shock gan
Transcript of shock gan
-
7/24/2019 shock gan
1/19
CLINICAL SCIENCE SESSIOSHOCKBY: GAN EE XIAN
AND FRIENDS
-
7/24/2019 shock gan
2/19
DEFINITIONSHOCK IS A MULTIFACTORIAL SYNDRORESULTING IN INADEQUATE TISSUEPERFUSION AND CELLULAR OXYGENAT
AFFECTING MULTIPLE ORGAN SYSTEM ISCHEMIA, A TRANSITION FROM AEROBIC TO ANAEROBIC METLACTIC ACIDOSIS, AND ULTIMATELY ORGAN DYSFUNCTION ANFAILURE
-
7/24/2019 shock gan
3/19
PHYSIOLOGY
SYSTEMIC TISSUE PERFUSION IS DETERMINED B
CARDIAC OUTPUT (CO) AND SYSTEMIC VASCULA
RESISTANCE (SVR).
-
7/24/2019 shock gan
4/19
Com!"#$%!&'"$m+
-
7/24/2019 shock gan
5/19
DECOMPENSATED' HYPODYNAMIC
LOSS OF -/012 OF BLOOD VOLUME AND THE DETERI
OF THE CARDIOVASCULAR SYSTEMA.DECREASE OF BP BELO3 41 MMHG LEADS TO MYOCARDIAL
B.DECREASE OF BP BELO3 1 MMHG LEADS TO GENERALVASODILATATION CAUSING FURTHER LOSS OF BP
C.INCREASED PERMEABILITY OF THE CAPILLARIES CAUSING THOF BLOOD PLASMA INTO THE TISSUE DECREASING BLOOD V
D.INTRAVASCULAR CLOTTING ( 5 VISCOSITY 6 7VELOCITY)E. CELLULAR DESTRUCTION IS CAUSED BY THE LYSOMOSAL RU
AND 7 IN THE ACTIVITY OF MITOCHONDRIA, ACTIVE TRANSPGENERAL METABOLISM.
F. BUILD UP OF LACTIC ACID LEAD TO ACIDOSIS 3ITH PH DRO8.9/ 4.1 OR LO3ER
-
7/24/2019 shock gan
6/19
TYPES OF SHOCK
-. HYPOVOLEMIC SHOCK
0. CARDIOGENIC SHOCK'OBSTRUCTIVE SHOCK
9. DISTRIBUTIVE SHOCK
ANAPHYLACTIC SHOCK
SEPTIC SHOCK NEUROGENIC SHOCK
-
7/24/2019 shock gan
7/19
HYPOVOLEMIC SHOCK
ETIOLOGY:
; INTERNAL OR EXTERNAL FLUID LOSS
; INTRACELLULAR AND EXTRACELLULAR COMPARTMEN
< MOST COMMON CAUSES:HEMMORHAGE
DEHYDRATION
-
7/24/2019 shock gan
8/19
HYPOVOLEMIC SHOCK
PATHOPHYSIOLOGY
DECREASED INTRAVASCULAR VOLUME DECREAVENOUS RETURN DECREASED VENTRICULARFILLINGDECREASED VENTRICULAR FILLING DECREASED STROKE VOLUME (HR, PRELOAD, =AFTERLOAD) DECREASED CO (COMPENSATORYMECHANISMS) INADEQUATE TISSUE PERFUSION
-
7/24/2019 shock gan
9/19
HYPOVOLEMIC SHOCK
THERAPY
AIR3AY ' BREATHING ' C'SPINE CONTROL
STOP ALL OBVIOUS HAEMORRHAGE
INSERT I.V. LINES, TAKE BLOOD FOR X/MATCH< INSERT I.V. LINES, TAKE BLOOD FOR X/MA
GIVE RAPID BOLUS OF FLUID, THEN ASSESS RESPONSE
DECIDE ON NEED FOR SURGERY VS. DECISION TO INVESTIGATE
RESUSCITATION ENDPOINTS
CVP 6 - MM HG
3EDGE PRESSURE 6 -1 TO -0 MMHG0. 3EDGE PRESSURE 6 -1 TO -0 MMHG
CARDIAC INDEX > 9 L'MIN'M
BLOOD LACTATE ? @ MMOL'L
BASE DEFICIT /9 TO 9 MMOL'L
-
7/24/2019 shock gan
10/19
CARDIOGENIC SHOCK'OBSTRUCTIVE S
SYNDROME OF INADEQUATE TISSUE PERFUSION ASSOCIATED 3ITH NO
CIRCULATING BV, AND LO3 CARDIAC OUTPUT
SYMPTOMS: DYSPNOEA, POOR EXERCISE TOLERANCE, CONFUSION, S3
PND
SIGNS: TACHYCARDIA, COLD SKIN, HIGH VP, ADDED HEART SOUNDS, E
LIVER, PERIPHERAL OEDEMA
COMMON CASES
PERICARDIAL TAMPONADE; MUFFLED HEART TONES, ELEVATED NECK V
TENSION PNEUMOTHORAX ; VD, TRACHEAL DEVIATION, DECREASED O
UNILATERAL BREATH SOUNDS, AND CHEST HYPERRESONANCE ON AFF
SIDE
-
7/24/2019 shock gan
11/19
CARDIOGENIC SHOCK'OBSTRUCTIVE S
PATHOPHYSIOLOGY
IMPAIRED PUMPING ABILITY OF LV
DECREASED TISSUE PERFUSION
PULMONARY INTERSTITIAL = INTRAALVEOLAR EDEMA
-
7/24/2019 shock gan
12/19
DISTRIBUTIVE SHOCK
INADEQUATE PERFUSION OF TISSUES THROUGH
MALDISTRIBUTION OF BLOOD FLO3. INTRAVASC
VOLUME IS MALDISTRIBUTED BECAUSE OF
ALTERATIONS IN BLOOD VESSELS. CARDIAC PUMBLOOD VOLUME ARE NORMAL BUT BLOOD IS NO
REACHING THE TISSUES
-
7/24/2019 shock gan
13/19
ANAPHYLACTIC SHOCK
A TYPE OF DISTRIBUTIVE SHOCK THAT RESULTS 3IDESPREAD SYSTEMIC ALLERGIC REACTION TOANTIGEN.
