Shock & Management Concept

Shock and Management Concept

Hardi Darmawan, MD, MPH&TM, FRSTM Dept of Physiology ,Sriwijaya Medical School RK Charitas Hospital Palembang

What is shock?

SHOCK SYNDROME 

Shock is a condition in which the

cardiovascular system fails to perfuse tissues adequately   An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues  Inadequate tissue perfusion can result in:  – generalized cellular hypoxia (starvation)  – widespread impairment of cellular metabolism  – tissue damage organ failure death

Definition Shock is a major critical illness that involves almost every organ system. It is not simply a problem of decreased blood pressure. Rather, it is a problem of inadequate tissue perfusion (Rice,1991)

Inadequate peripheral perfusion leading to failure of tissue oxygenation  may lead to anaerobic metabolism

Definisi • Hipotensi  – Tekanan Darah Sistolik < 90 mmHg  – Tekanan Darah Sistolik berkurang > 40 mmHg

• Hipoperfusi  – Perubahan status mental  – Oliguria  – Asidosis laktat

Diagnosis of Shock  

MAP < 60 Clinical s/s of hypoperfusion of vital organs

PATHOPHYSIOLOGY OF SHOCK SYNDROME Impaired tissue perfusion occurs when an imbalance develops between cellular oxygen supply and cellular oxygen demand.  All types of shock eventually result in impaired tissue perfusion & the development of acute circulatory failure or shock syndrome.

Oxygen transport and utilization

Limited to 180 beats/min before decreased CO due to decreased diastolic filling time

CARDIAC OUTPUT = HR X SV

Increased contractility Sympathetic n. Sympathetic system Catecholamine

Increase EDV via: Venoconstriction A r t e r io io l a r c o n s t r i c t i o n R e n al a l r ea ea b s o r p t i o n

PATHOPHYSIOLOGY OF SHOCK SYNDROME Cells switch from aerobic to anaerobic metabolism lactic acid production Cell function ceases & swells membrane becomes more permeable electrolytes & fluids seep in & out of cell Na+/K+ pump impaired mitochondria damage cell death

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS) Adrenal Response

SNS - Neurohormonal response Stimulated by baroreceptors

Increased heart rate Increased contractility Vasoconstriction (SVR-Afterload) Increased Preload

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS) Adrenal Response SNS - Hormonal: Renin-angiotension system

Decrease renal perfusion angiotension I Releases renin potent vasoconstriction & angiotension II releases aldosterone adrenal cortex sodium & water retention

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS) Adrenal Response SNS - Hormonal: Antidiuretic Hormone  Osmoreceptors  ADH

in hypothalamus stimulated

released by Posterior pituitary gland

Vasopressor effect to increase BP  Acts on renal tubules to retain water

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS) Adrenal Response

SNS - Hormonal:  Adrenal Cortex  Anterior

pituitary releases adrenocorticotropic hormone (ACTH)

 Stimulates

adrenal Cx to release glucorticoids

 Blood

sugar increases to meet increased metabolic needs

Failure of Compensat Compensatory ory Response

Decreased blood flow to the tissues causes cellular hypoxia metabolism begins  Anaerobic metabolism Cell swelling, mitochondrial disruption, and eventual cell death If Low Perfusion States persists: IRREVERSIBLE IRREVERSIB LE

DEATH IMMINENT!!

Dampak Syok Hypovolaemia and Shock decreased blood volume

septic shock

decreased cardiac output decreased oxygen delivery

impaired macro macrocirculation circulation vasoconstriction Inadequate perfusion Erythrocyte aggregation

impaired micro circulation tissue ischemia

organ failure

endotoxin release bowel kidney

Shock 

Microcirculatory Failure Systemic Inflammatory Response

Reduced GI Perfusion Mucosal Ischaemia Compromised Mucosal Integrity

Translocation Impaired Gut Barrier Function

Perfusi normal



Pompa jantung



 Volume sirkulasi



Tahanan pembuluh darah perifer

Pathophysiological causes of shock. Reduced Cardiac Output

pump problem

(Cardiogenic Ischaemic)

Reduced fluid Intravascular volume problem

(Hypovolaemi c)

Reduced Vascular Resistance

(Neurogenic Septic  Anaphylactic)

pipe problem

 After about an hour most patients will demonstrate a dysfunction of all components and it may be difficult to identify the original cause.

