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b io crisis

b io crisis

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BI OLOG IC CRI SI S

Dr. Anthony Toledo MD,RN

MAIN MENU
SHOCK ARRHYTHMIAS
HEART BLOCK/STROKE

DM/DKA
KIDNEY FAILURE (ERDS) PULMONARY EDEMA PULMONARY EMBOLISM

BURNS

HEPATIC COMA/ENCEPHALOPATHY

CLICK TOPIC

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Wh at is Sh ock ?

A condition in which systemic BP is adequate to deliver oxygen and nutrients to support vital organs and cellular functions. Maintenance of tissue perfusion depends on adequate cardiac pump, effective vasculature or circulating system and sufficient blood volume. Widespread serious reduction of tissue perfusion ( lack of O2 )

Cla ss ifica tion of s hock
A. 

HY PO VO LEMI C SHO CK Loss of circulating volume due to excessive blood loss, loss of body fluids and third spacing of fluids. Most common type of shock. Characterized by decreased intravascular volume of 15-25%.

 

HYP OVO LEM IC SH OCK

Predi spos in g fa ct or s:
External:FluidLoss Internal:FluidShift
trauma  surgery  vomiting  diarrhea  diuresis  diabetes insipidus

a. hemorrhage b. burns c. ascite d. peritonitis e. dehydration

Med ica l M an agemen t
GOALS:  restore intravascular volume  redistribute fluid volume  correct the underlying cause Fl ui d and Bl ood re plac ement : • Lactated Ringer’s solution, colloid, and 0.9% NaCl (normal saline) to restore intravascular volume. • Blood replacement for extensive and rapid blood loss; auto-transfusion methods may be considered for closed cavity hemorrhage. Red ist ri but ion of Flui ds • Patients is positioned in trendelenburg to assist in fluid redistribution. •Military antishock trousers (MAST) are used in extreme emergency situations when bleeding cannot be controlled

Ph arma colog ic Ex am
   

Desmopressin Insulin Anti-emetic Anti-diarreal

Nu rs in g M anagemen t

Closely monitor px at risk for fluid deficits(younger than 1y/o or 65 years of age) Assist with fluid replacement Ensure safe administration of of prescribe fluids and medications, and document effects Monitors and report signs of complications and effect of treatment. Monitor for cardiovascular overload and pulmonary edema: hemodynamic pressure, VS, ABG, and fluid IO. Reduce fear and anxiety about the need for oxygen mask by giving px explanations and frequent reasurance

 

Ca rdiog en ic Sh oc k

Ca rdiog en ic Sh oc k

The ability of the heart to pump blood is impaired that causes a decrease in cardiac output. Causes of cardiogenic shock are either coronary or noncoronary Coronary cardiogenic shock is more common and seen most often in px with myocardial infarction. Noncoronary causes include tension pneumothorax, sever metabolic problem, cardiac tamponade, cardiomyopathy, valvular damage and dysrhythmias.

Pa th oph ysi o o f C ar di ogen ic Shock

Clin ica l M anif estation :

Dysrhythmias are common and result from a decrease in oxygen to the myocardium. Angina pain Hemodynamic instability Classic sign like low blood pressure, rapid and weak pulse. Cerebral hypoxia and manifested by confusion and agitation. Deceased urinary output and cold clammy skin.

Med ica l M an agemen t
 

correction of underlying cause initiation of first line treatment Ø Ø Ø Ø Ø Ø supplemental oxygen controlling chest pain selected fluids support vasoactive medications controlling heart rate mechanical cardiac support e.g intra-aortic balloon counterpulsation, ventricular assist sysytem.

 

Coronary cardiogenic shock is treated with thrombolytic theraphy, angioplasty, or CABG Noncoronary cardiogenic shock is treated with cardiac valve replacement or correction of dysrhythmias.

Ph arma colog ic
    

Dobutamine Dopamine Anti-arrythemic meds Nitroglycerine Vasoactive meds

Nu rs in g M anagemen t
Preventing cardiogenic shock Administering meds and IV fluids Maintaining mechanical devices Enhancing safety and comfort

Distri buti ve Shock (

Sho ck / V aso genic Ci rcu latory Shock )

Result from profound vasodilation Three classification of distributive shock: Septic shock, Anaphylactic shock and Neurologic shock

Sep tic Sh ock

Sep tic Sh ock

The most common type of distributive shock, is caused by widespread infection. Gram-negative bacteria are the most common pathogens. Gram-positive bacteria and viruses and fungi, can also cause septic shock

Ris k f act or s:
        

Immunosuppression Extremes of age ( younger than 1y/l and older than 65y/o) Alcoholism Extensive trauma of burns Malnutrition Diabetes Malignancy Chronic illness Invasive procedures

Pathop hysiolog y

Microorganism invasion causes immune response that activates biochemical mediators associated with inflammatory response and produces a variety of effects leading to shock. There is an increase in the capillary permeability, with fluid loss from the capillaries and vasodilatation, result in inadequate perfusion of oxygen and nutrients to the tissue and cell.

Clin ica l M anifes tatio n
Fir st ph as e: Hyperd ynami c o r Prog res sive phas e
     

High cardiac output with vasodilation Hyperthermia (febrile) with warm, flushed skin, bounding pulses Heart and respiratory rate elevated Blood pressure may remain within normal limits, or subtle changes in mental status. Decreased urinary output or normal Gastrointestinal status compromised (eg, decreased bowel sounds, n/v or diarrhea) Low cardiac output with vasoconstriction Decreased blood pressure Skin cool and pale Temperature normal or below normal Rapid respiratory and heart rate Anuria and multiple organ dysfunction

Late ph as e: Hypody nami c or Ir re vers ib le p hase
     

Sep tic Sh ock

Med ica l M an agemen t

Urine, blood, sputum, and wound drainage specimens are collected to identify and eliminate the causes of infection. Begins immediately a broad-spectrum antibiotic therapy Fluid replacement and aggressive nutritional supplement (high protein) is provided. Enteral feedings are preferred.

Nu rs in g M anagemen t
 

Identify px at risk for sepsis and septic shock Monitor for sign of infection at intravenous lines, arterial and venous puncture sites, surgical incisions, trauma wounds, urinary catheters and pressure ulcer Reduce px temp. when ordered for temp above 104.8F (40.8C) monitor closely for shivering Administered prescribed intravenous fluids and medications Monitor and report blood levels (antibiotics, BUN, creatinine, WBC ) and hemodynamic status, fluid IO and nutritional status. Monitor daily wts. And serum albumin levels to determine daily protein requirements

 

NE UR OLOG IC SHO CK / S PI NAL SHOC K

There is loss of vasomotor tone that includes arteriolar and venous dilatation .

Predi spos in g fa ct or s:

Spinal cord injury Spinal anesthesia Depressant meds Hypoglycemia

Med ica l M an agemen t

Restoring sympathetic tone

Nu rs in g M anagemen t

Elevate the head of the bed 30 degrees ( in spinal / epidural anesthesia ) Immobilize the patient ( in spinal cord injury ) Elastic compression stockings Feet elevation Heparin / low molecular weight heparin Pneumatic compression of the legs Passive ROM

An aphylactic S hock

An aphylactic S hock

An antigen-antibody reaction brought about by severe allergenic reaction provokes mast cell to release chemical mediators like histamine and bradykinin widespread vasodilatation and capillary permeability.

Predi spos in g fa ct or s:
   

Drug sensitivity Transfusion reaction Bee sting allergy Latex sensitivity

Med ica l M an agemen t

Rremoval of causative agent Restore vascular tone ( epinephrine ) Antihistamines and bronchodilators

Nu rs in g M anagemen t

Assess for previous hypersensitivity reactions Prevention of future exposure to antigens Identification of new antigens Patient education

Sta ges of Sh ock
INITI AL STAG E / C OMP EN SATED / NONPR OGRESS IVE SH OCK

BP is maintained within normal limits due to the effect of normally functioning regulatory mechanisms Blood loss less than 10%

Sig ns an d Symp tom s
      

Apprehension and restlessness ( 1st sign of shock ) Increase heart rate Cool, pain skin Metabolic acidosis Fatigue Tachypnea Mental status change

Med ica l M an agemen t
  

Identify the cause of shock Correction of shock Support of the regulatory mechanisms

Nu rs in g M anagemen t

Monitoring tissue perfusion

Ø Ø Ø Ø Ø
 

LOC V/S Urine output Skin Laboratory values

Reducing anxiety Promoting safety

Pr ogr essi ve Sta ge / Dec om pen sa te d

Exhaustion of the compensatory mechanism Myocardial depression Increased capillary permeability

Sign s an d Sy mptoms
A. Re spi ra tory ef fect s

Ø hypoxemia and hypercarbia Ø intense inflammatory response Ø decreased surfactant production Ø acute respiratory distress syndrome ( acute lung injury, shock lungs, non cardiogenic pulmonary edema ) Ø Ø Ø Ø Ø Ø Ø dyshrythmias myocardial infraction cardiac depression

B. Ca rd iova scu la r ef fect s

C. Neu rologi c ef fec ts

decreased cerebral perfusion mental status change behavioral change papillary dilation

Sign s an d Sy mptoms
D. Renal effects Ø MAP<80mmHg Ø Acute renal failure E. Hepatic effects Ø Decreased blood flow Ø Less ability to perform hepatic functions F. gastrointestinal effects Ø Decreased blood flow Ø PUD Ø Bloody diarrhea Ø Sepsis

Med ica l M an agemen t

Depends on the type of shock Depends of the decompensation of the organ systems

Irr ev ersib le St age

Sever organ damage Can no longer respond to treatment Survival is less likely

Med ica l M an agemen t

Same with progressive stage

Nu rs in g M anagemen t
Same with progressive shock Moral support to the family Ethical issue ( living will )

