Shock

Physiology
Pathway of blood through the Heart and Lungs
Pathway of blood through the Heart and Lungs

• Right atrium  tricuspid valve  right ventricle

• Right ventricle  pulmonary semilunar valve 
pulmonary arteries  lungs
• Lungs  pulmonary veins  left atrium
• Left atrium  bicuspid valve  left ventricle
• Left ventricle  aortic semilunar valve  aorta
• Aorta  systemic circulation
 Cardiac Output (CO)
• Cardiac Output is the amount of blood
pumped by each ventricle in one minute
– CO is the product of heart rate (HR) and stroke
volume (SV)
• HR : the number of heart beats per minute
• SV : the amount of blood pumped out by a ventricle
with each beat
Cardiac Output (CO)
 Regulation of Stroke Volume
• Stroke Volume = EDV - ESV
– EDV (End Diastole Volume) = amount of blood
collected in a ventricle during diastole
– ESV (End Sistole Volume) = amount of blood
remaining in a ventricle after contraction
 Factors Affecting Stroke Volume
• Preload – amount ventricles stretched by
contained blood
• Contractility – cardiac cell contractile force
due to factors other than EDV
• Afterload – back pressure exerted by blood in
the large arteries leaving the heart
 Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac
muscle cells before they contract is the critical
factor controlling stroke volume
• Slow heartbeat and exercise increase venous
return to the heart, increasing SV
• Blood loss and extremely rapid heartbeat
decrease SV
Preload and Afterload
 Extrinsic Factors Influencing SV
• Contractility is the increase in contractile strength,
independent of stretch and EDV
• Increase in contractility comes from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
• Agents/factors that decrease contractility include:
– Acidosis
– Increased extracellular K+
– Calcium channel blockers
 Contractility and Norepinephrine
Sympathetic stimulation
releases norepinephrine
and initiates a cyclic AMP
second-messenger system
 Regulation of Heart Rate
• Positive chronotropic factors increase HR
– Caffeine
• Negative chronotropic factors decrease HR
– Sedatives
 Blood Pressure
• BP : Cardiac Output (CO) x Total Peripheral
Resistance (TPR)

• Regulation of BP :
– RAA System mechanism
– Neural Regulation
– Hormonal (Epinephrine & Norepinephrine)
RAA System
 Definition of Shock
• The state in which profound and widespread
reduction of effective tissue perfusion leads
first to reversible, and then if prolonged, to
irreversible cellular injury (Kumar and Parrillo,
1995).
 Stages of Shock
• Consist of 4 stages :
– Initial
– Nonprogresif
– Progresif
– Refractory/Irreversible

• Initial
- Aerob metabolism  anaerob metabolism
- Lactic acid 
- No clinical changes
• Non-progresif (compensated) : improving metabolic
disorder
– Peripheral vasocontriction and priority bloodflow to
vital organs  improving brain and heart circulation
– Decrease in coroner bloodflow  anaerob
metabolism & arterial dilatation
– Kidney  hormon release
• Epinefrin, norepinefrin
• Glukokortikoid
• Renin – angiotensin – aldosteron (RAA system)
– Anterior pituitary: secretion of ADH
• Progresive (decompensated) : if compenstated fails
– Vasocontriction  tissue oerfusion inadequate
and hypoxia
– Systemic anaerob metabolism  lactic acid 
metabolic asidosis
– Decrease production of ATP  transport
membran distrubed  cell edema, cell rupture
– Renal response continues
– Heart function decrease

• Refractory/irreversible : irreversibel damage to cell

and organs
 Types of Shock
• Hypovolemic shock  due to decreased circulating
blood volume in relation to the total vascular
capacity and characterized by a reduction of
diastolic filling pressures
• Cardiogenic shock  due to cardiac pump failure
related to loss of myocardial contractility/functional
myocardium or structural/mechanical failure of the
cardiac anatomy and characterized by elevations of
diastolic filling pressures and volumes
 Types of Shock
• Extra - cardiac obstructive shock  due to
obstruction to flow in the cardiovascular
circuit and characterized by either impairment
of diastolic filling or excessive afterload
• Distributive shock  caused by loss of
vasomotor control resulting in
arteriolar/venular dilatation and characterized
(after fluid resuscitation) by increased cardiac
output and decreased SVR
Work Up
Hypovolemic Shock
 Causes
Nonhemorrhagic
• External fluid loss Hemorrhagic
– Dehydration • Trauma
– Vomiting
• Gastrointestinal
– Diarrhea
– Polyuria • Retroperitoneal
• Interstitial fluid redistribution
– Thermal injury Increased vascular capacitance
– Trauma (venodilatation)
– Anaphylaxis • Sepsis
• Anaphylaxis
• Toxins/drugs
 Signs & symptom
• Low blood pressure
• Tachycardia/bradycardia
• Cyanosis
• CRT > 2 seconds
 Therapy
• Goal :
– improve normal blood pressure, pulse, tissue
perfussion
– stop the bleeding

