Shock

Shock

Decreased cellular perfusion

Anaerobic Metabolism (so you don’t have good perfusion you don’t have good oxygenation)

Cellular death

Can lead to MODS (multiple organ dysfunction syndrome)

Homeostatic regulation fails

Cardiac output (cardiogenic shock extension of CHF)

Circulating blood volume (if you don’t have enough)

Vasomotor tone (You can have way to much vasodilation need some vasoconstriction to maintain blood flow to you head)

Cardiac output

Amount of blood ejected by the heart per minute

4-8 liters per minute

CO= HR X SV

Stroke volume

Determinants of stroke volume

• Preload

• Afterload

• Contractility (how well the heart can handle this)

Determinant of stroke volume: Preload

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

PRE-load = VOLUME load

High preload

Everything came back and don’t know what to do with it

Congestive heart failure

Cardiogenic shock

Renal failure (fluid overload)

Because the heart is failing and kidneys didn’t get rid of the fluid

Low preload

Bleeding

Dehydration (People who fall at home and can’t get up might not be found for days so they aren’t eating or drinking until they are found)

Over diuresis (too much fluid came out and concentration in blood stream)

Tamponade (no stretch- can’t fill)

Tension pneumo (put in a chest tube, if it get back to much pressure in lungs won’t let heart fill)

Measuring preload

Echo - can measure the end-diastolic volume

PCWP (pulmonary Capillary Wedge Pressure)- measure 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

Bowtie: Your patient was adm with an MI. They called because thtey are very SOB. You find them flat in bed, gasping for air, with rales in all lung fields. They are using all their accessory muscles. They cough up pink, frothy sputum. Skin cool/clammy VS: 37, 120, 36, 100/70

This is high preload

What are priority interventions: Diuretics and positioning

What do you monitor for: Lung sounds and I&Os

Why might you add a nitro drip

It dilates both veins and arteries increase supply to the heart decreases preload and decreases afterload

Determinant of stroke volume: Afterload

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

Afterload = pressure load

Main determinants of afterload

Aortic valve stiffness (First door out of the heart, plaque in arteries and valves)

Atherosclerosis in teh arteries (increases pressure, tension from muscle portion)

Tension in the arterioles (Generally what we work on for afterload it releases tension, makes it easier for heart to pump, can be fixed with meds)

High Afterload

Hypovolemia (SNS, RAAS) (these kick in and increase tension in the arterioles)

Cardiogenic shock (compensatory mechanisms increases afterload)

Hypothermia

Vasopressor medication (why we give it to increase tension and afterload)

Low Afterload

Sepsis & Anaphylaxis (Cause too much vasodilation, enough volume but arteries loose tension)

Vasodilator medication (arteriole vasodilator medications)

Contractility

How well the heart pumps, might need to increase force of contraction to but it increases oxygen demand

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

MAP

Normal 60 or 70-100

Represents a continuous perfusion pressure

Ejection fraction

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

Hemodynamic changes with shock

Decreased CO (except septic shock) (at the beginning, CO can be high up to 10L per pump)

Decreased SV

Decreased MAP (adjust based on MAP)

Increased HR (except neurogenic shock)

• High pulse low pressure bad, shock is one of those causes

Summary of background information

Systemic imbalance of oxygen supply and demand causing decreased cellular perfusion usually due to decreased cardiac output

Results: Anaerobic metabolism resulting in cellular death

Sympathetic nervous system tries to compensate- can’t fix underlying cause

SNS tries to compensate

Restless/anxious? Figure out why (pt can seem confused is the first sign)

Resting tachycardia Figure out why

Resting tachypnea Figure out why

Pulse up, pressure up SNS is winning

Pulse up pressure down SNS tried but failed

Diagnostic studies in shock

Physical exam: cellular death occurring or coming soon to any/all organs (end organ failure)

History or recent events (Recent accident like a GI bleed)

Arterial line, pulmonary artery monitoring (line in artery usually radial, measures blood gas, can put BP on the screen)

CXR (chest x ray to see where everything is coming from)

