the ventricular muscle
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Right Ventricle Mitral Valve
Pulmonary Valve Left Ventricle
f. Heart Rate
Normal - Adult 60-100 ; Children 80-120 ;Newborn 120-160
Tachycardia
Bradycardia
g. Arterial Pressure
Blood Pressure/ Arterial Pressure pressure of blood
against arterial walls. Systolic Pressure maximum pressure of blood against
the arterial walls when the heart contracts ( normally100-140mmHg)
Diastolic Pressure force of blood exerted against theartery walls during the hearts relaxation (or filling)phase (normally 60-90mmHg)
II. Risk Factors of Coronary Heart Disease
A. Two ( 2) Categories of CHD Risk Factors
a. Non- modifiable Factorsb. Modifiable Risk Factors
Non-Modifiable Risk Factors Modifiable risk Factors
Heredity, including race Cigarette Smoking/Habits
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AgeGender
HypertensionElevated Serum CholesterolDiabetes MellitusPhysical InactivityObesity
B. Contributing Risk Factors include:
a. Response to Stressb. Homocysteine Levelsc. Inflammatory Responsesd. Menopause
III.Coronary Artery Diseases (CAD) / Coronary Heart Diseases (CHD)
Arteriosclerosis
Atherosclerosis
Angina Pectoris
Myocardial Infarction
Transient Ischemic AttackARTERIOSCLEROSIS:
When the arteries become obstructed with plaque andcholesterol, they harden and constrict, and the circulation ofblood through the vessels becomes difficult, forcing the bloodthrough narrower passageways. As a result, blood pressurebecomes elevated.
Arteriosclerosis occurs when lipids in the blood, includingcholesterol, accumulate inside the walls of blood vessels andreduce the size of the veins or arteries through which bloodflows.
ATHEROSCLEROSIS:
A degenerative condition of the arteries characterized bythickening due to localized accumulation of fats, mainlycholesterol. The term atherosclerosis refers to a condition inwhich fatty deposits build up in and on the artery walls,interfering with the normal flow of blood and oxygenthroughout the body. When this happens, the heart has to work
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harder to pump blood through the narrowed blood vessels, anda heart attack or a stroke may result.
Predisposing factors:
cigarette smoking high fat levels in the blood high cholesterol high blood pressure obesitySigns and symptoms:
The symptoms of atherosclerosis depend on the part of the body
where the condition is taking place. Sometimes there aren't any
noticeable symptoms until the condition has advanced to a very
serious stage. When the arteries of the heart are affected, one of
the first symptoms is chest pain, often called angina. A person
with clogged arteries of the heart may also have occasional
difficulty in breathing and may experience unusual fatigue after
short periods of exertion.
Medical & Surgical Interventions for Athero and
Arteriosclerosis:
a. Lifestyle Modification ; Reduce Risk Factorsb. Coronary Artery Bypass Graft (CABGc. Percutaneous Transluminal Coronary Angioplasty (PTCA)d. Directional Coronary Atherectomy (DCA)
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e. Intracoronary Stents
Nursing Intervention:
a. Health Teachingb. Reduce Risk Factors
c. Restore Blood Supplyd. Pre & Post-op Care for Surgical Patients
ANGINA PECTORIS: - insufficient coronary blood flow, thus inadequate O2 causes
intermittent chest pain.
-the result of myocardial ischemia caused by an imbalance
between myocardial blood supply and oxygen demand. Angina
is a common presenting symptom (typically, chest pain)
among patients with coronary artery disease. It is caused bychemical and mechanical stimulation of sensory afferent nerve
endings in the coronary vessels and myocardium.
- Angina pectoris can be relieved with rest. It lasts only for 1-5
minutes and taking up of nitroglycerine will be beneficial for
the client.
Signs and symptoms:
Patient experiences retrosternal chest discomfort ratherthan flank pain. Usually described as pressure, heaviness,squeezing, burning and choking sensation.
It localize primarily in the epigastrium, back neck jaw or inthe shoulders. The typical location for radiation of pain is in thearms, shoulders and the neck.
Precipitating factor:
over exertion
eating
exposure to cold
emotional stress
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The New York Heart Association classification is used to quantifythe functional limitation imposed by patients symptoms asfollows: (Killips)
Class I no limitations of physical activity (ordinary physical
activity does not cause symptoms).
Class II slight limitation of physical activity (ordinary physicalactivity does cause symptoms).
Class III moderate limitation of activity (patient is comfortable
at rest, but less than ordinary activity can cause symptoms).
Class IV unable to perform any physical activity without
discomfort, therefore severe limitations (patient may be
symptomatic even at rest).
Nursing Interventions:
a. Assess pain location, character, ECG (ST elevation),precipitatingfactors
b. Help client to adjust lifestyle to prevemt anginaattack avoid excessive activity in cold weather,avoid overeating, avoid constipation, rest aftermeals, exercise
c. Teach patient how to cope with angina attack
nitroglycerin every 5 mins upto 3x, if still not relievedgo to the hospital
Diagnostic Assessment:
a. ECGb. Stress Testc. Radioisotope Imagingd. Coronary Angiography
Medical Management:
a. Opiate Analgesic MoSo4b. Vasidilators Nitroglygcerin, Isosorbide
Mononitrate/Dinitratec. Calcium Channel Blockers Dlitiazem, Nifedipined. Beta Blocking Agents Propanolol
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===============================================================================
MYOCARDIAL INFARCTION- process by which myocardial tissue is destroyed due toreduced coronary blood flow.