As ses smen ts
A. Ea rl y Ø Ø Ø Ø Ø stage s Restlessness, confusion Increase RR and PR, respiratory alkalosis Diaphoresis, cool clammy skin/warm, flushed skin in septic shock Normal to decreased urine output, thirst, dry mucous membrane Hypokalemia

B. La te sta ges Ø Shallow respiration, decreased BP, increased PR, hypothermia Ø Oliguria, Anuria Ø Hyperkalemia Ø Metabolic acidosis Ø Edema Ø Cool clammy skin- hypovolemic, cardiogenic and septic shock Ø Lethargy, dilated pupils Ø Decreased bowel sounds Ø Cyanosis Ø DIC

Interv en tion s
A. Promoti ng flu id s balance Ø Blood transfusions Ø IV fluids B. A ssistin g wit h car diac support Ø Intraaortic balloon pump ( IABP) Ø Medical anti-shock trousers Ø Modified trendelenburg position C. As sis ti ng res pira to ry suppo rt Ø O2 therapy Ø Mechanical ventilator Ø Deep breathing, coughing excercises Ø Suction as necessary

In terven tion s
D. Ass istin g wi th renal support Ø Monitor I and O, BUN and creatinine Ø Diuretics E. Ass is tin g with GI sup port Ø NGT Ø H2 blockers and antacids F. Promotin g sa fety Ø Soft restraints as needed Ø Practice strict asepsis Ø Prevent complications of immobility Ø Protect from chills

Drug Th er apy
         

Vas oco nst ri ct ors: Norepi ne phr ine / epi nep hri ne, do pa min e, dobu tam Vaso dila tors: Nitr ate s lik e nitr ogly cer ine an d Iso so rb ide Na+ bicarbonate to reverse acidosis Antibiotics to control sepsis Heparin to treat DIC Steroids to reduce inflammation H2 antihistamines, Ranitidine, cimetidine Glucose 50% or glucagons to increased blood sugar Narcotics for pain Antidysrrhythamic drugs
End of the slides

Arrh yth mia s

Card ia c Arr hythmia s
It is an abnormal electrical conduction or automaticity causing changes in the heart rate and rhythm.

Predi spos in g fa ct or s:
        

Congenital Myocardial Ischemia MI Organic heart disease Drug effect and toxicity Conductive tissue degeneration Electrolyte imbalance Acid-base imbalance Cellular hypoxia

Pathop hysiolog y
Result in the disturbance in the excitability, automaticity, or conductivity Heart rate and rhythm are altered, reducing cardiac output

As ses smen t
        

Asymptomatic Palpitation Chest pain Dizziness Weakness, fatigue Feeling of impending doom Irregular heart rhythm Bradycardia or tachycardia hypotension

      

Syncope LOC Diaphoresis Pallor N/V Cold, clammy skin Life-threatening: pulselessness, (-) respiration, no palpable blood pressure

Di agn osi s

ECG- change in heart rate, rhythm Blood chemistry : electrolyte imbalance

Nor ma l Sin us R hyth m

Nor ma l Sin us R hyth m
Occurs when the electrical impulse starts at the regular rate and rhythm n the sinus node and travels at through the normal conduction pathway

Ch aract erist ics :
     

Vent ri cula r a nd a tri al ra te : 60 to 100 in adult Vent ri cula r a nd a tri al rhyt hm : Regular QR S d ura tion: Usually normal, but may be regularly abnormal P w ave : Normal and consistent shape; always in front of QRS PR int erva l: Consistent interval between 0.12 and 0.20 seconds P: QRS ratio 1:1

Typ es o f S inus n ode Dy srh ythm ias
A. Sinus Bra dyc ar dia
occurs when the sinus node creates an impulse at a slower rate than normal.

Ch aract erist ics :

 

Vent ri cula r a nd atr ia l r ate : Less than 60 in adult Vent ri cula r a nd atr ia l r hyt hm : Regular QR S d ura tion: Usually normal but may be regularly abnormal P w ave : Normal and consistent interval between 0.12 and 0.20 seconds P: QRS ratio 1:1

Sin us B rad yca rdia

Managemen t

The urgency of treatment depend is on the effect of the slow rate on maintenance of Cardiac output Atropines, 0.5 to 1.0 mg given IV push block vagal stimulation to the SA Node & therefore accelerate heart rate. If the bradycardia persists a pacemaker may be required.

Types of Sinus Node Dysrhythmias
B. Sinus Tac hyc ar dia

Occur when the sinus node create an impulse at a faster than normal rate. It may be caused by acute blood loss, anemia, shock, hypervolemia, hypovolemia CHF, pain, hypermetabolic states, fever, anxiety or sympathomimetic medication.

Characteristics:
Vent ri cular and atri al ra te: Greater than 100 in the adult  Vent ic ula r and atr ia l rhyt hm : Regular  QRS dura tio n: Usually normal, but may be regularly abnormal  P wave : Normal and consistent shape, always in front of the QES, but may be buried in the preceding T wave.  P: QRS ratio 1:1

Sinus Tachycardia

As the heart rate increases, the diastolic falling time decreases, result in reduced cardiac output and subsequent symptoms of syncope and low blood pressure. If the heart cannot compensate for the decreased ventricular falling the px may develop acute pulmonary edema

Ma nag eme nt

It is usually directed at abolishing its causes. Calcium channel blockers and Beta-blockers may be used to reduce the heart rate quickly.

Ty pes of Sin us n od e Dysrh yth mia s
C. Si nus Ar rhyt hmi as Occur when the sinus node create an impulse at an irregularly rhythm; the rate usually increase with inspiration and decrease with expiration. Non respiratory cause includes heart disease and valvular disease, but these are rarely seen.

Ch aract eris tics :
     

Ven tricu lar an d at ria l rat e : 60 to 100 in the adult Ven tricu lar an d at ria l rhyt hm : Irregular QRS du rat io n: Usually normal, but may be regularly abnormal P wa ve : Normal and consistent shape, always in front of the QRS. PR i nter va l : Consistent interval between 0.12 and 0.20 second P: QRS ratio: 1:1

*Sinus Arrhythmia does not cause any significant hemodynamic

effect and usually is not treated.

Atria l D ysrhythmia s
A. Pr emat ure At ria l Com plex

Premature Atrial Complex Is a single ECG complex that occur when an electrical impulse start in the atrium before the next normal impulse of the sinus node. The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety hypokalemia (low potassium level), hyper metabolic states or atrial ischemia, injury or infarction.

Ch aract erist ics :
       

Ven tricu lar an d at ria l rat e : Depend on the underlying rhythm Ven tricu lar an d at ria l rhyt hm : Irregular QRS du rat io n: The QRS that follows the early P wave is usually normal, but it may be abnormal. P wa ve : An early and different P wave may be seen or may be hidden in the T wave; Other P wave in the strip is consistent. PR i nter va l: The early P wave has a shorter than normal PR interval, but still between 0.12 And 0.20 seconds P : QRS ratio: Usually 1:1

Managemen t

If PACs are in frequent, no treatment is necessary. If they are frequent (more tan 6 per minute) this may herald a worsening diseases state or the onset of more serious dysrhythmias, such as atrial fibrillation. Treatment is directed toward the cause. PAC’s should be monitored for increasing frequency

At ria l F lu tter

Atria l Dysrhythmia s
B. At ri al Fl utt er
 Occur in the atrium and creates impulse at an atrial rate between 250 and 400 time per minute.

Because the atrial rate is faster than the AV node can conduct, not all atrial impulse are conducted into the ventricle causing a therapeutic block at the AV node.

At ri al Flu tter

Ch aract erist ics :
     

Vent ri cula r a nd atr ia l r ate: Atrial range between 250 and 400 ventricular rates usually Range between 75 and 150 Vent ri cula r a nd atr ia l r hyt hm : Usually Regular P w ave : Saw –toothed shape. These waves referred to as F wave PR i nt erva l; Multiple F waves may make it difficult to determine the PR interval. P : QRS ratio: 2:1, 3:1, or 4:1

Sign and Sy mptoms
Chest pain  Shortness of breath  Low blood pressure.

Ma nag emen t

The urgency of treatment depend on the ventricular response rate& resultant symptoms A Calcium channel blocker such as Diltiazem (cardizem) may be use to slow AV Nodal conduction used with caution in the patient with CHF, hypotension Digitalis & Quinidine preparation may be used. A beta –adrenergic block drug such as Esmolol may be used. If drug therapy is un successful, trial flutter will often respond to cardivertion. Small doses of electrical current are often successful

 

At ria l Fi brilla tion

Atria l Dysrhythmia s
C. At ri al Fibr ill at ion

May occur for a very short time (paroxysmal) or it may be chronic It is the most common dysrhythmias that cause patients seek medical attention The shorter time in diastole reduce the time available for coronary artery perfusion, there by increasing the risk for myocardial ischemia. The erratic atrial contraction promotes the formation of a thrombus within the atria increasing the risk of stroke (brain attack).

Ch aract erist ics :
   

 

Vent ri cula r a nd atr ia l r ate: Atrial rate is 300 and 600 in untreated atrial fibrilation Vent ri cula r a nd atr ia l r hyt hm : Highly irregular QR S s ha pe a nd d ura tion: usually normal but may be abnormal P w ave : No discernible P waves; irregular undulating waves are seen and are referred to as fibrillatory or waves. PR i nt erva l: Cannot be measured P : QRS ratio: many:1

Managemen t

Cardiovertion may be indicated for atrial fibrillation that has been present for less than 48 hours, a condition termed acute onset of atrial fibrillation Acute onset, the medication quinidine, Ibutilide,flecanide, dofetilide, profafenon, procanamide, dysopyramide or amiodirone may be given to achieve convertion to sinus rhythm Intravenouse adenosine (adenocard,adenescan) has also been use for convertion, as well as to assist in the diagnosis. Calcium channel blocker and beta blocker are effective in controlling the ventricular rate in atrial fibrillation Use Digoxin is recommended to control the ventricular rate those patient with poor cardiac function Aspirin may be substituted for warfarin.

