1. Discuss the indicators of, and the treatment for, various presentations of shock
2. Identify acid-base imbalances
3. Identify terminology used with ventilator management
4. Identify labs used for specific disease processes
5. Identify normal values and appropriate treatment abnormal values for:
6. Right atrial pressure (RA / CVP)
7. Pulmonary artery pressure S,D,M
8. PAOP (PCWP) aka "wedge" pressure
9. Cardiac output (CO)
10. Cardiac index (CI)

 

1. Discuss the indicators of, and the treatment for, various presentations of shock

Collaborative Care: General Measures

 Successful management of the patient in shock includes the following: (1) identification of patients at risk for the development of shock; (2) integration of the patient's history, physical examination, and clinical findings to establish a diagnosis; (3) interventions to control or eliminate the cause of the decreased perfusion; (4) protection of target and distal organs from dysfunction; and (5) provision of multisystem supportive care.

• General management strategies for a patient in shock begin with ensuring that the patient has a patent airway and oxygen delivery is optimized. The cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion with the administration of the appropriate fluid.

• The primary goal of drug therapy for shock is the correction of decreased tissue perfusion. Vasopressor or vasodilator therapy is used according to patient needs to maintain the mean arterial pressure at the appropriate level.

• Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in shock; nutrition is vital to decreasing morbidity from shock.

SHOCK

• Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply of and demand for oxygen and nutrients.

• The four main categories of shock are cardiogenic, hypovolemic, distributive (includes septic, anaphylactic, and neurogenic shock), and obstructive.

Cardiogenic Shock

Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in reduced cardiac output (CO).

• Causes of cardiogenic shock include acute myocardial infarction (AMI), cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, and myocardial depression from metabolic problems.

• Clinical manifestations include tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, diaphoresis, decreased capillary refill

Hypovolemic Shock

• Hypovolemic shock occurs when there is a loss of intravascular fluid volume.

• Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis.

• Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space, such as with sepsis and burns.

• Clinical manifestations depend on the extent of injury or insult, age, and general state of health and may include anxiety; an increase in heart rate, CO, and respiratory rate and depth; and a decrease in stroke volume, pulmonary artery wedge pressure (PAWP), and urine output.

Neurogenic Shock

• Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in response to spinal anesthesia.

• Clinical manifestations include hypotension, bradycardia, temperature dysregulation (resulting in heat loss), dry skin, and poikilothermia.

Anaphylactic Shock

• Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom).

• Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability resulting in fluid leaks from the vascular space into the interstitial space.

• Clinical manifestations can include anxiety, confusion, dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria, and angioedema.

Septic Shock

• Sepsis is a systemic inflammatory response to a documented or suspected infection. Severe sepsis is sepsis complicated by organ dysfunction.

• Septic shock is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of inadequate tissue perfusion.

• In severe sepsis and septic shock, the body's response to infection is exaggerated, resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis.

• Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression.

• Patients often have hypotension, respiratory failure, alteration in neurologic status, decreased urine output, and GI dysfunction.

Collaborative Care: Specific Measures: Cardiogenic Shock

• The overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand.

• Definitive measures include thrombolytic therapy, angioplasty with stenting, emergency revascularization, and valve replacement.

• Care involves hemodynamic monitoring, drug therapy (e.g., diuretics to reduce preload), and use of circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device).

Collaborative Care: Specific Measures: Hypovolemic Shock

• The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume.

Collaborative Care: Specific Measures: Septic Shock

• Patients in septic shock require large amounts of fluid replacement; the goal is to achieve a target central venous pressure (CVP) of 8 to 12 mm Hg.

• Vasopressor drug therapy may be added once CVP is ≥8 mm Hg; vasopressin may be given to patients refractory to vasopressor therapy.

• Intravenous corticosteroids are only recommended for patients who cannot maintain an adequate blood pressure (BP) with vasopressor therapy, despite fluid resuscitation.