• Patent a secure airway

• Venous acces
• Catheter  monitor urine output
• Control the bleeding :
– absorbent dressing & elevation of the bleeding
area
– dressing & bandage
– arterial tourniquet
• 0.9% Normal Saline (alternative)
• Blood transfusion
• Vasopressor
Cardiogenic Shock
 Causes
1. Myopathic 1. Pharmacologic
– Myocardial infarction – Anthracycline cardiotoxicity
(hibernating myocardium) – Calcium channel blockers
– Left ventricle 2. Mechanical
2. Right ventricle – Valvular failure (stenotic or
3. Blunt Cardiac Injury regurgitant)
(trauma) – Hypertropic
4. Myocarditis cardiomyopathy
– Ventricular septal defect
5. Cardiomyopathy
3. Arrhythmic
6. Post-ischemic myocardial
stunning – Bradycardia
– Tachycardia

7. Septic myocardial
depression
 Signs & symptom
• Poor tissue perfusion (oliguria, agitasi,
peripheral cyanosis)
• Tachycardia
• Hypotension
• Dyspnoe
• Diaphoresis
• Faint
 Therapy
• Goal : improve oxygen supply to myocardium and
peripheral tissue perfussion

• Vasopressor and inotropic  adequate cardiac

preload
• Inadequate CO : inotropic
• Hypotension : dopamine/norepinephrine
• Pulmonary congestion : Dobutamine and
nitroglycerin/sodium nitropruside
 Distributive Shock
• Result from excessive vasodilation and the impaired
distribution of blood flow.

• Etiologi :
- Sepsis
- SIRS
- TSS
- Adrenal insufficiency
- Anaphylaxis
- Neurogenic shock
 Septic Shock
Septic shock is systemic inflammatory response
syndrome (SIRS), which is organ injury or
damage in response to infection, leads to
dangerously low blood pressure and
abnormalities in cellular metabolism.
It can cause multiple organ dysfunction
syndrome and death
• The primary infection is most commonly by
bacteria, but also be by viruses, fungi or
parasites.
• Temp >38°C Septic
or <36°C Sepsis Shock
• Tachycardia • Sepsis
(HR >90) • End organ
• Tachypnea • SIRS
dysfunction • Sepsis
(RR>20 OR • Infection
(presumed or • Hypotension
PaCO22 <32
• WBC >12.000 known)
Severe
or <4000, 10%
bands Sepsis

SIRS
Pathophysiology
 Sign & symptoms
Hyperdynamic (warm shock)
- Hypotensive
- Tachycardia
- Tachypnea
- Bounding pulse
- Warm, well perfused extremities
- Skin flushed, moist
 Sign & symptoms
Hypodynamic (cold shock) :
- Hypotensive
- Tachycardia
- Tachypnea
- Narrow, thready pulse
- Cold, poorly perfused extremities
- Skin pale, dry
Therapy
 Anaphylactic Shock
• Anaphylaxis is an acute, potentially fatal,
multiorgan system reaction caused by type 1
hypersensitivity.
Causes
Therapy
 Neurogenic Shock
• Caused by stimulates parasympathetic activity
or inhibits sympathetic activity of vascular
smooth muscles, which results in widespread
and massive vasodilation.
• Etiology:
- Spinal cord injury above T5
- Spinal anesthesia
- Vasomotor center depression (e.g., severe pain,
drugs, hypoglycemia)
 Sign & symptoms
• Low systemic vascular resistance
• Excessive parasympathetic activity
• Bradycardia
• Hypotension
 Therapy
• ABCDE
• Fluid resuscitation
- Keep MAP at 85-90 mmHg for first 7 days
- Thought to minimize secondary cord injury
- If crystalloid is insufficient use vasopressors
• Search for other causes of hypotension
• For bradycardia
- Atropine
- Pacemaker
• Methylprednisolone
– Use only for blunt spinal cord injury
– High dose therapy
– Must be started within 8 hours
– Controversial risk for infection, GI bleed
 Obstructive Shock
• Obstruction to the outflow due to impaired
cardiac filling and excessive afterload.

• Etiology:
- Cardiac tamponade
- Tension pneumothorax
- Pulmonary embolism
Pathophysiology
Structural
compression

Venous return 

Stroke volume 

Cadiac output 

Oxygen supply 

Perfusion of tissue


Metabolism cell
damage
 Therapy
• Treat underlying cause
- Pericardial tamponade  pericardiocentesis,
surgical drainage (if needed)
- Pulmonary embolism  heparin, thrombolytic
therapy, embolectomy surgery
• Monitoring
• Fluid therapy
• Vasoactive agents