shock ppt

1. SHOCK:
ALTERATION IN
TISSUE PERFUSION

2. OBJECTIVES
• Describe shock and underlying pathophysiology
• Compare clinical findings of compensatory, progressive, and irreversible stages of shock
• Describe differences and similarities in shock states related to hypovolemia,
cardiogenic, neurogenic, anaphylaxsis and sepsis
• Discuss complications of shock
• Discuss nursing interventions and evaluate outcomes of patients experiencing shock

3. SHOCK… A CLINICAL SYNDROME
• Life threatening response to alterations in circulation… hemodynamic changes
• Inadequate tissue perfusion
• Imbalance between cellular O2 supply & demand
• Inadequate end-organ perfusion (liver, kidney, intestine, heart, lungs, brain)
• Results in ↓ supply of O2 & nutrients required to sustain normal cellular metabolism.
IMPACTS ALL BODY SYSTEMS  MOF  DEATH
Influenced by...
• Functioning of compensatory mechanisms
• Successful /timely interventions

5. CARDIOVASCULAR SYSTEM
Closed system: heart, blood, vascular bed
• Vascular bed: arteries, arterioles, capillaries, venules, veins
Functions:
• Delivery of oxygen and nutrients to cells
• Removal of metabolic waste products
• Regulation of blood volume, HR, BP
• Constricts/dilates to regulate blood flow

6. PATHOPHYSIOLOGY:
• Shock begins with CARDIOVASCULAR SYSTEM FAILURE.***
Alterations in at least ONE of four components:
• Blood volume (preload)
• Myocardial contractility CO
• Blood flow
• Vascular Resistance / Afterload (vasoconstriction vs. vasodilation)

7. REGULATION OF BLOOD FLOW:
• BP= product of CO & SVR
• When CO or SVR is low… BP ↓
Decreases in BP = Decreases in CO / SVR
• Leads to vasoconstriction
(attempting to ↑ venous return / BP)
• ↓ flow through the vessel resulting in the
inability to keep the vessel open.
• Compensatory mechanisms:
vasoconstriction, ↑ HR

9. COMPENSATORY
MECHANISMS:

11. • ↑ afterload (resistance) = ↓ SV and ↓ CO
• ↑ CO = ↓ afterload / PVR / SVR
• ↑ HR

12. STAGES OF
SHOCK:
• Initial—hypoperfusion
• Compensatory—sustained
reduction of tissue perfusion
• Progressive
• Irreversible / Refractory

13. STAGES OF SHOCK
Stage I Initiation:
↓ tissue oxygenation due to…
HYPOVOLEMIC: ↓ intravascular volume
CARDIOGENIC:
↓ myocardial contractility = ↓ preload (EDV) / ↑ afterload (resistance) = ↓ SV = ↓ CO
OBSTRUCTIVE: blockage of blood flow
DISTRIBUTIVE: ↓ vascular tone
• Mediator release (sepsis)
• Histamine release (anaphylactic)
• Suppression of SNS (neurogenic)

14. STAGES OF SHOCK
Stage II Compensatory: Sustained reduction in tissue perfusion.
• Initiation of compensatory mechanisms:
1) Neural (SNS): baroreceptors and chemoreceptors
- ↑ HR, ↑ contractility
- Vasoconstriction  blood shunted to essential organs.
- Bronchodilation
2) Endocrine:
- RAAS, ADH, ACTH  cortisol/glucocorticoid release.
- Vasoconstriction
3) Chemical:
• Low oxygen tension
• Hyperventilation / respiratory alkalosis

15. STAGES OF SHOCK
Stage III Progressive:
↑ capillary hydrostatic pressure:
• “leaky capillary syndrome”
• Fluid moves from vascular bed into
tissues.
• Intravascular fluid shifts:
-Causes interstitial edema, anasarca
-↓ circulating intravascular volume
• Decreased coronary perfusion
-MDF released by pancreas.
-↓ myocardial contractility

16. Stage IV Refractory:
Prolonged inadequate tissue perfusion
• Unresponsive to therapy
• Contributes to M.O.Ds and death
STAGES OF SHOCK

17. STAGES OF SHOCK

18. MAINTAIN HOMEOSTASIS: HEMATOLOGIC
• Activation of the coagulation cascade
• ↑ coagulopathy (DIC)
• Vasoconstriction to maintain BP.
• Fibrin deposition
• Enhanced clotting
• Inhibited fibrinolysis (can’t break up clots)
• Depletion of clotting factors.
- We are using all of the mature clotting factors…
immature clotting factors don’t sustain clotting.
• Platelet activation.
• Clotting in the microcirculation.
-MICROEMBOLI  peripheral ischemia / digit necrosis

19. MAINTAIN HOMEOSTASIS: CARDIOVASCULAR
• ↑ HR, ↑ myocardial contractility
• Vasoconstriction  Redistribution of blood to vital organs
HEMODYNAMICS:
-Hypovolemia/distributive shock = Low CVP
-Cardiogenic shock = High CVP
-Obstructive shock = High CVP
• Pulmonary artery catheter (PAC) to assess PAWP, PAP, and CVP
• Useful in all shock states for hemodynamic monitoring.