• Antibiotics are an important component of therapy and should be started within the first hour of septic shock.

Collaborative Care: Specific Measures: Neurogenic Shock

• The treatment of neurogenic shock is dependent on the cause. In spinal cord injury, general measures to promote spinal stability are initially used.

• Treatment of hypotension and bradycardia involves the use of vasopressors and atropine, respectively. Fluids are administered cautiously; the patient is monitored for hypothermia.

Collaborative Care: Specific Measures: Anaphylactic Shock

• Epinephrine is the drug of choice to treat anaphylactic shock.

• Maintaining the airway is critical; endotracheal intubation or cricothyroidotomy may be necessary.

• Aggressive fluid replacement, predominantly with colloids, is necessary.

Collaborative Care: Specific Measures: Obstructive Shock

• The primary strategy in treating obstructive shock is early recognition and treatment to relieve or manage the obstruction.

 

2.Identify acid-base imbalances

Acid-Base Regulation

- normal metabolic processes produce acids, and the body must neutralize and excrete them to maintain a normal balance between acids and bases

- the body has 3 mechanisms by which is regulates the acid-base balance to maintain the arterial pH between 7.35 and 7.45

- these systems are THE BUFFER SYSTEM, THE RESPIRATORY SYSTEM, AND THE RENAL SYSTEM

- they all react at different speed

- buffers react immediately

- respiratory system responds in minutes and reaches maximum effectiveness in hours

- the renal response takes 2-3 days to respond maximally but the kidneys can maintain balance indefinitely in chronic imbalances

Alterations in Acid-Base Balance

- acid base imbalances result when there is an alteration in the ratio of 20:1 between base and acid content ((((20 base, 1 acid)))))

- this occurs when COMPENSATORY MECHANISMS FAIL!!

- occurs when a primary disease or process alters one side of the ratio (CO2 retention in pulmonary disease) and the compensatory processes that maintain the other side of the ratio (increased renal bicarb reabsorption) either fail or are inadequate

- compensatory process may be inadequate because either the pathophysiologic process is overwhelming or there is insufficient time for the compensatory process to function

- acid-base imbalances are classified as respiratory or metabolic

- respiratory = excess/retention of CO2, altering carbonic acid concentration

- metabolic = effect the kidney base bicarbonate

- acidosis; caused by increase in carbonic acid (respiratory) or by a decrease in bicarb (metabolic)

- alkalosis; caused by a decrease in carbonic acid (respiratory) or by an increase in bicarbonate (metabolic)

- acute or chronic (chronic imbalances allow greater time for compensatory changes)

Clinical Manifestations of Acid-Base Imbalance

- in both respiratory and metabolic, the CNS is depressed

- decreased levels of consciousness, headache, weakness, confusion develop and will lead to coma and death

- in both types of alkalosis (metabolic/respiratory), irritability of the CNS occurs causing tingling and numbness of fingers, restlessness and tetany

- compensatory mechanisms also produce specific clinical manifestations (ex: deep, rapid respirations of a patient with metabolic acidosis are an example of respiratory compensation)

- in alkalosis, HYPOCALCEMIA occurs because of increased calcium binding with albumin, lowering the amount of ionized biologically active calcium

- hypocalcemia accounts for many of the clinical manifestations of alkalosis

 

3.Identify terminology used with ventilator management

Mode

• This determines the types of breaths that the patient receives via the Ventilator. There are 3 Major Modes: Control, Assist Control & SIMV.

Control Mode

• This mode allows the patient to only receive Mechanical Breaths. Spontaneous Breaths from the patient are ignored by the ventilator.

Assist Control

• This mode allows the patient to receive Mechanical Breaths by the Ventilator as well as extra breaths that the patient may trigger as long as the patient has the right amount of effort to trigger. So patient may get the set amount of breathes from the vent & extra breaths as needed from patient effort.