 

At ria l Fi brilla tion

Juncti onal D ys rh ythmias
A.

Pr emat ure Junc ti on Co mpl ex
Is an impulse that starts in the AV nodal before the next normal sinus impulse reaches the AV node Premature junction complex are less common than PAC’s The criteria for premature junction complex are the same as for PACs except for the Pwave and the PR interval. The Pwave may be absent QRS, or may occur before the QRS but with a PR interval of less than 0.12 second Treatment for frequency premature junction complexes is the same as for frequent PACs.

Premat ure J unct ion

Juncti onal D ys rh ythmias
B. J un ct io nal Rhy thm Jucntional or idionodal rhythm occur when the AV node, instead of the sinus node, become the pacemaker of the heart.

Ch ara ct eris tics :
   

 

Vent ricul ar a nd a tri al ra te: 40 to 60 Vent ricul ar r hyth m : Regular QR S dura tion: Usually normal but may be abnormal P w ave : May be absent, after the QRS complex, or before the QRS; may be invented, especially in lead II PR int erva l: If P wave is in front of the QRS, PR interval is less than 0.12 second P: QRS ratio1:1 or 1:1

Juncti onal D ys rh ythmias
C. At ri ove nti cul ar Noda l Reentr y
Tachyc ardi a

Occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate. It has an abrupt onset and an abrupt cessation with a QRS of normal duration had been called paroxysmal atrial tachycardia (PAT)

Ch aract erist ics :
     

Vent ricul ar a nd a tri al ra te: atrial rate 150250; vent rate: 75-250 Vent ricul ar a nd a tri al rhyt hm : Regular; sudden onset and termination of the tachycardia QR S dura tion: Usually normal but may be abnormal P w ave : usually very difficult to discern PR int erva l: If P wave is in front of the QRS, PR interval is less than 0.12 second P: QRS ratio1:1 or 2:1

Ven tri cu lar Dysrhyt hmia s
A. Pr emat ure Ven tricu lar Co mp lex

Caused by acute MI other form of heart disease, pulmonary disease, electrolyte disturbance, metabolic instability and drug abuse The wave of impulse originates from an ectopic Focus (Foci) within the ventricles at rate faster than the next normally occurring beat. Because the normal conduction pathway is by passed configuration of the PVC is wider than normal and is distorted in appearance. PVC’s may occur in regular sequence with normal rhythm.

Prem ature Ve ntricu la r Com plex

Ch aract erist ics :

 

 

Vent ricul ar a nd a tri al ra te: Depend on the underlying rhythm. Vent ricul ar a nd a tri al rhyt hm: Irregular QR S dura tion: 0.12 second or longer shape is bizarre and abnormal P w ave : none PP int erval : If the P wave is in front of the QRS, the PR interval is less than 0.12 second P : QRS ratio 0:1, 1:1

Managemen t

The standard treatment is Lidocaine hydrochloride (Xylocaine) by IV push Be alert to the development of confusion, slurring of speech and diminished mentation because lidocaine toxicity affects the CNS. If ventricular premature beats occur in conjunction with bradysrhythmias, atropine may be chosen to accelerate the heart rate and eliminate the need for etopic beat. Atropine should be used with caution in acute MI. the injured myocardium may not be able to tolerate the accelerated rate.

Ven tri cu lar Dysrhyt hmia s
B. Ven tricu lar Ta chy car dia

Ventricular tachycardia (VT) is designed as three or more PVCs in a row, occurring at a rate exceeding 100 beat per minute. The causes are similar to those for PVC VT is an emergency because the patient is usually unresponsive and pulse less

 

Ch aract erist ics :
Vent ri cular and atri al rate: 100to200 beat per minute  Vent ri cular and atri al rhythm : Usually Regular  P wave : so atrial rate and rhythm may be indeterminable.  PR int erva l: Very Irregular  P: QRS ratio: difficult to determine

Ven tri cu lar Ta ch yca rdia

Managemen t

Cardiovertion may be the treatment of choice, especially if the patient is unstable. VT in a patient who is unconscious and without a pulse treated in the same manner as ventricular fibrillation immediate defibrillation is the action of choice.

Ven tri cu lar Dysrhyt hmia s
C. Vent ri cular Fibri ll at io n
Is a rapid but disorganized ventricular rhythm that cause of ventricular fibrillation are the same as for VT, it may also result from untreated or unsuccessfully treated VT. Other cause includes electrical shock and Brugada Syndrome.

Ventricu la r Fib ril lat ion

Ch aract erist ics :
Ven tri cula r rat e: Great er than 300 per minute  Ven tri cula r and a tri al rhyt m: Extremely irregular  QRS dura tio n Irregular

Managemen t
 

Immediately fibrillation and activation of emergency service The importance of defibrillation is evident in one of the recent change in basic life support. Placing a call for emergency assistant and calling for a defibrillator takes precedence over initiating Cardio pulmonary resuscitation in adult victim. Application of an automatic external defibrillator AED is included in basic life support classes Administering Vaso active and anti arrhythmia medication alternating with defibrillation are treatment used to try convert the rhythm to normal sinus rhythm.

Ven tri cu lar Dysrhyt hmia s
D. Idio vent ric ul ar Rhyt hm

Is also called ventricular escape rhythm, occur when the impulse starts in the conduction system below the AV node. Commonly cause the patient to lose consciousness and experience other sign and symptoms of reduced cardiac out put . Intervention may include identify the underlying cause, administering Intravenous atropine and vasopressor medication. Initiating emergency transcutaneous pacing. Bed rest is prescribed so as not to increase the cardiac work load

Ch aract erist ics :
Ven tri cula r and a tri al ra te : Between 20and 40 if the rate exceeds 40, is known (AIVR)  Ven tri cula r and a tri al rhyt hm: Regular  QRS dura tio n : Bizarre, abnormal, duration is 0.12 second or more.

Ven tri cu lar Dysrhyt hmia s
E. Vent ric ular As ys tol e

Commonly called flat line, ventricular a systole characterized by QRS complexes, all though P wave may be apparent for a short duration is two different leads. There is no heart beat, no palpable pulse and no respiration. Assessment to identify the possible cause which may be hypoxia, acidosis, severe electrolyte imbalance, drug overdose or hypothermia.

Ven tricu la r As ystole

Managemen t

CPR and emergency service as necessary to keep the patient alive. Transcutaneuos pacing may be attempted. A bolus of intravenous epinephrine should be ad minister and repeated 3to5 minutes interval

End of the slides

HEAR T BL OCK

Conduct ion Ab norm alit ies

The nurse first to identify is the underlying rhythm.(eg, sinus rhythmia) then the PR interval is assessed for the possibility of an AV block. AV block occur when the conduction of impulse through the AV nodal are is decreased or stopped. These block can caused by medication (eg,digitalis, calcium channel blockers, beta blocker). The Clinical sign and symptoms of a heart block vary with the resulting ventricular rate and the severity of any underlying disease processes. The treatment is based on the hemodynamic effect of the rhythm

Types of Con duct ion

Ab normalit ies

A. Fir st Degree Bloc k Occur when all the atrial impulse are conducted through the AV node into the ventricle at a rate slower than normal

Ch aract erist ics :
Vent ri cular and atri al ra te: Depend on the underlying rhythm.  Vent ri cular and atri al rhythm : Depend on the underlying rhythm.  QRS dura tio n ; usually normal  P wave : In front of QRS complex; shows sinus rhythm, regular shape.  P: QRS ratio1:1

Fir st D eg ree A V Block

Types of Con duct ion

Ab normalit ies

B.1 Seco nd Deg re e Atri oven tricu la r Block Type I
Second degree type I heart block occurs when all but one of the atrial impulse are conducted. Through the AV node into the ventricles. Each atrial impulse a take longer time for conduction than the one before, until one impulse is fully blocked.

Ch aract erist ics :
 

  

Ven tricu lar an d at ria l rat e: Depend on the underlying rhythm Ven tricu lar an d at ria l rhyt hm: The PP interval is regular if the patient has an underlying normal sinus rhythm; the RR interval characteristically reflect a pattern of change . QRS du rat ion: Normal may be abnormal P wa ve : In front of the QRS complex; shape depend on underlying rhythm PR i nter va l: PR interval become longer with each succeeding ECG complex until there is a P wave not followed by a QRS. P: QRS ratio 3; 2, 4:3, 5:4,

Second D egr ee A tri oventr ic ul ar Bl oc k Typ e I

Types of Con duct ion

Ab norm alit ies

B.2 Sec ond Deg re e Atr iov entr icul ar Bl ock Typ e II Occur when only some of the atrial impulses are conducted through the AV node into the ventricles

Se con d De gr ee Atriove nt ric ular Block T ype II

Ch aract erist ics :

Ventricular and atrial rate: Depend on the underlying rhythm Ventricular and atrial rhythm. The PP interval is regular if the patient has an underlying normal sinus rhythm.

Types o f Con duction

Ab normali ties

C. Thi rd Degree Atrio ve nt ri cular Blo ck
Occur when no atrial impulse is conducted through the AV node into the ventricle In the third degree heart block , two impulse stimulate the heart :one stimulate the ventricle ,represent by the QRS complex, and one stimulate the atria .

Thi rd Degr ee Atri oventr icu lar Bl ock

Ch aract erist ics :

 

Vent ri cula r a nd a tri al ra te: Depend on the escape and underlying atrial rhythm. Vent ri cula r a nd a tri al rhyt hm :The PP interval is regular and the RR interval is regular; however the PP interval is not Equal to the RR interval. QR S d ura tion : Depend on the escape of rhythm P w ave : Depend on the underlying rhythm P: QRS ratio: More P wave than QRS complexes

Managemen t

IF the patient is short of breath, complains of chest pain or lightheadedness, or has low BP: Intravenous bolus of Atropine is the initial treatment of choice. If the patient does not respond to atropine or has acute MI, trascutaneous pacing should be started. A permanent pacemaker may be necessary if the block persist.

