RESHAPING: Shock Syndromes

     Shock Syndromes  

a cellular disease due to either hypoperfusion (oxygen demand is greater than oxygen delivered) or lack of ability of cells to utilize the delivered oxygen (oxygen utilization, consumption), leading to an exaggerated response by the body. 

Inadequate tissue perfusion or impaired oxygen uptake —> decreased oxygen to cells —> anaerobic metabolism —> increased lactate and H+ production and decrease ATP production —> acidosis —> cell death 

       Three Phases of Shock 

     Compensatory Phase (BP maintained)   

• tachycardia  and tachypnea (respiratory alkalosis)  
• normal PaO2  
• oliguria  
• skin pale, cool (except in early sepsis) •restlessness, anxiety  
• complaints of thirst 
• BP maintained!   

     Progressive Phase (compensatory mechanisms failing)   

• acedemia (metabolic acidosis)
• hypotension 
• worsening tachycardia 
• oliguria 
• clammy, mottled skin  further change in LOC   

     Refractory phase of shock   

• not responsive to interventions  
• severe systemic hypoperfusion, multisystem organ  dysfunction  

may survive shock and die from organ failure: pulmonary (ARDS), kidney (acute tubular\necrosis), heart (failure, ischemia), hematologic (disseminated intravascular coagulation), neurological (encephalopathy, stroke), liver (failure)   

  -  Compensatory Phase

Happens due to stimulation of SNS and Activation of the RAAS system 

• SNS Activation: related to decreases in CO and increase oxygenation utilization 

• Renin-Angiotensin-Aldosterone System (RAAS): related to decreases in CO and increase oxygenation utilization 

Functions to elevate blood volume and arterial tone in a prolonged manner by increasing sodium reabsorption, water reabsorption and vascular tone . 

1. Overview of Shocks  

 

Type	Heart Rate	Blood pressure	SV	SVR	PCWP	MVO2
Cardiogenic	Elevated	Normal to low	Down, Down	Elevated	Elevated	Down
Septic Shock	Elevated	Normal to low	Elevated	Down, Down	Low	Elevated
Hypovolemic	Elevated	Normal to low	Down, Down	Elevated	Low or Normal	Elevated
Neurogenic	Bradycardia	Normal to low	-----	Down, Down	low	Low

 

When considering patients that have fallen into a shock, the above parameters can be used assess the potential cause for their hypoperfusion. Can also account that the use of Swan-Ganz or Pulmonary Artery Catheters can be used to diagnosis the etiology of the shock syndrome.     

   Pulmonary Artery Catheter Interpretation; 

• Right heart failure: high CVP, low CI, high PVR 

• Left heart failure: high PCWP, low CI, high SVR 

• Pericardial tamponade: high PCWP, high SVR, CVP = PCWP 

• Hypovolemia: low CVP, low PCWP, low CI, high SVR 

• Cardiogenic: high CVP, high PCWP, low CI, high SVR 

• Sepsis (Distributive): low CVP, low PCWP, high CI, low SVR 

          Obstructive Shock  

Refers to condition that physically impair blood flow by limiting venous return to the heart or limit the pumping o blood from the heart. The result is decreased cardiac output which is seen with the following: 

The obstruction of blood flow results in low cardiac output, inadequate tissue perfusion and compensatory increase in SVR. Initially this can be indistinguishable from hypovolemic. However there would be increased respiratory effort, cyanosis and signs of vascular congestion that becomes more apparent.  
 
The main objective in this type of shock is correct the cause of obstructive shock and restore both tissue perfusion and cardiac output.  

 -  Pneumothorax 
Air or blood within the pleural space accumulating fluid that causes increased pressure that obstruct venous blood retiring to the heart resulting in decreased filling  

• S/S: tracheal deviation, increase WOB, increase RR, RD, diminished lung sounds, JVD, bradycardia  

Treatment:  

needle decompression to 2nd intercostal space midclavicular line; Chest tube  

 - Pulmonary Embolism 
occlusion of pulmonary artery that creates dead space ventilation 

• S/S: decreased LOC, increased WOB, RR, tachycardia, cyanosis, chest pain, pleural effusion, JVD  

Treatment:  

• anticoagulants, fibrinolytic therapy, fluids, oxygen, IVC filter  

 - Cardiac Tamponade

accumulation of fluid or blood within the pericardial sac 

• S/S: restlessness, agitation, hypotension, JVD, muffled heart sounds, pulsus paradoxes (excessive drop in SBP when inhalation occurs), decreased peripheral pulses with poor cap refill, narrow pulse pressure, cool extremities  

Treatment:  

• Diuresis, and pericardiocentesis (6th rib sternal boarder)  

          Hypovolemic Shock “Volume” Issue 

Seen with hypoperfusion of the tissue that is seen due to a reduction in the blood return to the heart due to trauma, GI bleed, etc. Physiology wise there is a shift form the intravascular space into the extravascular space due to changes in osmotic pressure. 