SIMV

• Spontaneous Intermittent Mechanical Ventilation-This mode allows the patient to receive Mechanical Breaths from the Ventilator as well a extra breaths. The breaths that the patient receives though are all patient effort breaths without any help from the ventilator. In other words patient is breathing on their own as if they were not attached to the ventilator.

Tidal Volume

• This is the quantity of air that the patient's receives in Volume. This is one of the 2 ways for a patient to get air delivered to the lungs. Another way to get air delivered to the lungs is by Pressure Limit. Ex: 500cc

Pressure Limit

• This is the quantity that the patient receives in Pressure. This is one of the 2 ways for a patient to get air delivered to the lungs. Lungs are inflated to a pre-set pressure & once that pressure is reached the ventilator stops delivering the air per breath. Ex: 30 cmh2o.

Respiratory Rate

• This is the amount of breaths the patient receives per minute. Dr. recommends a certain amount per patient based on diagnosis. Ex: 20 BPM (Breaths Per Minute).

Flow

• This is the speed in which the patient receives their air in Flow (Liters Per Minute). It is one of the 2 ways to determine how fast the patient should receive their air. The other way is by I Time. Example For Flow: 60 I/m

I Time

• This is the speed in which the patient receives their in time (sec.). It is one of the 2 ways the patient receives their air. The other way is by Flow. Example for I Time: 1.0 sec.

Sensitivity

• This setting allows the patient to trigger extra breaths once the patient reaches the set sensitivity. The higher the number the less sensitive to trigger. The lower the number the easier it is to trigger. Ex: -5cmh2o.

PEEP

• Positive End Exhalation Pressure. This option allows the patient to not fully exhale all their air during the exhalation phase of a breathing cycle. This pressure is designed to improve oxygenation. It is very beneficial for patients sensitive to oxygen. Ex: 4cmh2o

Pressure Support

• It can only be used during one specific mode of ventilation which is SIMV Mode. It can not be used with any other mode. During a spontaneous breath, the patient receives a burst of air to help assist the patient inflate their lungs when their own effort is not sufficient enough. It only applies when the patient breathes on their own. Ex: 5cmh2o.

FiO2

• Stand for Fraction of Inspired Oxygen. It is used to determine how much oxygen is delivered to the patient in the form of a certain percentage of oxygen or a fraction of oxygen. There is approximately 20-21% oxygen in room air. If the Dr recommends additional oxygen then it must be added to the room air oxygen already available. The Formula to help convert FiO2 to Liters per minute is: 1 L/M=4% Oxygen. Ex: Dr prescribed 40% O2 for a pt. There is 20-21% in R/A so we need to add additional Oxygen to get 40%. 5X4%=20% +R/A (20-21%)=40-41%. It will take 5 L/M to get approximately 40% Oxygen to the patient.

High Pressure Alarm

• This alarm is triggered when too much pressure is needed to inflate the lungs. Usually this alarm is caused by an Obstruction. There are 4 major causes: Mucus Plug, Coughing, Kinked Tubing and Water in the Tubes. The gauge on the ventilator will show to what extent the pressure rises causing the high pressure alarm.

Low Pressure

• This alarm is triggered when the pt's pressure to inflate the lungs is too low. There is usually 1 major cause for this alarm and that is air leak.

Minute Ventilation

• Allows us to monitor the pt's Respiratory Rate and Lung Volume in calculated form. The formula is Vi or VE=RR X Vt (i or e). This allows us to make sure that the pt. is constantly inhaling the right amount of air at the proper respiratory rate. The volume is measured either during the Inhalation or Exhalation (i or e) phase.

High Minute Ventilation

• When the Minute Ventilation number rises past the limited range the High Minute Ventilation Alarm is triggered. If it's High Vi (Volume Inhaled) then either the Respiratory Rate is too high or the Volume of air is too high. The resulting calculated Vi number is high. High Ve (Volume Exhaled) does not apply to Volume since it can never go too high than the amount of air that the pt. can breathe. The only thing that can be measured too high for Ve would be high respiratory rate. Most vent's don't have high Ve when measuring exhaled Volume.