CLASSIFICATIONS OF SHOCK • •

•

Cardiogenic Hypovolemic Distributive   

•

Obstructive    

•

sepsis, anaphylaxis, and neurogenic (spinal or epidural anaesthesia, and spinal cord injury). pulmonary embolism, dissecting aortic aneurysm, pericardial tamponade and tension pneumothorax

Combined

Dissecting Throrecic  Aortic Aneurysm

Pulmonary Embolism

Pulmonary Emboli

Tamponade

Stages of Shock 

Initial stage - tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building



Compensatory stage - R eversible. SNS activated by low CO, attempting to compensate for the decrease tissue perfusion.



Progressive stage - Failing compensatory mechanisms: profound vasoconstriction from the SNS Lactic acid production is high



ISCHEMIA metabolic acidosis

Irreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur

DEATH IS IMMINENT!!!!

Pathophysiology Systemic Level Net results of cellular shock: systemic lactic acidosis decreased myocardial contractility decreased vascular tone decrease blood pressure, preload, and cardiac output

Tanda dan gejala syok Sistem Kardiovaskuler  Gangguan sirkulasi  Pucat, dingin, sianosis   Vena perifer kolaps  Nadi cepat dan halus  Tekanan darah rendah – kurang bisa  jadi pegangan   Vena jugularis – penting.  CVP

Tanda dan gejala syok 

Sistem Respirasi  Nafas cepat dan dangkal



Sistem susunan saraf pusat  Perubahan mental / kesadaran



Sistem saluran cerna  Mual dan muntah



Sistem saluran kencing  Produksi urin < ½ cc/kg/jam

Clinical Presentation: Generalized Shock

Mental status: (LOC)   restless, irritable, apprehensive  unresponsive, painful stimuli only

Decreased Urine output

Shock Syndromes Hypovolemic Shock  –blood VOLUME problem  Cardiogenic Shock  –blood PUMP problem 



Distributive Shock  [septic;anaphylactic;neurogenic]

 blood

VESSEL problem

Hypovolemic Shock

Loss of circulating volume “Empty tank ” decrease tissue perfusion general shock response ETIOLOGY:

 –Internal or External fluid loss

 – Intracellular and extracellular compartments 

Most common causes: Hemorrhage Dehydration

Hypovolemik Shock

 A 25 year old woman was admitted in the ER She had given birth 2 hours ago helped by “dukun” 

Hypovolemic Shock: External loss of fluid 

Fluid loss: Dehydration

– Nausea & vomiting, diarrhea, massive

diuresis, extensive burns



Blood loss:

– trauma: blunt and penetrating  – BLOOD

YOU SEE

 – BLOOD YOU DON’T SEE

BP 60, pulse just palpable, over 160 per minute Cold clammy skin, unconscious Multiple iv line were inserted and hemodilution started

Hypovolemic Shock:

Internal fluid loss 

Loss of Intravascular integrity



Increased capillary membrane permeability



Decreased Colloidal Osmotic Pressure (third spacing)

Pathophysiology of Hypovolemic Shock Decreased intravascular volume leads to….  Decreased venous return (Preload, RAP) leads to...  Decreased ventricular filling (Preload, PAWP) leads to….  Decreased stroke volume (HR, Preload, &  Afterload) leads to …..  Decreased CO leads to...(Compensatory mechanisms)  Inadequate tissue perfusion!!!!

 Assessment & Management S/S vary depending on severity of fluid loss: 15%[750ml]- compensatory

mechanism

maintains CO 15-30% [750-1500ml- Hypoxemia, decreased BP & UOP 30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis 40-50% - refactory stage:

loss of volume= death

On arrival

After infusion

Guidelines for the clinical use of red cell transfusions British Journal of Hematology 2001, 113, p24-31









15% loss (750 ml)  – crystalloids, no transfusion 15-30% loss (800-1500 ml)  – crystalloids, colloids, no transfusions 30-40% loss (1500-2000 ml)  – crystalloids, colloids, probably transfusion > 40% loss (> 2000 ml)  – crystalloids, colloids, requires transfusion

Clinical Presentation Hypovolemic Shock      

Tachycardia and tachypnea Weak, thready pulses Hypotension Skin cool & clammy Mental status changes Decreased urine output: dark & concentrated

Hypovolemic Shock: Hemodynamic Changes Correlate with volume loss    

Low CO Decreased RAP ( Preload) Decreased PAD, PAWP Increased SVR (Afterload)

Initial Management Hypovolemic Shock Management goal: Restore circulating volume, tissue perfusion, & correct cause: 

Early Recognition- Do not relay on BP!