22. MAINTAIN HOMEOSTASIS: PULMONARY
Early stages—
• Rapid, deep respirations
• Hyperventilation  respiratory alkalosis
• Response to shock and metabolic acidosis
• Metabolic acidosis results from HYPOPERFUSION & BUILD-UP OF LACTIC ACID.
Late stages—
• Shallow respirations
• Hypoventilation  respiratory acidosis
• Poor gas exchange
• Metabolic waste accumulation – muscle weakness

24. MAINTAIN HOMEOSTASIS: RENAL
• ↓ GFR
Activated R.A.A.S.
(renin-angiotensin-aldosterone system):
• Vasoconstriction (angiotension)
• Na+ retention
• Water reabsorption
• Oliguria

27. MAINTAIN HOMEOSTASIS: GI
Slowing intestinal activity
• Hypoactive bowel sounds
• Distention
• Nausea
• Constipation
***r/t hypoperfusion of GI tract.
• Vasoconstriction shunts blood away from GI tract  vital organs

28. MAINTAIN HOMEOSTASIS: HEPATIC
• Altered liver enzymes
• Clotting disorders
-Liver manufactures all coagulation factors.
-Assess metabolic panel
• Increased susceptibility to infection

29. MAINTAIN HOMEOSTASIS: SKIN
Integumentary:
• Skin color, temperature, texture, and turgor.
• Cyanosis is a late/unreliable sign.
• Skin turgor evaluation.
• Peripheral vasoconstriction  cool, clammy skin / weak, thready pulses.

32. ASSESSMENT:
CNS
• Most sensitive to early changes…
first system affected by changes in
cellular perfusion.
• Initial stage: restless, agitation,
anxiety r/t hypoxemia
• Late stage: confusion, lethargy,
coma r/t inadequate perfusion

33. ASSESSMENT: CARDIOVASCULAR
Initial compensatory stages—
• Normal or slightly elevated SBP
• Diastolic has to work harder at rest (↑ DBP)
=Narrow pulse pressure
Late stages—
• Drop in SBP
• Pulses: weak, thready r/t peripheral vasoconstriction
• Delayed capillary refill

36. GENERAL MANAGEMENT
OF SHOCK:
General management of shock:
• Treat underlying cause*
• Reverse altered circulatory component
COMBINATION THERAPY:
• Fluid
• Pharmacotherapy
• Mechanical therapy (mechanical ventilation)
• Minimize oxygen consumption

39. GENERAL MANAGEMENT
OF SHOCK:
MAINTAIN CIRCULATING VOLUME… Correct alterations in fluid balance.
• IV fluids to restore volume
• Maintain oxygen carrying capacity supplemental O2 or mechanical ventilation
• Restore hemodynamic stability  vasopressors
• Choice of fluid, volume, and rate of infusion:
-Depend on fluid lost & current hemodynamic status
-FVO vs FVD, treated very differently.

41. FLUID RESUSCITATION:
BLOOD PRODUCTS: PRBCs, FFP, Platelets, cryoprecipitate
• Treat major blood loss & provide clotting factors
CRYSTALLOIDS:
• 0.9% NS, 0.45% NS, LRs, 3% hypertonic saline, 5% Dextrose
- Inexpensive and readily available
- Classified by tonicity (volume expanders, etc)
- Large volumes precipitate hemodilution… assess Hgb/Hct
- Need to give blood products along with crystalloids to
prevent hemodilution.
COLLOIDS: Albumin
- Avoided w. ↑ capillary permeability.
2 Large-Bore IVs:
• Peripheral: 14 / 16 gauge
• Central Access

44. HEMODYNAMICS
Physical Factors Regulating Blood Flow…
Cardiac Output (CO):
• Amount of blood pumped by the heart per minute.
• (Normal: 4-8 L/min)
Cardiac index (CI):
• Amount of blood pumped by the heart per minute per BSA (height/weight)
• (Normal: 2.4-4 L/min/m2)
• More accurate, individualized.
Stroke Volume (SV):
• Amount of blood pumped out the heart with each beat.
• Measured by a PAC and is reported as C.O.

45. Five factors influence blood pressure:
• Cardiac output
• Peripheral vascular resistance
• Volume of circulating blood
• Viscosity of blood
• Elasticity of vessels walls
HEMODYNAMICS
BP INCREASES WITH…
↑ C.O.
↑ PVR
↑ BV
↑ blood viscosity
↑ rigidity / stenosis of vessels

46. C.O. = HR x SV
CI = (HR x SV) / BSA
• Both HR & SV affect C.O.
• Sepsis = initially ↑ C.O.
(Fever, vasodilation = less SVR).
• As sepsis progresses…SVR ↑ + C.O. ↓
HEMODYNAMICS
↑ HR, SV is unchanged = ↑ CO

47. COMPENSATORY CHANGES:
HEMODYNAMICS
Stroke volume: preload, afterload, contractility
PRELOAD:
Amount of stretch of the myocardium prior to contraction.
End diastolic pressure (EDBP)
Measured by PAC
• Right heart preload: CVP
Normal: 0-8 mmHg
• Left heart preload: PAOP/PAWP
Normal 8-12 mmHg
Tells us the FX of left-side of heart.

48. Afterload: the amount of work the heart has to do to eject blood.
• Resistance the heart encounters is from the blood vessels.
• Heart and lung afterload determined by:
- Diameter of the vessel
- Vasodilation / vasoconstriction
- Valves, Viscosity, and Flow Patterns
• Systemic vascular resistance (SVR): LEFT side of the heart.
• Pulmonary vascular resistance (PVR): RIGHT side of the heart
COMPENSATORY CHANGES:
HEMODYNAMICS

50. SVR & PVR
• MAP: True driving pressure for peripheral blood flow.
• Normal 60-100 mmHg
• MPAP: Mean pulmonary artery pressure
• SVR: LEFT side of the heart.
• PVR: RIGHT side of the heart
Close relationship btwn. SVR / PVR and C.O.
***When CO ↑…. SVR / PVR ↓
(Vasodilation)

