Glasgow Coma Scale – Patients with low scores(3-4) have high mortality and poor prognosis for cognitive recovery compared to patients with higher scores (8 and above)

Eye OpeningSpontaneously 4 Glasgow Coma Scale To speech 3 Maximum score: 15To pain 2None 1

Verbal responseOriented 5Confused 4Inappropriate 3Incomprehensible2None 1

Motor ResponseObeys Command 6Localizes pain 5Withdraws (pain) 4Flexion (pain) 3Extension (pain) 2None 1

P - Pattern Q - QualityR - ReactionS - SeverityT - Treatment done

AMPLE Mnemonic For Multiple Trauma

A=Allergies, M=Medication, P=Past medical history, L=Last food intake,

E=Events preceding the injury

A=Airway

B=Breathing

C=Circulation

D=Disability

E=Exposure

A=Is patient ALERT?

V=Is patient responding to VERBAL stimulus?

P=Is patient responding to PAINFUL stimulus?

U=Is patient UNCONCIOUS?

Components ScoreC - Circulation

Normal capillary refill and BP>=1002

Delayed capillary refill or BP>=85<100 1No capillary refill or BP<85 0

R - RespirationNormal 2Abnormal (labored or shallow) 1Absent 0

A - AbdomenAbdomen and thorax non-tender 2Abdomen and thorax tender 1Abdomen rigid or flail chest* 0

M - MotorNormal 2Responds only to pain

1(other than decerebrate)

no response (decerebrate) 0

S - SpeechNormal 2Confused 1No 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, LCARight 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%)

1. Consent2. Explain procedure – cooperation3. Trendelenberg position – lower

extremity source4. Assist during procedure – local

anesthesia5. Instruct for deep breath and hold;

neck flexion for PICC6. Correct reading 7. 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 Values

Arterial Venous

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 (mEq/L)

10 to 18 8 to 16

ANALYSIS OF ARTERIAL BLOOD GASES

COMPONENT

DESCRIPTION VALUES

pH Measures hydrogen ion (H+) concentration

7.35-7.45

Increase in ions, acidosis <7.35

Decrease in ions, alkalosis >7.45

pCO2

•Partial pressure of in CO2 arteries

•Respiratory component of acid-base regulation

35 to 45 mmHg

Hypercapnia, respiratory acidosis >45 mmHg

Hypoventilation, respiratory alkalosis

<35 mmHg

HCO3

•Measures serum bicarbonate•May reflect primary metabolic disorder or compensatory mechanism to respiratory acidosis

Normal: 22 to 26 mEq/L

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.

Initiating Mech. Ventilation/ Setting up machine1.Set up the machine

2. Plug to emergency outlet

3. Select ventilatory settings ( per doctor’s orders)

Tidal volume, FiO2, peak inspiratory flow rate, Mode ( A/C, IMV, SIMV, PSV), Sensitivity, Pressure limit, I:E ratio, respiratory rate.

Types of Ventilators1. Pressure- Cycled2. Volume- Cycled3. Time- Cycled

Nursing Care1.Note ETT position. Monitor cuff

pressure2. Restrain only if needed3. Administer sedatives prn.( To keep

patient calm)4. Auscultate breath sounds

5. Monitor ventilator settings6. Change tubings prn.7. Perform CPT as needed8. Monitor ABG, O2 sat. , V/S

9. Assess position change10. Provide alternate communication

measures11. Suctioning prn.12. Respond to alarms

Weaning Parameters:

PaO2 is over 70-80 mmHg PaCO2 = normal Acceptable general respiratory status Correction of underlying problem

Description: a visual representation of the electrical activity of the heart reflected by changes in the electrical potential at the skin surface

PP

QQSS

RR

TT

UU

PP

QQSS

RR

TT

UU

PP

QQSS

RR

TT

UU

PP

QQSS

RR

TT

UU

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)

Ectopic Foci- may arise from any part of the heart atria or ventricles causing abnormal heart rates and activity.

The following conditions can interfere with normal heart functioning:

A. Disturbances of rate or rhythm

B. Disorders of conductivityC. Enlarged heart chambersD. Presence of myocardial

infarctionE. Fluid and electrolyte

imbalances.