EKG monitoring for arrythmias

ABG- assessing for acidosis and also for pulmonary compromise

Foley catheter- need accurate I/O with severe illness

• One of the only times they will let you have a catheter in this situation, urine output is going to decrease cause CO to kidneys decrease)

Lactate level >3 meq/L indicates hypo perfusion and anoxia (anerobic metabolism)

Labs to assess organ failure: especially renal and liver

Cultures: blood, urine, sputum, wounds

WBC is differential

Lactate

Normal = 0.5-2.2 mmol/L

Elevated shows anerobic metabolism

General nursing care for all types of shock

Early recognition and treatment

Treat primary cause

Remember ABCs

IV fluids

Isotonic crystalloids (mostly what we give for volume replacement for dehydration)

• 0.9% NSS

• Lactated ringers

Colloids- conflicting evidence (depends on what we need to do)

• Albumin- restore circulating volume? or just fix low albumin level

  • Definitely use with liver failure pts

• Plasmanate- similar uses

Blood/blood products (if they’re bleeding we give this)

• Packed RBCs

• Clotting factors

Medications

Sympathomimetic / Vasopressors

Antibiotics, particulary for septic shock

Calcium gluconate (Lose Ca++ with blood loss and/or clot formation) (because the blood we give them doesn’t have enough calcium in it)

Magnesium Sulfate (Critically ill people frequently have low Mg+)

Insulin (if BG is elevated)

• Glucose if blood glucose is low- happens as liver fails

NaHCO3- only given when someone is acidotic, automatically given it causes hypernatremia and alkolosis

Antiarrhytmics if needed (if heart is affected)

Sympathomimetic meds

Meds that work on SNS and mimic it

Can stimulate either alpa or beta adrenergic receptors

Alpa= vasoconstriction (called a vasopressor)

Beta1= increased myocardial contractility

Beta2= bronchodilation

Meds which cause vasoconstriction are called vasopressors

Norepinephrine, Epinephrine, Phenylephrine (Vasoconstriction in your nose), Dopamine

Beta 1

Heart: beat faster and stronger

Increased workload for heart, May cause tachy-arrythmias

Beta 2

Lungs: bronchodilation, Increased RR

Vital areas: vasodilation (Blood to heart, head, lungs, etc)

Increased alertness

Can have hyperglycemic anxiety

Alpha

Vasoconstriction to non-vital areas

Increased workload for heart renal failure, liver failure, lose toes, etc

Classifications of shock

Distributive: neurogenic, septic (main focus), Anaphylactic

• Decreased afterload too far

Cardiogenic- decreased contractility; increased preload too far

Hypovolemic- decreased preload too far (hemorrhagic is a subset of this)

Distributive

Decreased vascular tone

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 the tissues (not enough blood pressure to go anywhere need vasconstriction)

Defintion of sepsis

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

Septic shock

• Patients with sepsis who develop underlying circulatory and meatbolic abnormalities

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

  • And having serum lactate level of >= 2 mmol/L despite adequate volume resuscitation

Patho 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 mutliple cellular components and signaling systems

Inflammatory things come out to fix the problem

How sepsis effects 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- decreased afterload too far (ON TEST)

Cardiovascular- hypotension due to vasodilation from nitrous oxide and protacyclin release

Patients at risk for septic shock

Immunosuppression

Trauma Victims

Chronic illness

Invasive procedure

Poor nutrition

Extremes of age

Manifestations of septic shock

Hypotension

Tachycardia

Fever

High-CO- body is trying to compensate (SNS is working to fix this)

Skin warm and dry; flushed

Mild hyperventilation (to get rid of CO2); respiratory alkalosis

Decreased LOC

Urine output adequate initially

• As long as your compensatory you’ll have urine output

Additional facts

Sepsis is associated with DIC (widespread clotting AND bleeding), ARDS (lungs failing), MODS, and death

1.7 million people have sepsis in 1 year

• Mortality rate is approx. 40-50%

Increased incidence as population is growing older

Initital resuscitations

Best practice- Treatment and initial resuscitation begin ASAP

• Cultures, if at all possible → blood cultures should be possible (gotta know what the bug is so they can treat it with a proper antibiotic)

