Shock

Shock

-Syndrome; not a disease

-Systemic imbalance of oxygen supply and demand

Results in:

-Decreased cellular perfusion

-Anaerobic metabolism

-Cellular Death

-Can lead to MODS (Multiple Organ Dysfunction Syndrome)

Homeostatic regulation fails effecting

-Cardiac Output

-Circulating blood volume

-Vasomotor tone: have too much vasodilation, need some amount of vasoconstriction to get blood to vital organs like the head

Cardiac Output

-Amount of blood ejected by the heart per minute

-4-8 liters per minute

-CO= HR x SV

Cardiac index

-Normal: 2.5-4 Liters per minute

-Cardiac output based upon body size

-Need to get their actual height and weight

-Referenced to body surface area

Stroke Volume (SV)

-Amount of blood ejected per heartbeat

-60-130 cc/beat

-Determinants of stroke volume: preload, afterload, and contractility

Preload

-Volume of blood during diastolic filling of the ventricles immediately before contraction

-Work generated by the volume in the heart BEFORE the heart beats, thus PRE-load

-Volume load, or work generated by the volume of blood

-Compliance of the ventricle and the pericardium may also affect preload

-Usually 120-150 cc of blood in the ventricles at end of diastole

High and Low Preload

High Preload

-Congestive heart failure

-Cardiogenic shock

-Renal failure

Low Preload

-Bleeding

-Dehydration

-Over-diuresis

-Tamponade (no stretch, can’t fill)

-Tension Pneumothorax

Measuring Preload

-Echo: can just measure the end-diastolic volume

-PCWP (Pulmonary Capillary Wedge Pressure): Measures left atrial pressure, reflecting left ventricular preload

-CVP (Central Venous Pressure): Measures pressure of blood returning to heart- not direct at all, but sometimes used since less invasive

Afterload

-Force of resistance against which the heart must pump against to eject blood

-Pressure load

-Systemic vascular resistance (SVR)

-Reflects vasomotor tone and a number of other things

Main Determinants of Afterload

-Blood viscosity

-Blood volume (no blood volume, no afterload)

-Aortic valve stiffness

-Aorta: plaque, stiffness

-Atherosclerosis in the arteries: will increase pressure, occupy space in the aeteries

-Tension in the arterioles: Release tension makes it easier for the heart to pump

High and Low Afterload

High Afterload

-Hypovolemia (SNS, RAAS)

-Hypothermia

-Vasopressor medication- usually given to increase afterload

Low Afterload

-Sepsis

-Spinal shock

-Hyperthermia

-Adrenal insufficiency

-Anaphylaxis

-Vasodilator medication- will decrease afterload

Contractility

-How well does the heart pump, might need to increase force of contraction to improve but then requires more oxygen

-Force of contraction of ventricles during systole

-Consumes oxygen (MVO2= Myocardial Volume of O2 Consumption)

-The contractile state can be supported by inotropic influences like meds

Mean Arterial Pressure

-MAP normal: 60 or 70-100

-Represents a continuous perfusion pressure

-Systole + 2x diastole divided by 3

Ejection Fracture

-Percentage represented by Stroke Volume (60-130) divided by EDV (120-150cc)

-60-70% is normal; some say 50-70% or as high as 74%

-Don’t want it to be 100%, want some blood to stay in the heart

Hemodynamic changes with shock

-Decreased CO (except septic shock)

-Decreased SV

-Decreased MAP

-Increased HR (except neurogenic shock)

Diagnostic Studies in Shock

-Physical exam: cellular death occurring or coming soon to any/all organs

-History of recent events

-Arterial line, pulmonary artery monitoring: line put into the artery, measures blood gas and BP

-Chest X-ray

-EKG monitoring for arrhythmias

-ANG: assessing for acidosis and also for pulmonary compromise

-Foley catheter: need accurate I/O with severe illness, Urine output can tell a lot about cardiac output, CO goes down, Urine output goes down 

-Lactate level >3 mEq/L indicates hypoperfusion and anoxia

-Labs to assess organ failure: especially renal and liver

-Cultures: blood, urine, sputum, wounds: see where the is an infection

-WBC with differential: another sign body is fighting infection

Lactate

-Normal: 0.5-2.2 mmol/liter

0Elevated: shows anaerobic metabolism, leaving cells in distress

-Reflects tissue hypoxia from any reason

-Lactate from anaerobic metabolism creates lactic acidosis

-Causes of elevation: sepsis, reduced O2 availability, impaired lactate clearance by the liver, some metabolic disorders or chronic diseases

