Shock & Management Concept

(1)

Shock

and

Management Concept

Hardi Darmawan,

MD, MPH&TM, FRSTMMD, MPH&TM, FRSTM

Dept of Physiology ,Sriwijaya Medical School

RK Charitas Hospital

Palembang

(2)

(3)

(4)

What is shock?

(5)

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

(6)

Definition

Inadequate peripheral perfusion

leading to failure of tissue oxygenation

anaerobic metabolism

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)

(7)

Definisi

• Hipotensi

– Tekanan Darah Sistolik < 90 mmHg

– Tekanan Darah Sistolik berkurang > 40 mmHg

• Hipoperfusi

– Perubahan status mental – Oliguria

(8)

Diagnosis of Shock

 MAP < 60

 Clinical s/s of

hypoperfusion of vital organs

(9)

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.

(10)

Oxygen transport

and utilization

(11)

(12)

CARDIAC OUTPUT = HR X SV

Sympathe

Sympathetic tic n.n.

system

Catecholamine

Increase EDV via:

V e n o c o n s t r i c t i o n V e n o c o n s t r i c t i o n A r t e r i A r t e r io l a r c o no l a r c o ns t r i c t i o ns t r i c t i o n R e n a R e n al r el r ea b s o r pa b s o r pt i o nt i o n Increased Increased contractility contractility Limited to 180 beats/min Limited to 180 beats/min before decreased CO before decreased CO due to decreased due to decreased

diastolic filling time

(13)

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

(14)

COMPENSATORY MECHANISMS:

Sympathetic Nervous System

(SNS)- Adrenal Response

SNS - Neurohormonal response

Stimulated by baroreceptors



Increased heart rate



Increased contractility



Vasoconstriction (SVR-Afterload)

(15)

COMPENSATORY MECHANISMS:

Sympathetic Nervous System

(SNS)- Adrenal Response

SNS - Hormonal:

Renin-angiotension system



Decrease renal perfusion



Releases renin angiotension I



angiotension II potent vasoconstriction &



releases aldosterone adrenal cortex

(16)

COMPENSATORY MECHANISMS:

Sympathetic Nervous System

(SNS)- Adrenal Response

SNS - Hormonal: Antidiuretic Hormone



Osmoreceptors in hypothalamus stimulated



ADH released by Posterior pituitary gland



Vasopressor effect to increase BP

(17)

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

(18)

Failure of

Compensat

ory

Response



Decreased blood flow to the tissues causesDecreased blood flow to the tissues causes

cellular hypoxia



Anaerobic meta Anaerobic metabolism beginsbolism begins



Cell swelling, mitochondrial disruption, andCell swelling, mitochondrial disruption, and

eventual cell death



If Low Perfusion States persists:If Low Perfusion States persists:

IRREVERSIB

(19)

Hypovolaemia and Shock

decreased blood volume

decreased cardiac output

decreased oxygen delivery

impaired

impaired macromacrocirculationcirculation

vasoconstriction vasoconstriction Inadequate perfusion Inadequate perfusion Erythrocyte aggregation Erythrocyte aggregation impaired

impaired micromicro circulationcirculation

tissue ischemia

tissue ischemia organ failureorgan failure

kidney kidney bowel bowel endotoxin endotoxin release release septic shock septic shock

Dampak Syok

(20)

Shock Shock Microcirculatory Microcirculatory Failure Failure Systemic Systemic Inflammatory Inflammatory Response Response Translocation Translocation Impaired Gut Impaired Gut Barrier Function Barrier Function Compromised Compromised Mucosal Integrity Mucosal Integrity Mucosal Mucosal Ischaemia Ischaemia Reduced GI Reduced GI Perfusion Perfusion

(21)

Perfusi normal



Pompa jantung



Volume sirkulasi

(22)

Pathophysiological causes of shock.

Reduced Cardiac Output pump problem (Cardiogenic -Ischaemic) Reduced Intravascular volume fluid problem (Hypovolaemi c) Reduced Vascular Resistance pipe problem (Neurogenic Septic - Anaphylactic)

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

(23)

CLASSIFICATIONS OF SHOCK

• Cardiogenic • Hypovolemic • Distributive  sepsis,  anaphylaxis, and

 neurogenic (spinal or epidural anaesthesia,

and spinal cord injury).

