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60 Cards in this Set

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PRE-LOAD
AMOUNT OF BLOOD AVAILABLE TO FILL THE VENTRICLES. END DIASTOLIC VOLUME, END DIASTOLIC PRESSURE
HOW MUCH BLOOD VOLUME IS HELD IN THE VENOUS SYSTEM
64%
FRANK-STARLING-MECHANISM
GREATER THE PRE-LOAD=GREATER THE STRETCH=GREATER THE FORCE OF CONTRACTION
AFTER-LOAD
RESISTANCE OR PRESSURE THE VENTRICLES CONTRACT OR PUMP AGAINST
CARDIAC OUTPUT
AMT OF BLOOD PUMPED IN ONE MINUITE, C.O.=S.V. X RATE
STROKE VOLUME
BLOOD EJECTED IN ONE CONTRACTION
BLOOD PRESSURE
PERIPGERAL VASCULAR RESISTANCE (AFTERLOAD) B/P=C.O. X P.V.R.
HOW DOES THE BODY COMPENSATE FOR BLOOD LOSS
BARORCEPTORS-SNS NERVES-ADRENAL MEDULA-NE AND EPINEPHRINE RELEASED-VASOCONSTRICTION-SVR AND PRELOAD INCREASE
HOW MUCH BLOOD VOLUME DO ARTERIES CONTAIN
13%
HOW MUCH BLOOD VOLUME DO CAPILLARIES CONTAIN
7%
HOW MUCH BLOOD CAN THE VENULES COMPENSATE FOR
500-1000 ML BLOOD LOSS, 15-20% OF VOLUME
AEROBIC METABOLISM
1.GLUCOSE BREAKDOWN YIELDS PYRUVIC ACID, 2.PYRUVIC ACID ENTERS THE KREB OR CITRIC ACID CYCLE, 3.PYRUVIC ACID IS DEGRATED TO CO2,H2O,ENERGY
ANAEROBIC METABOLISM
1.GLYCOLYSIS OCCURS AND PYRUVIC ACID IS PRODUCED, 2.PYRUVIC ACID DOES NOT ENTER KREB OR CITRIC ACID CYCLE, 3.PYRUVIC ACID DEGRADES INTO LACTIC ACID AND SMALL AMOUNT OF ENERGY
INADEQUATE PERFUSION LEADS TO:
BARORECEPTORS NOT BEING STRETCHED-STROKE VOLUME DECREASED-CNS ALERTED
RENIN
RELEASED FROM KIDNEYS DUE TO LOW PRESSURE. RENINACTS AS AN ENZYME TO CONVERT PLASMA PROTIEN ANGIOTENSIN TO ANGIOTENSIN 1 WICH IS CONVERTED TO ANGIOTENSIN 2 BY ANGIOTENSIN-CONVERTING ENZYME
ANGIOTENSIN 2
STIMULATES VASOCONSTRICTION THAT LAST ABOUT ONE HOUR, AND PRODUCES ALDOSTERONE
ALDOSTERONE
CAUSES KIDNEYS TO REABSORB Na+, REDUCES Na+/H2O LOSS FROM SWEATING AND GI TRACT=INTRAVASCULAR VOLUME MAINTAINED
POSTERIOR PITUITARY GLAND
STIMULATED BY HYPOTHALAMUS WHEN BP IS LOW, THE GLAND RELEASES ADH WICH CAUSES KIDNEYS TO REABSORBE Na=FLUID VOLUME MAINTAINED
SPLEEN
STORES 300 ML OF BLOOD IN VENOUS SINUS, DROP IN PRESSURE=SNS STIMULATES CONSTRICTION OF SINUS=UP TO 200ML ADDED TO CIRCULATION
WHAT % BODY FLUID IS IN INTERSTITIAL SPACE
88%
EYRTHROPOIETIN
RELEASED BY KIDNEYS IN RESPONSE TO HYPOXIA, ANEMIA ECT. CAUSES INCREASE PRODUCTION AND MATURATION OF RBC. CAN INCREASE BY 10 OVERTIME
COMPENSATED SHOCK HEART-
INCREASES RATE AND FORCE OF CONTRACTIONS
COMPENSATED SHOCK BLOOD VESSELS-
CONSTRICT=BP MAINTAINED
COMPENSATED SHOCK SKIN-
GETS COOL, CLAMY, PALE
COMPENSATED SHOCK RESPIRATIONS-
INCREASE TO GET RID OF CO2 AND INCREASE O2
COMPENSATED SHOCK URINARY SYSTEM-
PITUITARY RELEASES ADH/ADRENAL CORTEX RELEASES ALDESTRONE=DECREASED URINATION=MAINTAIN FLUID VOLUME
COMPENSATED SHOCK GI SYSTEM-
DIGESTION SLOWES DUE TO DECREASES BLOOD FLOW AND DECREASED GUT MOBILITY
DECOMPENSATED SHOCK
AKA:PROGRESSIVE SHOCK, MEDICAL INTERVENTION MAY STILL HELP, BODT CAN NO LONGER COMPENSATE, HEART NO LONGER PERFUSED VESSELS DIALATE=BP DROBS
IRREVERSABLE SHOCK
SELF NOR MEDS CAN CORRECT CONDITIONMULTIPLE ORGAN DISFUNCTION SYNDROME DUE TO MICRO EMBOLI, MASSIVE RELEASE OF NEURTROPHILS
HEART, LUNGS, BRAIN CAN LIVE