Each EKG should include identifying information of patient

The standard EKG is the 12-lead EKG. Bedside monitoring through

telemetry is more commonly seen in the clinical setting using 3-5 leads

A portable continuous monitor (Holter monitor) can be placed on the client to provide a magnetic tape recording; patient to record activities, medications and pain experiences

The EKG graph paper consists of small and large squares:

A. The small squares represent 0.04 seconds with five of these small squares combining to form one large square.

B. Each large square represents 0.20 seconds (0.04 seconds x 5). Five large squares represent 1 second.

Using Boxes – 300-150-100-75-60 Calculation of heart rate using the six-second

rule:1. The easiest means of calculating the heart

rate.2. Can not be used when the heart rate is

irregular.3. 30 large squares equal one-six second

interval.4. Count the number of R-R intervals in the 30

large squares, and multiply by ten to determine the heart rate for one minute (the R is the high peak on the strip).

1. P wave: atrial systoleA. Represents depolarization of the atrial

muscleB. Should be rounded without peaking or

notching.2. QRS complex: ventricular systole

A. Represents depolarization of the ventricular muscle.

B. Normally follows P wave.C. QRS interval measured from beginning of

the QRS to the end of QRS (normal:0.06-0.12 sec.).

T wave: ventricular diastole1.Represents repolarization of the

ventricular muscle.2.Follows QRS complex.3.Usually slightly rounded without

peaking or notching.

U wave – a small wave following the T-wave indicating potassium depletion

3. ST segment:A. Represents every ventricular

repolarization.B. Measured from the end of the S

wave to the beginning of the T wave.4. PR interval:

A. Represents the time required for the impulse to travel through the atria (SA node), through the A-V node, to the Purkinje fibers in the ventricles.

B. Measured from the beginning of the P wave to the beginning of the QRS complex.

C. Represents A-V nodal function (normal: 0.12 to 0.2 seconds)

5. U wave:A. Not always present.B. Most prominent in the presence of

hypokalemia.6. QT interval:

A. Represents the time required to completely depolarize and repolarize the ventricles.

B. Measured from the beginning of the QRS complex to the end of the T wave. (0.32-0.44 sec.)

7. R-R interval:A. Reflects the regularity of the heart

rhythm.B. Measured from one QRS to the next QRS.

Normal sinus rhythm (60-100) Sinus bradycardia (below 60) Sinus tachycardia (101-180) Sinus arrhythmia (irregular)

Normal Sinus Rhythm

Lead II

Look at the p waves: rate is 60-100/min cycle length do not vary by 10% PR interval is 0.12 sec. or more

Sinus Bradycardia

Regularly occurring PQRST Rate < 60 / min

Rate = 48/minRate = 48/min

Sinus Tachycardia

Regularly occurring PQRST Rate > 100 / min

Rate = 111/min Rate = 111/min Rate = 111/min

Sinus Arrhythmia

Identical but irregularlyoccurring PQRST

longest PP or RR > theshortest by 0.16 sec or more

Rate = 94/minRate = 71/min

Rate = 79/minRate = 94/min

PAC – P waves are premature Atrial tachycardia – (150-250) difficult

to distinguish P from T waves Atrial flutter – atrial (250-450) no p

waves but replaced by saw-toothed waves before a QRS

Atrial fibrillation- atrial (400-600) bizzare P waves before a QRS

Premature Atrial Contraction

Prematurely occurring PQRTS complex P wave different in configuration

from the sinus beat. PR interval often long. QRS narrow.

Multifocal Atrial Tachycardia

Impulses originate irregularly and rapidly at different points in the atrium

Varying P wave, PR, PP and RR intervals Ventricular rate > 100/min

Atrial Flutter

Atrial rate = 220-300/min( P as flutter waves )

Variable degree of AV block( irregular RR interval )

Atrial Fibrillation

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

At least 3 consecutive PVC’s Rapid, bizarre, wide QRS complexes

(> 0.10 sec) No P wave (ventricular impulse

origin)

Rate > 140 / min

Ventricular Fibrillation

First degree AV – Normal rate and rhythm with prolonged constant PR interval

Second degree AV 1 or 2– Atrial regular, ventricular irregular, more P waves than QRS , PR lengthens then drops a QRS periodically or QRS maybe absent

Third degree AV - Atrial -ventricular no relationship, more P waves than QRS , No PR ; QRS narrow or wide

FIRST DEGREE AV BLOCK

PR interval > 0.20 sec

0.28 sec 0.28 sec0.28 sec

Second Degree Atrioventricular Blocks

Do you have a normal P wave?