52. SWAN GANZ
CATHETER:
MEASURES MEAN
PULMONARY
ARTERIAL
PRESSURE (MPAP)

53. PHARMACOLOGICAL MANAGEMENT:
CARDIAC OUTPUT—
• Positive chronotropics (↑ HR)
• Inotropics (↑ contractility and SV)
-Dopamine, dobutamine, epi, N.E.
• Antidysrhythmics
-amiodarone, Cardizem, sotalol
• Dysrhythmias can alter blood flow
PRELOAD—
• To ↑ preload: fluid administration
• To ↓ preload: venous vasodilators (dobutamine) or diuretics

54. (↑ HR) (↓ HR)

55. AFTERLOAD—
• Vasoconstrictors / vasopressors for TX of LOW afterload.
• ↑ vascular tone = ↑ SVR = ↑ BP
• Contraindicated in hypovolemic shock…
-FVD… don’t have the volume needed to ↑ BP.
• Vasodilators to reduce HIGH afterload.
CONTRACTILITY—
• Positive inotropic agents (dopamine, dobutamine)
• ↑ contractile force
=↑ workload of heart  complications
PHARMACOLOGICAL MANAGEMENT:

56. Other medications:
• Sedatives:↓ HR / anxiety
• Analgesics: pain
• Insulin: BS rises when under stress
• Corticosteroids: assess hyperglycemia!
• Antibiotics
• Sodium bicarbonate: tx metabolic acidosis when pH<7.0
PHARMACOLOGICAL MANAGEMENT:

57. TYPES OF SHOCK:
• HYPOVOLEMIC = inadequate intravascular volume, FVD (trauma, surgery)  need
volume replacement
• CARDIOGENIC = inadequate myocardial contractility, poor pump, back-up of fluid
• OBSTRUCTIVE = obstruction of blood flow, blockage (tumors, etc)
• DISTRIBUTIVE = (neurogenic, anaphylactic, sepsis): inadequate vascular tone
- Maldistribution of circulating blood.
- Have right amt of volume, it’s just not in the right place.
- ↓ vagal tone.
Each has a unique mechanism causing an…
Alteration in Tissue Perfusion

60. HYPOVOLEMIC SHOCK
• Overall ↓ in vascular volume
• The most common shock syndrome
• Blood volume is insufficient to fill the intravascular space
ACTUAL HYPOVOLEMIA: EXTERNAL fluid loss, actual volume loss.
• Hemorrhage, surgery, trauma, diarrhea, diuresis, burns.
RELATIVE HYPOVOLEMIA: INTERNAL FLUID SHIFT from the
intravascular space into the interstitial or intracellular space.
• Third spacing, leaky capillary syndrome, pleural effusion
• Fluid moves out of vessels into tissues  ANASARCA

62. HYPOVOLEMIC SHOCK:
CLINICAL PRESENTATION
↓ BP
↓ CO, ↓CI
↓ RAP, PAP, PAOP
↓ SvO2
↓ Hct (if from blood loss)
↓ urine output
↑ HR
↑SVR
↑ RR
↑ Hct (if from dehydration)
• Oliguria
• Cool, pale skin
• Altered LOC
• Flat neck veins

63. PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK

64. MILD:
• Blood volume deficit of 0-10% or 500cc.
• ↓ venous return, ↓ CO
• ANS compensates: vasoconstriction & inc. myocardial
contractility to maintain MAP and CO.
MODERATE:
• Blood volume ↓ by 15-20% = ↓ CO and arterial pressure
• ↓ blood flow to the liver, pancreas, kidneys, GI tract:
• Oliguria, kidney failure, high BUN/creatinine
• Hypoactive bowel sounds, abd. distention
• Generalized venoconstriction: helps ↑ venous return
• Tachycardia (>100bpm) in attempts to ↑ blood volume
• Tachypnea
• ↓ pulse pressure
• Cool / clammy , mottled skin,↓ cap refill
• Anxiety = acidosis, low cerebral perfusion
SEVERE:
• Blood volume deficit >25%
• Other small losses create major
↓ in CO, BP, and tissue perfusion.
• Brain and myocardium are subject
to a fall in perfusion.
• All compensatory mechanisms are
functioning at MAX CAPACITY!!
• Significant tachycardia (>140 bpm)
• Increase RR respiratory failure
• Severe hypotension
• Anuria
• Confusion, anxious, agitated,
obtunded, eventually comatose.

66. NURSING INT:
HYPOVOLEMIC SHOCK
• Modified trendelenburg
• Control hemorrhage, apply pressure
• Infusion of blood products (O-neg universal donor)
FLUID REPLACEMENT:
• ISOTONIC CRYSTALLOIDS: ↑ preload, ↑ SV, ↑ CO
• NS (can cause ↑ Na+/Cl-) or LRs (can cause buildup
of lactate)
**will often switch btwn the two to avoid these issues.
• Colloidal solution (ALBUMIN):
• Pulls fluid back into intravascular space.
• Volume expander

67. 3:1 RULE FOR CRYSTALLOIDS:
• For every 1 mL of approximate blood
loss, 3 mL of crystalloid solution is
given.
• PRBCS: helps replace fluid and provides
Hgb, which will carry O2 to deprived cells
• Platelets: for uncontrolled bleeding to
help with thrombocytopenia.
• Fresh Frozen Plasma: for when the
patient needs clotting factors.
MONITOR FOR FVO:
• Elevated CVP or PAWP
• Crackles
• Edema
• JVD Collect labs:
Hgb/Hct, lactate level (status of cell’s metabolism),
blood gases (acidosis?), electrolytes, BUN/

