Shock
Dr. Imad AL – FahdConsultant SurgeonAssistant ProfessorGeneral Surgery Dept.Baghdad College Of MedicineTo understand:• The pathophysiology of shock and ischaemia–reperfusion injury• The different patterns of shock and the principles and priorities of resuscitation• The appropriate monitoring and endpoints of resuscitation LEARNING OBJECTIVES
SHOCK
Complex clinical syndrome : group of signs/symptoms that's form together a disorder can be observable and measurable May be life-threateningSHOCK
Definition- failure of circulatory system to maintain adequate perfusion of vital organs Leads to anaerobic cellular metabolism and accumulated waste products Results in inadequate tissue perfusion with decreased oxygenation at cellular levelClassifications of shock
Hypovolemic- most common type, inadequate circulating blood volume. Cardiogenic- inadequate pumping action d/t primary cardiac muscle dysfunction Distributive- d/t changes in blood vessel tone that changes size of spacePathophysiology
Adequate circulating blood volume depends upon three interrelated components; A minor impairment in one can be compensated for by the other two, but prolonged or severe impairments will lead to SHOCK. Heart Vascular tone Blood volume
Pathophysiology
Blood flows d/t driving force as leaves LV Continuous process whereby arterioles store blood and capillaries release it as needed Blood flow influenced by varying needs of cells located nearby Capillaries open on demand Larger blood vessels regulated by autonomic nervous systemPATHO
Sympathetic NS constricts blood vessels; parasympathetic dilates blood vessels Capillaries operate within own mechanisms using sphincters; different controls than autonomic nervous system Called: MICROCIRCULATIONMicrocirculation
Autonomy exists within capillaries No coordinated effort throughout body Governed by local vasoactive substances sensitive to blood flow adjusts moment to moment Capillaries meet with veins Veins are low pressure and have no musclesBlood flow
Two major receptors that sense blood flow and volume Arterial baroreceptors Atrial baroreceptorsArterial baroreceptors
Located in aortic archSense how “Full system is”Low pressure is sensed by receptorsReceptors stimulate sympathetic NSCardiac output is increased by: rate and stroke volumemuscle tensionArterial baroreceptors
Called systemic/peripheral vascular resistance
Atrial baroreceptors
Located on right side of heart Measures fluid volume returning to heart Stimulates sympathetic NS to constrict Constricts vessels in areas not considered VITAL to survival Brain HeartMean arteial pressure
MAPA MAP > 60 is necessary to perfuse coronary arteries, brain, and kidneys. Ideal for heart patients with LV disorders is 70-90
EXAMPLE: MAP
B/P = 120/60 MAP = 80 60 X 2 = 120 (plus +) 120 X 1 = 120 = 240 3 = 80Other mechanisms
Chemoreceptors located in aortic arch and carotid bodies sense decreased pH and increased PaCO2 Tissues not receiving enough O2 maintain metabolism using anaerobic functions Produces lactic acid as by-product Respiratory rate may change Increased CO2 leads to increased cardiac outputOther mechanisms
Juxtaglomerular receptor- located in kidney measures blood flow to kidney With lowered blood volume, renin is released Renin begins process leading to vasoconstriction ADH is released to prevent diuresis Leads to water conservation and increased blood volumeIf one of three components fail, others compensate Vasoconstriction and increased cardiac output used for decreased volume Two of three must adequately function Two or more fail---SHOCK
Types of shock
■ Hypovolaemic■ Cardiogenic■ Obstructive■ Distributive■ Endocrine Hypovolemic Cardiogenic Distributive Anaphylactic Neurogenic SepticHypovolemic shock
Most common type Inadequate circulating blood volume Caused by- Hemorrhage- loss of fluid and protein Burns-loss of fluids or fluid shifts Dehydration- loss of fluidsCardiogenic shock
Caused by inadequate pumping power 40% cardiac muscle dysfunction with 80% mortality rateDistributive shock
Due to changes in blood vessel tone that changes size by increasing vascular space without increasing blood volumeResults in “relative” hypovolemiaFluid remains same but is redistributedDistributive shock