Do you have a normal PR segment?

Do you have a normal PR interval?

Yes

No

NoWill there be intermittent P waves not followed by QRS complex? Yes (dropped beats)

Complete atrioventricular block

Impulses originate at both SA node and at

the subsidiary pacemaker below the block

THIRD DEGREE AV BLOCK

Atrial rate = 100 BPM Atrial rate = 100 BPM

Atrial rate = 100 BPM

Ventricular rate = 83 BPM Ventricular rate = 83 BPM

Do you have regularly occurring P waves and QRS complexes?Are the P waves related to the QRST complexes?Is the atrial rate < = > ventricular rate?

Yes

greaterNo

Frequent PVC’s, Salvo, V-tach - Lidocaine to regulate rhythm to normal; cardioversion

Asystole – epinephrine, atropine to initiate rhythm and contractions, then defibrillation if with pulse

Coarse V-Fibrillation with pulse – defibrillation, then medications to regulate rhythm

loss of oxygen and nutrients to myocardial tissue due to poor coronary blood flow. The most common cause is atherosclerosis ( fatty, fibrous, possibly calcium deposits in the lumen of coronary arteries)

Risk factors: Non- modifiable/ non-controllable: Heredity Age ( above 40), Sex/gender( more men , more likely in women

who smoke and those on oral contraceptive) Race ( more in blacks)

Coronary Artery Disease ( CAD)-

• Diet• Habit/ Lifestyle ( sedentary; smoking- risk drops

within 1 year of quitting)• Contributing: Obesity, Response to stress, other

diseases like DM, • Increased LDL ; decreased HDL; Hypertension; • Coronary artery spasm associated with

atherosclerosis or from unknown cause

A for aspirin and antianginal therapy,

B for beta-blocker therapy and BP control,

C for cigarettes and cholesterol,

D for diet and diabetes,

E for education and exercise.

The mnemonic A B C D E to control risk factors

a transient ischemic attack resulting from decreased blood supply through partially occluded coronary arteries. Precipitating factors include: extreme changes in temperature, physical exercise, emotional factors, eating a heavy meal, sexual intercourse, valsalva maneuver, cigarette smoking, stimulants.

Angina/ Angina Pectoris-

Percutaneous Transluminal Coronary Angioplasty (PTCA), Coronary Artery Bypass graft ( CABG), or Stress Test may cause angina.

Pain or chest discomfort may be described as burning, suffocating squeezing or crushing tightness in the substernal or precordial areas that radiates to the left arm ( or both), neck, jaw or shoulder blade.

Patient may clench his fist or rub his left arm when describing it. Commonly accompanied by nausea, vomiting, fainting, sweating, and cool extremities.

1. Stable ( chronic) Angina :

usually precipitated by physical exertion, emotional stress, or cold weather.

Has stable pattern of onset, duration and severity and relieving factors

pain or discomfort may vary from mild to severe and usually lasts for 1 to 5 minutes .

Relieved with rest and sublingual NTG, or both.

2. Unstable angina

Preinfarction angina, crescendo angina or intermittent coronary syndrome

Triggered by unpredictable degree of exertion or emotion, which may occur at night.

It must be treated as a medical emergency with the client receiving immediate medical attention

Often described as progressive, prolonged, or frequent angina with increasing severity.

Pain or discomfort is more intense lasting up to 30 minutes, often arouses patient from sleep.

Pain is not completely relieved with NTG, may require narcotics (like Morphine Sulfate)

Without significant EKG changes like ( T wave inversion =Ischemia ) diagnosis is based on history and clinical condition

10-30% of clients progress to having an MI in 1 year, and 29% die from MI in 5 years

3. Prinzmetal’s angina :

Variant angina similar to classic angina ; chest pain of longer duration; may occur at rest

Attacks tend to happen between midnight and 8am

Results from coronary artery associated with elevation of ST segment in the EKG

NTG generally yields quick relief. Calcium channel blockers ( Verapamil,

Nifedipine, Dialtezem ) are most effective Goal: vasodilation and reduce myocardial oxygen demands

When administering Nitroglycerin: Take baseline V/S, give it sublingually x 3 every 5 min. take V/S after each dosage.

