Beruflich Dokumente
Kultur Dokumente
A=Allergies,
M=Medication,
R - Respiration
Normal 2
Abnormal (labored or shallow)
1
Absent 0
A - Abdomen
Abdomen and thorax non-tender 2
Abdomen and thorax tender 1
Abdomen rigid or flail chest* 0
M - Motor
Normal 2
Responds only to pain
1
(other than decerebrate)
no response (decerebrate)
0
S - Speech
Normal 2
Confused 1
No intelligent words 0
Score <= 8: Major
Trauma
Score >= 9: Minor
Trauma
Pericardium – loose fitting of the heart
composed of membranes and 5-20ml
fluid
Cardiac layers – epicardium,
myocardium, endocardium
Chambers – right and left atria; right
and left ventricles
Valves –Tricuspid, bicuspid, semi-lunar
Coronary circulation
Left coronary – LAD, LCA
Right coronary
S3 Gallop- ventricular overload; heard
after S2; “ken-tuck-y”
S4 Gallop- increased resistance to
ventricular filling; heard late in
diastole; “ten-ne-see”
Splitting heart sounds –Aortic and
pulmonic valve does not close
simultaneously
Systolic Murmur- turbulent blood flow
Ultrasound
Coronary angiography
Electrocardiogram
Serum Studies
CK-MB – (3-4 days)
LDH – Lactate dehydrogenase (7-14
days)
Troponin –T (14-21 days)
Aspartate Transaminase (3-4 days)
C- Reactive Protein
Myeloperoxidase
Intra-arterial blood pressure(80-90
60-65
mmHg)
Central venous pressure ( 1-8 mmHg or
4-12 cm water)
Pulmonary artery pressure ( 8-12
mmHg)
Cardiac output (4-8 L/min)
Venous oxygen Saturation (60-80%)
Consent
Explain procedure – cooperation
Trendelenberg position – lower
extremity source
Assist during procedure – local
anesthesia
Instruct for deep breath and hold;
neck flexion for PICC
Correct reading
Sterile and Aseptic technique –
prevent infection.
Cannulation of central vein or arterial
wall
Pneumothorax and hemmorrhage
Infection by the indwelling invasive
device
Catheter occlusion
Ischemia distant to the site of catheter
Disturbance of cardiac rhythym
BLOOD GASES:
ARTERIAL/VENOUS
Normal Arterial Venous
Values
pH 7.35-7.45 7.31 to 7.42
PO2 80 to 100 35 to 45
PCO2 35 to 45 39 to 52
HCO3 (mEqL) 22 to 26 22 to 26
Anion gap 10 to 18 8 to 16
(mEq/L)
ANALYSIS OF ARTERIAL BLOOD GASES
COMPONE DESCRIPTION VALUES
NT Measures hydrogen ion (H+) 7.35-7.45
pH concentration
Increase in ions, acidosis <7.35
Decrease in ions, alkalosis >7.45
•Partial pressure of in CO2 arteries 35 to 45
•Respiratory component of acid- mmHg
base regulation
pCO2 Hypercapnia, respiratory acidosis
Hypoventilation, respiratory
>45 mmHg
<35 mmHg
alkalosis
•Measures serum bicarbonate Normal: 22 to
•May reflect primary metabolic 26 mEq/L
disorder or compensatory
HCO3 mechanism to respiratory acidosis
Metabolic acidosis <22 mEq/L
Metabolic alkalosis >26 mEq/L
The GOAL is to maintain alveolar ventilation, correct
hypoxemia and maximize O2 transport when client
cannot sustain spontaneous and effective respirations.
P T U
Q
S
R
P T U
Q
S
R
P T U
Q
S
R
P T U
Q
S
Leads 1,II, III, AVF, V6 – all waveforms
are upright
aVR – all waveforms are negatively
deflected
aVL – P and T are negative, QRS are
biphasic
V1,V2 – P and T positive, QRS
negative
V3, V4, V5 – P and T positive, QRS
biphasic
Atrial( 60-100 Bpm)
Junctional ( 40-60 Bpm)
Ventricular (30-40 Bpm and lower)
Lead II
Sinus Bradycardia
Rate = 48/min
Rate = 48/min
Sinus Tachycardia
No discernible P waves
Irregular RR interval
PVC – P wave absent with wide
Bizzare QRS
Ventricular Tachycardia- wide saw-
toothed QRS (200-250) without P or
PR
Ventricular Fibrillation- rate cannot be
determined, rapid and chaotic;
coarse or fine
Asystole- flat line
Premature Ventricular Contraction
Prematurely occurring complex.
