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Presentation on theme: "SHOCK DOOMSDAY."— Presentation transcript:


2 Vicken Y. Totten Shock lecture Thanks to David Cheng MD
And all who taught me

3 Definition SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand

Cells switch from aerobic to anaerobic metabolism lactic acid production Cell function ceases & cells swell membranes becomes more permeable electrolytes & fluids seep in & out of cell Cells Die in Many Organs Death

5 Stages of shock Compensated /Early Shock
Vasoconstriction  (renin & carotid sinus baroceptor Increase in HR and RR <- sympthatic activation) Normotensive usually <- (aldosterone/ADH Na+/h20 retention) Decompensated / late Shock Cool, clammy , hypotenisve. Vital organ preservation Worsening LOC Continued increase in HR and RR <-----(Chemreceptor respose to metabolic acidosis) Irreversible- HR and RR drop Multi Organ Failure Impending death) Compensated (early shock)-Body recognizes problem and triggers mechanisms to correct BP (autotransfusion) Vasoconstriction < (renin & carotid sinus baroceptor Increase in HR and RR < sympthatic activation) Normotensive usually <------(aldosterone/ADH Na+/h20 retention) Decompensated (late shock)-Compensatory mechanisms can not keep up and begin to fail (bld moves to vital organs) Signs and symptoms more profound (pale cool clammy hypoBP) Worsening LOC Continued increase in HR and RR <-----(Chemreceptor respose to metabolic acidosis) Irreversible-no longer be helped by compensatory mechanisms (HR and RR dropMOFImpending death)

6 Symptoms of Shock Fevers / Rigors (sepsis) SSCP (cardiogenic)
General Symptoms Specific Symptoms Fevers / Rigors (sepsis) SSCP (cardiogenic) Wheezing (anaphylaxis) Trauma pain (hypovolemia) Anxious Dizziness Weakness Faintness Thirsty “I am sick”

7 Early Signs of Shock in Non Complicated Patients
WARM EARLY STAGE / PRESHOCK Need high index of suspicion b/c lack of signs +/- tachycardia +/- orthostatics (HR more sensitive than BP) +/- pulse pressure narrowing +/-restless

8 “Hypoperfusion can be present in the absence of significant hypotension.” (Don’t only relay on BP for diagnosisng shock) -fccs course

9 Signs of Late Shock Hypotension
COLD LATE STAGE Cold, clammy and pale skin Rapid, weak, thready pulse Rapid breathing (blow off CO2 met acidosis) Cyanotic AMS->Coma Anuria

10 End Stage Clinical effects
Cardiovascular Myocardial depression Vasogenic effects Pulmonary ARDS Renal ARF GI Ischemic bowel Hepatic Increased LFT’s, liver failure Hematologic Neutropenia, Thrombocytopenia DIC (Gm- > Gm+) CNS coma

11 Multiple Organ Dysfunction Syndrome
Number of Organs Mortality (%) 0.8 1 6.8 2 26.2 3 48.5 4 68.8 5 83.3 *Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837

12 Circumferential Subendocardial Infarction due to Shock

13 Shock Lung

14 Acute congestion of liver due to shock

15 Acute tubular necrosis of the kidney due to shock

16 Intestinal mucosal hemorrhages due to shock

17 Adrenal gland hemorrhage due to shock

18 Remember History and Physical often limited by patient’s condition
Patient presentation can be variable secondary to Severity of the perfusion defect Underlying cause Prior organ dysfunction Exam should be tailored to be performed quickly with highest yield for uncovering the cause of shock.

19 Components (fluids, pump, pipes)

20 Components: Blood (fluid) Heart (pump) Blood Vessels (pipes)

21 Types of Shock Hypovolemic (fluids) Cardiogenic (pump)
Redistributive (pipes) (septic, neurogenic, anaphylactic)

22 Adequate circulating blood volume depends on 3 components; A minor impairment in one can be compensated for by the other 2 for a limited time. Prolonged or severe impairments will lead to SHOCK.