69. CARDIOGENIC SHOCK:
Primary dysfunction: inadequate
myocardial contractility / weak
pumping action of heart.
• Approx 80% of cases of cardiogenic
shock are fatal.
Most common etiology:
Damage from MI & impairment of the
myocardial pumping ability.
• Left ventricle is the primary pump
Left ventricular dysfunction:
• Measured by PAP/PAOP
• ↓ CO
• Blood backs up in to pulmonary system
• Pulmonary congestion occurs
Right ventricular dysfunction:
• Measured by RAP/CVP
• Blood backs up into venous circulation
• Reduces available SV for each heartbeat
• Systemic congestion occurs

70. CARDIOGENIC SHOCK:
CAUSES
• Myocardial infarction
• Cardiomyopathy
• Dysrhythmias:
- ↓ efficiency of myocardial contractions.
- ↓ amt of blood pumped out of the ventricle
per minute = inadequate organ perfusion
• CHF
• VSD
• Rupture of ventricular wall
• Disorder of the myocardium, valves, or
electrical conduction system
• Valvular dysFX
• In cardiogenic shock,
there is NOT an issue
with a loss of blood
volume.
• Blood volume is
normal.
• However, bc the heart is
not FX properly…blood
volume starts to back
up:
• Causes congestion in
the lungs & the right

71. CARDIOGENIC SHOCK:
PATHO. & HEMODYNAMICS
• Heart is unable to provide adequate SV and CO/CI
• ↓ SV = ↓ CO = ↓ TISSUE PERFUSION
SV: amt/ of blood pumped out of the heart with each beat… 65-135 ml)
• ↑ SVR
• Compensatory mechanisms (catecholamine release)
• ↑ PAOP (volume in the left ventricle at end of filling time)
• Distention of ventricle
• Transmits to pulmonary bed (↑ PAP and ↑ PAOP)
• JVD (backing all the way up into right side), peripheral
edema, systemic effects.
• Oxygen supply does not meet demand
• End-organ failure

73. ↑ HR
↑ RR
↑ RAP, PAP, PAOP
↑ SVR
CARDIOGENIC SHOCK:
CLINICAL PRESENTATION
↓ BP
↓ CO / CI
↓ SvO2
↓ urine output
• LV failure  RV failure
• Dysrhythmias
• Chest pain
• Oliguria (↓ kidney perfusion)
• Orthostatic hypotension
• Rapid, thready pulse
• Cool, pale skin

74. ↑ PAOP/PAWP (>18 mmHg):
• Normal 8-12 mmHg
• Swan-Ganz catheter is inserted through the right side of the heart &
wedged in pulmonary artery.
• Balloon is temporarily inflated to measure LEFT ATRIAL FILLING PRESSURE.
• >18 mmHg in cardiogenic shock bc blood is backing up in the heart & lungs
= HIGH PRESSURE IN LEFT ATRIUM.
↑ CVP/ RAP:
• Catheter used to measure the pressure in the right atrium and SVC.
• Normal: 2-8 mmHg
• Backflow of blood to the right side of the heart (right atrium into venous
circulation) leads to VENOUS CONGESTION = ↑ CVP.

75. PATHOPHYSIOLOGY OF
CARDIOGENIC SHOCK

77. CARDIOGENIC SHOCK—
DIAGNOSTICS
• CBC—assess Hgb / Hct levels
• EKG –assess area of heart being effected
• ABG –to correct imbalances
• Type and cross-match
• Blood chemistry (electrolytes)
-Hypokalemia: dysrhythmias
-Hyperkalemia: Peaked T-waves,indicates renal failure.
• Coronary angiography—assess obstructions in coronary
arteries, do they need a stent to inc. perfusion to
myocardium?
• Echocardiogram—structures / blood flow / valve FX /
myocardial contractility / size of chambers / estimates EF
• Nuclear scans

78. CARDIOGENIC SHOCK—
NURSING INT.
• HOB elevated –reduce afterload
• Bedrest: ↓ cardiac demand
• Supplemental O2: ↓ cardiac workload by reducing tissue demands, maintain oxygenation
due to pulmonary edema
• IV fluids (used with caution) – optimize preload
• Inotropic agents:↓ afterload & improves myocardial contractility = ↑SV, ↑CO
• Diuretics: ↓ pulmonary congestion & FVO.
• Use torsemide for pts who are insensitive to Lasix.
• Pain medication (morphine)  vasodilation
DO NOT PUT IN TRENDELENBURG… due to ↑ pulmonary congestion.
• This ↑ resistance for the heart to beat against (uphill)
• Will worsen tissue perfusion and pulmonary edema.

79. DIURETICS: cardiogenic shock doesn’t have a ↓ in blood volume. (same with neurogenic shock)
• Fluid backs up into lungs from an injured heart that is failing to pump blood forward.
• Furosemide (K+ wasting, monitor for hypokalemia): HELPS REMOVE EXCESS FLUID.
• ↓ preload = ↓ workload of heart
• Monitor for FVD and worsening hypotension
VASOPRESSORS: cause vasoconstriction = ↑ preload (venous return) = ↑ SV & CO
• Norepinephrine: ↑ tissue perfusion by ↑ BP
- Doesn’t cause tachydysrhythmias.
• Dobutamine: ↑ contractility & CO
- Can cause vasodilation  worsening hypotension
• Dopamine: ↑ contractility / BP / MAP
- Monitor for tachydysrhythmias

80. VASODILATORS: ↓ preload / afterload = ↑ SV = ↑ CO
• ↓ workload of heart by dilating the coronary arteries.
• CAN CAUSE HYPOTENSION!!!  MONITOR BP CLOSELY!
• May not be used if the pt is severely hypotensive
• Nitroglycerin or Sodium Nitroprusside
IV FLUIDS: used with EXTREME CAUTION r/t pulmonary edema!!!
• Normal saline (if even used)
• A fluid challenge is majorly used for the other types of shock when blood volume is the issue…
…remember in cardiogenic shock blood volume is NOT the issue.
Heart is a weak pump!! IABP for mechanical support