If the BP is less than 100mmHg or less than

25mmhg lower than the previous reading, do not give it, the nurse lowers the head of the bed and notifies the physician

ST segment depression and T-wave inversion occur with chest pain and return to normal when episode subsides; ST segment elevation ( Prinzmetal’s) which goes back to normal when spasm subsides.

Definition 1. Necrosis of myocardial cells is

life-threatening event 2. Loss of functional myocardium

affects heart ability to maintain effective cardiac output

Ulceration or rupture of complicated atherosclerotic lesion

Substances released which lead to platelet aggregation, thrombin generation, local vasomotor tone

Formation of clot which occludes vessel and blocks blood to myocardium distal to obstruction

Prolonged ischemia (>20 – 45 minutes): irreversible hypoxemic damage

Cellular metabolism shifts from aerobic to anaerobic metabolism producing hydrogen ions and lactic acid

Depth of Infarction Subendocardial or non-Q-wave infarction1. Damage is limited to subendocardial tissue2.Occurs within 20 minutes of injury3. Common complication is recurrent ischemia4. S-T segment depression with small infarct Intramural infarction – in myocardium ;

associated with angina pectoris Transmural infarction or Q- wave infarction1.All layers of myocardium to epicardium

affected within 1 to 6 hours2. Common complication is heart failure3. S-T segment elevation with large infarct

size

Pain: classic manifestation Lasts > 15 – 20 minutes Unrelieved by rest or nitroglycerine Onset sudden and usually not

associated with activity Described as crushing and severe; as

a pressure, heavy or squeezing sensation; tightness or burning in the chest

Location: center of chest (substernal) and may radiate to shoulders, neck, jaw, arms

Women and older adults have atypical chest pain with complaints of indigestion, heartburn, nausea, vomiting

No chest discomfort in 25% of clients with acute MI

Additional symptoms relate to sympathetic nervous system stimulation:

Cool, clammy, mottled skin Tachypnea Sense of impending doom and death

Depending on location and amount of infarct

Hypertension or hypotension Signs of heart failure Nausea and vomiting, bradycardia Hiccups Sudden death (large blood vessel

involvement)

Treatment goals:

Relieve chest 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-MBIsoenzyme of CK most sensitive indicator of MICK-MB elevation > 5% positive indicator of MI

Cardiac-specific troponin T (cTnT) andCardiac-specific troponin I (cTnI)

Proteins released during myocardial infarction; sensitive indicators for myocardial damage

Released and levels rise with necrosis of cardiac muscle

Sensitive enough to detect very small infarction and remain in blood 10 – 14 days post MI

Other laboratory tests

CBC, Erythrocyte Sedimentation Rate: WBC and ESR elevated of because of inflammation

Arterial Blood Gases: assessment secondary to physical effects of MI

Electrocardiography: T wave inversion;

Elevation of S-T segment; Formation of Q wave

Nursing Diagnoses:

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 Interventions1. Relief of 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. UrokinaseC. 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:1.Percutaneous Transluminal Angioplasty (

PTCA)- a non surgical procedure performed under fluoroscopy, that uses pressurized balloon catheter to expand stenotic coronary artery.

2.Intracoronary stents- placement of a tubular mesh or coilspring device which is place in the lumen of the coronary artery.

3.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.

ARDS is characterized by:1. Hypoxemia: PO2 below 50mmHg.2. Hypercapnia: PCO2 above 45 mmHg.

ARDS is an unexpected, catastrophic pulmonary complication occurring in a person with no previous pulmonary problems. The mortality rate is high (50%).

During acute failure, the pH falls below 7.30, indicating acidosis.