23 An Approach to Shock – Know this!
BP = SVR x CO BP = blood pressure CO = cardiac output (pump & fluids) SVR = systemic vascular resistance (pipes)

24 If the blood pressure is low, then either the:
An Approach to Shock If the blood pressure is low, then either the: CO is low or SVR is low BOTH

25 Low SVR There are only a few causes of low SVR.
They ALL cause vasodilation: Septic shock Neurogenic (spinal cord injury) shock Anaphylaxis Shock Vasodilator (antihypertensive) Posioning

26 Look at and feel the patient!
How do you assess SVR? Look at and feel the patient! Low SVR has the features: warm !!! pink Bounding pulses hyperdynamic heart (fast and pounding)

27 Cause of shock (low BP) is then:
What if the SVR is high? Pale Poor cap refill (>2 seconds) Cool arms/legs (>2 degree C difference) Thready pulses (narrow pulse pressure (incr DBP)) Cause of shock (low BP) is then: low CO

28 CO = HR x SV What are factors of CO? CO = cardiac output
HR = heart rate SV = stroke volume

29 HR Problems Heart Rate problems are easy to diagnose
Rate: bradycardia versus tachycardia

30 Most difficult to diagnose and manage
Low SV (stroke volume) Most difficult to diagnose and manage

31 Stroke Volume depends on
Preload--is the ventricle full? Hypovolemic Shock Obstructive Shock (ie Tension PTX, Tamponade) Cardiac function SqueezeContractility– can the ventricle contract? Can blood get out?  Valve function: normal? regurgitation? stenosis?

32 Perfusion (blood pressure) depends on:
BP = CO x SVR CO = HR x SV SV = preload & cardiac contractility-valve

33 Components of BP summary

34 Why Monitor? Essential to understanding their disease
Describe the patient’s physiologic status Serial monitoring Facilitates diagnosis and treatment of shock

35 Monitoring clinical shock parameter
Noninvasive: Blood pressure (SBP, MAP) Urine output Heart rate Shock index Invasive: Pulmonary artery catheter: CVP, PAWP, CO, SVR, DO2I, VO2I, SvO2 Arterial catheter: ABP, Serum lactate, Base deficit

36 Diagnosis of Shock MAP < 60 or decrease of 20 from baseline
systolic BP  90  systolic BP > 40 mm Hg from the patient’s baseline pressure Shock index (HR>SBP) Clinical s/s of hypoperfusion of vital organs

37 Mean Arterial Pressure
MAP is the mean perfusion pressure for the tissues Most require a MAP of 60 or greater! Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial tree MAP = (2 x DBP) + SBP 3

38 Pulse Pressure=SBP-DBP
Pulse Pressure=SBP-DBP The difference between the systolic (fxn of ejection fraction) and diastolic pressures (function of SVR and distensibility (elastic recoil) of the aorta Wide Normal mmHg Commonly seen with fever, anemia, exercise and hyperthyroidism AR (aortic regurgitation) is also a cause Narrow May indicate an increase in vascular resistance with decreased stroke volume (ie aortic stenosis or decreased intravascular volume)

39 Invasive Markers Global Markers Regional Markers Base Deficit Lactate
Gastric pH Sublingual CO2

40 Base Deficit Inadequate tissue perfusion leads to tissue acidosis
Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 Normal range +3 to –3 mmol per L Elevated base deficit correlates with the presence and severity of shock

41 Base Deficit Inadequate tissue perfusion leads to tissue acidosis
Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 Normal range +3 to –3 mmol per L Elevated base deficit correlates with the presence and severity of shock

42 Initial Lactate Weil and Afifi. (Circulation 1970)

43 Lactate and Outcomes Adult Patients
A peak blood lactate level of >4.0 mmol/L was identified as a strong independent predictor of mortality and morbidity and suggests that tissue hypoperfusion Demmers Ann Thorac Surg 70:2082-6:2000


45 Gastric Intramucosal pH
Blood flow is not uniformly distributed to all tissue beds Regions with inadequate tissue perfusion may exist while global markers are ‘normal’ Gut mucosa among the first to be affected during shock and the last to be restored to normal Intramucosal pH falls when perfusion becomes inadequate

46 Sublingual capnometry:
A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock hypercarbia is a universal indicator of critically reduced tissue perfusion.