Low Minute Ventilation

• When the Minute Ventilation number falls below the limited range then the low Minute Ventilation Alarm is triggered. If it's Low Vi (Volume Inhaled) the the measured Volume is too low. The Respiratory Rate can not fall because it always has a set prescribed respiratory rate from the Dr orders. So it usually applies to Volume Inhaled only. The same is true for Low Ve (Volume Exhaled). If the Volume measured on exhalation is too low then the calculated Ve will drop causing a low Ve Alarm to be triggered.

4.Identify labs used for specific disease processes

5.Identify normal values and appropriate treatment abnormal values for:

 

Hemodynamic Monitoring is a direct system of measuring:

-Heart/Blood Pressure

-Pulmonary Artery Pressure (AP)

-Central Venous Pressure (CVP, RA)

-Intra-Arterial Pressure

-Wedge Pressure

 

Right atrial pressure (RA / CVP)

• -Assesses right ventricular function and venous return to the right side of heart
• -Proximal port of the pulmonary artery catheter (in RA)
• -Direct method of measuring right ventricular filling pressure (preload)

What is the CVP (volume)?

-The pressure within the superior vena cava; it reflects the pressure under which the blood is returned to the superior vena cava and right atrium (preload)

-The CVP is measured with a central venous catheter in the superior vena cava

-Normal CVP is 3-8 mm Hg

Elevated CVP indicates:

-An increase volume (sodium and water retention)

-Decreased contractility

-Excessive IV fluids

-Kidney failure

Decreased CVP indicates

-Decrease in intravascular volume

-Hemorrhage

-Severe vasodilation

-Pooling of blood in the extremities

How do you measure the CVP?

-Identify the level of the right atrium

-Patient supine

-Zero the transducer to the right atrium

-Patient relaxed

-If on ventilator reading is taken at the point of end expiration

 

What does Pulmonary Artery Pressure assess and diagnose?

-Assesses LV function

-Diagnosis of etiology of shock

-Assesses response to interventions such as administration of volume and medications that are vasoactive

How is PAWP or PCWP (pulmonary artery wedge pressure or pulmonary capillary wedge pressure) achieved?

• Wedge is achieved by momentary inflation of the balloon and watching the waveform dampen

What is the normal Wedge Pressure?

• Wedge pressure is normally 4-12 mm Hg and is reflective of the LV function

What is the normal Cardiac Output?

• 4-7 Liters per Minute

How is the Cardiac Index calculated and what is the normal Cardiac Index?

• Cardiac Index is calculated using BSA (CO/BSA)
• Normal is 2.5-4 L/min/m2
• Calculates out patients size

Step-by-step explanation

Stages of Shock

• The initial stage of shock that occurs at a cellular level is usually not clinically apparent.

• The compensatory stage is clinically apparent and involves neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis.

• The progressive stage of shock begins as compensatory mechanisms fail and aggressive interventions are necessary to prevent the development of multiple-organ dysfunction system (MODS).

• In the irreversible stage, decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism. The patient will demonstrate profound hypotension and hypoxemia, as well as organ failure; at this stage, recovery is unlikely.

Diagnostic Studies

• There is no specific diagnostic study to determine shock. The diagnosis depends on the history and physical.

• Studies that assist in diagnosis include a serum lactate, base deficit, 12-lead ECG, continuous cardiac monitoring, chest x-ray, continuous pulse oximetry, and hemodynamic monitoring.

 

What causes an increase in Right Arterial Pressure?

• Increase in RA due to right ventricular failure, hypervolemia or decreased contractility

 

How does the PA catheter calculate the Cardiac Output?

• There is a temperature probe (thermistor) at the end of the PA catheter and in the pressure tubing. The cardiac output monitor measures the difference in the two temperatures and calculates the cardiac output