Anaphylactic- Acute allergic reaction from exposure to substance client has been exposed to Bee stings, snake bite, chocolate, iodine Re-exposure to foreign substances leads to antigen binding to IgE on mast cells Mast cells release histamine, prostagladins,etc. S/S- massive vasodilation, uticaria (hives), laryngeal edema, bronchial constrictionDistributive shock
Neurogenic- Injury to spinal cord Autonomic nervous system affected by loss of sympathetic vasoconstriction and smooth muscle Leads to pooling of blood in veins Decreased venous return to heart Decreased cardiac outputDistributive shock
Septic- Sepsis is systemic response to infection Begins with growth of bacteria Bacteria release substances called endotoxins Once released, lead to process and shock Very lethal- mortality rate 20-80% Most common causitive organism is gram + staph, strep, fungusSeptic shock
Conditions predisposing clients include: UTI URI Contaminated blood Extreme ages Immunosuppressed clients Steroid use Surgery- GU, GI Invasive devices- IV, catheter Men with benign prostatic hypertrophyStages of shock
Initial stage (early compensation stage) Nonprogressive stage (compensatory) Progressive stage (intermediate) Refractory stage (irreversible)Initial stage
Cardiac output is d/t loss of actual or relative blood lossMAP from baseline to < 10mm/HgCompensatory mechanisms are able to maintain perfusion to tissuesSystemic and microcirculation work togetherInitial
aerobic metabolism with anaerobic metabolismProduction of lactic acid C.O. results in hydrostatic capillary pressureFluid moves from interstitial to capillary to increase volumeInitial
Vascular constriction and increase heart rate help to maintain B/PS/S: increase heart rate from client’s baseline or slight increase in diastolic B/P may be only manifestation
Nonprogressive-compensatory
MAP 10-15 mm/Hg from baselineMust activate kidney and chemical mechanisms to maintain B/PKidneys and baroreceptors sense vascular volumeRelease of renin; ADH; Aldosterone; epinephrine; norepinephrineSystemic and microcirculation no longer work in unisonNonprogressive
Renin secretion begins reaction- leading to urine output, sodium absorption, widespread vasoconstrictionADH causes water reabsorption and vasoconstriction in skinTissue hypoxia is present in kidneys and skinAnaerobic metabolism results in lactic acid productionNonprogressive
Acidosis (pH< 2.45)Hyperkalemia (K+ >5.0 mEq/l) heart rate, B/P, urine outputStimulation of thirst mechanismProgressive stage
Sustained decrease of MAP < 20 mm/Hg Tissue hypoxia has worsened Vital organs are hypoxic and non-vital organs become anoxic leading to ischemia Ischemia will lead to cell destruction and death Increased lactic acid production causes increased capillary permeabilityProgressive
Increased blood in capillaries increase hydrostatic pressure Fluids moves from vascular to interstitial space Microcirculation reverses with pooling of blood in capillaries Increases vascular spaceProgressive stage
Increased vascular space; decreased blood volume; decreased heart action—all reduces MAPAll lead to venous pooling, decreased venous return, decreased cardiac outputNo mechanisms to change pattern at this point, therefore events become more severeVital organs can tolerate this for a brief time without permanent damageProgressive stage
Immediate interventions are necessary to preserve life Tolerance varies with individuals LIFE-THREATENING GENERALLY HAVE 1 HOUR AFTER SYMPTOMS BEGIN TO REVERSE PATTERN
Refractory stage
Vital organs experience drastic changes including cell destructin and death Body is unable to reverse sequence Metabolism is strictly anaerobic Underlying cause may not be more severe Cellular ischemia and necrosis leads to organ failure Therapy is ineffective---DEATHEffects on body systems
Respiratory- tissue hypoxia leading to anoxia major cause of death ARDS (acute respiratory distress syndrome)Effects
Acid-base- Oxygen needed for ATP production (energy) Without O2 cells use anaerobic metabolism, producing lactic acid Lactic acid causes cellular acidity which damages cells and decreases C.O. Circulation is disrupted, blood pools, decreased venous return VICIOUS CYCLEEffects
Chemoreceptors sense decreased pH, respirations increase in rate and depth to compensate for respiratory acidosis Respiratory alkalosis ensues. Cellular hypoxia is not caused by inadequate ventilation, but instead by inadequate tissue perfusion.Effects