Wide, bizarre looking QRS complex.
Usually no preceding P wave.
T wave opposite in deflection to the QRS
complex.
Complete compensatory pause following
every premature beat.
Ventricular Tachycardia
Relievechest pain
Reduce extent of myocardial damage
Maintain cardiovascular stability
Decrease cardiac workload
Prevent complications
Rapid assessment and early diagnosis
key:
“Time is muscle”
Initiation of definitive treatment
within 1 hour of entry into health care
system
Major problem: delay in seeking
medical care post onset of symptoms
(44% wait > 4 hours to seek
treatment)
Serum cardiac markers: Proteins
released from necrotic heart muscle;
ordered on admission and for 3
succeeding days
a. Creatine phosphokinase (CK)
Appears 4 – 6 hours postacute MI; peaks
12 –24 hours; declines over next 48 –
72 hours
b. CK-MB
Isoenzyme of CK most sensitive indicator
of MI
CK-MB elevation > 5% positive indicator of
Cardiac-specific troponin T (cTnT) and
Cardiac-specific troponin I (cTnI)
Acute Pain
Ineffective Tissue Perfusion: obtain
12-lead ECG to assess significant
chest pain
Ineffective Coping: overuse of denial
may interfere with learning and
compliance with treatment
Fear
Nursing Interventions
2. Reliefof pain- MONA is the guide of
treatment of clients with chest pain.
M for Morphine sulfate,
O for Oxygen therapy,
N for nitrates and
A for aspirin.
2. Promote measures to maintain cardiac
parameters-
• Cardiac monitoring ( place client on Lead II),
• Report changes in LOC, Heart /Lung sounds,
• Peripheral pulses, Capillary refill time (less
than 3 sec),
• JVD (jugular vein distention),
• Monitor Pulmonary artery wedge
pressure( PAWP) if patient has a
Swan- Ganz catheter (PAWP less
than 18 mmHg shows volume
depletion and PAWP more than 18
mmHg signifies pulmonary
congestion or cardiogenic shock
• Monitor urinary output, Decreased
activity level, Schedule rest periods,
Adm. stool softeners.
Promote measures to maintain
adequate O2 and carbon dioxide
exchange
• O2 Administration,
• Pulse oximetry, Monitor ABG
results, Monitor secretions by
coughing and suctioning,
• Prepare for intubation as necessary.
Thrombolytics- agents which cause
lysis of a pathogenic clot and a
hypercoagulable state in the entire
circulatory system. For coronary
artery thrombi treatment should be
initiated within 4-6 hours from onset
of symptoms.
A. Streptokinase (SK)
B. Urokinase
C. Anisoylated Plasminogen –Streptokinase
Activator Complex ( APSAC)
D. Tissue Plasminogen Activator (t-PA) or
recombinant tissue-type plasminogen
activator ( rt-PA)
E. Retavase
Other Medications: used to reduce
oxygen demand and increase oxygen
supply
Analgesics – Morphine Sulfate
Angiotensin converting enzyme
inhibitor-vasodilation
Beta adrenergic blockers- decrease
contractility & O2 demand; increase
coronary blood flow
Anticoagulants( Heparin, Coumadin)
Calcium channel blockers (Verapamil)
Antidysrhythmic drugs( Lidocaine is
the most common)
Other Medical Interventions:
2.Percutaneous Transluminal Angioplasty (
PTCA)- a non surgical procedure
performed under fluoroscopy, that uses
pressurized balloon catheter to expand
stenotic coronary artery.
3.Intracoronary stents- placement of a
tubular mesh or coilspring device which
is place in the lumen of the coronary
artery.
4.Laser surgery- coronary artery is dilated
with use of laser.
4. Intra-aortic Balloon Pump ( IABP)-
inflation of a balloon in the coronary
artery during diastole and deflated
during sysytole.
5. Coronary Artery Bypass Graft(
CABG)-diversion of blood flow
around an occluded artery. This
conduit is accomplished through
anastomosing of the saphenous
vein or internal mammary artery.
1. Dysrhythmias – due to myocardial
irritability ; Fibrillation is the most
common.