(30% fld loss) Control hemorrhage  Restore circulating volume  Optimize oxygen delivery  Vasoconstrictor if BP still low after volume loading 

Penanganan Syok Hipovolemik •

•

Mengembalikan volume intravaskuler  – 

Tekanan Darah

 – 

Nadi

 – 

Perfusi organ

Pilihan cairan  – 

Kristaloid

 – 

Koloid

 – 

PRC

American Soc of Anesthesiologists 1996

1

Hemorrhage 1. Loss of IVF 1. Poor sluggish perfusion 2. Increasing pulse rate 3. Decreasing BP 2. Partially compensated by ISF (transcapillary refill)

2

Ringer Lactate Ringer Acetate NaCl 0.9%

Crystalloids for hemorrhage 1. Rapid Infusion to normalize IVF 2. After IVF stabilized, infusion is intended for ISF 3. Volume required thus 2-4x initially lost IVF

1

2

Pulmonary Edema Neurogenic

Treatment 

Impaired perfusion secondary to reduced volume  restore volume  Restoration of circulating volume can be achieved by the infusion of 3 mL of balanced electrolyte solution for each milliliter of blood lost.  Fluids are infused through two largebore intravenous lines

Treatment  Administration of supplemental oxygen  Control bleeding  Foley catheter to monitor renal function 

 establishment of urine output at approximately 50 cc/hr for the adult

Penanganan Syok Hipovolemik 

Pasang jalur IV satu/lebih no. 18 / 16



Infus cepat Kristaloid / kombinasi+ koloid



Bila perdarahan, ambil contoh darah



Bila vena sudah terisi, peningkatan isi nadi dan tekanan darah, infus lambatkan



Jangan kelebihan cairan

Cardiogenic Shock DEFINISI 

Simply stated, cardiogenic shock is lack of perfusion from pump failure.



Cardiogenic

shock

is

related

to

the

inability of the myocardium to produce sufficient

flow

and/or

pressure

maintain adequate tissue perfusion.

to

Cardiogenic Shock 









The impaired ability of the heart to pump blood Pump failure of the right or left ventricle Most common cause is LV MI (Anterior) Occurs when > 40% of ventricular mass damage Mortality rate of 80 % or >

Etiologies of Cardiogenic Shock I. Ischemic heart disease  A. Acute myocardial infarction, usually anteroseptal B. Ventricular septal defect C. Papillary muscle rupture D. Ventricular aneurysm

II. Valvular heart disease  A. Acute mitral or aortic insufficiency B. Severe aortic stenosis

Etiologies of Cardiogenic Shock III. Arrhythmias  A. Supraventricular B.  Ventricular IV.Trauma  A. Tension pneumothorax B. Pericardial tamponade, may include nontraumatic causes C. Cardiac contusion

Cardiogenic Shock: Pathophysiology Impaired pumping ability of LV leads to…  Decreased stroke volume leads to…..  Decreased CO leads to …..  Decreased BP leads to…..  Compensatory mechanism which may lead to …  Decreased tissue perfusion !!!!

Cardiogenic Shock: Pathophysiology Impaired pumping ability of LV leads to…  Inadequate systolic emptying leads to ...   Left ventricular filling pressures (preload) leads to...  Left atrial pressures leads to ….  Pulmonary capillary pressure leads to …  Pulmonary interstitial & intraalveolar

Diagnosa Syok Kardiogenik • Cardiac Output berkurang • LV filling pressure meningkat • SVR meningkat

Clinical Presentation Cardiogenic Shock 





Similar catecholamine compensation changes in generalized shock & hypovolemic shock May not show typical tachycardic response if on Beta blockers, in heart block, or if bradycardic in response to nodal tissue ischemia Mean arterial pressure below 70 mmHg compromises coronary perfusion  – (MAP = SBP + (2) DBP/3)

Cardiogenic Shock: Clinical Presentation  Abnormal heart sounds

  

Murmurs Pathologic S3 (ventricular gallop) Pathologic S4 (atrial gallop)

Clinical Presentation Cardiogenic Shock Pericardial

tamponade

 – muffled heart tones, elevated neck veins Tension

pneumothorax

 – JVD, tracheal deviation, decreased or absent unilateral breath sounds, and chest hyperresonance on affected side

CLINICAL ASSESSMENT 

    

Pulmonary & Peripheral Edema JVD CO Hypotension Tachypnea, Crackles



  PaO2   UOP   LOC



Hemodynamic changes:

 

PCWP,PAP,RAP & SVR

COLLABORATIVE MANAGEMENT

Goal of management   

Treat Reversible Causes Protect ischemic myocardium Improve tissue perfusion

Treatment is aimed at 



Early assessment & treatment!!! Optimizing pump by:  – Increasing myocardial O2 delivery  – Maximizing CO  – Decreasing LV workload (Afterload)