47 Sublingual CO2 Decrease gut perfusion Non-invasive, hand held monitor
Gastric tissue = esophagus = sublingual tissue Non-invasive, hand held monitor Rapid measurement Sensitive marker of decreased blood flow

48 Sublingual capnometry:
A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock P SL CO2 provides a prompt indication of the reversal of tissue hypercarbia when circulatory shock is reversed

49 Direct arterial pressure A-line

50 Pulmonary Artery Catheter
INDICATIONS volume status cardiac status COMPLICATIONS technical anatomic physiologic

51 Swan-Ganz Catheter


53 Correct PA-C Position From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm.

54 Standard Parameters Measured Calculated Blood pressure
Pulmonary A. pressure Heart rate Cardiac Output Stroke volume Wedge pressure CVP Calculated Mean BP Mean PAP Cardiac Index Stroke volume index SVRI LVSWI BSA

55 Why Index? Body habitus and size is individual
“Indexing” to patient with BSA allows for reproducible standard PATIENT A 60 yo male 50 kg CO = 4.0 L/min BSA = 1.86 CI = 2.4 L/min/m2 PATIENT B 60 yo male 150 kg CO = 4.0 L/min BSA = 2.64 CI = 1.5 L/min/m2


57 PA Insertion 20 15 10 5 RA = 5 RV = 22/4 PA 19/10 PAOP(wedge) = 9

58 CVP CVP of SVC at level of right atrium pre-load “assessment”
normal mm Hg

59 PAOP (wedge) End expiration Wedge adjustment with positive pressure
Measured PAOP - ½ PEEP = “real PAOP”

60 Vascular Resistance PULMONARY (PVR) SYSTEMIC (SVR) MAP - CVP
MPAP - PAOP CO PVR = constriction PE, hypoxia SYSTEMIC (SVR) MAP - CVP C0  SVR = vasoconstriction  SVR = vasodilation x 80 x 80 Vascular resistance = change in pressure/blood flow

61 Cardiac Cycle pulmonary Right ventricle Left ventricle systemic MPAP
PVR MPAP pulmonary PCWP RVSW Right ventricle Left ventricle LVSW MAP CVP systemic SVR

62 Swan Ganz interpretation

63 Too Many Numbers

64 Definitions O2 Delivery - volume of gaseous O2 delivered to the LV/min. O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min. consumption > demand = anaerobic metabolism

65 Mixed venous oxygen saturation
Reflects difference between oxygen delivery and consumption Normal – 65-75% Measurement taken from the distal port of a PA catheter

66 SvO2: Low Values (< 60%)
 CO/CI SV/SVI  Hgb  SaO2  O2 consumption

67 SvO2: High Values (> 75%)
Sepsis AV shunts/fistulae

68 Oxycalculations

69 Break Time…

70 Goals of Shock Resuscitation
Restore blood pressure Normalize systemic perfusion Preserve organ function

71 Parameters of Adequate Resuscitation
Urine output ( ml/kg/hr) acceptable renal perfusion Reversal of lactic acidosis (nl. pH) improved perfusion Normal mental status adequate cerebral perfusion

SHOCK: an EMERGENCY !!! Goal RAPIDLY RESTORE TISSUE PERFUSION Recognize it !!! Immediate stabilization: ABC ……. SHOTGUN approach Normalization of BP, pulse, UOP Hemodynamic parameters Restoration of aerobic metabolism, elimination of tissue acidosis, repayment of O2 debt Treat the cause

73 “Shock is a symptom of its cause.”
-fccs course

74 In general, treat the cause...

75 Management Re-assess every 5-15 minutes
ABC’s Maintain airway Decrease work of breathing & Optimize 02 Circulation & Control Hemorrhage includes: Direct pressure Pressure points Fluids & Drugs Must address and treat: PRELOAD AFTERLOAD PUMP Re-assess every 5-15 minutes (the sicker the patient, the shorter the interval