Nur si ng A ss ess ment

Major assessment include all possible cause of the dysrhythmia and the dysrhythmia’s effect on the heart’s ability to pumped an adequate blood volume. When cardiac output is reduced, the amount of O2 reaching the tissue and vital organ is diminished. This diminished oxygenation produces the s/sx associated with dysrhythmia. A health history is obtained to identify any previous occurrence of decreased cardiac output such as syncope (fainting), lightheadedness , dizziness , fatigue, chest discomfort and palpitation Coexisting condition that could be a possible cause of heart block or dysrhythmia (heart disease, chronic obstructive

Nur si ng A ssess me nt

All medications prescribed and over the counter (supplements herbs and nutritional) may be reviewed. The nurse conducts physical assessment to the patient with diminished cardiac output especially the level of LOC . the nurse directs attention to the skin which may be pale and cool. Sign of fluid retention, such as neck vein distention and crackles and wheezes auscultated in the lungs. The nurse auscultates for extra heart sounds ( especially S3 and S4 ) and for heart murmur, measure blood pressure indicates reduced cardiac output.

Nu rs in g D ia gnos is
  

Decreased cardiac output Anxiety related to fear of the unknown Deficient knowledge about the dysrhythmias and its related treatment. Collaborative Problems and Potential Complication May developed over time a heart failure Thromboembolic

 

Nu rs in g I nter ven tion
1. Mo ni torin g an d man ag in g the dy sr hyt hmia s

Regularly evaluate the blood pressure, pulse rate and rhythm, rate and depth of respiration and breath sounds to determine the hemodynamic effects. Obtain a 12 lead ECG, continuously monitor the patient and analyze rhythm of the strips to track dysrhythmias. Use an antiarrhythmias medications and the nurse assess and observe for the beneficial and adverse effects of each medications ad prescribed. Assist the patient in developing a plan to make a lifestyle change that eliminates or reduced the risk factors.

Nu rsing In terv en tion
2. Mi nimi ze anxie ty
 

Maintain a calm and reassuring attitude Emphasized with the patient to promote a sense of confidence in living the disease. Goal is to maximize the client’s controls and to make the unknown less threatening.

3. Pr omo ti ng Home and Commu ni ty Based Car e

Explain the importance of maintaining therapeutic serum levels of the medications so that the patients understand why medications should be taken regularly each day.

Adju ncti ve M oda li ti es a nd Man agemen t

Pacema ker the rapy – is an electronic device that provide electrical stimulation to the heart muscles. Used when the patient has a slower than normal impulse formation or conduction disturbance causing symptoms.

Permanent pacemaker- are used commonly irreversible complete heart block. Temporary pacemaker- are used to support patients until they improve or receive a permanent pacemaker.

Pa cema ker D es ig n a nd types

Pacemaker consist of 2 components : an electronic pulse generator and pacemaker electrodes, which are located on leads or wire. The generator contains the circuitry and batteries that generate the rate and strength of the electrical impulse delivered to the heart. The pacemaker electrodes convey the heart’s electrical activity through a lead to the generator ; the generator’s electrical response to the information received is then transmitted to the heart. Leads can be threaded through a major veins into the right ventricles (endocardial leads) or they can be lightly sutured onto the outside the heart and brought the chest wall during open heart surgery.

Pa cema ker D es ig n a nd types

Epicardial wires are always temporary and are removed by a gentle tug within a few daysafter surgery. Endocardial leads may be temporarily placed with catheters through the femoral, antecubical, brachial or jugular veins, usually guided by fluoroscopy. The energy source for permanent generators are: mercury-zinc batteries (which last 3 to 4 years), lithium cell units (up to 10 years), nuclear powered source such as plutonium (up to 20 years).

Clin ica l M anifes tatio n
Block AV block usually 3 bundle branch block  Symptomatic Bradycardia  Arrhythmia during surgery  Sick sinus syndrome

Nu rsing In terv en tion

Mo nito ri ng Pacema ke r fun ct io n- observe the presence of the pacemaker spikes in the ECG, monitor for the pacemaker malfunctions, weakness, dizziness, fainting, hypotension, shortness of breath, chest pain, ankle swelling. Pr ev en t in fecti ons- changes the dressing regularly and inspects the insertion site for redness, swelling, soreness or any unusual drainage and increase the temperature should be noted.

Nu rsing In terv en tion

Cl ie nt t each in g ab out pace make rinstruct the patient how to check pulse at home, inform to report any changes in the heart rate, avoid contact sports, carry ID, instruct to report sign of battery failure, wear loose fitting clothes, remind that most electrical appliances can be used without interference the functions of the pacemaker, avoid MRI, transmitter tower and anti theft device, move away from electrical appliances that cause disturbances and emphasize regular follow up check up.

End of the slides

STROKE

St rok e
Disrup tion of cereb ral circul at ion that resul ts in mot or and sensor y de fici ts
Caus es:  Cerebral
      

arteriosclerosis

Syphilis Trauma Hypertension Thrombosis Embolism Hemorrhage Vasospasm

Ty pes of S trok e
1. Ische mic St roke

Larg e Artery Thr omb otic Strokes - are due to atherosclerotic
plaques in the large blood vessel of the brain. Thrombus formation and occlusion at the site of the atherosclerosis result in ischemia and infraction and occur in older patients.

Sma ll Penetratin g Artery Thr omb otic Strokes - affect one
or more vessels are the most common type of ischemic stroke. Also called lacunar strokes. Occur in young ones.

Ty pes of S trok e

Ca rd iogen ic Emb oli c Stroke sare associated with cardiac dysrhythmias, usually atrial fibrillation. Emboli originated from the heart and circulate to the cerebral vasculature, most commonly in the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented by the use of anticoagulant therapy in patients with atrial fibrillation.

Cr ypt ogen ic St ro ke -

which have no known cause and other stroke from cause of cocaine used, coagulopathies, migraine and spontaneous dissections of the carotid or vertebral arteries.

Clin ica l M anifes tatio n

Numbness or weakness of the face, arm or leg especially on one side of the body. Confusion or change in mental status Trouble speaking or understanding speech Visual disturbance Difficulty walking, dizziness or loss of balance or coordination Sudden severe headache

Clinical Man ifesta ti on
Mot or l oss

 

A stroke is a lesion of the upper motor neurons and result in loss of voluntary control over motor movements. Upper motor neuron decussate (cross) a disturbance of voluntary motor control on one side of the body may reflect damage to the upper motor neuron on the opposite side of the brain. Most common motor dysfunction is hemi pl eg ia ( paralysis of one side of the body) due to the lesion of the opposite side of the brain. He mip ar es is or weakness of one side of the body Fl acc id pa ral ysi s and loss or decrease of deep tendon reflex.

Clinical Man ifesta ti on
Com munic ati on Lo ss

Dysa rthi a

( difficulty in speaking), caused by paralysis of the muscles responsible for producing speech.

Dysp ha si a or apha si a Ap ra xia

(defective speech or loss of speech) which can be ex pr es siv e aph asia , rece pt ive aphasia or globa l (m ixe d) aphasia ( inability to perform a previously learned action) as may be seen when a patient picks up a fork and attempts to comb.

Clinical Man ifesta ti on
Percept ua l Di stur ba nce
   

Perception is the ability to interpret sensation Visual perceptual dysfunction are due to disturbance of the primary sensory pathways between the eye and visual cortex. Hemianopsia (loss of half of the visual fields) may be occur from the stroke and may be temporary or permanent. Disturbance in visual spatial relation ( perceiving the relation of two or more objects in spatial areas) frequently seen in patient with right hemispheric damage.

Se nsory Loss

Sensory loss from stroke may take the form of slight impairment of touch or may be more severe, with loss of proprioception ( ability to perceive the position and motion of the body parts) as well as difficulty in interpreting visual, tactile and auditory stimuli.

Clinical Man ifesta ti on
Sensor y Loss

Sensory loss from stroke may take the form of slight impairment of touch or may be more severe, with loss of proprioception ( ability to perceive the position and motion of the body parts) as well as difficulty in interpreting visual, tactile and auditory stimuli.

Clinical Man ifesta ti on
Cogni ti ve Im pairm ent

Such dysfunction may be attention span, difficulties in comprehension, forgetfulness and lack of motivation, which cause these patients to become frustrated in their rehabilitation program.

Nu rs in g D ia gnos is

    

Impaired physical mobility related to hemiparesis. Loss of balance and coordination, spasticity and brain injury. Acute pain (painful shoulder) related to hemiplegia and disuse Self care deficit ( hygiene, toileting, grooming and feeding) related to stroke sequelae Disturbed sensory perception related to altered sensory reception, transmission and integration. Impaired swallowing Incontinence related to flaccid bladder, detrusor instability confusion or difficulty in communicating.

Nu rs in g D ia gnos is
Disturbed thought process related to brain damage, confusion or inability to follow instruction. Impaired verbal communication related to brain damage Risk for impaired skin integrity related to hemiparesis/ hemiplegia or decreased mobility. Interrupted family process related to catastrophic illness and care giving burdens Sexual dysfunction related to neurologic deficit or fear of failure

 

Di ag nos ic Te st F in din gs
LP: increase pressure, bloody CSF  CT scan: intracranial bleeding, infarct, or shift of midline structures.  EEG : focal slowing in area of lesion  MRI : intracranial bleeding, infarct, or shift of

midline structures  Brai n sc an: decreased perfusion

Digit al subtr acti on Ang iography:
occlusion or narrowing of vessel

Med ica l M an agemen t

Platelet inhibiting medication decrease the incidence of cerebral infraction in patients who have experience TIA from embolic or thrombotic cause Thrombolytic agents are used to treat ischemic by dissolving the blood clot that is blocking blood flow to the brain. Recombinant t-PA is genetically engineered form t-PA thrombolytic substance made naturally by the body. It works by binding to fibrin and converting plasminogen to plasmin which stimulate fibrinolysis of the atherosclerosis lesion. The dose of t-PA minimum dose is 0.9mg/kg, the maximum dose is 90 mg. The loading dose is 10% of the calculated dose and is administering over 1min. the remaining dose is administered over 1 hr via an infusion pump. Then flushed the line with 20 ml of normal saline solution.