• Obstructive

 pulmonary embolism,

 dissecting aortic aneurysm,  pericardial tamponade and  tension pneumothorax

(24)

Dissecting Throrecic Aortic Aneurysm

(25)

(26)

(27)

(28)

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 ISCHEMIA

Lactic acid production is high metabolic acidosis

 Irreversible or refractory stage - Cellular necrosis

and Multiple Organ Dysfunction Syndrome may occur

(29)

Pathophysiology Systemic

Level

Net results of cellular shock:



systemic lactic acidosis



decreased myocardial contractility



decreased vascular tone



decrease blood pressure, preload,

and cardiac output

(30)

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

(31)



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

(32)

Clinical Presentation:

Generalized Shock



Mental status: (LOC)



restless, irritable, apprehensive



unresponsive, painful stimuli only

(33)

Shock Syndromes



Hypovolemic Shock

–blood VOLUME problem



Cardiogenic Shock

–blood PUMP problem



Distributive Shock

[septic;anaphylactic;neurogenic] 

blood VESSEL problem

(34)

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

(35)

(36)

A 25 year old woman was admitted in the ER

(37)

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}

(38)

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

(39)

Hypovolemic Shock:

Internal fluid loss



Loss of Intravascular integrity



Increased capillary membrane

permeability



Decreased Colloidal Osmotic Pressure

(40)

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)

(41)

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:

(42)

On arrival

(43)

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)

(44)

Clinical Presentation

Hypovolemic Shock



Tachycardia and tachypnea



Weak, thready pulses



Hypotension



Skin cool & clammy



Mental status changes



Decreased urine output: dark &

(45)

Hypovolemic Shock:

Hemodynamic Changes

Correlate with volume loss



Low CO



Decreased RAP ( Preload)



Decreased PAD, PAWP

(46)

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

(47)

Penanganan Syok Hipovolemik

•

Mengembalikan volume intravaskuler

–

Tekanan Darah

–

Nadi

–

Perfusi organ

•

Pilihan cairan

–

Kristaloid

–

Koloid

–

PRC

(48)

(49)

(50)

(51)

(52)

(53)

2

1 Hemorrhage

1. Loss of IVF

1. Poor sluggish perfusion 2. Increasing pulse rate

3. Decreasing BP

2. Partially compensated by ISF (transcapillary refill)

(54)

2

1 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

Ringer Lactate Ringer Acetate NaCl 0.9%

(55)

(56)

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 large-bore intravenous lines

(57)

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

(58)

 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

(59)

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 to maintain adequate tissue perfusion.

(60)

(61)

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

(62)

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

(63)

Etiologies of Cardiogenic Shock

III. Arrhythmias

A.

Supraventricular

B.

Ventricular

IV.Trauma

A.

Tension pneumothorax

B.

Pericardial tamponade, may

include nontraumatic causes

(64)

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 …

(65)

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

(66)

Diagnosa Syok Kardiogenik

• Cardiac Output berkurang

• LV filling pressure meningkat

(67)

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

(68)

Cardiogenic Shock:

Clinical Presentation

Abnormal heart sounds



Murmurs



Pathologic S3 (ventricular gallop)



Pathologic S4 (atrial gallop)

(69)

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

(70)

CLINICAL ASSESSMENT

 Pulmonary & Peripheral Edema  JVD  CO  Hypotension  Tachypnea,  Crackles  PaO2  UOP  LOC  Hemodynamic changes: PCWP,PAP,RAP & SVR

(71)

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)

(72)

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

(73)

Management Cardiogenic

Shock

OPTIMIZING PUMP FUNCTION:

– Pulmonary artery monitoring is a necessity !!

– Aggressive airway management: Mechanical Ventilation

– Judicious fluid management – Vasoactive agents

Dobutamine Dopamine

(74)

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

(75)

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

(76)

Treatment of

Cardiogenic Shock

Determinants of Myocardial

Oxygen Consumption

I. Heart rate II. Contractility

III. Wall tension, preload IV. Afterload

(77)

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.

(78)

Treatment



Broadly based on four methods

(a) increasing contractility

(b) altering preload and afterload (c) providing mechanical support (d) controlling arrhythmias.