As pH of cell decreases, lysosomes within cell explode releasing destructive enzymes Enzymes destroy cell membrane and digest cell contents Once this process begins, cellular changes are irreversibleEffects
Myocardial deterioration- as shock progresses, heart muscle and function deteriorates Myocardial depressant factor (MDF)- released d/t ischemia in GI tract. Causes reduced C.O.Effects
Disseminated Intravascular Coagulaion- DIC Sluggish blood movement & anaerobic metabolism (lactic acid) make blood hypercoagulable Accompanied by hemolysis (destruction of red blood cells) Widespread intravascular clotting occurs Multiple thrombi or emboli formEffects
Leads to occluded circulation to organsBody attempts to break down clots but not specific—all clots are broken downLeads to bleeding; further decreasing vascular volume and tissue perfusionOften fatalEffects
Vasoconstriction- increased CO2 dilates arterioles in active tissues (heart) Increased heart activity increases CO2 which dilates coronary arteries CO2 is powerful vasoconstrictor in sympathetic nervous system Blood in inactive tissues is shunted to tissues which need it mostEffects
Catecholamines- epinephrine and norepinephrine are released related to fight or flight response Effects are to increase blood flow to brain, heart, and skeletal muscle Decrease blood flow to skin, kidneys, GI tractEffects
Histamine – causes vasodilationIncreased capillary membraneBronchoconstrictionCoronary vasodilationCutaneous reaction (flares, wheals)Effects
Vasoactive polypeptides- Bradykinin- vasodilation, capillary permeability, pain, acti6ve in late shock Angiotension- vasoconstriction and increased SVR MDF- depresses cardiac muscle contraction
Effects
Adrenal medulla releases epinephrine and norephinphrine Increases respiratory and heart rates, increased B/P Release of mineralocorticoids- aldosterone and glucocorticoids- desoxycorticosterone; effects fluid and electrolyte balance through sodium and water, energy in tissueEffects
ADH- also called vasopressin; from pituitary gland; tells kidneys to conserve water MANY OTHER EFFECTS ON BODY!!!!General clinical manifestations
Shock had many diverse S/S Subjective complaints are usually nonspecific Observable and measurable are often conflictingS/S
Tachypnea- Rapid, shallow respirations (tachypnea) d/t tissue hypoxia
S/S
Tachycardia- Generally pulse rate increases Becomes weak and thready May be unreliable due to pain, fear, anxiety Be aware of clients taking beta-blockers and elderly with heart block
S/S
Hypotension- Systolic B/P indicates integrity of heart, arteries, and arterioles Diastolic B/P indicates peripheral vascular resistance (vasoconstriction) When diastolic falls significantly, indicates vasoconstriction in being lost as a compensatory measure
S/S
B/P usually falls when total blood volume is decreased by 15-20%In young adults, falling B/P is a sign of late shockWith progression, both fall, but systolic falls morePulse pressure narrows- systolic – diastolicTherefore pulse pressure is more significant in late shock than B/P
S/S
It parallels stroke volume- if stroke volume falls, it means volume of blood ejected is less Pulse pressure may decrease before B/P and can be a more reliable indicator or severity of condition Minimum of 60-70 mm Hg systolic to maintain coronary circulation Must know baseline B/P to interpret findings Hypotension by itself does not indicate shock
S/S
In early shock, systolic B/P is unreliable; may be elevated due to compensation Assess strength of femoral pulses
S/S
Level of consciousness Early shock produces stimulation of SNS leading to feelings of anxiety, fear, irritability Dizziness, faintness, unconsciousness (if sudden onset) Apathy, confusion, restlessness, increased alertness ( if gradual onset) With narcotics, must be careful not to mask situations
S/S
Oliguria- Fall in UO is often the earliest sign; one of the most sensitive indices in shock However, if shock occurs suddenly, other S/S will present before urine output decreases UO must be kept above 0.5 ml/kg/hr (35 ml/hr)
Hypovolemic shock