COLLABORATIVE MANAGEMENT Limiting/reducing myocardial damage during Myocardial Infarction:  Increased pumping action & decrease workload of the heart



 – Inotropic agents  – Vasoactive drugs  – Intra-aortic balloon pump  – Cautious administration of fluids  – Transplantation Consider thrombolytics, angioplasty in specific cases

Management Cardiogenic Shock OPTIMIZING PUMP FUNCTION:  – Pulmonary artery monitoring is a necessity !!  – Aggressive airway management: Mechanical  Ventilation  – Judicious fluid management  – Vasoactive agents  Dobutamine  Dopamine

Management Cardiogenic Shock OPTIMIZING PUMP FUNCTION (CONT.):  – Morphine as needed (Decreases preload, anxiety)  – Cautious use of diuretics in CHF  – Vasodilators as needed for afterload reduction  – Short acting beta blocker, esmolol, for refractory tachycardia

Hemodynamic Goals of Cardiogenic Shock Optimized Cardiac function involves cautious use of combined fluids, diuretics, inotropes, vasopressors, and vasodilators to : Maintain adequate filling pressures (LVEDP 14 to 18 mmHg) Decrease Afterload (SVR 800-1400) Increase contractility Optimize CO/CI

Treatment of Cardiogenic Shock Determinants of Myocardial Oxygen Consumption I.

Heart rate

II.

Contractility

III.

Wall tension, preload

IV.

 Afterload

Treatment 

Cardiogenic shock cannot be managed appropriately without the ability to measure right and left ventricular filling pressures, cardiac index, and arterial blood pressure or the ability to calculate oxygen delivery, oxygen consumption, and pulmonary and systemic vascular resistance. The pulmonary artery catheter,therefore, is mandatory.

Treatment 

Broadly based on four methods (a) increasing contractility (b) altering preload and afterload (c) providing mechanical support (d) controlling arrhythmias.

Treatment 

Increasing Contractility  The three drugs commonly used to increase cardiac contractility are dobutamine, dopamine, noradrenalin and isoproterenol.



Reducing Preload and Afterload  Diuretics may be used as an adjuvant in the treatment of cardiogenic shock but not as a primary agent.  vasodilator therapy may be added to reduce preload and afterload, thereby enhancing cardiac output and reducing myocardial oxygen needs

Treatment 

Mechanical Interventions  tension pneumothorax, relief of tension in the chest cavity  pericardiocentesis in the case of pericardial tamponade  intraaortic balloon pump

Treatment Common Drugs for Arrhythmias 

Supraventricular tachycardia  Digitalis   Verapamil  Propanolol  Procainamide  Quinidine



 Ventricular ectopy  Lidocaine  Procainamide  Bretylium  Quinidine

DISTRIBUTIVE SHOCK  

 

Maldistribution of blood to the tissues.  Acute vasodilation without concommitant increase in intravascular volume. Inadequate tissue perfusion. This type of shock is seen in :  sepsis,  anaphylaxis, and  neurogenic (spinal or epidural anaesthesia, and spinal cord injury).

Mechanism of distributive shock

Sepsis

 Anaphylaxis

Neurogenic

Septic Shock DEFINISI  Result of the systemic effects of infection, primarily with bacterial or fungal organisms  inadequate oxygen delivery  supernormal oxygen demand by the increased metabolism of septic cells  metabolic derangement of cellular metabolism such that cells cannot utilize oxygen

Pathophysiology Early Septic Shock (Warm Shock)  low systolic blood pressure  a relative normal pulse pressure and stroke volume  normal or high cardiac output  Because these patients tend to be vasodilated and have a low systemic vascular resistance, the skin is usually warm (or even flushed) and dry. (a "relative" hypovolemia)

Pathophysiology Early Septic Shock (Warm Shock)  Tachycardia and tachypnea   Arterial blood gases usually reveal a moderate respiratory alkalosis  Lactate levels are usually normal or only mildly increased initially

Pathophysiology Late Septic Shock (Cold Shock)

 Impaired organ function  intravascular fluid retention  depletion of the functional extracellular fluid volume  Cardiac index usually falls below normal  Lactate levels begin to rise rapidly  bicarbonate levels fall

Pathophysiology Late Septic Shock (Cold Shock)  pH becomes increasingly acidotic  The skin becomes cold, clammy, mottled, and cyanotic  Oliguria and depressed mental status are common accompaniments of severe sepsis.