General Nursing Care for All types of Shock

-Early recognition and treatment: look at SNS and what it is doing

-Treat primary cause

-Remember ABCs

-Oxygen to maintain saturation >90%

-2 large bore IV catheters >16g

-Stabilize BP with IV fluids (isotonic) and drug treatment (caution with cardiogenic shock)

-Foley

-Position supine, HOB flat once BP drops

-Frequent total system assessment

-Assess for Mental Status changes: starts with restless/anxious

-Assess for Respiratory distress: as patient tires, may need intubation

-Frequent VS

-Temperature WNL

IV Fluids

-Isotonic crystalloids: 0.9% normal saline (NNS), Lactated Ringers

-Colloids: Conflicting evidence

• Albumin: restore circulating volume, just fix low albumin levels, Definitely use with liver failure pts

• Plasmanate: similar use

-Blood/blood products: Packed RBCs, Clotting factors (FFP)

Medications

-Sympathomimetics/Vasopressors

-Antibiotics, particularly for septic shock

-Calcium gluconate (lose Ca with blood loss and/or clot formation)

-Magnesium Sulfate (critically ill people frequently have los Mg)

-Insulin: if blood glucose elevated

-Glucose: if blood glucose low- happens as liver fails

-NaHCO3: sodium bicarbonates, given if acidotic

-Antiarrhythmics if needed

Sympathomimetic Medication

-Mimics the SNS

-Can stimulate either alpha or beta adrenergic receptors

-Alpha: vasoconstriction

-Beta 1: increased myocardial contractility

-Beta 2: Bronchodilation

-Meds which cause vasoconstriction are called vasopressors

- Norepinephrine, Epinephrine, Phenylephrine, Dopamine

Beta 1

-Heart: beat faster and stronger

-Increased workload for heart

-May cause tachy-arrhythmias

Beta-2

-Lungs: bronchodilation, increased RR

-Vital areas: vasodilation

-Make more glucose available

-Increased alertness

-Can have hyperglycemia, anxiety

Alpha

-Vasoconstriction to non-vital areas

-Increased workload for heart

-Renal failure, Liver failure, lose toes

Classifications of Shock

-Distributive: neurogenic, septic, anaphylactic

• Decreased afterload too far

-Cardiogenic: decreased controactility; increased preload too far

-Hypovolemic: decreased preload too far, Hemorrhagic is a subset of hypovolemic shock

Distributive Shock

-Decreased vascular tone

-Decreased afterload

-Altered distribution of blood volume (no loss of total blood volume)

-Can be complicated by loss of intravascular volume from increased capillary permeability

-Therefore, decreased blood flow to tissues

Neurogenic Shock

-Impairment of Autonomic Nervous system

-Caused by disease or injury to spinal cord above or at T6, spinal anesthesia, severe stress or pain

-Can last from hours to weeks

-Hypotension and Bradycardia

Sepsis

Life-threatening organ dysfunction caused by dysregulated host response to infection

Septic Shock

-Patients with sepsis who develop underlying circulatory circulatory and metabolic abnormalities

-Hypotension that requires vasopressors to maintain a MAP >= 65 mmHg

-Serum lactate level >2 mmol/L despite adequate volume resuscitation

Pathophysiology of Sepsis

-When an infection occurs, the body’s host response system attempts to contain the infection to a localized area. This is a complex process regulated by multiple cellular components and signaling systems

-This is an inflammatory process mediated by pro- and anti-inflammatory cellular mediators, that should balance each other, neutralize the infectious insult and lead to restoration of the cell

-Occurs when pro-inflammatory mediators in the cell triggered by an infection cause a systemic, generalized immune response

-This response causes cellular injury throughout the body which leads to organ dysfunction

-The mechanisms and risk factors for sepsis are not fully understood. Each pt’s response is different

How Sepsis can effect the body?

-Tissue ischemia: micro vascular legions interfere with tissue oxygen exchange

-Apoptosis (programmed cell death to get rid of excess cells): but in sepsis, leads to multi-system organ failure

-Cytopathic Injury: cellular injury leads mitochondrial DNA breakdown

-Massive vasodilation from overall immune response process, decreases afterload too far

-Cardiovascular: Hypotension due to vasodilation from nitrous oxide and prostacyclin release