- Myocardial infarction (MI) is the rapid development ofmyocardial necrosis caused by a critical imbalance betweenthe oxygen supply and demand of the myocardium.
- This usually results from plaque rupture with thrombusformation in a coronary vessel, resulting in an acute reductionof blood supply to a portion of the myocardium.
Causes:
1. Atherosclerotic heart2. Coronary Artery Embolism
Pathophysiology:
- The most common cause of MI is narrowing of the epicardial
blood vessels due to atheromatous plaques. . This can result in
partial or complete occlusion of the vessel and subsequent
myocardial ischemia. . Total occlusion of the vessel for more
than 4-6 hours results in irreversible myocardial necrosis, but
reperfusion within this period can salvage the myocardium andreduce morbidity and mortality.
- MI is a leading cause of morbidity and mortality in the United
States.
- Male predilection exists in persons aged 40-70 years. Evidence
exists that women more often have MIs without atypical
symptoms. The atypical presentation in women might explain
the sometimes delayed diagnosis of MIs in women.
- MI occurs most frequently in persons older than 45 years. Apositive family history includes any first-degree male relative
aged 45 years or younger.
Signs and symptoms :
1. chest pain heavy (viselike, crushing, squeezing)
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usually across the anterior pericardium typically isdescribed as tightness, pressure, or squeezing.
Pain may radiate to the jaw, neck, arms, back, andepigastrium. The left arm is affected more frequently;however, a patient may experience pain in both arms.
2. Dyspnea, Orthopnea sense of suffocation
3. Nausea and/or abdominal pain- gas pains around theheart4. Anxiety5. Light headedness with or without syncope6. Cough7. Nausea with or without vomiting8. Cold diaphoresis, gray facial color,9. Wheezing10.Weakness and altered mental status common in
elderly patients.11.Rales may be present in congestive heart failure.12.Neck vein distention represents right pump failure.
13.Dysrythmias - an irregular heart beat or pulse, usuallytachycardic.14. Oliguria urine less than 30 ml/hr15. Apprehension
Risk factors:
Age , Male gender, Smoking, DM, Family history, Sedentarylifestyle, obesity, diet, stress, hypertension, Type A personality
DIAGNOSTICS:
Lab studies:
Troponin - is a contractile protein that normally is notfound in serum. It is released only when myocardial necrosisoccurs.
- have the greatest sensitivity and specificity in
detecting MI. The test result is both diagnostic as well as
prognostic of outcome.
Creatine kinaseMB (CK-MB)
Myoglobin - a low-molecular-weight heme protein found incardiac and skeletal muscle, is released more rapidly frominfarcted myocardium.CBC is indicated if anemia is suspected as a precipitant.
Transfusion with PRBC may beindicated.
Potassium and magnesium level should be monitoredand corrected.
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Creatinine level
C Reactive protein (CRP) - is a marker of acuteinflammation.
Erythrocyte sedimentation rate (ESR)
Serum lactate dehydrogenase (LDH)
Imaging studies:
Chest radiography or chest x-ray reveals pulmonaryedema secondary to heart failure.
CT scan
Radionuclide Imaging
Positron Emission Imaging
Transesophagial Echocardiography
Magnetic resonance imaging (MRI) - can identify wallthinning, scar, delayed enhancement (infarction), and wallmotion abnormalities (ischemia).
Electrocardiogram (ECG) - ST-segment elevation greaterthan 1 mm.
- the presence of new Qwaves.
- intermediate probability of MI are ST-segmentdepression, T-wave inversion, and other
nonspecific ST-T wave abnormalities.
Immediate emergency intervention:
IV access thrombolytic agents e.g. heparin
supplemental oxygen
pulse oximetry maintain oxygen saturation at >90%
Immediate administration of aspirin en route
Nitroglycerin for active chest pain, given sublingually or byspray
ECG
Treatment is aimed at:
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1) Restoration of the balance between the oxygen supply anddemand to prevent further ischemia.
2) Pain relief3) Prevention and treatment of complications.
Drug of choice for patient with MI:
Antithrombotic agents -These agents prevent the formation of thrombusassociated with myocardial infarction and inhibit platelet function. (aspirin,-heparin)
Vasodilators - Opposes coronary artery spasm, which augments coronaryblood flow and reduces cardiac work by decreasing preload and afterload. It iseffective in the management of symptoms in AMI.
- can be administered sublingually by tablet or spray,topically, or IV.