2. Heart Failure.
3. Cardiogenic Shock- due to massive
left ventricular failure.
4. Ventricular aneurysm- a healing
necrotic tissue can cause thinning
and weakening of the
ventricular wall.
5. Pericarditis-an inflammatory
response to myocardial damage.
6. Dressler’s syndrome ( AKA post-
myocardial infarction syndrome)- a
late Pericarditis, with precordial pain,
friction rub, fever, peuritis and/or
pleural effusion.
7. Pulmonary embolism.
8. Interventricular septal rupture.
9. Papillary muscle rupture.
Description: the exchange of oxygen for
carbon dioxide in the lungs is inadequate
for oxygen consumption and carbon
dioxide production within the body’s
cells.
3. COPD 1. Emboli
4. Pneumonia 2. Drug overdose
5. Tuberculosis 3. Fluid overload
6. Contusion 4. DIC
7. Aspiration 5. Shock
8. Inhaled toxins
Nursing assessment
• Dyspnea, tachypnea
• Intercoastal retractions
• Cyanosis
• Hypoxemia: PO2< 50 mmHg
with FiO2 > 60%
• Diffuse pulmonary infiltrates
seen on chest x-ray as “white-
out” appearance
• verbalized anxiety; restlessness
(Nursing Diagnoses)
Description: Widespread,
serious reduction of tissue
perfusion (lack of oxygen and
nutrients), which, if prolonged,
leads to generalized impairment
of cellular functioning.
At risk for developing shock
include:
2.The very young or the very old client
3.Post-MI clients
4.Clients with severe
dysrhythmia
6.Clients with adrenocortical
dysfunction
8.Persons with a history of
recent hemorrhage or
blood loss.
11.Clients with burns
TYPES OF SHOCK
TYPE DESCRIPTION
HYPOVOLEMI
C Related to external or
internal blood/fluid loss
(most common cause of
CARDIOGENI
C/OBSTRUCTI
shock);
Related hemorrhage, burns, to
VE dehydration
ischemia/impairment in
tissue perfusion from
myocardial infarction, serious
arrhythmia, or congestive
heart failure. All of these
Distributiv Results from inadequate
e
SHOCK
vascular tone.
Blood volume remains
normal
Vascular space increases
dramatically because of
massive vasodilation
1.Neuroge Blocking of the sympathetic
nic
NS in SCI leads to massive
peripheral vasodilation from
an unopposed
parasympathetic NS.
2. Related to allergens
VASOGENI
C (anaphylaxis), spinal cord
ANAPHYLACT
IC
injury, or peripheral
neuropathies, all resulting in
venous pooling and
decreased blood return to
the heart, which decreases
cardiac output over
3. time.Warm
Related to skin,
endotoxins
SEPTIC bronchoconstriction
released from rashes
bacteria,
may
which be causes
observed with
vascular
products
pooling, of inflammation
diminished venous
STAGES OF HYPOVOLEMIC SHOCK
STAGE SIGNS AND CLINICAL DESCRIPTION
SYMPTOMS
Vital Signs:
4.Tachycardia (>100 bpm)
5.Tachypnea (>24 cpm)
6.Blood pressure decreased
(systolic <80 mmHg)
Mental Status Exam:
9.Early shock: restless, hyper-alert
10.Late shock: decreased alertness,
lethargy, coma
Skin Changes:
2.Cool, clammy (warm skin in vasogenic
and early shock)
3.Diaphoresis
4.Pale
Fluid Status (acute tubular necrosis
can happen quickly in shock):
• Urine output decreases or an
imbalance between intake and output
occurs
• Abnormal CVP (>4 cm of H2O).
• Urine specific gravity >1.020
(Nursing Diagnosis)
4. Decreased cardiac
output
6. Altered thought
process
Nursing Diagnoses
10. Potential for injury
11. Alteration in tissue perfusion
Nursing Plans and Interventions
2. Monitor client for bleeding.
3. Monitor vital signs.
4. Protect client from injury and bleeding:
• Provide gentle oral care with mouth
swabs
• Minimize needle sticks, use smallest
gauge needle possible.
• Turn frequently to eliminate pressure
points.
• Minimize number of blood pressures
taken by cuff.
4. Administer Heparin IV
during the first phase to
inhibit
coagulation.
5. If in hemorrhagic phase,
administer clotting factors