Med ica l M an agemen t

Vital sign monitored q 15min for the first 2 hrs,q30 min for the next 6 hrs. Bleeding is the most common side effects of t-PA administration and the patient should be closely monitored. Other treatment are anticoagulant administration for ischemic stroke and careful maintenace of cerebral hemodynamics to maintain cerebral perfusion. Elevation of the head of the bed to promote venous drainage and to lower increased ICP.intubation with an endotracheal tube to established a patent airway. Endarterectomy for prevention of ischemic stroke is the removal of an atherosclerotic plaques orthrombus from the carotid artery to prevent stroke in patients with occlusive disease of the ectracranial cerebral arteries

Nu rs in g I nter ven tion
1.

Imp rovi ng mo bi li ty and pr even ting jo int def ormi ties
 

 

correct positioning is important to prevent contractures Prevent adduction of the affected shoulder while the patients is in bed, a pillow is placed in the axilla when where is limited external rotation; this keep the arm away from the chest. Positioning the finger so that they are flexed while the hand placed on slight supination which it is most functional position. The patients position should be changed every 2 hrs. toplace a patient in a lateral position position, a pillow is placed between the legs before the patients is turned. A full range of motion 4 to 5 times a day to maintain joint mobility and regain motor control, prevent contractures, prevent further deterioration of the neurovascular system Preparing for ambulation, the patient is taught to maintain balance while sitting and then learn to balance while standing in a gradual manner until the patient can walk.

Nu rs in g I nter ven tion
1

Prev ent ing Shoul der pa in
To prevent shoulder pain, the nurse should never lift the patient by the flaccid shoulder or pull on the affected arm shoulder. If the arm is paralyzed, subluxation at the shoulder can occur from over stretching the joint capsule and masculature by the force of gravity. Amitriptyline hydrochloride used because of its sedating effects. Some clinicians advocate the use of a properly worn sling when the patients first becomes ambulatory to prevent upper extremity from dangling without support. ROM is important in preventing painful shoulder

Nu rs in g I nter ven tion
3. M an ag e D ysph agia

ET is reduced the risk of aspiration while the patient is in ET tube elevate the head of the bed at least 30 degree to prevent aspiration, check the proper position of the ET tube before feeding the patients, ensure the cuff of ET is inflated and give the formula slowly. Intermittent catheterization is used with patient with bladder distention. And increased high fiber diet and adequate fluid intake with patient with constipation

STRO KE
ISCHEMIC STROKE

HEMORRHAGIC STROKE

Hemor rh agic St ro ke

Primarily caused by an intracranial or subarachnoid hemorrhage, bleeding into the brain tissue, the ventricles, or subarachnoid space. Intracerebral hemorrhage from spontaneous rupture of small vessels account approximately 80% of hemorrhagic strokes and caused by uncontrolled hypertension. Secondary intracerebral hemorhage is associated with arteriovenous malformation, intracranial aneurysm, or certain medications (anticoagulants and amphetamines)

Hemor rh agic St ro ke

Pathop hysiolog y
Intr acere bral h emorrh age

Bleeding into the brain substance, common in patients with hypertension and cerebral atherosclerosis that causes rupture of the vessel Brain tumor and the use of medicines( oral anticoagulants, amphetamines and illicit drugs such as crack and cocoaine). Bleeding occur mostly in the cerebral lobes, basal ganglia, thalamus, brain stem (mostly pons) and cerebellum

Intr acrani al (Cereb ral) An eury sm
 

Dilation of cerebral artery wall causes of weakness in the arterial walls. An aneurysm due to atherosclerosis, vascular disease, head trauma or advance aging.

Pathop hysiolog y
Art eri oven ous Ma lfo rmat ion
 Due to an abnormality in embryonal development that leads to a tangle of arteries and viens in the brain without acapillary bed. A cause of hemorrhagic in young peoples.

Sub ara ch no id Hemorrh ag e

May occur as a result of an AVM, intracranial, aneurysm, trauma or hypertension There is a leaking aneurysm in the area of the circle of Willis or a congenital AVM of the brain.

S T R O K E

Clin ica l man if es tati ons

Sudden, unusually severe headache and often loss of consciousness for a variable period. Pain and rigidity at the bask of the neck (nuchal rigidity) and spine due to meningeal irritation. Visual disturbance: loss of vision, diplopia, and ptosis occur when the aneurysm is adjacent to the oculomotor nerve. Tinnitus, dizziness and hemiparesis may also occur.

Ass essmen t

Altered level of consciousness Sluggish papillary reaction Motor and sensory dysfunction Cranial nerve deficit (EOM, facial droop, presence of ptosis) Speech difficulties and visual disturbance Headache and nuchal rigidity or other neurologic deficit

Nu rs in g D ia gnos is

Ineffective cerebral tissue perfusion related to bleeding Disturced sensory perception related to medically imposed restrictions (aneurysm precautions) Anxiety related to illness and / or medically imposed restrictions.

Med ica l M an agemen t

Bed rest with sedation to prevent agitation and stress management of vasospasm and surgical and medical treatment to prevent rebleeding Analgesic prescribed for head and neck pain Elastic compression stockings to prevent DVT. Adequate hydration must be ensured to reduced blood viscosity and improve cerebral blood flow. IV administration of calcium channel blockers, nimodipine which delay the ischemic deterioration. Mannitol is given to reduced ICP, it acts by pulling water out of the brain tissue by osmosis as well as reducing total body water through diuresis.

  

Nu rs in g I nter ven tion
Opti mizing Cerebra l Tis sue Pe rfusion

Monitor blood pressure , pulse , level of responsiveness, papillary reaction and motor functions hourly. Respiration status is monitored becaused reduction of O2 in the areas of the brain with impaired autoregulation increased chances of cerebral infraction.

Nu rs in g I nter ven tion
Imp lement in g An eury sm preca ution
  

CBR with quite, non stressfull environment HOB elevated 15 to 30 degree to promote venous drainage and decrease ICP. Avoid Valsalva maneuver, straining , forceful sneezing, pushing up to bed, acute flexion or rotation of the head and neck. No enemas are permitted but stool softener and mild laxative is prescribed. Dim light is helpful because of photophobia Coffee , tea, unless decaffeinated is usually eliminated. Wear antiemboic stocking to prevent DVT Observed for the s/sx of deep vein thrombosis such as tenderness, swelling, warmth, discoloration, positive Homan’s sign report any abnormal findings
End of the slides

    

BURNS

Bu rns

 

 

Burns are caused by a transfer of energy from a source to the body. Categorized as thermal, radiation or chemical burn. There is a disruption in the skin that leads to increased fluid loss, infection, hypothermia, scarring, compromised immunity and changes in function, appearance, and body image. Young children and older people are at high risk for burn injury Younger than 5 years and older than 40 y/o are at high risk for death after burn trauma.

Med ica l M an agemen t
Four major goals relating to burn:  Prevention  Institution of life saving measure for the severely burned person  Prevention of disability and disfigurement  rehabilitation

Pathop hysiolog y
Caused by transfer of energy form a heat source to the body Thermal, radiation or chemical burn Tissue destruction results from coagulation, protein denaturation, or ionization of cellular contents. Depth of the injury depends on the temperature of the burning agent and the duration of contact with the agent
Disruption of the skin can lead increased fluid loss, infection, hypothermia scarring compromised immunity, and changes in function, appearance, and body image.

Skin and the mucosa of the upper airways are the sites of tissue destruction

Deep tissue can be damaged by electrical burns or through prolonged contact with a heat source

Clas si fica tio ns of B ur n Ac co rd ing to D epth o f Ti ssu e Destr uc tio n
A.

Superficial Partial-Thicknes Burn (first degree burn)
The epidermis and possibly a portion of the dermis are injured The damaged skin may be painful and appear red and dry, as in sunburn, or it may blister.

Firs t D egree Bu rn

Classi fica tio ns of Bur n Ac co rdi ng to D epth o f Ti ssu e Destr uc tio n
B. Deep Partial – Thickness (second degree burn)

 

The epidermis and upper to uper deeper portion of the dermis are injured. eg, scald The wound is painful, appears red, and exudes fluid. Capillary refill follows tissue blanching. Hair follicles remain intact. Deep partial-thickness burns take longer to heal and are more likely to result in hypertrophic scars.

Secon d D egree Bu rn

Cl assi fica tio ns of Bur n Ac co rdi ng to D epth o f Ti ssu e Destr uc tio n
C. Full – Thickness Burn (third degree burn)
 

 

Burn from a flame or electric current The epidermis, entire dermis, and sometimes the underlying tissue are injured Wound color ranges widely from white to red, brown, or black. The burned area is painless because nerve fibers are destroyed. And the wound appears leathery; hair follicles and sweat glands are destroyed

Th ir d D eg re e Bu rn

Exten t of Bod y S ur face Ar ea In ju red
A. In ner zo ne  known as the area of coagulation, where cellular death occurs  sustains the most damage. B. Mi dd le zo ne  has a compromised blood supply, inflammation, and tissue injury. C. Outer zo ne  the zone of hyperemia which sustains the least damage.