-nitroglycerine
Beta-adrenergic blockers - reduce blood pressure, which decreasesmyocardial oxygen demand. (-metoprolol)
Platelet aggregation inhibitors inhibits platelet aggregation.-clopidogrel(plavix)
Analgesics reduce pain which decreases sympathetic stress.-morphine sulfate
Angiotensin converting enzyme (ACE) inhibitors prevents conversion ofangiotensin I to ngiotensin II, a potent vasoconstrictor. -captopril(capoten)
Complications of MI:
DysrhytmiasCardiogenic ShockHeart FailurePulmonary EdemaPulmonary EmbolismRecurrent MIComplications due to Necrosis VSD, rupture of the heart,
ruptured papillary musclesPericarditis
Recommendations:
- All MI patients should be admitted in the ICU.- Patient should remain on complete bed rest during his stayin the hospital and avoid straining activities.
Nursing interventions for MI
1. Earlya. Treat arrythmias promptly lidocaine
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b. Give analgesic- morphinec. Provide physical restd. Administer O2 via cannulae. Frequent VSf. Nifedipineg. Propanolo HCLh. Emotional Support
2. Latera. Give stool softenerb. Provide low fat, low cholesterol, low sodium diet, soft foodc. Commoded. Self-caree. Plan for rehabilitation
Exercise program
Stress management
Teach risk factors
f. Psychological supportg. Long-term drug therapy
Antiarryhtmics- quinidine, lidocaine
Anticoagualnt heparin, aspirin
Antihypertensives propanolol, chlorathiazide
3. TRANSIENT ISCHEMIC ATTACK (TIA)
- temporary episode of neurological dysfunction lasting only a fewminutes or seconds (in a day/ 24hrs) due to decreased blood flowto the brain.
- A warning sign of stroke especially in first 4 weeks after TIACauses:
1. Atherosclerosis2. Microemboli from atherosclerotic plaque
Manifestations:
1. Sudden loss of visual function2. Sudden loss of sensory function
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3. Sudden loss of mmotor function
Management: - Surgical Carotid Endarterectomy (bypass)
1. Post-op focus assess neurologic deficits; avoid flexingneck
Inability to swallow, move tongue, raise arm, smile may
indicate
problem in the specific cranial nerve.
2. Anticoagulant therapy: aspirin, etc.
4. Arrythmias
a. Review of Conduction System
Heart Conduction System
The sinoatrial node (SAN), located within the wall of the right atrium (RA), normally
generates electrical impulses that are carried by special conducting tissue to the
atrioventricular node (AVN).
Upon reaching the AVN, located between the atria and ventricles, the electrical impulse
is relayed down conducting tissue (Bundle of HIS) that branches into pathways that
supply the right and left ventricles. These paths are called the right bundle branch
(RBBB) and left bundle branch (LBBB) respectively. The left bundle branch further
divides into two sub branches (called fascicles).
Electrical impulses generated in the SAN cause the right and left atria to contract first.
Depolarization (heart muscle contraction caused by electrical stimulation) occurs nearly
simultaneously in the right and left ventricles 1-2 tenths of a second after atrial
depolarization. The entire sequence of depolarization, from beginning to end (for one
heart beat), takes 2-3 tenths of a second.
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All heart cells, muscle and conducting tissue, are capable of generating electrical
impulses that can trigger the heart to beat. Under normal circumstances all parts of the
heart conducting system can conduct over 140-200 signals (and corresponding heart
beats) per minute.
The SAN is known as the "heart's pacemaker" because electrical impulses are normally
generated here. At rest the SAN usually produces 60-70 signals a minute. It is the SAN
that increases its' rate due to stimuli such as exercise, stimulant drugs, or fever.
Should the SAN fail to produce impulses the AVN can take over. The resting rate of the
AVN is slower, generating 40-60 beats a minute. The AVN and remaining parts of the
conducting system are less capable of increasing heart rate due to stimuli previously
mentioned than the SAN.
The Bundle of HIS can generate 30-40 signals a minute. Ventricular muscle cells may
generate 20-30 signals a minute.
Heart rates below 35-40 beats a minute for a prolonged period usually cause problems
due to not enough blood flow to vital organs.
Problems with signal conduction, due to disease or abnormalities of the conducting
system, can occur anyplace along the heart's conduction pathway.
Abnormally conducted signals , resulting in alterations of
the heart's normal beating, are called arrhythmias or
dysrrythmia.
By analyzing an EKG a doctor is often able to tell if there
are problems with specific parts of the conducting system
or if certain areas of heart muscle may be injured.
b. Basic ECG Interpretation
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Electrocardiogram (ECG):
-An electrocardiogram (ECG) is a test that records the electrical
activity of the heart.
-is used to measure the rate and regularity of heartbeats as well as
the size and position of the chambers, the presence of any damage tothe heart, and the effects of drugs or devices used to regulate the
heart.
The ECG Waves:
P wave - represents the wave of depolarization that spreads from the
SA node throughout the atria, and is usually 0.08 to 0.1 seconds (80-
100 ms) in duration.
P R interval - the period of time from the onset of the P wave to
the beginning of the QRS complex, which normally ranges from 0.12
to 0.20 seconds in duration. This interval represents the time
between the onset of atrial depolarization and the onset of ventricular
depolarization.
QRS complex - represents ventricular depolarization. The duration
of the QRS complex is normally 0.06 to 0.1 seconds.