76 Management priorities in hypoperfused states
BP potency: Dopamine...NE…Vasopressin/Phenylephrine When in doubt, try a little more volume

77 Hypovolemia

78 Time Outcomes of same vol. lost over diff. periods of time. Slow losses (III, IV) allow compensations to take effect. Rapid loss (I, II) of same vol. is fatal 5

79 Classes of Hypovolemic Shock

80 Clinical Signs of Acute Hemorrhagic Shock
% Blood loss Clinical Signs < 15 Slightly increased heart rate 15-30 Increased HR, increased DBP (narrow pp), prolonged capillary refill, flat neck veins 30-50 Above findings plus: hypotension, confusion, acidosis, decreased urine output > 50 Refractory hypotension, refractory acidosis, death

81 Hypovolemic Shock Causes hemorrhage vomiting diarrhea dehydration
third-space loss burns Signs  cardiac output  PAOP/CVP  SVR

82 Treatment - Hypovolemic
Reverse hypovolemia & hemorrhage control Crystalloid vs. Colloid 1 L crystalloid  250 ml colloid Watch for fluid overload by reassessing lung sounds 3:1 Rule (3cc crystalloid for 1cc bld loss) Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused Best to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolus Colloids: (ex: albumin) Will increase osmotic pressure, watch for pulm edema Remain in vascular space longer (several hrs) NOT increase survival prbc sooner than later 500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4% Increases oxygen carrying capacity Used with acute hemorrhaging (mntn Hct 24% and Hgb 8g/dL) NOT FOR VOLUME FFP for coagulopathy (all factors) Factor vii PLT for thrombocytopenia Pressors?

83 Resuscitation Transport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial. Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.

84 Role of PASG? Higher mortality rate in penetrating thoracic, cardiac trauma Role undefined in rural, blunt trauma Splinting role

85 Cardiogenic Shock Mech Signs
defect in cardiac function (lost > 40% Fxn) Signs  cardiac output  PAOP/CVP  SVR  left ventricular stroke work (LVSW)

86 Cardiogenic Shock Myocardial failure (MI) Severe Arrhythmia
Severe Valvular dysfunction Reduction in cardiac output: >Decreased oxygen delivery

87 Symptoms of Cardiogenic Shock
Skin: progressive peripheral vasoconstriction results in cool, moist, pale skin with mottling CHF Sx JVD, HJR, APE, pedal edema Heart: Sounds: d/t enlargement and congestion you can hear murmurs or S3 or S4 Pulse: rapid rate and thready/weak pulse BP: decreased BP and MAP UO: decreases early d/t decreased renal perfusion

88 Cardiogenic Shock Assess for: Signs of heart failure
Signs of tamponade Cardiac dysrrhythmia Myocardial infarction Tachycardia Muffled heart sounds or third heart sound Engorged neck veins with hypotension Dyspnea Edema in feet and ankles

89 Coronary Perfusion Pressure
Coronary PP = DBP - PAOP coronary perfusion =  P across coronary a. GOAL - Coronary PP > 50 mm Hg

90 Treatment of Cardiogenic Shock
Increase oxygen supply to the heart Decrease O2 consumption (pain meds/sedation) Increase O2 delivery (Mech vent, reperfusion of the coronary arteries) Maximize the cardiac output Mntn normal rhythm (dysrhythmics, pacing, cardioversion) Diastolic Vasopressors (dopamine, epi, norepi, vasopressin) Improve myocardial contractility--Inotropes dobut and amrinone Decrease the afterload (workload of the LV) IABP LVAD

91 The Failing Heart Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient. Fluids first, then cautious pressors Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure) If inotropes and vasopressors fail, intra-aortic balloon pump & LV assist devices

92 Intra-Aortic Balloon Pump

93 Distributive Shock Types Signs Sepsis Anaphylactic
Acute adrenal insufficiency Neurogenic Signs ± cardiac output  PAOP SVR