Common causes of respiratory failure include:

1. COPD2. Pneumonia3. Tuberculosis4. Contusion5. Aspiration6. Inhaled toxins

7. Emboli8. Drug overdose9. Fluid overload10. DIC11. Shock

Nursing assessment

1.Dyspnea, tachypnea2.Intercoastal retractions3.Cyanosis4.Hypoxemia: PO2< 50 mmHg

with FiO2 > 60%5.Diffuse pulmonary infiltrates

seen on chest x-ray as “white-out” appearance

6.verbalized anxiety; restlessness

(Nursing Diagnoses)

1.Impaired gas exchange2.Ineffective airway clearance3.Ineffective breathing

pattern4.decreased cardiac output5.Fluid volume excess

Nursing Plans and Interventions

1. Maintain client on a ventilator with the correct settings.

2. Provide care for either an oral airway or a tracheostomy. (Suction ONLY when secretions are present)

3. Monitor breath sounds for pneumothorax especially when positive end expiratory pressure (PEEP) is used to keep small airways open. The amount of pressure can be set with the ventilator and is usually around 5-10 cm of water.

4. Provide emotional support to decrease anxiety and allow ventilator to “work” the lungs.

5. Monitor client hemodynamically with essential vital signs and cardiac monitor.

6. Monitor ABGs routinely.7. Monitor vital organ status:

central nervous system, level of consciousness, renal system output and myocardium (apical pulse, blood pressure).

8. Monitor fluid and electrolyte balance.

9. Monitor metabolic status through routine laboratory work.

Artificial Surfactant (Survanta/Beractant) ?

Nitric Oxide –pulmonary vasodilator ? Dobutamine/Dopamine for fluid

instability Steroids Antibiotics Ventilatory support with PEEP

Baro trauma, VA pneumonia, pulmonary fibrosis, Pulmonary embolism

Stress ulcers, GIT hemorrhage Arrhythmias ARF Pneumothorax and tracheal stenosis Malnutrition and electrolyte inbalance MOSF – from endothelial damage by

circulating immune complexes

Description: Widespread, serious reduction of tissue perfusion (lack of oxygen and nutrients), which, if prolonged, leads to generalized impairment of cellular functioning.

SHOCK

At risk for developing shock include:

1.The very young or the very old client2.Post-MI clients3.Clients with severe dysrhythmia4.Clients with adrenocortical dysfunction5.Persons with a history of recent hemorrhage or blood loss.6.Clients with burns7.Clients with massive/overwhelming

infection.

TYPES OF SHOCKTYPE DESCRIPTION

HYPOVOLEMIC Related to external or

internal blood/fluid loss (most common cause of shock); hemorrhage, burns, dehydration

CARDIOGENIC/

OBSTRUCTIVE

Related to ischemia/impairment in tissue perfusion from myocardial infarction, serious arrhythmia, or congestive heart failure. All of these result in decreased cardiac output.

Distributive

SHOCK

Results from inadequate vascular tone.Blood volume remains normalVascular space increases dramatically because of massive vasodilation

1.Neurogenic

Blocking of the sympathetic NS in SCI leads to massive peripheral vasodilation from an unopposed parasympathetic NS.

2. VASOGENI

CANAPHYLACT

IC

Related to allergens (anaphylaxis), spinal cord injury, or peripheral neuropathies, all resulting in venous pooling and decreased blood return to the heart, which decreases cardiac output over time.Warm skin, bronchoconstriction rashes may be observed with products of inflammation

3. SEPTIC

Related to endotoxins released from bacteria, which causes vascular pooling, diminished venous return and reduced cardiac output. S/S with fever

STAGES OF HYPOVOLEMIC SHOCKSTAGE SIGNS AND

SYMPTOMSCLINICAL DESCRIPTION

STAGE I: INITIAL STAGEBlood loss of less than 10%. Compensatory mechanisms triggered.

Apprehension and restlessness (first signs of shock)Increased heart rateCool, pale skinFatigue

Arteriolar constrictionIncreased production of ADHArterial pressure is maintainedCardiac output usually normal (for healthy individuals)Selective reduction of blood flow to skin and muscle beds

STAGE II: COMPENSATO

RY STAGEBloodvolume reduced by 15 to 25%. Decompensation begins.