RU LE O F NI NE
9 9 18 18 9
1

An estimation of the TBSA involved in a burn is simplified by using the rule of nines. It is a quick way to calculate the extent of burns. The system assigns percentage in multiples of nine to major body surfaces. PARKLAND FORMULA Computation of fluids Most commonly used in burned patient Formula: TBSA x 4ml x kg body weight 1st 8hrs give 50% of the formula 2nd 8hrs give 25% of the formula 3rd 8hrs give 25% of the formula

18

18

Meth ods i n D eter mi nin g Extent of Su rfac e Ar ea Bu

the rned

Ru le of Nine : an estimation of the total body surface area (BSA) burned by dividing the body into multiples of nine. Lund and Browd er Me th od : a more precise method of estimating the extent of the burn; the percentage of the surface area is represented by various anatomic parts (head and legs) changes with growth. Pa lm Met hod : used to estimate percentage of the scattered burns; using the size of the px palm (abt. 1% of body surface area) to assess the extent of burn injury.

Ass essmen t

Review the initial assessment data obtained by prehospital providers. Assess the time of injury, mechanism of burn whether the burn happened in a closed space, the possibility of inhalation of noxious chemicals, and any related trauma. Focus on the major priorities of any trauma patient: ABC, disability, exposure, and fluid resuscitation. Assess respiratory status as first priority (airway patency and breathing adequacy) Note any increased hoarseness, stridor, abnormal respiratory rate, and depth, or mental changes from hypoxia. Evaluate circulation (apical, carotid, and femoral pulse) Check V/S frequently, using an ultrasound device if necessary. Check peripheral pulses on burned extremities hourly; use Doppler as needed

  

Ass essmen t
         

  

Review the initial assessment data obtained by perhospital providers Focus on the major priorities of any trauma patient (ABC) Assess respiratory status as first priority Note any increased hoarseness, stridor, abnormal respiratory rate and depth or mental changes from hypoxia Evaluate circulation (apical, carotid and femoral pulses) Check V/S frequently Check pheripheral pulses on burned extremities hourly Monitor fluid intake and output measure hourly Arrange for patients with facial burns to be assessed for corneal injury Assess body temperature, body weight, hx of preborn weight, allergies, tetanus immunization, past medical surgical problems, current illnesses and use of medication Assess depth of wound and identify areas of full and partial thickness injury Assess neurologic status Assess patient’s and family understanding of injury and treatment

Dia gnos is

Impaired gas exchange r/t carbon monoxide poisoning, smoke inhalation, and upper airway obstruction Ineffective airway clearance r/t edema and effects of smoke inhalation Fluid volume deficit r/t increased capillary permeability and evaporative fluid loss from burn wound. Hypothermia r/t loss of skin microcirculation and open wound Pain r/t tissue and nerve injury and emotional impact of injury. Anxiety r/t fear and emotional impact of injury

 

  

Nu rs in g I nter ven tion
1.

Promoti ng Gas Exc hanage and Air way Cl earan ce

 

 

Provide humidified oxygen, and monitor arterial blood gas (ABGs), pulse oximetry, and carboxyhemoglobin levels Assess breath sound, respiratory rate, rhythm, depth, and symmetry; monitor for hypoxia. Observed for sign of inhalation injury: blistering of lips or buccal mucosa Report labored respiration, decreased depth of respirations; prepare to assist with intubations and escharotomies Monitor patient with mechanical ventilation. Institute aggressive pulmonary care measures; turning coughing, deep breathing, using spirometry and tracheal suctioning. Maintain proper positioning t promote removal of secretions and patent airway, optimal chest expansion. Maintain asepsis to prevent contamination of the respiratory tract and infection, which increase metabolic requirements

Nu rs in g I nter ven tion
2. Rest oring Flu id an d Ele ctr olyt e Bal an ce
 

  

Insert large-bone IV catheter and indwelling urinary catheter Monitor V/S and urinary IO (hourly), note sign of hypovolimia or fluid overload. Provide IV fluids as prescribe; document IO and daily weight. Elevate head of bed and burned extremities Monitor serum electrolyte levels (eg, sodium, potassium, calcium, phosphorus, bicarbonate); recognizing developing electrolyte imbalance

3. Mai nta in ing Norma l Body Te mp er at ure
  

Provide warm environment; use heat shield, space blanket, and heat lights Assess core body temp. frequently Work quikly when wounds must be exposed to minimize heat loss from the wound

Nu rs in g I nter ven tion
4. Mi ni mi zin g Pa in and An xi et y
 

Use pain sclae to asses pain

Perform respiratory assessment before giving analgesic agent to nonventilated px. Admistered IV analgesic as prescribe and assess response to medication Assess px and family understanding of burn injury, coping strategies, family dynamics, and anxiety levels. Provide emotional support, reassurance and simple explanation about procedures Provide pain releif, and give antianxiety med if px remain highly anxious and agitated.

 

Nu rs in g I nter ven tion
5. Mon ito r an d Ma nagi ng Pote nti al Comp lica ti on s

   

Ac ute Re spir atory Failu re : assess for increasing dyspnea. Stridor, changes in respiratory patterns; monitor arterial blood gas (ABGs), pulse oximetry to detect problematic oxygen saturation and increasing carbon monoxide; monitor chest x-rays for cerebral hypoxia Dis tri bu tiv e Shock : monitor for early signs of shock or progressive edema. Administered fluid resuscitation as ordered in response to physical findings; continue monitoring fluid status Ac ute Re nal Fa ilu re : monitor and report abnormal urine output and quality Com pa rtme nt Syndr ome : assess nuerovascular status of extremities hourly; report any extremity pain, loss of peripheral pulse or sensation Paralyt ic Ileu s: NGT and maintain in low intermittent suction until bowel sound resume Cu rli ng’ s Ulce r: assess gastric aspirate for blood and pH; assess stools for occult blood; administerd antacids and histamine blockers (eg, ranitidine, (zantac)) as prescribed.

Acu te and In term edi ate P ha se

It b egins 42 to 72 hours aft er t he b urn inju ry. Burn pai n cont ro l are the p riori ties i n thi s st ag e

wo und care and

Assessment
- Focus on hemodynamic changes - Measure V/S frequently - Assess peripheral pulses frequently - Observe electrocardiogram for dysrhythmias resulting from potassium imbalance - Assess residual gastric volume and pH in px with NGT - Note and report blood in gastric fluid or stool. - Assess wound: size, color, eschar, exudate, abscess formation under the eschar, epithelial buds, bleeding granulation tissue appearance - Focus on pain and psychosocial response - Assess for excessive bleeding adjacent to areas of surgical exploration and debridement

Dia gnos is

Excessive fluid volume related to resumption of capillary integrity Risk for infection related to loss of skin barrier and impaired immune response Impaired skin integrity related to open burn wounds Imbalance nutrition: Less than body requirements Impaired physical mobility r/t burn wound edema, pain, and joint contractures Ineffective coping r/t fear and anxiety Deficit knowledge about the burn treatment

Nu rs in g I nter ven tion
1. Re sto ri ng Fl ui d Balanc e  Monitor IV and oral fluid intake  Measure IO and daily weight  Report in changes in hemodynamic  Administered low dose of dopamine as prescribe to increase perfusion and diuretics to promote increased urine output 2. Prevent ing inf ection  Provide a clean and safe environment  Caution px to avoid touching wounds or dressings, bathed unburned areas and change linens regularly  Closely scrutinized wound t detect early sign of infection 3. Maint ain A deq uat e Nut ri tion  Initiate oral fluid slowly when bowel sound resume  Collaborate with dietitian  Document caloric intake  Weight px daily and graph weights  Encourage px with anorexia to increase food intake, provide pleasant surroundings

Nu rs in g I nter ven tion
4. Promot e Sk in Int eg ri ty  Asses wound status  Support px during distressing and painful wound care  Coordinate complex aspects of wound care  Assess and record any changes and progress in wound healing  Assist, instruct, support, and encourage px and family to take part in dressing changes and wound care. 5. Re lievi ng Pai n and Dis co mfo rt  Teach px relaxation technique  Use guided imagery to alter px perception and responses to pain  Administer minor antianxiety med and analgesic agent before becomes too severe  Promote comfort during healing phase

Nu rs in g I nter ven tion
6. Promot ing Mob ili ty  Prevent complications for immobility  Modify intervention to meets patient’s need  Make aggressive effort to prevent contractures and hypertrophic scaring of the wound area after wound closure for a year or more  Initiate passive ROM  Apply splits or functional devices to extremities for contracture control 7. Moni tori ng and Manag ing Po tential Co mplic at ion  Heart failure: assess for decreased cardiac output. Oliguria,edema, or onset of S3 or S4 heart sound  Pulmonary edema: assess fro increasing central venous pressure (CVP)  Sepsis  ARDS  Visceral damage (frm electrical burns)

Rehabi litatio n an d Lon g-Te rm Ph ase
Re habil ita ti on ph ase sh ou ld begi n imm edia te ly after th e bu rn has occ urr ed .