• At least 30 ml/kg crystalloids within the first 3 hours - frequently lactated ringers

  • 100 kg pt x 30cc = 3 liters (to increase pressure and fill everything back up)

• Guide resuscitation to decrease serum lactate levels (if high, anerobic metabolism and cell death, can measure how well we are doing)

• Use capillary refill to guide resuscitation (abnorm >2-3 secs)

• If receiving large amounts of crystalloids, consider albumin

For patients not responding to fluid resuscitation (MAP <65 mmHg). Add a vasopressor - norepinephrine (the reason we pick norepinephrine, because the heart is struggling to get anything done and need some support, very good vasopressor)

Within first hour (“1 hour bundle”)

Measure lactate level (tells how we’re doing if better or worse)

• Remeasure if initial lactate is elevated (.2mmol/L)

Obtain blood cultures before administering antibiotics (cultures first then broad spectrum antibiotic then getting results specific antibiotic)

Administer broad spectrum antibiotics

Begin rapid fluid administration (may need up to 3L)

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

Apply vasopressor if hypotensive during or after fluid administration to maintain MAP >= 65 mm Hg

Infection

Begin antibiotic within the first hour if septic or has septic shock

• Cultures first, if at all possible

• Beta-lactam antibiotics (pencillins cephalosporin, carbapenems)

Continuously look or 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 patient is stable (whatever else we need to do)

• Tylenol for fever and therefore comfort

• Target Hgb 7-9 g/dl

• Manage glucose if 2 consecutive levels >180 mg/dl (under stress body may become hypoglycemic)

• DVT prophylaxis

• Stress ulcer prophylaxis

• Begin oral or enteral feedings

  • Should provide low dose feeding in the first week (up to 500kcal/day)

Anaphylactic shock

Acute and life-threatening allergic reaction

Massive dilation, increased capillary permeability, microvascular leakage

Histamine release: bronchospasm and laryngospasm

Serotonin release: pulmonary edema

Allergic reaction also calling massive vasodilation

Caused by histamine release

Treatment of anaphylactic shock

Airway maintenance (main focus stridor or can’t get air moving trachea is swollen get intubated)

Support circulation

Antihistamine (because thats the cause)

Epi. (gives you bronchodilation then Benadryl that's the antihistamine)

Patient usually recovers quickly

Hypovolemic shock chart

Hypovolemic shock → Blood loss, Fluid loss, Fluid shift

Blood loss → Trauma surgery → Absolute

Fluid loss → Diarrhea, vomiting, DI, Diuretics → Absolute

Fluid shift (fluid is in the third space) → Burn, ascites → relative

Pathophysiology og hypovolemic shock

Decreased intravascular volume

Decreased venous return (preload) low

Decreased SV (nothing to pump out cause nothing came back)

Decreased CO

Inadequate tissue perfusion

Anoxia

Treatment of hypovolemic shock

Rapid volume replacement until CO, Hgb, ABG’s, and BP is normaland UO 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

Just an extension of CHF
Patient at risk: myocardial infarction, cardiomyopathies, VSD, Dysrhythmias, electrolyte imbalances, medications

Caused by pump failure

Patho: decreased SV

Decreased CO

Decreased BP

Decreased organ perfusion

Decreased coronary artery perfusion which causes myocardial ischemia and infarction

Patho: increased LV pressure

Increased LA pressure, Increased pulmonary capillary wedge pressure (because you can’t pump out, pump is failing, backs up into lungs)

Increased pulmonary venous pressure

Movement of pulmonary capillary fluid causing interstitial edema and intraalveolar edema

Treatment

Goal is to increase CO, reduce preload and reduce afterload

IV medications: inotropes, vasodilators, diuretics

Cautious fluid replacement

Antiarrhtythmic

IABP (balloon pump) and VAD (Ventricular assits devices) (both help the heart pump easier)

Dobutamine and Milrinone (doesn’t work on sns)`