Patients at Risk for septic shock

-Came in with an infection

-Immunosuppression

-Trauma Victims: too many open areas

-Chronic illness

-Invasive procedures

-Poor nutrition

-Extremes of age

Manifestations of Septic Shock

-Hypotension

-Tachycardia

-Fever

-High CO: body is trying to compensate

-Skin warm, dry, flushed

-Mild hyperventilation; respiratory alkalosis

-Decreased LOC

-Urine output adequate initially

National Early Warning Score (NEWS) for Sepsis

-An aggregate score made up of 6 physiological parameters

-Aimed at improving detection and response to clinical deterioration

-Respiratory rate

-Heart rate

-LOC (APVU score)

-Systolic BP

-Temperature

-O2 Saturation

Initial Resuscitation for Sepsis

-Treatment and initial resuscitation begins ASAP

-Cultures, if possible

-At least 30 ml/kg crystalloids within first 3 hours- frequently lactated ringer’s

-Guide resuscitation to decrease serum lactate levels; If high, anerobolic metabolism and cell death; can measure how well we are doing 

-Use capillary refill to guide resuscitation

-If receiving large amounts of crystalloids, consider albumin

-For pts not responding to fluid resuscitation (MAP <65 mmHg), add a vasopressor: norepinephrine

-Heart is stuggling, need some beta and good alpha for vasoconstriction 

Within First Hour (1 hour bundle) of Sepsis

-Measure Lactate level: remeasure if initial lactate is elevated (>2 mmol/L)

-Obtain blood cultures before administering antibiotics

-Administer broad spectrum antibiotics

-Begin rapid fluid administration: May need up to 3L

• 30 ml crystalloid for hypotension or lactate level > 4 mmol/L

-Apply vasopressors if hypotensive during or after fluid administration to maintain MAP >= 65 mmHg

Infection

-Begin antibiotics within the first hour if septic or has septic shock

-Cultures first

-Beta-lactam antibiotics (penicillins, cephalosporins, carbapenems)

-Continuously look for other causes if not certain it is an infection. If another reason is identified stop antibiotics immediately

-There are a lot of specific guidelines related to the type of antibiotics to use

Treatment of Septic Shock: Additional considerations once the pt is stable:

-Tylenol for fever and therefore comfort

-Target Hbg 7-9 g/dl

-Manage glucose if 2 consecutive levels >180 mg/dl

-DVT prophylaxis

-Stress ulcer prophylaxis

-Begin oral or enteral feedings: should provide low dose feedings in the first week (up to 500 kcal/day

Anaphylactic Shock

-Caused by histamine release

-Acute or life-threatening allergic reaction

-Massive dilation, increased capillary permeability, microvascular leakage

-Histamine release: bronchospasm and laryngospasm

-Serotonin release: pulmonary edema

Treatment of Anaphylactic Shock

-Airway maintenance

-Support circulation

-Antihistamines: epi, bronchodilator, then Benadryl

-Epinephrine

-Occurs in 1 out of 3000 patients and accounts for 500 deaths annually

-Patients usually recovers quickly

Hypovolemic Shock

-Have some fluid loss

-Blood loss→ trauma, surgery→ absolute

-Fluid loss → Diarrhea, Vomiting, DI, Diuretics→ Absolute

-Fluid shift (third space)→ burns, Ascites→ Relative

Pathophysiology of Hypovolemic shock

-Decreased Intravascular volume

-Decreased venous return (preload)

-Decreased SV

-Decreased CO

-Inadequate tissue perfusion

-Anoxia: absence of O2 in the tissue

Treatment of Hypovolemic Shock

-Rapid volume replacement until CO, Hgb, ABG, and BP is normal and Urine output is at least 0.5 cc/kg/hr

-Dopamine can be administered if extremely hypotensive, only after fluid administration; fill up the tank first

Cardiogenic Shock

-Extension of CHF

-Patients at risk: MI, Cardiomyopathies, VSD, dysrrhythmias, electrolyte imbalances, medications

-Caused by pump failure

Pathophysiology of Cardiogenic Shock

-Decreased SV

-Decreased cardiac output

-Decreased BP

-Decreased organ perfusion

-Decreased coronary artery perfusion which causes myocardial ischemia and infarction

-Increased LV pressure

-Increased LA pressure, pulmonary capillary wedge pressure; pump is failing so you back up into the lungs

-Increased pulmonary venous pressure

-Movement of pulmonary capillary fluid causing interstitial edema and intralveolar edema

Treatment of Cardiogenic Shock

-Goal is to increased CO, Reduced Preload and Reduce Afterload

-IV medications, inotropes, vasodilators, diuretics

-Cautious fluid replacement

-Antiarrhythmics

-IABP (balloon pump) and VAD (ventricular assistance device): physical things we put in the body to help the heart beat right