94 Anaphylaxis

95 Anaphylactic Shock Rapid onset
Diffuse vasodilation mechanism from histamine & bradykinin Edema from increased capillary permeability Bronchoconstriction

96 Symptoms Onset within seconds and progression to death in minutes
Cutaneous manifestations urticaria, erythema, pruritis, angioedema Respiratory compromise stridor, wheezing, bronchorrhea, resp. distress Circulatory collapse tachycardia, vasodilation, hypotension CNS apprehension->ams->coma

97 Diagnosis History and physical alone make the diagnosis
Lab values serve no role Histamine levels are elevated for about 30 min, tryptase for several hours.

98 Treatment Remove the antigen ABC’s
IV Fluids, O2, cardiac monitor, pulse ox First line Rx: Epinephrine For severe bronchospasm, laryngeal edema, signs of upper airway obstruction, respiratory arrest or shock: IV epi 100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 10 mL of NS, give over 5-10 min) If less severe, can give mL 1:1000 SC

99 Treatment 2nd line: H1 blocker: Diphenhydramine 25-50 mg IV
H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.) Steroids (Methylprednisolone 125 mg IV or Prednisone mg po) Albuterol For patients taking Beta-blockers with refractory hypotension, think about glucagon

100 Septic Shock

101 SEPSIS Systemic Inflammatory Response (SIRS) manifested by two or > of following: Temp > 38 or < 36 centigrade HR > 90 RR > 20 or PaCO2 < 32 WBC > 12,000/cu mm or > 10% Bands (immature wbc)

102 Risk factors of Sepsis Extreme age: <1 and >65 years
Surgical / invasive procedures Malnutrition Chronic illness DM, CRF, Hepatitis Compromised immune status AIDS, immunosuppressives, EtOH, malignancies Drug resistant organisms

103 What is Sepsis? SIRS  Sepsis  Severe Sepsis  Septic Shock
Sepsis is the combination of the Systemic Inflammatory Response Syndrome (SIRS) & a confirmed or presumed infectious etiology. Severe Sepsis: SIRS criteria, source of infection and infection-induced organ dysfunction or hypoperfusion abnormalities (sepsis + lactic acidosis/oliguria/AMS/etc.) Septic Shock: SIRS criteria, source of infection, and hypotension not reversed with fluid resuscitation and associated with organ dysfunction or hypoperfusion abnormalities A long line sepsis trials…but first, what is sepsis? SIRS, or Systemic Inflammatory Response Syndrome, is the overall inflammatory response of a host. We often think that “sepsis” implies that someone is close to death. This isn’t true. But they may be…Someone with sepsis can be as benign as a strep pharyngitis with a fever of 102.2, HR of 125, and WBC=16 or it can be a hypotensive patient with meningococcemia who will die in the next several hours.

104 Septic Shock Bacterial, viral, fungal infection
“Warm shock” is early stage Fever, tachycardia, tachypnoea, leucocytosis, inadequate oxygen extraction (High SvO2, Metabolic acidosis) in infected tissues “Cold shock” is late stage

105 Septic/Inflammatory Shock
Signs: Early– warm w/ vasodilation, often adequate urine output, febrile, tachypneic. Late-- vasoconstriction, hypotension, oliguria, altered mental status. Monitor/findings: Early—hyperglycemia, respiratory alkylosis, hemoconcentration, WBC typically normal or low. Late – Leukocytosis, lactic acidosis Very Late– Disseminated Intravascular Coagulation & Multi-Organ System Failure.

106 Septic Shock TX Prompt volume replacement - fill the tank
Early antibiotic administration - treat the cause If MAP < 60 Dopamine = g/kg/min Norepinephrine = titrate (1-100 g/min)

107 Neurogenic shock

108 Neurogenic Shock Essential derangement: paralysis of the sympathetic chain which controls vascular tone from injury to thoracic or cervical level spinal cord injury. Produces decreased SVR from loss of vascular tone and bradycardia from unopposed parasympathetic input to SA node.