ST segment - following the QRS is the time at which the entire
ventricle is depolarized and roughly corresponds to the plateau phase
of the ventricular action potential. The ST segment is important in
the diagnosis of ventricular ischemia or hypoxia because under those
conditions, the ST segment can become either depressed or elevated.
T wave - represents ventricular repolarization and is longer in
duration than depolarization.
Q T interval - represents the time for both ventricular
depolarization and repolarization to occur, and therefore roughly
estimates the duration of an average ventricular action potential.
This interval can range from 0.2 to 0.4 seconds depending upon heart
rate.
Abnormal ECG results may indicate the following:
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V1: Fourth intercostal space to the right
of the sternum.
V2: Fourth intercostal space to the Left of
the sternum.
V3: Directly between leads V2 and V4.
V4: Fifth intercostal space at
midclavicular line.
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Myocardial (cardiac muscle) defect Past heart attacksEnlargement of the heart Present orimpending heart attackCongenital defects Inflammation ofthe heart (myocarditis)Heart valve diseaseArrhythmias (abnormal rhythms)
Tachycardia (heart rate too fast) or bradycardia (too slow)Coronary artery
How to perform ECG Using Disposable Electrodes.
Skin Preparation:
Clean with alcohol or usual skin prep, if necessary. If the patients are very hairy shave
the electrode areas.
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Trouble Shooting.
When no signal or a poor signal is observed the following should be considered:
1. Have the cables been correctly connected?2. Is the equipment functioning correctly?
3. Could external electrical equipment interference be a problem?
4. Was skin preparation adequate?
5. Could the electrodes suffer from
a) gel dry out?
b) Poor adhesion?
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12 Lead (10 Electrode) Placement Guide:
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Normal adult 12-lead ECG
The diagnosis through electrocardiogram is made by excluding any recognised
abnormality. It's description is therefore quite lengthy.
normal sinus rhythmo each P wave is followed by a QRS
o P waves normal for the subject
o P wave rate 60 - 100 bpm with 10% = sinus
arrhythmia normal QRS axis
normal P waveso height < 2.5 mm in lead IIo width < 0.11 s in lead II
for abnormal P waves see right atrial hypertrophy, left atrialhypertrophy, atrial premature beat, hyperkalaemia
normal PR interval
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o 0.12 to 0.20 s (3 - 5 small squares) for short PR segment consider Wolff-Parkinson-White
syndrome or Lown-Ganong-Levine syndrome (other causes- Duchenne muscular dystrophy, type II glycogen storagedisease (Pompe's), HOCM)
for long PR interval see first degree heart block normal QRS complex
o < 0.12 s duration (3 small squares)
for abnormally wide QRS consider right or left bundlebranch block, ventricular rhythm, hyperkalaemia, etc.
o no pathological Q waveso no evidence ofleft or right ventricular hypertrophy
normal QT intervalo Calculate the corrected QT interval (QTc) by dividing the QT
interval by the square root of the preceeding R - R interval.Normal = 0.42 s.
o Causes oflong QT interval myocardial infarction, myocarditis, diffuse myocardial
disease hypocalcaemia, hypothyrodism subarachnoid haemorrhage, intracerebral haemorrhage drugs (e.g. sotalol, amiodarone) hereditary
Romano Ward syndrome (autosomal dominant)
Jervill + Lange Nielson syndrome (autosomalrecessive) associated with sensorineural deafness
normal ST segmento no elevation or depression
causes of elevation include acute MI (e.g. anterior, inferior),left bundle branch block, normal variants (e.g. athleticheart, Edeiken pattern, high-take off), acute pericarditis
causes of depression include myocardial ischaemia, digoxineffect, ventricular hypertrophy, acute posterior MI,pulmonary embolus, left bundle branch block
normal T wave causes of tall T waves include hyperkalaemia, hyperacute
myocardial infarction and left bundle branch block
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causes of small, flattened or inverted T waves arenumerous and include ischaemia, age, race,hyperventilation, anxiety, drinking iced water, LVH, drugs(e.g. digoxin), pericarditis, PE, intraventricular conductiondelay (e.g. RBBB)and electrolyte disturbance.
normal U wave1. Different kinds of Arrythmias
a. Atrial tachycardia sudden onset of atrial rates 140 250 per minute.
rhythm: regular
P waves: present before QRS complex.
PR interval: usually not measurable.
QRS complex: normal in shape (0.06 0.10 secs.)
T wave: distorted in appearance.
b. Atrial flutter atrial stretching or enlargement, MI, CHF. rate 250 400 beats per minute
rhythm: regular or irregular
P wave: not present; replaced by a saw toothed pattern (F waves).
PR intervals: not measurable.
QRS complex: normal shape and time.
T wave: present but may be obscured by flutter waves.
ECG TRACING OF AN ATRIAL FLUTTER
c. Ventricular tachycardia life threatening dysrythmias thatoriginates from an irritable focus within the ventricle.
o metabolic acidosis (lactic acidosis)o electrolyte imbalanceo digitalis toxicity
rate: 140 220 bpm.
rhythm: usually regular but may be irregular
P wave: not present.