     Treatment:  

FLUIDS FIRST, with adequate placement of two short large bore IVs in large veins, then consider inotropes and vasopressors if needed to manage hemodynamic stability, PRBCs and FFP should be consider when levels of h/h are considered lower than or at 7 mg/dL – considering potential transfusion reactions that can occur.  

Priorities for the type of blood or blood products used In order of preference are the following: 

• Crossmatched  
• Type specific 
• Type O-negative preferred for females and either O+ or O- for males  

Issues that common along with blood product, particularly in large volume can produce the following: 

• Hypothermia 
• Myocardial dysfunction  
• Ionized hypocalcemia  
• Infusion reactions  

To minimize these problems, warm blood and blood products if possible, calcium administration if the child becomes hypotensive and there can also be empirical infusion of calcium replacements.  

          Cardiogenic Shock “Pump” problems 

Preload is variable, contractility decreased, and afterload is increased  
Seen with hypoperfusion of the tissue that is assed with arterial constriction that leads to increased systemic vascular resistance, which incorporates with a decrease in CO and a tachycardia response.  Can be seen with heart disease, myocarditis, cardiomyopathy, arrythmias, sepsis, poisoning or drug toxicity or myocardial injury (e.g. trauma) 

   Note on Pulmonary Edema  

• Backward flow of blood leading to pulmonary congestion and pressure changes: increased pulmonary artery wedge pressure (e.g 20 to 30 indicates heart failure) 

• Consequence: Cardiogenic pulmonary edema  esulting from myocardial failure and high ventricular end diastolic, left arterial and pulmonary venous pressures and from increased venous tone and fluid retention 

 
   Treatment 

placement of CVLs and infusion of inotropes or vasopressor medications to correct hemodynamics, further management can be done through placement of invasive monitoring or interventional equipment being arterial lines, PA or Swan-Ganz Catheters and intra-aortic balloon pumps. The key in this management is to increase cardiac output – which is the perpetrating issue.  

•  Enhance Effectiveness of Pump   

Positive inotropic support: -Norepinephrine (Levophed), Dopamine, Dobutamine, milrinone (Primacor)   AVOID negative inotropic agents!   

• Decrease Demand on Pump   

Preload reduction (or optimization Afterload reduction Mechanical ventilation Treat pain  IABP for short term support Ventricular assist device (VAD)   

     Note on Fluid Resuscitation  

Remember that rapid volume resuscitation of cardiogenic shock in the setting of poor myocardial function can further deteriorate function and lead to aggravated pulmonary edema  

          Distributive Shock  

Refers to a clinical state characterized by reduced systemic vascular resistance leading to maldistribution of blood volume and blood flow. This group includes  

   Overview (Septic Shock) 

• SIRS (temp, HR increased, RR increased, WBC increase, bands >4000, 10% shift) + infection 
• Treatment: Crystalloids, norepi (first line), epi, vasopressin, ATB

   Overview (Anaphylactic Shock) 

   Overview (Neurogenic Shock) 

• rapid loss of sympathetic stimulation; massive vasodilation and decrease PVR Treatment 
• unlikely to be corrected with fluid; need dopamine and vasopressin, steroids 

In this type of shock, it is known that there is maldistribution of blood flow which leads to varying levels of cardiac output but overall having decreased tissue perfusion. Often it is seen that there will be a high cardiac output and low SVR often observed in distributive shock differing from the low cardiac output and high SVR that is seen in other shock states.  

     Warm versus Cold Shock (Pediatric Population)  
 
Early in the clinical course, a person with distributive shock can present with decreased SVR and increased blood flow to the skin, this produces warm extremities and bounding peripheral pulses “warm shock”.  
  