Flattened neck veins and delayed venous filling timeIncreased pulse and respirationsPallor, diaphoresis and cool skinDecreased urinary outputSunken soft eyeballsConfusion

Marked reduction in cardiac outputArterial pressure decline (despite compensatory arteriolar vasoconstriction)Massive adrenergic compensatory response resulting in: tachycardia, tachypnea,cutaneous vasoconstriction, and oliguriaDecreased cerebral perfusion

STAGE III: PROGRESSIVE STAGE

EdemaIncreased blood viscosityExcessively low blood pressureDysrhythmia, ischemia and MIWeak, thready, or absent peripheral pulses

Rapid circulatory deteriorationDecreased cardiac outputDecreased tissue perfusionReduced blood volume

STAGE IV: Irreversible STAGE

Profound hypotension, unresponsive to vasopressor drugsSevere hypoxemia, unresponsive to oxygen administrationAnuria, renal shutdownHeart rate slows, BP falls, with consequent cardiac and respiratory arrest

Cell destruction so severe death is inevitableMultiple organ system failure

Nursing Assessment

Vital Signs:1.Tachycardia (>100 bpm)2.Tachypnea (>24 cpm)3.Blood pressure decreased (systolic <80 mmHg)Mental Status Exam:1.Early shock: restless, hyper-alert2.Late shock: decreased alertness,

lethargy, coma

Skin Changes:1.Cool, clammy (warm skin in vasogenic

and early shock)2.Diaphoresis3.PaleFluid Status (acute tubular necrosis

can happen quickly in shock):1.Urine output decreases or an

imbalance between intake and output occurs

2.Abnormal CVP (>4 cm of H2O).3.Urine specific gravity >1.020

(indicates hypovolemia)

(Nursing Diagnosis)

1. Fluid volume deficit

2. Decreased cardiac output

3. Altered thought process

4. Anxiety (family and individual)

1. Monitor arterial pressure by understanding the concepts related to arterial pressure

2. Monitor vital signs and arrhythmias every 15 minutes or more often depending on the stability of the client.

3. Assess urine every hour to maintain at least 30 ml/hr. Notify healthcare provider if urine output drops below 30 ml/hr

4. MAST, IABP, External counterpulsation devise

5. Administer fluids as prescribed by provider: blood, colloids, or electrolyte solutions until designated CVP is reached. (In shock, the healthcare provider often orders fluids to elevate CVP 16-19 cm of H2O as compensation for decreased cardiac output).

6. Place client in modified Trendelenburg’s position (feet up 30-45 degrees, head flat).

7. Administer medications IV (not IM or subQ) until perfusion improves in muscles and subcutaneous tissues.

HINT: If cardiogenic shock exists with the presence of pulmonary edema, i.e. from pump failure, position client to REDUCE venous return (high-Fowler’s with legs down) in order to decrease venous return further to the left ventricle.

8. Keep client warm (increase heat in room or put warm blankets in client, but not too hot).

9. Keep side rails up during all procedures (clients in shock experience mental confusion and may easily be injured by falls).

10.Obtain blood for laboratory work as prescribed: CBC, electrolytes, BUN, creatinine (renal damage), and blood gases (oxygenation).

Drugs of choice for shock:1. Digitalis preparations:

increase contractility of the heart muscle

2. Vasoconstrictors ( Dopamine): generalized vasoconstriction to provide more available blood to the heart to help maintain cardiac output.

Vasodilators – for blood supply to important organs and in cardiogenic shock

Steroids Heparin Naloxone- reverses the effects of

hypotension as an opiate antagonist Epinephrine- for anaphylactic shock H2 receptor antagonists – ulcers Opioids – for cardiogenic shock Calcium gluconate- for blood clotting

and muscular function

Blood- whole ( to replace large volume loss), packed RBC 9 for moderate blood loss bec they replenish RBC and improve oxygen –carrying capacity without adding excessive volume), autotransfusion (trauma). As a rule of thumb, Hct. Rises about 4% and Hgb rises about 1 g % for each unit of packed RBC administered.