PR interval: immeasurable. .
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T wave: usually deflected opposite to the QRS complex.
d.Atrial fibrillation rapid and chaotic firing of atrial impulses.a. fibrotic changes associated with aging process.
b. AMIc. valvular diseased. digitalis
rate: immeasurable because fibrillatory waves replace P waves;ventricular rate may vary from brady to tachycardia.
Rhythm: irregular
P wave: replaced by fibrillatory waves (little f waves)
PR interval: immeasurable
QRS complex: normal
T wave: normal
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e.Ventricular fibrillation random and chaotic discharging ofimpulses within the ventricles at rates that exceeds 300 bpm.
a. produces clinical death and must be reversedimmediately.b. AMIc.Acidosisd.Electrolyte disturbance
rate: immeasurable because of absence of well formed QRS complex.
rhythm: chaotic
P wave: not present
PR interval: not present
QRS complex: bizarre, chaotic, no definite contour
T wave: not apparent
ECG TRACING OF A VENTRICULAR FIBRILLATION
a. Premature atrial contraction ectopic beat that originates inthe atria and is discharged at a rate faster than that of the SAnode
the atrial beat occurs sooner than the next normalbeat and is said to be early or premature.
Occurs in healthy or diseased heart (ischemia) Precursor of more serious dysrhytmias
rate: slow or fast
rhythm: irregular because of the early occurrence of the PAC
P wave: present for each normal QRS complex; the P wave of thepremature contraction
will be distorted in shape.
PR interval: may be normal or shortened depending on where in theatria the impulses originated; the closer the site of atrial impulse formation tothe AV node, the shorter the PR interval will be.
QRS and T wave: normal
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g.Premature ventricular contraction ectopic beat originating in theventricle and is being
discharged at a rate faster than that of the nextnormally occurring beat.
most common dysrythmias in the hospital
AMI
All other forms of heart disease Pulmonary disease
Electrolyte disturbances
Metabolic instability
Drug abuse
rate: slow or fast
rhythm: irregular because of the premature firing of the ventricularectopic focus.
P wave: absent since the impulse originates in the ventricle, bypassingthe atria and the AV
node.
PR interval: immeasurable QRS complex: QRS of the PVC will be widened (>0.12 sec.), bizarre in
appearance whencompared to normal QRS complex.
T wave: usually deflected opposite to the QRS.
ECG TRACING OF A PREMATURE VENTRICULAR CONTRACTION
4. Heart Block
a. transmission of the wave of impulse from the SA node through thenormal conduction
pathway is altered at the level of AV node.
b. the altered state does not allow the impulse to be conducted ontime or at all.
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TYPES:
a. First degree AV block the impulse is transmitted normally
but, but is delayed longer at the level of the AV node.
c. may be a sign of CAD, acute rhuematic carditis,electrolyte imbalance.
rate: usually normal but may be slow.
Rhythm: regular
P wave: present for each QRS complex and isidentical.
PR interval: >20 sec.
QRS complex: normal (0.06 0.10 sec.)
T wave: normal
b. Second degree AV block the AV node becomes selective aboutwhich impulses are conducted to the ventricles.
c. Third degree AV block complete heart block.d. no relationship between the atrial and ventricular activity
Acute Inferior Myocardial Infarction
ST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads
Acute Anterior Myocardial Infarction
ST elevation in the anterior leads V1 - 6, I and aVL
reciprocal ST depression in the inferior leads
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Acute Posterior Myocardial Infarction
(hyperacute) the mirror image of acute injury in leads V1 - 3
(fully evolved) tall R wave, tall upright T wave in leads V1 -3
usually associated with inferior and/or lateral wall MI
Old Inferior Myocardial Infarction
a Q wave in lead III wider than 1 mm (1 small square) and a Q wave in lead aVF wider than 0.5 mm and a Q wave of any size in lead II
Acute myocardial infarction in the presence of left bundle branch block
Features suggesting acute MI
ST changes in the same direction as the QRS (as shown here)
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ST elevation more than you'd expect from LBBB alone (e.g. > 5 mm inleads V1 - 3)
Q waves in two consecutive lateral leads (indicating anteroseptal MI)
5. Difference between Angina Pectoris, Myocardial Infarction, TransientIschemic Attack
Angina Pectoris MyocardialInfarction
TIA
Definition - insufficient
coronary bloodflow, thusinadequate O2causesintermittentchest pain.
-can be relievedwith rest andnitroglycerine
- process by
which myocardialtissue isdestroyed due toreduced coronaryblood flow.
- not relieved withrest andnitroglycerine
- needs immediatemedicalintervention
- temp
orary episode ofneurologicaldysfunctionlasting only a fewminutes orseconds (in aday/ 24hrs) dueto decreasedblood flow to thebrain.
- A warning signof stroke
especially infirst 4 weeksafter TIA
Signs andSypmtomsChest pain
pressure,heaviness,
squeezing, burningand chokingsensation
localized primarilyin the epigastrium,back neck jaw or inthe shoulders.
The typical location
viselike, crushing,squeezing
Pain may radiateto the jaw, neck,arms, back, andepigastrium.