81. CARDIOGENIC SHOCK—
NURSING INT.
High cardiac markers:
• ↑ troponin: released if there is injury to heart cells.
• ↑ BNP: released by the cells that make up the ventricles when they stretch due to high BV.
• Pulmonary edema on chest x-ray
• Echocardiogram will show a low E.F.
• Acid-base levels will demonstrate acidosis
• Serum lactate >4 mmol/L
• Cells switch from aerobic  anaerobic metabolism, which will produce lactic acid.
• pH <7.35
• ↑ lactic acid = ↓ O2 perfusion

82. Intra-aortic balloon pump (IABP):
• Mechanical device used to ↓ myocardial
oxygen demand while ↑ CO.
• ↑ CO = ↑ coronary blood flow and
myocardial oxygen delivery.
• Used in cardiogenic & other shock states.
↓ workload of heart
↓ afterload
↓ myocardial oxygen consumption
↑ CO
↑ coronary artery perfusion
INFLATES during diastole:
displaces / pushes blood out to coronary arteries.
DEFLATES during systole:
helps empty coronary arteries

83. OBSTRUCTIVE SHOCK:
• Blockage (physical obstruction) of circulation
prevents venous return.
↓ preload (venous return) = ↓ CO
• No ↓ in intravascular volume or vasodilation
of the intravascular space.
• ↓ CO from a drop in preload
(rather than myocardial dysfunction).
• Impaired venous return because of high
pressure surrounding right atrium.
• Need to alleviate or repair the obstruction.
Mostly surgical interventions.
Examples:
- P.E.
- Dissecting aortic aneurysm
- Atrial tumor
- Pericardial tamponade 
creates pressure around heart
- Tension pneumothorax 
displaces great vessels,
tracheal shift, ↑ ITP = ↓ CO
- Ruptured diaphragm with
evisceration of contents into
the abdominal cavity:
**will hear bowel sounds
in the chest.

85. ↑ HR
↑ or normal RAP, PAP, PAOP
↑ PVR and SVR
↓ BP
↓ CO / CI
↓ SvO2
↓ urine output
↓ LOC
• Dyspnea
• Dysrhythmias
• Chest pain
• Oliguria (↓ kidney perfusion)
• Cool, pale skin
• JVD
OBSTRUCTIVE SHOCK:
CLINICAL PRESENTATION

86. OBSTRUCTIVE SHOCK:
CLINICAL PRESENTATION
CARDIAC TAMPONADE:
• Muffled heart sounds
• Pulsus paradoxus (↓ SBP >10 mmHg during inspiration)
• Tx: pericardiocentesis
TENSION PNEUMOTHORAX:
• Diminished / absent breath sounds on affected side
• Tracheal shifting away from affected side.
• TX: Emergency decompression: chest tube, thoracentesis

87. P.E.
• Right ventricular failure
• SOB
• Hemoptysis
• TX: fibrinolytics & anticoagulants
AORTIC DISSECTION:
• Ripping chest pain
• Pulse difference btwn left & right side
• Widened mediastinum
OBSTRUCTIVE SHOCK:
CLINICAL PRESENTATION

88. DISTRIBUTIVE / VASOGENIC SHOCK:
Septic, Neurogenic, Anaphylactic:
• Systemic vasodilation = ↓ SVR
• Maldistribution of blood flow / intravascular volume
• Loss of intravascular volume from ↑ capillary permeability and ↓ vascular tone
Massive vasodilation = larger vascular capacity = RELATIVE HYPOVOLEMIA =
↓ preload = ↓ CVP, ↓ PAOP = ↓ CO
• Major goal: stop the cause of vasodilation & return the circulating volume to the intravascular
space to improve tissue perfusion.
• FLUID RESUS. FIRST…THEN VASOPRESSORS (want vessels to constrict to ↑ tissue perfusion)

89. PATHOPHYSIOLOGY OF
CIRCULATORY SHOCK

90. Loss of sympathetic vasoconstrictor tone in
the vascular smooth muscle
• Impaired autonomic function
• Body unable to use compensatory
mechanisms (increasing HR) r/t a
sympathetic blockade and dominance of
the PSNS.
Bradycardia  ONLY SHOCK
STATE WITH BRADYCARDIA.
• ↓ preload (venous return) = ↓ SV and CO
NEUROGENIC SHOCK:

92. CAUSES: Disease / injury to the spinal cord  an interruption of impulses from the SNS.
• SCI at or above T6
• General or spinal anesthesia, epidural block
• Drugs that cause CNS depression: barbiturates, phenothiazines, etc.
• Severe pain
• Hypoglycemia
FIRST-LINE TX:
• Fluid replacement (monitor carefully)
• Maintain MAP >65: higher than other shock states bc we really want to ↑ cerebral perfusion
• Epi/ N.E. –stimulate SNS to ↑ HR & BP through vasoconstriction
NEUROGENIC SHOCK:

93. • Bradycardia with hypotension
• Warm, dry, flushed skin due to lack
of vascular tone  vasodilation
• Hypothermia due to impaired
thermoregulation (damaged
hypothalamus)
NEUROGENIC SHOCK:
CLINICAL PRESENTATION
↓ HR
↓ BP
↓ temp.
↓ CO/CI
↓ RAP, PAP, PAOP
↓ SVR
↓ SvO2
↓ urine output

94. • Immobilization of spinal injuries (backboard, cervical collar)
• Maintain MAP and adequate HR
• IV fluids for hypotension
• Vasopressors (only after volume replaced)
• Slow rewarming to prevent further vasodilation  EVEN LOWER BP.
• VTE prophylaxis
NEUROGENIC SHOCK:
NURSING INT.