Asse ssmen t

Obtain information about patient’s educational level, occupation, leisure activities, cultural background, religion and family interactions Assess self-concept, mental status , emotional response to injury and hospitalization, level of intellectual functioning, previous hospitalization, response to pain and pain relief measures and sleep pattern Perform ongoing assessments relative to rehabilitation goal Document participation and self care abilities in wound care and ambulation Maintain comprehensive and continuous assessment for detection of early complication

 

  

Dia gnos is

Activity intolerance r/t to pain on exercise, muscle wasting, and limited endurance Disturbed body image r/t altered appearance and selfconcept Deficient knowledge of postdischarge home care and followup needs

Nu rs in g I nter ven tion
1. Pr omo ting Activi ty Toler an ce
   

Schedule care to allow periods of uninterrupted sleep Administer hypnotic agents as prescribed Communicate plan of care to family and other caregivers Reduce metabolic stress by relieving pain, preventing chilling or fever and promoting integrity of all body systems to help conserve energy Incorporate physical therapy exercises to prevent muscular atrophy and maintain mobility required for daily activities Support positive outlook and increase tolerance for activity by scheduling diversion activities in periods of increasing duration

Nu rs in g I nter ven tion
2. Imp rovi ng Body Imag e and Sel f-Co ncep t
    

Refer patient to support group to develop coping strategies Assess patient’s psychosocial reactions Support patient through small gestures Teach patient ways to direct attention away from a disfigured body to the self within Coordinate communications of consultants

3. Mo nit oring and ma na gin g poten tial compl ica ti on
Contr actu res  Provide early and aggressive physical and occupational therapy  Support patient if surgery is needed to achieve full ROM

Impa ir ed ps yc hologi ca l adapt ation to th e bu rn in ju ry  Obtain psychological or psychiatric referral as soon as evidence of major coping problems appears

Dia betes M ellit us

-Diabetes Mellitus is a group of metabolic disorders characterized by elevated blood glucose hyperglycemia) resulting from defects in insulin production and secretion, decreased cellular response to insulin, or both. -This leads to hyperglycemia, which may lead to acute metabolic complications, such as diabetic ketoacidosis (DKA),and hyperglycemic hyperosmolar nonketonic syndrome (HHNS) -Long term hyperglycemia may contribute to chronic microvascular complications (kidney and eye disease) and neuropathic complications -Diabetic is also associated with an increased occurrence of CAD, CVA, and peripheral disease

Ty pes of D ia betes
1. Type 1 (Form erl y Insul in-D epen dent D iabetes Me lli tus)

About 5%-10% of diabetic patient have type 1 diabetes. Beta cells of the pancreas that normally produce insulin are destroyed by an autoimmune process. Insulin injections are needed to control the blood glucose Type 1 diabetes has a sudden onset, usually before the age of 30 years About 90%-95% of diabetes has type 2 diabetes. Results from a decreased sensitivity to insulin (insulin resistance) or from a decreased amount of insulin production First treated with diet and exercise, then oral hypoglycemic agents as needed Occurs most frequently in patients older than 30 years of age and in obese patients Characterized by an degree of glucose intolerance with onset during pregnancy (second or third trimester) It occurs in women 25 years of age or older, women younger than 25 years of age who are obese, women with a family history of diabetes

2. Type 2 (Form erl y Non -I ns ulin -D ependent Diab etes Mell it us )

 

3.G esta ti on al D iabete s
 

Clin ica l M anifes tatio n
 

Polyuria, polydipsia and polyphagia Fatigue and weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, sores that heal slowly and recurrent infections Onset of the type 1 diabetes may be associated with the nausea, vomiting, or stomach pains Type 2 diabetes results from slow, progressive glucose intolerance and results in long-term complications if diabetes goes undetected for many years. Complications may have developed before the actual diagnosis is made Signs and symptoms of DKA include abdominal pain, nausea, vomiting, hyperventilation, and fruity breath odor.

As sess men t an d D ia gn osti c Meth od s

High blood glucose levels: fasting plasma glucose levels 126 mg/dL or more, or random plasma glucose levels more than 200 mg/dL on more than one occasion Evaluation for complications

Pr even tio n

For obese patients(especially those with type 2 diabetes): weight loss is the key to treatment and the major preventive factor for the development of diabetes

Managemen t

Primary treatment of type 1 diabetes is insulin. Primary treatment of type 2 diabetes is weight loss Exercise is important in enhancing the effectiveness of insulin Use of oral hypoglycemic agents if diet and exercise are not successful in controlling blood glucose levels. Insulin injections may be used in acute situations Because treatment varies throughout course because of changes in lifestyle and physical and emotional status as well as advances in therapy.

Nu rs in g M anagemen t

Maintain fluid and electrolytes balance. Improve nutritional intake Reduce anxiety Monitor and Manage potential complications Teaching patient about self care

Dia betic Ket oacid os is

Caused by an abs ence of in ade qu ate amou t of in su li n. This res ult s in di sor der s in th e met abol is m of ca rboh ydr ates , prote in , and fat.

The three main clinical features of DKA :
(5)

Hyperglycemia, due to decreased use of glucose by the cells and increased production of glucose by the liver; Dehydration and electrolyte loss, resulting from polyuria, with a loss of up to 6.5 liters of water and up to 400 to 500 mEq each of sodium, potassium, and chloride over 24 hours; and Acidosis, due to an excess breakdown of fatty acids and production of ketone bodies, which are also acids. Three main causes of DKA are decreased or missed dose of insulin, illness or infection, and initial manifestation of undiagnosed or untreated diabetes.

(7)

(9)

Clin ica l M anifes tatio ns
    

Polyuria, polydipsia (increased thirst) Blurred vision, weakness, and headache Orthostatic hypotension in patient with the volume depletion Weak rapid pulse GI symptoms, such as anorexia, nausea/vomiting, and abdominal pain Acetone breath Kaussmauls respiration Mental status changes

  

As sess men t an d D ia gn osti c Fi ndin gs

Blood glucose level:300-800mg/dL Lower serum bicarbonate level: 0-15mEq/L Low pH: 6.8-7.3 Low pCO2: 10-30 mmHg Low sodium and potassium Elevated creatinine, BUN, hemoglobin, and hematocrit

Nu rs in g M anagemen t
     

Administer fluid as ordered Monitor fluid volume status Monitor for sign of fluid overload *Monitor carefully for hypokalemia due to rehydration and insulin treatment. Promote electrolyte and acid-base balance -Observe frequently for signs of hyperkalemia (ie, tall, peaked T waves on the ECG) and obtain frequent (every 2-4 hours) potassium values during first 8 hours of treatment.

Teach the patient about “sick-day rules” which are strategies to help prevent diabetic complications.

 

Do not eliminate insulin doses when nausea and vomiting occur Take usual insulin dose or previously prescribed sick-day doses and attempt to consume frequent small portions of carbohydrates Drink fluids every hour to avoid dehydrations Check blood glucose level every 3-4 hours

End of the slides

Hepatic En ce phalop ath y

ammonia (cerebral toxin) It is a potentially reversible neuropsychiatic abnormality in the setting of liver failure. It can be diagnosed only after exclusion of other neurological, psychiatric, infectious and metabolic etiologies

Clin ica l M anifes tatio n
Early signs:
    

minor mental changes and motor disturbance Slight confusion and mood alteration Patient is unkempt Disturbance in sleep pattern (sleeps during the day) Restlessness and insomnia at night

As coma progresses the px may be difficult to awaken.  asterisxis (flapping tremor of the hand)  Reflexes are hyperactive; with worsening encephalopathy reflexes disappear and extremities become flaccid  Slowing and increase in amptitude of brain waves (EEG)  Fetor hepaticus: breath odor like freshly mowed grass, acetone or old wine  Gross disturbances of consciousness and complete disorientation  With further progression, frank coma and seizure occurs

Dia gnos is
  

Liver enzymes- All increase SGPT (ALT) SGOT (AST)  Serum cholesterol & ammonia increase

Indirect bilirubin increase CBC – pancytopenia PTT – prolonged Hepatic ultrasonogram – fat necrosis of liver lobules

Med ica l M an agemen t
    

Administer lactulose (cephulac) to reduce serum ammonia level Reduce protein intake Give enema as prescribed to reduce ammonia absorption from GIT Administer nonabsorbable antibiotics (neomycin) as an intestinal antiseptic Monitor serum ammonia level daily; monitor electrolyte status and correct if abnormal Discontinue medications that may precipitate encephalopathy (eg, sedative medication, tranquilizers, analgesic agents) Other treatment include administration of IV glucose, vitamins and oxygen

Nu rs in g M anagemen t

Assess neurologic status frequently. Keep daily record of handwriting and performance in arithmetic to monitor mental status Monitor fluid IO and body weight daily Monitor for peritoneal, pulmonary, or other infection Instruct family to observe subtle sign of recurrent encephalopathy Maintain low protein, high calorie diet

End of the slides

En d- St age R enal Dis eas e

Chronic renal failure or ESRD is a progressive irreversible deterioration in renal function in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia and azotemia

CAUSE S
         

Diabetes mellitus Hypertension Chronic glomerulonephritis Pyelonephritis Obstruction of the urinary tract Hereditary lesions (eg. Polycystic kidney disease) Vascular disorder Infections Medications / toxic agents Environmental and occupational agents (eg. Lead, cadmium, mercury, chromium)

Pathop hysiolog y
Renal function declines End product of CHON metabolism accumulates in the blood Uremia develops Affects every system in the body

St ages of Kid ney Fa ilu re
Sta ge I - (Redu ced ren al res erv e)  Loss of nephron function (40% - 70%)  Px usually does not have sx because the remaining nephrons are able to carry out the normal function of the kidney Sta ge II - (Re nal in suffici en cy )  Nephron function is lost (75% - 90%)  Serum creatinine and blood urea nitrogen rise  Kidney loses it’s ability to concentrate urine and anemia develops  Px may report polyuria and nocturia Sta ge III - (ES RD )  Final stage of chronic renal failure  Loss of nephron function (10%)  All of the normal regulatory, excretory and hormonal function of the kidney are severely impaired  Elevated creatinine and BUN levels as well as electrolyte imbalances  Dialysis is indicated

Clin ica l M anifes tatio n

Ca rd iva scu la r : hypertension, pitting and periorbital edema, pericardial friction rub,
pericardial tamponade, hyperkalimia

Integu me ntary: ecchymosis, purpura, thin brittle nails, coarse thinning hair, gray-bronze
skin color, dry flaky skin

Pulmonary: crackles, thick tenacious sputum, depressed cough reflex, shortness of
breath, tachypnea, kussmaul type of respiration, uremic pneumonitis

Ga str oin test in al: ammonia odor of breath, metallic taste, mouth ulceration and
bleeding,N/V, constipation or diarrhea, bleeding in GIT

Nu er ologic : weakness, fatigue, confusion, disorientation, tremors, seizure, burning of sole
of feet, behavioral change

Musculos kel eta l: muscle craps, loss of muscle strength, renal osteodystrophy, bone
pain, fracture, foot drop

 

Rep rodu cti ve: amenorrhea, testicular atrophy, infertility, decrease libido Hem atologic : anemia,thrombocytopenia