The left arm isaffected morefrequently;
Sudden loss ofvisual function
Sudden loss ofsensoryfunction
Sudden loss ofmotor function
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for radiation of painis in the arms,shoulders and theneck
however, apatient mayexperience painin both arms.
=====================================================
6. Acute Respiratory Failure
Pulmonary edema
- often occurs when the left side of the heart is distended and fails topump adequately
Clinical Manifestation
Constant irritating cough, dyspnea, crackles, cyanosis
Pathophysiology
Fluid accumulation in the alveolar sacs due to hypovolemia, fluid
congestions in the lungs, alveoli are congested
Diagnostic Tests
CXR
Medical Surgical MgtDiuretics, low sodium diet, I&O
Nursing Mgt
1. promote effective airway clearance, breathing patterns andventilation
2. Monitor VS3. Psychological support4. Administer medications
------------------------------------------------------------------------------------------------
-------------------7. Acute Respiratory Failure
Pneumonia
- inflammtory process of lung parenchyma assoc. w/ marked increase inalveolar and interstitial fluid
Risk factors:
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1. Smoking, air pollution2. URTI3. Altered conciousness4. Tracheal intubation5. Prolonged immobility6. lowered immune system7. malnutrition, DHN,8. Chronic Diseases:DM, Heart dse, renal dse, cancer9. inhalation toxicity/ aspiration
Clinical Manifestationo Chest pain, irritability, apprehensiveness, irritability, restlessness,
nausea, anorexia, hx of exposureo Cough- productive , rusty/ yellowish/greenish sputum, splinting of
affected side, chest retration (infants)o Sudden increased fever, chills
o Nasal Flaring, circumoral cyanosis
o Tachypnea, vomiting
Pathophysiology
Caused by infectious or non-infectious agents, clotting of an exudate rich
fibrogen, consolidated lung tissue
Diagnostic Tests
CXR, sputum culture, Blood culture, increased WBC, elevated
sedimentation rate
Medical Surgical Mgt
AntibioticsRest
Nursing Mgt
1. Promote adequate ventilation- positioning, Chest physiotherapy,IPPB2. Provide rest and comfort3. Prevent potential complications4. Health teaching
-------------------------------------------------------------------------------------------------------------------
8. Acute Respiratory Failure
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Asthma
- increased responsiveness of the trachea and bronchi to various stimuli,with difficulty in breathing, caused by narrowing of airways
Types:
- Immunologic asthma occurs in childhood- Non-immunologic asthma occurs in adulthood and assoc w/ recurrent
resp infections.Usually >35 y/o
- Mixed, combined immunologic and non-immunologic
** Status Asthmaticus
- a life-threatening asthmatic attack in w/c symptoms of asthma continues andso not respond to treatment
Clinical Manifestation
History of rhinitis, allergies, family hx of asthmaIncreased tightness of chest, dyspnea
Tachycardia, tachypneaDry, hacking, persistent cough(+) wheezes, cracklesPallor, cyanosis, diaphoresis, Chronic barrel chest, elevated shoulders,distended neck veins, orthopnea
Tenacious, mucoid sputum
Pathophysiology
Bronchial smooth muscles constrictsBronchial secretions increaseMucosa swell and narrows airway passageHistamine is produced in the lungsBronchospasm, production of large amount of thick mucous andinflammatory response contribute to resp. obstruction
Diagnostic Tests
ABG (elevated PCO2, dec PO2 and pH)Vital capacity reduedForced expiratoryVolume decreasedResidual Volume increased
Medical Surgical Mgt
Steroids,
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Antibiotics,Bronchodilators, expectorantsO2, nebulization
Nursing Mgt
a. Promote pulmonary ventillationb. Facilitate expectorationc. Health teachingd. Breathing techniquese. Stress management
-------------------------------------------------------------------------------------------------------------------Chronic Obstructive Pulmonary Disease
o a group of conditions assoc. w/ chronic obstruction of airflow
entering or leaving the lungs
a. Major diseases
1. Pulmonary Emphysema airway is obstructed due to destroyedalveolar walls
2. Chronic Bronchitis- increased mucus production that obstructsairway
3. Asthma
b. Clinical Manifestation
Shortness of breath, productive cough, hypoxia, wheezes/rales,
decreased exercise tolerance
c. Diagnostic Tests
Same w/ asthma
d. Medical Surgical Mgt
Antibiotics, expectorants, O2 at low flow, nebulization
e. Nursing Mgt
a. Promote pulmonary ventillationb. Facilitate expectorationc. Health teachingd. Breathing techniquese. Stress management
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-------------------------------------------------------------------------------------------------------------------
1. Acute Respiratory Failure
a. Acute Respiratory Distress
Syndrome
- noncardiogenic pulmonary infiltrations resulting in stiff, wet lungs andrefractory hypoxemia in previously healthy adult. Arf w/o hypercapnia
b.Risk Factors:
a. Primary- Shock, multiple trauma- Infections- Aspirations, inhalation of chemical toxins- Drug overdose- DIC- Emboli, esp Fat embolib. Secondary- Overaggressive fluid administration- Oxygen toxicity
c. Clinical Manifestation
Restlessness, anxiety, hx of risk factors, severe dyspnea cyanosis,tachycardia, hypotension, hypoxemia, acidosis, crackles
d. Pathophysiology
Damage to alveolar capillary membrane
Increased Vascular Permeability to pulmonary edema
Impaired Gas exchange
Decreased surfactant prduction
Potential Atelectasis
Severe hypoxia
May lead to death
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e. Diagnostic Tests
CVP, Pulmonary Wedge Capillary Pressure, ABG
f. Medical Surgical Mgt
ICU, strict monitoring, O2, suction, bronchodilator, anitibiotics, ETventilator
g. Nursing Mgt
a. Assist in respirationsb. Prevent complicationsc. Environment, fluid balance, bleeding tendencies
d. Health teaching
2. Ventilation Therapy:
b. Mechanical Ventilation a
means of augmenting respiratory gas exchange using a
mechanical device, equipped to deliver negative or positive
pressure that can maintain ventilation and O2 delivery for a
prolonged period of time.