95. ANAPHYLACTIC SHOCK:
Acute / potentially life-threatening massive allergic reaction:
• Sensitized person is exposed to an antigen.
• Reaction causes direct damage to the vascular wall.
• Cells throughout the body release vasoactive mediators (histamines &
prostaglandins) that trigger a systemic response.
↑ capillary permeability = mvmt of fluid into the interstitial space =
RELATIVE HYPOVOLEMIA
• Vasodilation = ↓ BP = ↓ CO = hypoperfusion
• Bronchospasms may occur from release of chemical mediators

96. ↑ HR
↑ IgE
• Dysrhythmias
• Chest pain
• Tachypnea, dyspnea
• Flushed, warm-hot skin
• Oliguria
• Restless, ALOC
• Seizures
• Cough, stridor, wheezing, dysphagia
• Urticaria, angioedema
• N/V/D, abdominal cramps
↓ BP
↓ CO/CI
↓ RAP, PAP, PAOP
↓ SVR
↓ SvO2
↓ urine output

97. Signs and symptoms:
• Bronchospasm
• Laryngeal edema, stridor, wheezing
• Rash, urticaria, angioedema
• Flushed skin
• Generalized edema (r/t ↑ capillary
permeability & fluid shifts)
Hemodynamics:
• ↓ BP (vasodilation) = ↓ CO
• Compensatory ↑ in HR (to maintain CO)
• ↓ SVR due to ↓ CO
TX: EPINEPHRINE—
• Reverses symptoms of anaphylaxis.
• Reverses vasodilation, ↑ BP
• Reduces edema
• Dilates bronchioles
Positive inotropic effect:
• ↑ contractility of myocardium
• inhibits further mediator response
ANAPHYLACTIC SHOCK:

98. ANAPHYLACTIC SHOCK:
• Epi
• Benadryl
• Steroids (↓ inflammation) –
solumedrol, methylprednisone
• PPIs—histamine blockers &
combat stress ulcers from
steroids

99. SEPTIC SHOCK
• Most common type of
circulatory shock.
• 750,000 cases of
sepsis/septic shock per year
• Incidence is on the rise.
• 30 % mortality rate
• Nosocomial infection
• Critically ill pts at high risk
INCREASING INCIDENCE R/T…
• Elderly
• Immunocompromised pts
• Comorbidities
• More extensive utilization of long-
& short-term invasive devices
(catheters, indwelling devices,
central lines)
• Resistant organisms

100. SEPTIC SHOCK
• Microorganism invades the body
• Triggers immune response  activation of
biochemical inflammatory mediators
• Inflammation = ↑ capillary permeability 
fluid seeping from the capillaries
• Vasodilation & ↓ BP = inadequate perfusion =
↓ O2 and nutrients to the cells  MODS

101. WARM STAGE:
Hyperdynamic / Progressive
• ↑ CO
• ↑ HR
• ↑ RR
• Systemic vasodilation
• Hyperthermia / febrile / flushed
• Mental Status changes
• U/O normal or ↓
• GI: N/V/D, hypoactive bowel sounds
COLD STAGE:
Hypodynamic / Irreversible
• Low CO
• Rapid HR/RR
• Vasoconstriction, hypoTN (↓BP)
• Skin cool and pale
• ↓ temp.
• Oliguria (<400cc/day)  Anuria
• MSOF: can lead to cardiogenic shock!!!
-The more organs that begin to fail, the
higher the morbidity/mortality rate.
TWO PHASES OF SEPSIS:

104. SEPTIC SHOCK:
ASSESSMENT
PULMONARY:
• Respiratory failure  may require
mechanical ventilation
• ↓ O2 sats (SaO2)
• Breath sounds:
• crackles and wheezes r/t
pulmonary congestion.
• Assess pt response to mechanical
ventilation & ventilator changes.
• ABGs
CARDIOVASCULAR:
• Persistent hypoTN: SBP <90 or
dropped 40 from baseline SBP)
• Pale / Cool / clammy skin
• ↓ capillary refill
• ↑ CO
• ↓ SVR
Progressive sepsis:
• ↓ CO, ↑ CVP, ↑ PAP caused
by fluid backup in lungs

105. SEPTIC SHOCK:
ASSESSMENT
HEMATOLOGIC:
• Hypocoagulable state bc using up all
the clotting factors.
• Increased risk bleeding, immature
clotting factors  DIC
• Bruising, petechiae
• Hematuria
• Guaic stool (can have GI bleeding)
• ↓ Hgb/Hct
RENAL:
• Monitor U/O q1-2h
• Assess peripheral edema
• Monitor BUN/Creatinine, GFR
• Is kidney FX improving?
Getting worst?
• Dehydration can cause elevated
BUN / creatinine  IVF
• If creatinine continues to ↑…
there is ↓ in KIDNEY PERFUSION.

106. SEPTIC SHOCK:
ASSESSMENT
GI: FX is interrupted
• Sepsis  hyperglycemia  DKA / HHS
• Elevated bilirubin, glucose and LFT’s from liver dysfx  hematological changes
• NUTRITION IS A PRIORITY enteral preferred over parenteral
• Enteral gives bacteria in gut something to work on.
• Prevents bloodstream infections from GI bacteria.
• Assess residual  should be <300cc
• If ↑ residual… stop tube feeding, then reassess volume.
• If ↓ residual… run tube feeding at a lower rate.
• Consult w dietician… what type of enteral feedings will be best for this pt?