(79)

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

(80)

Treatment



Mechanical Interventions



tension pneumothorax, relief of

tension in the chest cavity



pericardiocentesis in the case of

pericardial tamponade

(81)

Treatment

Common Drugs for Arrhythmias



Supraventricular

tachycardia

 Digitalis  Verapamil  Propanolol  Procainamide  Quinidine 

Ventricular ectopy

 Lidocaine  Procainamide  Bretylium  Quinidine

(82)

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

(83)

Mechanism of distributive

(84)

(85)

(86)

(87)

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

(88)

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

(89)

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

(90)

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

(91)

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

(92)

Diagnosa Syok Distributif

• Cardiac Output normal atau meningkat

• LV filling pressure normal atau rendah

• SVR berkurang

(93)

Gambaran Hemodinamik Syok

Jenis Syok PAOP Cardiac_Output SVR Kardiogenik Hipovolemik Distributif / nl / nl / Obstruktif  Tamponade Jantung  Emboli Paru / nl

(94)

Hipotensi

•

Biasanya (tidak selalu) cardiac output

berkurang, kecuali Sepsis berat

•

Tidak selalu berarti syok

•

Hipertensi bisa CO rendah dan

hipoperfusi organ (Gagal Jantung)

(95)

PRINCIPLES OF MANAGEMENT



identify cause



establish adequate ventilation and

oxygenation



restore optimum intravascular

volume



maintain adequate cardiac output

and renal perfusion



maintain optimum internal

(96)

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

(97)

Penanganan Syok Distributif

Syok Septik

I. Correct primary process

A. Antibiotics B. Drainage

II. Resuscitation

A. Ventilatory support and 02, as needed

B. Fluids

C. Inotropes

(98)

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 output in hypotensive vasodilated patients.

(99)

Syok Anafilaktik

– Epinephrine SQ – Resusitasi cairan – Epinephrine IV

(100)

Terapi Cairan

• Mengganti volume intravaskuler • Menentukan status volume cairan

pasien

– Vena leher

– Auskultasi paru – CVP

(101)

Resusitasi Cairan

• Koreksi hipotensi • Turunkan HR

• Koreksi hipoperfusi

– Oliguria

– Perubahan status mental – Asidosis laktat

(102)

Prioritas dalam Terapi Cairan

 EMERJENSI :

 VOLUME INTRAVASKULAR

 CURAH JANTUNG

 PERFUSI ORGAN VITAL

 SUB-EMERJENSI :

 INTERSTITIAL

 INTRASEL

 TANDA-TANDA VITAL  PROD. URIN

(103)

Jenis Cairan

 Kristaloid

 Ringer Asetat / Ringer Laktat

 Normal Saline

 Koloid

 Hetastarch

 Albumin 5%

 PRC

 Meningkatkan kapasitas angkutan O₂

 Fresh-frozen plasma

(104)

TERAPI CAIRAN

ASERING

RINGER LAKTAT NORMAL SALINE

RESUSITASI

KRISTALOID _KOLOID _ELEKTROLIT _NUTRISI

MENGGANTIKAN KEHILANGAN AKUT CAIRAN DEXTRAN- 40

MEMENUHI KEBUTUHAN HARIAN ELEKTROLIT DAN NUTRISI

KA-EN 1B KA-EN 3A KA-EN 3B KA-EN 4A KA-EN 4B AMIPAREN AMINOVEL- 600 PAN- AMIN G KA-EN MG 3 Martos -10 TRIPAREN I TRIPAREN II RUMATAN

KONSEP MEDIS

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

(105)

TREATMENT CONCEPT OF SHOCK ENHANCING PERFUSION / OXYGEN DELIVERY

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

Cardiac output

Arterial O₂ content

Fluids Transfuse Partially dependent on FIO₂ and pulmonary status Inotropes DO₂ = CO x CaO₂

(106)

C a r d i ac O ut p u t x S VR Pipe = Vasc ular

Pump = Heart Volume = B l o o d H y p o v o l e m i c S h o c k C a r d i o g e n i c S h o c k D i s t r i b u t i v e S h o c k I n o t r o p e s

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

F l u i d s O b s t r u c t i v e S h o c k Release t a m p o n a d e , e t c B l o o d P r es s u r e