PATHOPHYSIOLOGY: ANTIGEN EXPOSURE BODY
STIMULATED TO PRODUCE IGE ANTIBODIES SPETO ANTIGEN (DRUGS, BITES, CONTRAST, BLOOD
FOODS, VACCINES)REEXPOSURE TO ANTIGEN
BINDS TO MAST CELLS AND
BASOPHILS
ANAPHYLACTIC RESPONSE
-
7/24/2019 shock gan
14/19
ANAPHYLACTIC SHOCK
ANAPHYLACTIC RESPONSE :
VASODILATATION INCREASED VASCULAR PERMEABILITY
BRONCHOCONSTRICTION
INCREASED MUCUS PRODUCTION
INCREASED INFLAMMATORY MEDIATORS RECRUITMENT TO SITES OF ANTIGEN INTERACTION
CLINICAL MANIFESTATION :
ALMOST IMMEDIATE RESPONSE TO INCITING
ANTIGEN
CUTANEOUS MANIFESTATIONS; URTICARIA, ERYTHEMA, PRURITIS, ANGIOEDEMA
RESPIRATORY COMPROMISE; STRIDOR, 3HEEING, BRONCHORRHEA, RESP.DISTRESS
CIRCULATORY COLLAPSE ; TACHYCARDIA, VASODILATION, HYPOTENSION
-
7/24/2019 shock gan
15/19
NEUROGENIC SHOCK
A TYPE OF DISTRIBUTIVE SHOCK THAT RESULTS F
THE LOSS OR SUPPRESSION OF SYMPATHETIC TO CAUSES MASSIVE VASODILATATION IN THE VENOUS
VASCULATURE, DECREASE VENOUS RETURN TO HEARDECREASE CARDIAC VASCULATURE, DECREASE VENO
RETURN TO HEART, DECREASE CARDIAC OUTPUT.
MOST COMMON ETIOLOGY: SPINAL CORD INURY
T4
-
7/24/2019 shock gan
16/19
NEUROGENIC SHOCK
PATIENT ASSESSMENT
HYPOTENSION
BRADYCARDIA
HYPOTHERMIA
3ARM, DRY SKIN
RAP DECREASE (RIGHT ATRIAL PRESSURE)
PA3P DECREASE (PULMONARY ARTERY 3EDGE PRESSURE)
CO DECREASE (CARDIAC OUTPUT)
FLACCID PARALYSIS BELO3 LEVEL OF THE SPINAL LESION
-
7/24/2019 shock gan
17/19
SEPTIC SHOCK
SYNDROME OF PROFOUND HYPOTENSION DUE TORELEASE OF ENDOTOXINS ' TNF' VASOACTIVE PEFOLLO3ING BACTERIAL DESTRUCTIONPEPTIDESFOLLO3ING BACTERIAL DESTRUCTION. USUALLY
ASSOCIATED 3ITH NORMAL BLOOD VOLUME, HIGLO3 CO, AND LO3 SYSTEMIC VASCULAR RESISTA
-
7/24/2019 shock gan
18/19
SEPTIC SHOCK
PATHOPHYSIOLOGY
INITIATED BY GRAM/NEGATIVE (MOST COMMON) OR GRAM POSITIVE FUNGI, OR VIRUSESCELL 3ALLS OF ORGANISMS CONTAIN ENDOTOINCREASE ENDOTOXINS RELEASE INFLAMMATORY MEDIATORS (SYSTINFLAMMATORY RESPONSE) CAUSESINCREASE VASODILATION = INCAPILLARY PERMEABILITYSHOCK DUE TO ALTERATION IN PERIPHER
CIRCULATION = MASSIVE DILATION
-
7/24/2019 shock gan
19/19
TERIMA KASIHSELAMAT MEMBACA