Primary event is large reduction in blood volume Urine osmolality and specific gravity increase d/t water and Na+ retention Stimulation of SNS leads to diaphoresis, losing more fluid- skin feels cool, clammy, pale Increase heart and respiratory rateHypovolemic
Cyanosis is a LATE sign Decreased pulse pressure; normal is 30-50 Decreased LOC Decreased DTRSeptic shock
Caused by bacterial infectionEarly stages body experiences massive vasodilationWarm, dry, flushed skin d/t increased C.O. and increased perfusion of skinOften referred to as “warm shock”Later stages show pale, cold, clammy, mottled skin; decreased body temp.; crackles and wheezes in lungs; drowsiness and stuporSeptic shock
Referred to as “cold shock”May eventually develop ARDSpulmonary failure following successful resuscitation from hypotensiondevelops 1-6 days after treatmentclient looks well, but hyperventilation, cough, elevated PCO2, & low PO2treated with ventilatory support (PEEP), oxygen, diuretics, heparin, and steroidshigh mortality rate with ARDSSeptic shock
Toxins and endotoxins secreted by bacteria lead to whole body inflammatory response Systemic inflammatory response syndrome (SIRS)- alter microcirculation, increase capillary permeability, cause cell injury, clot formation, and anaerobic metabolismSeptic shock
Capillary leak syndrome- fluid shift from intravascular to interstitial spaces is a complicationDiagnosis
Assess oxygenationSpirometry measurementsPulse oximeterABG’sPCO2 is key to detecting compensatory acidosisRising PCO2 with low pH & bicarbonateIndicates respiratory assistance is neededDiagnosis
Cardiac monitoring EKG Labs CBC Lytes Body fluid cultures obtain culture and sensitivity (C&S) before antibiotics are started.Treatment
It is difficult to ascertain when shock begins. Therefore tx. Should be instituted when at least two of the following are present Systolic B/P of 80 mm HG or less Pulse pressure of 20 mm Hg or less Pulse rate of 120 or moreTreatment
Maintain patent airway Supplemental O2 Modified trendelenberg- lower extremities elevated 30-45 0, knees straight, trunk horizontal, head level with chest Promotes venous return by not compressing diaphragm, mobilizes pooled bloodTreatment
REPLACE FLUIDSUse IV therapy with large bore catheter or central lineCarefully monitor infusion of fluidsWhen UO is 60ml/hr or>, B/P is >100 systolic, or heart rate is 60-100, fluids should be tapered offGeneral rule is 3:1 : for a client’s blood loss, 3 times as much fluid should be givenTypes of fluid
Crystalloid or balanced salt solutions: D5W should not be used 2/3 crystalloid solution will leave ECF to Interstitial Use NS, RL, 1/2NS RL or NS expand volume, reduce viscosity, prevent sludging With liver dysfunction, using lactate will increase acidosis, so consider other fluids than RLTypes of fluids
Colloid solutions- contains proteins to increase osmotic pressure in ECFPlasma- Fresh Frozen Plasma (FFP)- requires thawing for 15-30 min.Albumin- may move into pulmonary space and contribute to ARDSDextran- can rapidly expand ECF, but interferes with type and crossmatch of bloodBlood products- PRBC’s or whole bloodTypes of fluids
Fluids given in excess of normal volume should be other than blood so they can easily be removed by kidneysOther treatments
Monitor urinary output Use indwelling catheter Diuretics usually used Dialysis with tubular necrosis of kidney (ATN) Oliguria does not contraindicate large volumes of fluidsOther treatments
Perfusion to GI will be decreased. May result in inadequate perfusion, delayed emptying, vomiting, & possible aspiration Insert NG tube with suctioning Assess periodically for bloodOther treatments
Do not apply heat to skin, heat dilates and draws blood away from vital organsHeat also increases metabolism and need for more O2 & adds strain to the heartDo not allow to become cold- chilling requires extra energy, contributes to sludging of blood, slows heart rate, inhibits body’s reparative processesMultiple organ failure syndrome
Sequential organ failure of lung, liver, and kidney, usually followed by death. 50-90% mortality. All three organs involved: 100%Several etiologies:Dead tissue, injured tissue, infectionPersistent inflammation- pancreatitis, pneumonitisAcute lung injury – usually presentMOFS
Clients at high risk- Impaired immune response Elderly Chronic illnesses Malnutrition Cancer Severe trauma Sepsis