Through the progression of this shock there can be concomitant hypovolemia and/or myocardial dysfunction produce a decrease in cardiac output, SVR can then increase resulting In the pulling of blood flow from secondary organs leading to “cold shock” showing a picture similar to hypovolemic and cardiogenic shock  

     Warm Shock 

• Vasodilation, low systemic vascular resistance, high cardiac output 
• Warm extremities, flash capillary refill < 1 sec, “bounding” pulses 
• Decreased diastolic blood pressure, wide pulse pressure ( > 40 mm Hg) 

     Cold Shock 

• High systemic vascular resistance, low cardiac output 
• Cold extremities, prolonged capillary refill ( > 3 seconds) 
• Faint pulses 
• Normal or increased diastolic blood pressure 
• Narrow pulse pressure (< 30 mm Hg) 

 

WARM SHOCK	COLD SHOCK – LOW BP	COLD SHOCK – NORMAL BP
Titrate NOREPINEPHRINE      Second line:  Add epinephrine,   or vasopressin	Titrate EPINEPHRINE      Second line:  Add norepinephrine,   or dobutamine	If in shock (i.e., ScvO2 < 70%), titrate EPINEPHRINE    Consider:  Dobutamine or Milrinone starting dose

 

          Neurogenic Shock  

Seen with injury that affects the neurologic center and coined to be “loss of vascular tone” leading to hypoperfusion of the peripheral system. Autonomic dysfunction resulting in VASODILATION, bradycardia, and hypothermia – loss of sympathetic tone. (Compensatory tachycardia does not occur due to failure of autonomic system) 

     Peripheral vasodilation that is accompanied with the following: 

• Bradycardia and Hypotension leading to reduced cardiac output: less than 5 
• irregular temperature control 
• Decreased right atrial pressure or CVP and decreased PAWP < 8-12 mmHg 

Note: injury at T6 or above results in autonomic dysreflexia; further more spinal shock is loss of motor and sensory function including all reflexes below the SCI whereas neurogenic shock is inadequate perfusion to vital organs and associated with autonomic instability  

     Treatment:

manage with treating the spinal injury and use of support to manage airway, circulation and breathing. Dopamine is the preferred vasopressor for this type of distributive shock  

• Administer a trial of fluid therapy (isotonic crystalloid) and assess response  
• For fluid refractory use vasopressors as indicated  
• Provide supplementary warming or cooling as needed.  

Septic Shock  

• Systemic inflammatory response syndrome (SIRS) – systemic inflammation with leukocytosis, fever, tachycardia, tachypnea, elevated WBC or elevated WBC band– when this is resulted form an infection this is known as sepsis.  
  
  
• Sepsis is a life-threatening organ dysfunction with source of infection caused by a dysregulated host response to infection then when accompanied with an elevated lactate (>2 - 4mM/L) and more than dysfunction in one or more organs this is severe sepsis 

• When severe sepsis is accompanied by hypotension that is caused by volume infusion this is called septic shock 

• Inflammatory injury involving more than one viral organ is called MODS 

 
Responses are due primarily to compensatory mechanisms that counterbalance the profound vasodilation due to increased capillary permeability , blood maldistribution, and decreased contractility associated with inflammatory mediators. 

Early recognition and treatment of septic shock are critically important determinants of outcome thus evaluate temperature, heart rate, systemic perfusion, blood pressure and clinical signs of end-organ function  
 
     Treatment: 

• Fluids (30 mL per kg) FIRST and then Vasopressors  
• Trending Lactate, WBC and Blood Cultures  
• Oxygenation delivery and utilization management  

   Disseminated Intravascular Coagulation  

There will be cytokines that produce vasodilation and damage of the blood vessel lining and activates a coagulation cascade and may result in microvascular thrombosis and disseminated intravascular coagulation (DIC). This microvascular thrombosis and hemorrhage can lead to adrenal insuffiency leading to contributions of a low SVR and myocardial dysfunction  
When this occurs, there is widespread microvascular thrombosis, which contributes to microcirculatory dysfunction, and produces ischemia of the fingers and toes.  
 
Polycythemia does not occur in DIC. DIC does not cause coagulation factor overproduction; rather, it causes consumption and lysis of coagulation factors, which can lead to severe bleeding. Severe bleeding results from the consumption of coagulation factors and not from liver inflammation 

   DIC Panel 

• low platelet count 
• elevated D-dimer concentration,  
• decreased fibrinogen concentration 
• prolongation of clotting times such as prothrombin time (PT). 

 
 Treatment 

•  find the underlying cause, always a secondary issue