-The volume of air delivered by the ventilator is relativelyconstant, assuring consistent adequate breaths despite varyingairway pressure.
c. Types:
1. Pressure cycled it permits air to flow into theclients lungs until a predetermined pressure is reached.-the volume of air or O2 can vary as the clients airwayresistance changes.
Birds
Bennett
2. Volume cycled delivers a predetermined volumeof gas into the patients lungs with each breath.-preset volume of air, ordered by the physician.
Engstron Bennett
Ohio and Emerson
d. Indications:
continues decrease in oxygenation (paO2)
increase in arterial carbon dioxide levels (paCO2)
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persistence of acidosis (decrease in blood pH)
e. Respiratory conditions
needing the aid of the mechanical ventilators:
post operative thoracic or abdominal surgery drug overdose
neuromuscular disease
inhalation injury
COPD
multiple trauma
shock
multi-system failure
coma
e. Mode or Breath Pattern:
- what causes the ventilator to cycle from inspiration
Mandatory (controlled) - which is determined by the respiratory rate.
Assisted (as in assist control) - synchronized intermittent mandatoryventilation, pressure support.
Spontaneous - no additional assistance in inspiration, as in CPAP.
CMV - Conventional controlled ventilation, without allowances forspontaneous breathing.
Many anesthesia ventilators operate in this way.
Assist-Control - Where assisted breaths are facsimiles of controlled
breaths. Intermittent Mandatory Ventilation - which mix controlled breath
and spontaneous breath.
Pressure Support - Where the patient has control over all aspects ofhis/her breath except the pressure limit.
Positive End Expiratory Pressure (PEEP) a method of maintaining apressure higher than the atmospheric pressure in the lungs in the end ofeach expiration.
Continues Positive Airway Pressure (CPAP) a non mechanicalmeans of ventilation. It provides a continues positive airway pressure inthe lungs at the end of expiration.
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Bennett MA-1 Bennett Puritan
=====================================================
3. SHOCK
- is defined as failure of the circulatory system to maintain adequateperfusion of vital organs.
A. Pathophysiology of Shock
The three major components of the circulatory system are the heart,
large blood vessels and microcirculation. As long as two of these factors
canmaintain a satisfactory compensatory action, adequate blood
circulation can be maintained even if the third factor is not functioning
normally.
However, if compensatory mechanisms fail or if more than one of these
three factors necessary for adequate circulation malfunction, circulatry
failure results and shock develops.
(see matrix and stages)
B. Classification of Shock
Classification Etiology
1. Hypovol Blood loss: Massive Trauma, GI Bleeding,
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emic Shock
- due to inadequatecirculationg bloodvolume
Ruptured AorticAneurysm, Surgery, Erosion of
Vessesl due to lesion, tubes or other devices,DIC
Plasma loss: Burns, Accumulation of intra-abdominal fluid,
malnutrition, severe dermatitis,DIC
Crystalloid loss: Dehydration, ProtractedVomiting, Diarrhea, nasogastric suction
2. Cardiogenic Shock
- due to inadequatepumping action ofthe heart becauseof primary cardiacmuscle dysfunctionor mechanicalobstruction of bloodflow caused by MI orvalvular insufficiency
Myocardial disease: Acute MI, MyocardialContusion,
Cardiomypathies
Valvular Disease or injury: Ruptured AorticCusp, Ruptured
Papillary muscle, Ballthrombus
External Pressure on the Heart interferes with heart
filling or emptying:Pericardial Tamponade due to Trauma,
aneurysm,cardiac surgery, pericarditis,
massivepulmonary embolus, tension
pneumothorax
Cardiac Dysrhtymias: Tachyarrhythmias,Bradyarrythmias,
Electromechanicaldissociation
3. Neurogenic Shock- interferencewith nervous
system control ofthe blood vessels
Spinal: Spinal anesthesia, spinal cord injury
Vaso-vagal reaction: Severe pain, severeemotional stress
4. Anaphylactic Shock- severehypersensitivity
reactionresulting in
Allergy to food, medicines, dye, insect bites orstings
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massivesystemicvasodilation.