As sess men t an d D ia gno stic Fi nd ings
1. Gl omeru lar filt ration rate

 

24ᵒ urinalysis for creatinine clearance = decrease GFR Increase BUN level Serum creatinine (most sensitive indicator of renal function

2. Na and H2O rete ntion

  

Kidney cannot concentrate or dilute urine normally Retain Na and H2O = increase risk for edem, heart failure and HPN Other px tends to lose salt and develop hypotension and hypovolemia Vomiting and diarrhea may produce Na and H2O depletion which worsen the uremic state

3. An emia
 

Inadequate erythropoietin production Producing fatigue, angina and shortness of breath

4. Ca a nd Phosp or ous imb alanc e  Body does not normally respond to the increased secretion of parathormone  Active metabolite of vitaminD normally manufactured by the kidney decreases  Uremic bone disease develops from the complex changes in Ca, PO4 and parathormone balance

Med ica l M an agemen t
1. Me di cat io ns

 

Antihypertensive - to manage HPN

An ti sei sure agen ts - ( Diazepam, Phenytoin) Er yt hropo iet in (Epoge n ) - to manage anemia Administer via IV or SubQ tid A/E: HPN, increased clotting of vascular access sites, seizure and depletion of iron stores Iron suppl em ent PO4 bi ndi ng agen ts - suitable for or select not to participate in dialysis or transplantation Antacids Hyperphosphatemia and hypocalemia are treated with aluminium based antacid Magnesium based antacid should be avoided to prevent magnesium toxicit

 

  

Med ica l M an agemen t
2. Di et ther ap y
     

Vitamin supplementation CHON restriction Potassium restriction Adequate caloric intake Fluid intake to balance fluid loses Na intake to balance Na loses

3. Dial ys is
 

Used to remove fluid and uremic waste products from the body when the kidney cannot do so. Used to treat px with edema that does not respond to tx, hepatic coma, hyperkalemiam hypercalcemiam HPN and uremia

Ty pes of D ia lys is

Med ica l M an agemen t

Meth ods of Thera py

Complication includes:
           

1. Hemod ial ysis

Commonly used method of dialysis  Used for acutely ill and require short term dialysis (days to weeks)  Used for ESRD who require long term or permanent therapy to prevent death  Uses dial yz er (synthetic semipermeable membrane replacing the renal glomeruli and tubules as the filter for the impaired kidneys) Dialysis disequilibrium

Hypertriglyceridemia Heart failure Coronary heart disease Angina pain Stoke Peripheral vascular insufficiency Hypotension Painful muscle cramping Exsanguinations Dysrhythmias Air embolism Dialysis disequilibrium

Hemod ia ly sis

Nu rs in g Dia gnos is

Excess fluid volume r/t decreased urine output, dietary excesses and retention of Na and H2O Imbalance nutrition: less than body requirements r/t anorexia, N/V, dietary restriction and altered oral mucous membranes Deficient knowledge regarding condition and tx regimen Activity intolerance r/t fatigue, anemia, retention of waste product and dialysis procedure Low self-esteem r/t dependency, role changes, change in body image and sexual dysfunction

 

Nu rs in g M anagemen t
  

Assessing fluid status and identifying potential source of imbalance Implementing dietary program to ensure proper nutritional intake Promoting positive feelings by encouraging increase self-care and greater independence Report the health care provider the s/sx of decreased renal fxn
  

Worsening s/sx of renal failure (N/v, change in usual output, ammonia odor or breath s/sx of hyperkalemia s/sx of access problem (clotted fistula or graft and infection)

Multiple dietary restrictions is required, including fluid intake, NA, K and CHON restriction
End of the slides

PUL MONARY EDE MA

Pulmon ary Ed ema

Defined as abnormal accumulation of fluid in the lung tissue and alveolar space Fluid may accumulate in the interstitial spaces. It is a severe life threatening condition.

CAUSES: • • • Hypovolemia Sudden increased in intravascular pressure in the lung Inadequate liver function

Pathop hysiolog y
pulmonary edema most commonly occurs as a result of increased microvascular pressure from abnormal cardiac function an acute event that results from HF, It can occur acutely, such as with MI, or it can occur as an exacerbation of chronic HF The backup of blood into the pulmonary vasculature resulting from inadequate left ventricular function causes an increased microvascular pressure and fluid begins to leak into the interstitial space and the alveoli.

Clin ica l M anifes tatio n

Decreased cerebral oxygenation Sudden onset of breathlessness Patient hands become cold and moist the nailbeds are cyanotic Neck veins are distended Very anxious and often agitated Confused and stuporous Pink foamy or frothy secretions by blood tinged

Pulmon ary Ed ema

Ass essmen t

Auscultation reveals crackles in the lung bases that rapidly progress toward the apices of the lungs. Crackles are due to the movement of air through the alveolar fluid Chest x-ray reveals increased interstitial marking Tachycardia, the pulse oximetry values begins to fall and arterial blood gads analyzing demonstrates increased hypoxemia

Med ica l man agemen t

Improving ventricular function and increased respiratory exchanged Goal mgt. Accomplish through a combination of oxygen medical therapies and nursing support.

Pulmon ary Ed ema

Ph arm acolog ic M anagemen t
1.Ox yg en thera py  oxygen administered in concentration adequate to relieve hypocemia and dyspnea 2. Morp hin e  administered intravenously in small doses(2-5mg) to reduce peripheral resistance and venous return so that blood can be redistributed from the pulmonary circulatiuon to the parts of body. 3. Diu ret ic s  promote the excretion of sodium and water by the kidneys 4. Dobutamin e  intravenous medication given to patient with significant left ventricular dysfunction. 5. Mi lri non e  a phospodieterase inhibitor that delays the released of calcium from intracellular reservoir and prevents the uptake of extracellular calcium by the cells. 6. Ne siri ti de  indicate for acutely decompensate HF

Nu rs in g ma nagemen ts

Administration of oxygen and intubation and mechanical ventilation if respiratory failure occurs. Positioning the patient to promote circulation Monitor I and O Monitoring pulse rate and blood pressure Examining skin turgor and mucous membranes for signs of DHN. Assessment symptoms of fluid overload.

 

End of the slides

PULMON ARY EMB OLI SM

Pu lmon ary E mbolis m

Pulmonary Embolism refers to the obstruction of the base or one or more branches of the pulmonary arteries by the thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart. Gas exchange is impaired in the lung mass supplied by the obstructed vessel. Massive pulmonary embolism is life threatening and can cause death within the first 1 to 2 hours after the embolic event. It is a common disorder associated with trauma, surgery (orthopedic, major abdominal, pelvic, gynecologic), pregnancy, oral contraceptive use, congestive heart failure, age older that 50 years, hypercoagulable states, and prolonged immobility. Most thrombi originates in the deep veins of the legs.

Clinica l M anifes tation s

Symptoms depend on the size of the thrombus and the area of the pulmonary artery occlusion. Dyspnea is the most common symptom. Tachypnea is the most frequent sign Chest pain is common, usually sudden in onset and pleuritic in nature; it can be substernal and may mimic angina pectoris Fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, syncope, shock, and sudden death may occur Multiple small emboli in the terminal pulmonary arterioles stimulate symptoms of bronchopneumonia or heart failure

As sess men t an d D ia gno stic Met hods
Ventilation-perfusion scan, pulmonary angiography, chest radiograph Electrocardiogram (ECG), tachycardia, PR interval and T-wave changes, peripheral vascular studies, impedance plethysmography, and arterial blood gas (ABG) analysis (for hypoxemia)

Prev ention
Ambulation or leg exercises in patients on bed rest Anticoagulant therapy before abdominothoracic surgery and every 8 to 12 hours until discharge from hospital Application of intermittent pneumatic leg compression devices

Med ica l M an agemen t
 

Stabilize the cardiorespiratory system Nasal oxygen is administered immediately to relieve hypoxemia, respiratory distress, and cyanosis An infusion is started to establish an intravenous route for drugs or fluids Pulmonary angiography, spiral CT, perfusion lung scans, hemodynamic measurements, and ABGs are performed An indwelling urethral catheter is inserted to monitor urinary output Infusion of dobutamine or dopamineECG is monitored continuously for dysrhythmias and right ventricular failure Administration of digitalis glycosides, intravenous diuretic, and antiarrythmic agents Administer small doses of intravenous morphine are given to relieve anxiety,

 

 

Med ica l M an agemen t
Anti coa gu lation Ther apy  The partial thromboplastin time (PTT) is maintained at 1.5 to 2.5 times normal, prothrombin time (PT) 1.5 to 2.5 time normal, or an ANR of 2.0 to 3.0  Heparin id administered for 5 to 7 days  Warfarin (Coumadin) is begun within 24 hours following the start of heparin therapy and continued for 3 to 6 months Throm boly ti c Thera py  Thrombolytic therapy may include urokinase alteplase, anistreplase and streptokinase (tissue plasminogen activator). It is reserved for pulmonary embolism affecting a significant area and causing hemodynamic instability  Bleeding is a significant side effect; nonessential invasive procedures are voided Surgi ca l Managem ent  Embolectomy by means of thoracotomy with cardiopulmonary bypass technique  Transvenous catheter embolectomy with or without insertion of an inferior vena caval filter (eg. Greenfield)

Nu rs in g In ter ven tion s
  

Providing general care.. Encourage deep-brathing exercises Preventing thrombus formation. Encourage ambulation Monitoring anticoagulant and thrombolytic therapy. Advise bed rest, monitor VS every 2 hours, limit invasive procedures Minimizing chest pain, pleuritic. Administer analgesics as prescribed for severe pain Alleviating anxiety. Encourage patient to express feeling and concerns Managing oxygen therapy. Assess for hypoxia Providing postoperative nursing care. Measure pulmonary arterial pressure and urinary output

  

THANK YOU!
END OF THE SLIDE

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