107. SURVIVING
SEPSIS
CAMPAIGN
CARE BUNDLES
WITHIN 3 HRS OF SEVERE SEPSIS…
1. Measure lactate levels to determine the
presence of tissue hypoperfusion.
• Normal: 0.3-0.8 mmol/L
• Lactic acidosis > 4mmol/L
2. Obtain blood cultures x2 BEFORE administration of ABX.
3. Administer broad-spectrum ABX
• Covers both gram+ and gram-
• Adjust ABX when results of culture & sensitivity are in.
4. Give 30 mL/kg crystalloids for hypotension or lactate >4
• 2.5L of fluid usually required

108. SURVIVING
SEPSIS
CAMPAIGN
CARE BUNDLES
WITHIN 6 HRS OF INITIAL S&S OF SEPTIC SHOCK…
5. Administer vasopressors for…
• hypoTN that does not respond to initial fluid resuscitation
to maintain MAP ≥ 65.
• MUST BE GIVEN VIA CENTRAL LINE…caustic to veins.
• Hemodynamic monitoring in place.
6. In the event of persistent arterial hypotension despite
volume resuscitation (septic shock) or initial lactate ≥4
mmol/L (36 mg/dL):
• Measure CVP & central venous O2-sat
7. Remeasure lactate level if initial level was elevated.
• LACTATE SHOWS PERFUSION. Did the fluids help?
Goal of fluid resuscitation:
• CVP >8 mmHg
• central venous O2-sat of >70%
• return of lactate level to normal.

110. • Hand Hygiene
• Aseptic technique
• Identify cause of infection (culture blood, body fluids, devices, catheter tips, etc).
• Remove / replace access devices
• Antibiotic therapy
• Fluid replacement
• Drain abscesses (drains)
• Goal directed therapy
GREATEST RISK: immunocompromised & the elderly
SEPTIC SHOCK: MANAGEMENT

111. QSOFA—HELPS NURSES IDENTIFY
PTS WITH SUSPECTED SEPSIS.
• Quick
• Sepsis-Related
• Organ
• Failure
• Assessment
Measured by 3 Criteria:
• Altered Mental Status
• Increased RR
• Decreased BP

112. QSOFA—HELPS NURSES IDENTIFY
PTS WITH SUSPECTED SEPSIS.

113. • Physiologic imbalance btwn. compensatory inflammatory &
anti-inflammatory response to immune system activation
Three main processes occur:
• Inflammation
• Hypercoagulation
• Impaired fibrinolysis
• Endothelial activation
SEPTIC SHOCK: PATHO.

114. • WBCs release cytokines
• Myocardial depressant factor (MDF) released
causes ↓ E.F.
• ↓ response to fluid resuscitation
• Excessive inflammation and coagulation
damages the endothelium resulting in
capillary leak.
• Fluid shifts into the tissues causing more
inflammation and edema.
• Difficulty maintaining homeostasis
• Resulting organ dysfunction
1) INFLAMMATION

115. • Inflammation initiates coagulation cascade
• Endothelial injury and cytokine release
• Thrombin production
• Further inflammation
• Unregulated thrombin
• Thrombin transforms soluble fibrinogen into fibrin
• Fibrin combines with circulating platelets to form clots
• Clots become microemboli
Fibrin + platelets  clot formation  microemboli clogging
up capillaries  necrosis of digits
2) HYPERCOAGULATION

116. • Epithelial injury in sepsis impairs fibrinolysis.
• The balance between clot removal and clot
development is delayed.
• Alteration of coagulation cascade leads to DIC
3) IMPAIRED FIBRINOLYSIS

120. COMPLICATIONS OF SHOCK
Systemic
Inflammatory
Response Syndrome
(SIRS)
Multisystem Organ
Dysfunction
Syndrome
(MODS)

121. SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)
• Widespread systemic inflammatory response
Associated with diverse disorders:
• Infection
• Trauma
• Shock
• Pancreatitis
• Ischemia
**Most frequently associated with sepsis.
SIRS is a precursor to MOFS

122. SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)
• Normally localized process becomes systemic.
• SIRS is a precursor to MOFS
• Release of mediators:
• ↑ endothelial & capillary permeability
• Fluid shifts into intravascular spaces
• ↓ intravascular volume = RELATIVE
HYPOVOLEMIA

123. SIRS
CRITERIA:
• Tachycardia (HR>90)
• RR >20 or PaCO2 < 32 mmHg
• Hyperthermia (>38 C) or Hypothermia(<36 C)
• WBC count >12,000 or <4,000
• Hypotension
• Hyperglycemia
• ↓ U/O
• Peripheral edema
• Mottling (r/t vasoconstriction in skin)
• Mental status changes
(poor brain perfusion irritability, confusion)
AT RISK POPULATIONS:
• <1 y.o. and >85 y.o.
• Immunocompromised
• Trauma
• Intra-abdominal surgery
• Gastric bypass**
• Pancreatitis
• Cirrhosis
• Meningitis
• Chronic disease (CV, renal, diabetes)
• Cellulitis
• UTI
• Burns

124. DISSEMINATED INTRAVASCULAR
COAGULOPATHY (DIC)
• Acquired Syndrome
• Secondary to another primary illness
• Intravascular stimulation (activation)
of the clotting cascade
• Severe Thrombosis
• Depletion of mature clotting factors 
hemorrhage

125. DIC: PATHO.
• Systemic disorder
• Generation of intravascular fibrin with the consumption of coagulation factors / platelets
• Initiation of coagulation through endothelial or tissue injury
• Clots are formed in the absence of injury, thrombin production is uncontrolled
• Stable clotting cannot form  hemorrhage
• Platelet aggregation
• Consumption of coagulation factors
• Excessive plasmin is produced in response to intravascular thrombi
• Degradation of fibrinogen, fibrin, and other coagulation factors
• Fibrinolysis enhances hemorrhage
Positive D-dimer: evidence that DIC is present

127. DIC: PATHO.

128. CAUSES OF DIC:
• Systemic infections (sepsis)
• SHOCK
• ARDS
• Trauma (burns, crush injuries)
• Hematological disorders
• Oncological disorders
• Obstetric conditions
- Abruptio placentae, amniotic fluid
embolus, retained dead fetus.