5. SepticShock- systemicreactionvasodilation dueto infection
Gram-negative septicemia but also caused byother organisms
MATRIX: PATHOPHYSIOLOGY OF SHOCK
CIRCULATORY SYSTEM
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HEART LARGE BLOOD VESSELS
MICROCIRCULATION
Myocardial disease Blood loss Plasma loss
Crystalloid loss
External Pressure on the Heart interferes with heart filling or emptying
S inal cord in ur
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Compensated Decompensated
(body is able to maintain tissue (systemic circulation µcirculationperfusion to the vital organs) no longer work in unison)
C. Stages of Shock
1. Nonprogressive Stage - cardiac output is slightly decreasedbecause of loss
of actual or relative blood volume.
- body responds to compensate for the
hypovolemia
to maintain blood pressure.
cardiac output sympatheticstimulation
capillary blood flow epinephrine and
hydrostatic pressure within norepinephrinereleased
capillaries lower thansurrounding tissues vasoconstriction
fluid moves from tissues tachycardia systemic vascularinto vascular system resistance
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Non-progressive
Stage
vasoconstriction continues microcirculationNormal State
decreased venous return decreased circulation ofdeoxygenated blood
Inadequate tissue perfusion
Pro ressive Sta e
Cellular IschemiaNecrosis
Organ FailureDEATH
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circulating volume blood pressuremaintained
2. Progressive Stage - the compensatory mechanisms are notadequate to
compensate for the loss of blood volume.- blood declines to a very low level that is not
adequate
to maintain blood flow to the cardiac musclethus
heart begins to deteriorate.
persistent compensatory vasoconstriction
dilation in microcirculation
venous return
cardiac output
arterial blood pressure
venous poolingcoronary artery
tissue perfusionfillingpooling of bloodin microcirculation damage to microcirculationmyocardial
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functionaccumulation of cellular hypoxia and release ofmetabolites in cell vasoactive substances
metabolic acidosis capillary permeability
venous return
3. Irreversible Stage occurs if the cycle of inadequate tissueperfusion is
not interrupted
- cellular ischemia and necrosis lead to organ
failure
D. Physiologic Manifestations of Shock
Early signs
1. tachycardia2. tachypnea3. oliguria
Late signs
4. cold moist skin5. color ashen: pallor
6. hypotensive, tachycardia
E. Effects of Shock in Different Organs
a.Respiratory system
- shock leads to hypoxia, with blockage of normal aerobicmetabolism.
- lactic acid accumulates, resulting to tissue acidosis.
b. Cardiovascular System1. Myocardial deterioration2. Disseminated Intravascular Coagulation
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c. Neuroendocrine System1. General Adaptation Response
- neuroendocrine responses during shock are defensivereactions that
occur during the bodys stage of resistance2. Adrenal Response
- increase in adrenocortical mineralocorticoid hormonesoccurs
- helps increase intravascular fluid volume by stimulating thekidneys
to retain sodium and water3. Pituitary response
-ADH is released and carried to the kidneys where it causesthe body
to retain water4. Metabolic Response
- during the initial phase of shock, the bodys small stores ofavailable
carbohydrates are rapidly depleted. Protein and fats arethen
metabolized to meet bodys energy requirements.
d. Immune System- all forms of shock depresses the macrophages located both in the
bloodstream and tissues.- A person in a state of shock is more susceptible to bacterial
endotoxins.
e. GI Sysytem- vagal stimulation to the GI tract slows down or stops, resulting to
absenceof peristalsis
- liver loses ability to detoxify and may release vasoactivesubstances .
- during shock, pooling of blood occurs in the liver or portal bed
f. Renal System1. Altered Capiillary blood pressure and glumerular filtration2. Renal Ischemia
F. Medical Surgical Management
1. Improve oxygenation- supplemental oxygen is administered to protect againsthypoxemia- via O2 cannula, ET tude, tracheostomy tube
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2. Restore and maintain adequate perfusion
3. Administer vasoactive medications or emergency drugs
- Atropine, dopamine, epinephrine, isoproterenol ( to increaseStroke volume), Lidocaine( for
dysrrhythmias), Metaraminol ( promotes vasoconstriction),Levophed, Na bicarbonate
4. Assist circulation-use of intra aortic balloon pump, medical anti shock trousers(MAST suit)- modified trendelenberg position- administer blood products properly typed and crossmatched
5. Fluid replacement Colloid or balanaced salt solution, colloidsolution, blood,
6. Prevent complications such as renal impairment and GI bleeding
G. Nursing Intervention
1. Assessment:
Vital signs, Airway, breathing, circulation, LOC, state ofhydration, Pane, presence of any laceration or deformity(if any)
2. Diagnosis
Ineffective airway clearance, impaired gas exchange,decreased cardiac output, etc..
3. Planning
Plans of intervention R/T diagnosis and state of theclient
4. Intervention
Assess and monitor client, stop bleeding (if present),Administer medications and fluids, Refer accordingly,position client appropriately, maintain safety of thepatient
FEU-MTA baylon vt3
-
8/9/2019 ABC Revised
45/45
45
5. Evaluation