109 Neurogenic (Vasogenic) Shock
Caused by: Spinal cord injury loss of SNS Massive venous pooling & arteriolar dilatation Signs and Symptoms: Hypotension without tachycardia Warm pink skin from cutaneous vasodilation Low BP w/ minimal response to fluids Accompanying Neurologic deficit Spinal shock is not Neurogenic shock Spinal Shock: the temporary loss of spinal reflex activity that occurs below a total or near total spinal cord injury

110 Treatment of Neurogenic Shock
Increase vascular tone and improve CO Increase preload with fluids CVP PAWP Increase vascular tone Vasopressors Maintain heart rate Treat bradycardia if symptomatic Maintain adequate oxygenation Watch with SCI because of the disruption of O2 to the medulla Initiate therapy to prevent DVT Sluggish venous flow will increase risk factors Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4 mg/kg/hr x 23 hours) There are contradicting studies, all of which have flaw The symptoms of neurogenic shock typically last 1-3 weeks

111 Obstructive Shock Causes Signs Treatment Needle decompression
Cardiac Tamponade Tension Pneumothorax Massive Pulmonary Embolus Signs  cardiac output  PAOP/CVP  SVR Treatment Needle decompression Embolectomy / TPA

112 Adrenal Crisis Distributive Shock
Causes Autoimmune adrenalitis Adrenal apoplexy = B hemorrhage or infarct This is suspected when patient is non-responsive to fluids, vasopressors and antibiotics. Electrolytes may reveal hypoNa+ & hyperK+ Steroids may be lifesaving in patient who is unresponsive to fluids-inotropic-vasopressor (hydrocortisone 100mg IV)

113 Vasopressor Agents? Augments contractility, after preload established, thus improving cardiac output. Risk tachycardia and increased myocardial oxygen consumption if used too soon Rationale, increased C.I. improves global perfusion

114 Vasopressors & Inotropic Agents
Norepinephrine Epinephrine Amrinone Dopamine Dobutamine

115 Dopamine Low dose (0.5 - 2 g/kg/min) = dopaminergic
Moderate dose (3-10 g/kg/min) = -effects High dose (> 10 g/kg/min) = -effects SIDE EFFECTS tachycardia > 20 g/kg/min  to norepinephrine

116 Dobutamine -agonist 5 - 20 g/kg/min
potent inotrope, variable chronotrope caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension

117 Norepinephrine Potent -adrenergic vasopressor
Some -adrenergic, inotropic, chronotropic Dose g/min Unproven effect with low-dose dopamine to protect renal and mesenteric flow.

118 Epinephrine - and -adrenergic effects
potent inotrope and chronotrope dose g/min increases myocardial oxygen consumption particularly in coronary heart disease

119 Amrinone Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects increased cardiac stroke output without an increase in cardiac stroke work most often added with dobutamine as a second agent load dose = mg/kg  g/kg/min drip main side-effect - thrombocytopenia

120 vasopressin V1 vascular smooth muscle receptor vasoconstriction
units/min Risk: coronary, mesenteric ischemia, hyponatremia, skin necrosis

121 Calcium Sensitisation by Levosimendan
Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca2+ Clinical trials status Ultimately, the binding of levosimendan to troponin C evokes a stabilising, prolonged conformational change that occurs when calcium binds to troponin C. This is an enhancement of calcium's effects, and it thus increases the force of contraction. Sensitising the filaments to calcium rather than increasing calcium levels means that there is less potential for arrhythmia and increased contractile force with less energy consumption (i.e., myocardial oxygen demand is not increased).

122 Endpoints? ACS / ATLS - restoration of vital signs and evidence of end-organ perfusion Swan-guided resuscitation C.I.  4.5, DO2I  670, VO2I  166 Lactic Acid clearance Gastric pH

123 Shock: “rude unhinging of the machinery of life.”
Don’t forget... Shock: “rude unhinging of the machinery of life.” -Samuel D. Gross, 1872

124 ??????????? For the human speaker

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