129. ACUTE:
• Sepsis
• Massive trauma
• Rapid initiating event
• Rapid change in lab values
• Generalized bleeding
• Petechiae to exsanguination
• Microcirculatory &
macrocirculatory thrombosis
• Hypoperfusion, infarction,
and organ damage
CHRONIC:
• Retained dead fetus
• Cancer
• Large abdominal aneurysm
• Mildly reduced platelets
• Slightly increased D-dimer level
• May have little bleeding or no
symptoms at all.
DIC: ACUTE VS CHRONIC

130. ASSESSMENT OF DIC:
Overt bleeding or oozing:
• Epistaxis
• Hematuria
Signs of platelet deficiency:
• Petechiae
• Ecchymosis / Mottling
• Microhemorrhages
• Broken blood vessels
• Pinpoint red dots
Hypoperfusion of organs:
• Mental status changes
• Infarction of tissues in extremities
• Hemodynamic instability / shock

131. • ↓ platelets
• ↓ fibrinogen
• Prolonged PT, aPTT, thrombin time
• Elevated FDP & FSP
• ↓ in coagulation factors
• ↓ Hgb/Hct
• ↑ d-dimer
DIAGNOSTICS OF DIC:

133. • Correct underlying cause
• Administer blood products
- Platelets
- FFP
- RBCs
- Cryoprecipitate (frozen coag. factors)
- Take 20 mins to thaw.
- Thaw bags back-to-back to prevent delay in care.
• Stop abnormal coagulation
• Prevent injury & bleeding
TREATMENT OF DIC:

134. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)
• Altered organ function
Primary MODS:
• Direct tissue insult…leads to impaired perfusion or ischemia.
Secondary MODS:
• Inadequate tissue perfusion r/t secondary disease process.
• Septic shock
• SIRS
AT RISK PTS:
• advanced age, malnutrition, co-morbidities contribute to development of MODS

135. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)
Maldistribution of blood flow to various organs:
• Impaired tissue perfusion
• Decreased oxygen supply to cells
Organs severely affected / first organs compromised:
• Lungs
• Splanchnic bed
• Liver
• Kidneys
Respiratory failure  kidney failure

137. MODS: CLINICAL
MANIFESTATIONS
• Restlessness / agitation
• Mental status changes
• Tachypnea & hypoxemia
• Tachycardia
• Hypotension
• Petechiae/bleeding
• Jaundice (eyes first, then skin)
• Abdominal distention / rigidity
• Oliguria  anuria
• Hyperglycemia
• Elevated lactic acid  metabolic acidosis, poor tissue perfusion
• Skin breakdown (r/t vasoconstriction. dec. blood flow to skin / poor NX)

138. MODS:
NURSING INT.
• Treat the underlying cause / infection
• Provide adequate oxygenation, may
need mechanical ventilation
• Provide adequate tissue perfusion
• Volume resuscitation
• Placement of a central line
• Support organ function
• Supportive care
• Nutritional support: albumin

140. Cause vasoconstriction = ↑ preload (venous return) & ↑ CO
Alpha Receptor’s
• Blood vessel
• A1: Smooth muscle constriction / vessels
• A2: Smooth muscle constriction / vessels and inhibits neurotransmitters
Beta Receptor’s (1 heart / 2 lungs)
• Cardiac
• B1: ↑ HR / ↑ contractility
• B2: Smooth muscle relaxation / bronchodilator
VASOPRESSORS

142. VASOPRESSORS
NOREPINEPHRINE***
first line TX in most shocks
• Sepsis, cardiogenic shock
• Undifferentiated shock
• 1-30 mcg/min
• ↑ tissue perfusion by ↑ BP
- Doesn’t cause tachydysrhythmias.

143. VASOPRESSIN:
used for shock & with GI bleeds 
DOSAGES ARE ENTIRELY DIFFERENT
• Septic shock (2nd line)
• Vascular , GI smooth muscle & anti-
diuretic effects
• Coronary & splachnic constriction
• 0.01-0.04 units/min (no titration)
VASOPRESSORS

144. VASOPRESSORS
DOPAMINE:
• Cardiogenic shock
• Septic shock (2nd line)
• Increased risk tachy-arrhythmias
• 1-20 mcg/kg/min
• Not always best drug…
↑ contractility / workload of heart
High doses: ↑ SVR and BP

145. PHENYLEPHRINE:
• Neurogenic shock (already
have a reflex bradycardia)
• Septic shock
• 20-300 mcgs/min
• Causes reflex bradycardia
VASOPRESSORS

146. DOBUTAMINE:
• Neurogenic shock
• Cardiogenic shock
• Low output Septic shock
• 2.5-20 mcg’s/kg/min (not titrated
to MAP)
• Risk of tachy-arrhythmias
• ↑ contractility & CO
- Can cause vasodilation 
worsening hypotension
VASOPRESSORS

147. SEPSIS EMERGENCY
• https://www.youtube.com/watch?v=rSIoG_QuMmg
• https://www.youtube.com/watch?v=nw_WIl89LWo
• http://www.sepsisalliance.org/video/video_emergency.swf?width=480&h
eight=330
• http://www.sepsisalliance.org