Diagnosa Syok Distributif • Cardiac Output normal atau meningkat • LV filling pressure normal atau rendah • SVR berkurang

Gambaran Hemodinamik Syok Jenis Syok

PAOP

Cardiac Output

Kardiogenik Hipovolemik Distributif

/ nl

Obstruktif  Tamponade Jantung  Emboli Paru

/ nl

/ nl /

SVR

Hipotensi •

Biasanya (tidak selalu) cardiac output berkurang, kecuali Sepsis berat

•

Tidak selalu berarti syok

•

Hipertensi bisa CO rendah dan hipoperfusi organ (Gagal Jantung)

•

Penting pemeriksaan fisik

PRINCIPLES OF MANAGEMENT  







identify cause establish adequate ventilation and oxygenation restore optimum intravascular volume maintain adequate cardiac output and renal perfusion maintain optimum internal metabolic environment

Penanggulangan Syok 

Prinsip dasar  Meningkatkan O2 delivery  Cara 

resusitasi cairan



meningkatkan kontraktilitas jantung



meningkatkan SVR

 Memperbaiki kelainan irama  Optimalisasi O2 content darah  Pasang kateter urin The goal of all treatment is to maintain adequate tissue perfusion and treat the underlying cause

Penanganan Syok Distributif Syok Septik I.

II.

 Correct primary process  A.

Antibiotics

B.

Drainage

Resuscitation  A.

Ventilatory support and 02, as needed

B.

Fluids

C.

Inotropes

D.

Vasodilators or vasopressors

Resuscitation 

increase vascular volume

 crystalloid solutions are preferred for raising intravascular volume 

severe acidosis may impair cardiac function if the arterial pH is < 7. 1, bicarbonate may be required.



Dopamine in doses of 5 to 15 ug/kg/min seems ideal for improving myocardial contractility and cardiac patients.

output

in

hypotensive

vasodilated

Penanganan Syok Distributif Syok Anafilaktik  – Epinephrine SQ  – Resusitasi cairan  – Epinephrine IV

Terapi Cairan • Mengganti volume intravaskuler • Menentukan status volume cairan pasien  –  Vena leher  –  Auskultasi paru  – CVP

Resusitasi Cairan • Koreksi hipotensi • Turunkan HR • Koreksi hipoperfusi  – Oliguria  – Perubahan status mental  –  Asidosis laktat

• Pantau perburukkan oksigenasi

Prioritas dalam Terapi Cairan 

EMERJENSI :   VOLUME INTRAVASKULAR





CURAH JANTUNG



PERFUSI ORGAN VITAL

SUB-EMERJENSI :  INTERSTITIAL  INTRASEL 

TANDA-TANDA VITAL



PROD. URIN

Jenis Cairan 

Kristaloid  Ringer Asetat / Ringer Laktat  Normal Saline



Koloid  Hetastarch   Albumin 5%



PRC  Meningkatkan kapasitas angkutan O 2



Fresh-frozen plasma  Tidak diindikasikan untuk mengganti volume

KONSEP MEDIS TERAPI CAIRAN

RESUSITASI

- NaCl 3 % - MgSO4 20 % - Mannitol 20 %

RUMATAN

KOREKSI KRISTALOID  ASERING RINGER LAKTAT NORMAL SALINE

KOLOID DEXTRAN- 40

MENGGANTIKAN KEHILANGAN AKUT CAIRAN

ELEKTROLIT KA-EN 1B KA-EN 3A KA-EN 3B KA-EN 4A KA-EN 4B

NUTRISI  AMIPAREN  AMINOVEL- 600 PAN- AMIN G KA-EN MG 3 Martos -10 TRIPAREN I TRIPAREN II

MEMENUHI KEBUTUHAN HARIAN ELEKTROLIT DAN NUTRISI

TREATMENT CONCEPT OF SHOCK ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2 Arterial O2 content

Cardiac output

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2

Inotropes

Fluids

Transfuse

Partially dependent on FIO2 and pulmonary status

Cardiogenic Shock

Distributive Shock

Inotropes (Dob,Dop,Adr,Amr) Release tamponade,etc

Vaso pres so r ( NE,PE,A DR,Dop )

Pump = Pipe = Vasc ular

B l o o d P r es s u r e

Heart C a r d i ac O u t p u t x S V R

Obstructive Shock Volume = Blood

Fluids

Hypovolemic Shock

John Collin Warren (1800s)

 “momentary pause in the act of death.” 

Samuel D. Gross (late 19th century)

 “rude unhinging of the machinery of life.” 

Arthur C. Guyton