Fluid replacement- Crystalloids ( for F/E replacement) ,Colloids( plasma protein fraction, fresh-frozen plasma, albumin, dextran, hetasarch ( plasma expander) are used to restore plasma volume and colloidal osmotic pressure bec. they contain large molecules usually proteins or starches)

•Isotonic solutions:1.Normal saline (0.9% NS)2.Lactated Ringers (LR)3.5% dextrose in water (D5W is on the low end of isotonic-some sources classify as hypotonic)

Hypotonic solutions:1.0.3 % NaCl2.0.45 NS3.D 2.5 in H20

•Hypertonic saline solutions are available but used only when serum osmolality is dangerously low

1.5% dextrose in LR (D5LR)

2.5% dextrose in 0.45% saline (D5 ½ NS)3.5% dextrose in 0.9% saline (D5NS)

Description: a coagulation disorder with paradoxical thrombus and hemorrhage. DIC is an acute complication of conditions such as hypotension and septicemia, suspected when there is bloody oozing from two or more unexpected sites. The first phase involves abnormal clotting factors, and results in an inability to form clots and hemorrhage occurs.

The diagnosis is based on laboratory findings:

1. Prolonged PT2. Prolonged PTT3. Decreased fibrinogen4. Decreased platelet count5. Increased Fibrin Degradation

(split) Products (FDP)

Nursing Assessment1. Petechiae, purpura, hematomas2. Oozing from IV sites, drains, gums

and wounds3. GI and GU bleeding4. Hemoptysis5. Hypotension, tachycardia6. Pain

Nursing Diagnoses1. Potential for injury2. Alteration in tissue perfusion

Nursing Plans and Interventions1. Monitor client for bleeding.2. Monitor vital signs.3. 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.• Use gentle suction to prevent trauma to

mucosa.• Apply pressure to any oozing site.

4. Administer Heparin IV during the first phase to inhibit coagulation.

5. If in hemorrhagic phase, administer clotting factors

6. Provide emotional support to decrease anxiety.

Description: dilation of the abdominal aorta caused by an alteration in the integrity of its wall.

Most common cause of AAA is atherosclerosis It can also be a late manifestation of syphilis Without treatment, rupture and death will

occur It is often asymptomatic Most common symptom is abdominal pain or

low back pain with the complaint that the client can feel “heart beating”.

Those taking antihypertensive drugs are at risk of developing AAA.

Nursing Assessment1. Bruit (swooshing sound heard over a

constricted artery when auscultated) heard over abdominal aorta, pulsation in upper abdomen.

2. Abdominal or lower back pain.3. Abdominal x-ray will confirm diagnosis

if aneurysm is calcified (aortagram, angiogram, abdominal ultrasound).

4. Symptoms of rupture: hypovolemic or cardiogenic shock with sudden, severe abdominal pain.

Nursing Diagnosis1. Activity intolerance2. Impaired skin integrity3. Anxiety

Nursing Plans and Interventions

1. Assess all peripheral pulses and vital signs regularly

2. Observe for signs of occlusion after graft

3. Observe renal functioning for signs of kidney damage (artery clamped during surgery may result in kidney damage).

4. Observe for postoperative ileus

MOSF= Multiple Organ System Failure Multiple Organ Dysfunction Syndrome ( MODS)

a syndrome that occurs when one or more than one system/organ cannot support its activities.

Factors Influencing the development of MODS: Gram negative sepsis ( #1 risk), immunosuppressants, traumatic injury, sleep deprivation, malnutrition, blood transfusions, age over 65.

Pathophysiology: the 3 Is of MODS are: persistent Inflammation,

Infection (sepsis), Ischemia.

The precursor of MODS is systemic inflammatory response syndrome ( SIRS)

1. Stimulation of the inflammatory-immune response ( IIR) which

2. Sympathetic nervous system stimulation and release of catecholamines

3. Endothelial damage and embolus formation. Complement activation occurs

GOAL: is to induce inflammation, the goal of inflammation is to protect the body, limit injury extent , and promote healing at the damaged site)

Other Mediators involved in the IIR are WBC, platelet, T cells, B cells, and histamine.

Altered perfusion r/t to small microvasculature emboli and respiratory insufficiency causes shunting of blood to major organs until compensatory mechanisms fail.

The organs affected are usually the lungs, liver kidney, heart and brain.