4-6 MIN WITH OUT O2
LIVER, KIDNEYS, GI TRACT CAN LIVE
45-60 MIN WITH OUT O2
MUSCLE, SKIN, BONE CAN LIVE
2-3 HOURS WITH OUT O2
HYPOVOLEMIC SHOCK
FLUID LOSS CAUSED BY HEMORRHAGE, BURNS, DEHYDRATION
IF FLUID LOSS IS NONTRAUMATIC OR PT IS NOT SHOWING SIGNS OF SHOCK YOU SHOULD
TAKE ORTHOSTATIC VITALS, POS. IF PULSE INCREASE OR BP DECREASES 10-20 = 500-1000 CC LOST
CAPILLARY BLEEDING=
OOZES, CLOTS QUICKLY,BRIGHT RED
VENOUS BLEEDING=
FLOWS STEADY, DARK RED
ARTERIAL BLEEDING=
RAPID, SPURTING, BRIGHT RED
HEMOSTASIS VASCULAR PHASE
VESSSEL CUT-SMOOTH MUSCLES AROUND VESSEL CONTRACT-REDUCING LUMEN SIZE AND BLOOD FLOW, SUSTAINED FOR UP TO 10 MIN. MAY NOT WORK IF CUT NOT CLEAN
HEMOSTASIS PLATLET PHASE
1-5 SEC. POST INJURY, PLATLETS STICK TO COLLAGEN-PLATLETS STICK TO PLATLETS-RAPID CONTROL BUT CLOTS ARE UNSTABLE
HEMOSTASIS COAGULATION PHASE
DISRUPTION OF INTIMA EXPOSES COLLAGEN AND OTHER PROTEINS- THIS LEADS TO COAGULATION, IN 3-6 MIN. VESSES IS FILLED
WHAT MEDS. LOWER COAGULATION PHASE
COUMADIN, HEPARIN, FIBRONOLYTICS
STAGE 1 BLEEDING
NO RESPONSE, LOSS OF <15% VOLUME, 500-700 ML,
STAGE 2 BLEEDING
COMPENSATED, 15-25% LOSS OF VOLUME, 750-1,250 ML, TACHYCARDIC, NARROWING BP, COOL&CLAMMY, RESTLESS, THIRST
STAGE 3 BLEEDING
DECOMPENSATED, 25-35% LOSS, 1,250-1,750 ML, TACHYCARDIC, BP DROPSPULSE BARELY PALPABLE, ANXIETY, LOC DECREASE, COOL, PALE, LOW URIN OUTPUT
STAGE 4 BLEEDING
>35% LOSS, 2,000 ML, PULSE BARLEY PALPABLE, RR SHALLOW, UNRESPONSIVE, SKIN COLD-MOTTLED, URIN CEASES, SURVIVLE UNLIKELY
PREGNANT WOMEN HAVE
50% MORE VOLUME, MAY NOT HAVE EARLY SIGNS
ATHLETES HAVE
MORE VOLUME AND CARDIAC NERVES, MAY MOVE SLOWER THROUGH STAGES
OBESE PATIENTS HAVE
LESS VOLUME, SMALL LOSS MAY BE SERIOUS
INFANTS AND CHILDREN HAVE
20% MORE VOLUME THAN ADULTS, CAN COMPENSATE WELL-CRASH QUICKLEY
ELDERLY HAVE
LOWER VOLUME RESERVES, COMPENSATORY SYSTEMS LESS RESPONSIVE, LOWER PAIN PERCEPTIONS/MENTAL ACUITY
NEUROGENIC SHOCK
OCCURS AFTER SPINAL INJURY, CORD CUT BELLOW C-5= PHRENIC NERV INTACT=DIAPHRAGMATIC BREATHING
ANAPHYLACTIC REACTION
EXTREME SYSTEMIC REACTION, MASSIVE DUMPUNG OF HISTAMINE, PT HAVE SENSE OF IMPENDING DOOM
ANAPHYLACTIC SHOCK
COMPRISED OF HYPOVOLEMIC, CARDIOGENIC, NEUROGENIC, RESPIRATORY SHOCK, PT DIES FROM CIRCULATORY, RESPIRATORY FAILURE
SEPTIC SHOCK
PT HAVE HISTORY OF ILNESS/INFECTION, PT HAS HIGH FEVERS, PALE, INFECTS LUNGS, BRAIN
CARDIOGENIC SHOCK
DUE TO POOR CONTRACTILITY, AMI, USUALY RESULTS WHEN 40% OR MORE OF LEFT VENTRICLE IS DAMAGED, MORTALITY RATE OF 80-90%
MULTIPLE ORGAN DYSFUNCTION SYNDROME
due to irreversable shock,ischemia and infection of organs
WHAT IS TACHY PULSE RATE DUE TO HYPOVOLEMIA
>100-ADULTS, >120-SCHOOL AGE, >140-PRESCHOOLER, >160-INFANTS
WHAT BP IS USUALY SUFFICIENT TO MAINTAIN LOC
88-100 mmHg
CONTRAINDICATIONS OF PASG
ABSOLUTE-PULMONARY EDEMA, CARDIOGENIC SHOCK, RELATIVE-PREGNANCY, EVISCERATION, IMPALED OBJECT IN ABD, SUSPECTED DIAPHRAGMATIC RUPTURE, DO NOT INFLATE UNLESS BP <90 OR LOSS OF PULSES
IV COMPLICATIONS
PYROGENIC REACTION, CATHETER SHEAR, ARTERIAL PUNCTURE, CIRCULATORY OVERLOAD, THROMBOPHLEBITIS, AIR EMBOLISM, PAIN, HEMATOMA, INFILTRATION, LOCAL INFECTION