Modified APACHE II Criteria for Diagnosing Multiple Organ System Failure ( Black and Jacobs, 1997)

I. Cardiovascular Failure ( presence of one or more of the ff)

HR less than 54 beats / min Mean arterial pressure equal or less that

49 mm Hg (systolic pressure of equal or less than 60mmHg)

Occurrence of Ventricular Tachycardia/ Fibrillation

Serum pH of equal or less than 7.24 with a PaCo2 of equal or less than 40 mmHg

II. Respiratory Failure ( presence of one or more of the following)

RR of less than or equal to 5/min. equal to or greater than 49/min, PaCO2 equal or greater than 50mmHg

Alveolar Arterial Oxygen difference equal or greater then 350mmHg calculated as follows: (713 x % Oxygen in inspired gas)- PaCO2- PaO2

Dependent on ventilator on the 2nd day

III. Renal Failure ( presence of one or more of the ff)

*Urine output equal or less than 479 ml/24 hrs. or equal or less than 159ml/8 hrs.

* Serum BUN equal to or greater than 100mg/dl

* Serum Creatinine equal to or greater than 3.5 mg/dl

IV. Hematologic Failure ( presence of one or more of the ff)

*WBC equal or less than 1000/ul ( Normal is 4,000 to 10,000/ ul)

*Platelet equal or less than 20,000 /mm3

* Hematocrit equal or less than 20%

V. Neurologic Failure

Glasgow coma score equal or < than 6 ( in the absence of sedation )

VI. Hepatic Failure Serum Bilirubin equal or greater than

6 mg/dl Prothrombin Time equal to or greater

than 4 sec over control in the absence of systemic anticoagulation

Assessment:

Early: Vasodilation and ↓ PR With normal BP, Cardiac output increases to maintain blood pressure= initial hyperthermia ( skin warm, pink, and dry with shaking chills although the reverse may occur in the elderly) ,

Increase renal blood flow ( polyuria), Hyperventilation (Causes resp alkalosis), Signs of tissue hypoxia manifest due to

oxyhemoglobin dissociation ; Hemoglobin is reluctant to release oxygen to cells.

Late: Hypotension due decreased cardiac output ( PR is ↑ via catecholamine release due to sympathetic nervous system stimulation) ;

Pulse becomes weak and thready; ST and T wave changes on ECG ( due to ↓ myocardial perfusion);

Cold, moist, pale skin, mottling and cyanosis, hematologic changes( DIC or primary bleeding problem),

Hypoxia (↑HR,↑RR, restlessness, diaphoresis, lethargy, confusion, and pallor) and

↓perfusion evident metabolic acidosis develops.

Others: Glucose: initially increased,

gluconeogenesis occurs leading to lactic acidiosis; protein catabolism causes negative nitrogen balance and proteinuria

Generalized acidotic state and decreased cellular energy cause cell death and organ failure

Mortality is up to 90%

Management:

Monitor V/S, Neuro status, Measure I/O, Bowel sounds/ Abdominal distention, Abdominal girth, Occult blood

Ventilatory support, ABG monitoring, pulse oximetry

Maintain + nitrogen balance ( enteral feeding)

MEDICATIONS : antibiotics, antacids, histamine

antagonists, analgesics, anti-anxiety agents, sedate as ordered to ↓ metabolic needs, anti-inflammatories, vasoactive agents, inotropes, fluids , steroids ( not proven to be beneficial)

FUTURE TRENDS in therapy: Cyclosporine vs. FK-586; monoclonal/polyclonal antibodies.

Sample QuestionsWhich of the following nursing orders

would be found on the care plan for a client for the first 24 hours after an MI?

A. Utilize bedside commode for bowel movements

B. 200 calorie soft dietC. Feed the patientD. Administer promethazine daily

Which of the following would be included in the discharge plan for a client after MI?

A. Don’t begin sexual intercourse until after 3 months

B. Begin walking frequentlyC. Take one aspirin every 8 hours

as orderedD. Continue previous lifestyle

when ready

To prevent the leaking of blood into surrounding tissue following blood extraction for ABG determination, the nurse should implement which nursing measure:

A. Apply ice to the puncture siteB. Maintain manual compression

over the puncture site for at least one minute

C. Elevate the limb on several pillows

The client is an asthmatic and in acute respiratory distress. The nurse auscultates the lungs and notes no inspiratory wheezing. What should this finding suggest to the nurse?

A. Airway constriction requiring intensive interventions

B. An appropriate reaction to the medications used in the management of the client

C. The need to assess the client further for signs of pleural effusion

D. Overuse of the intercostal muscles resulting in poor exchange