Hemodynamic Monitoring/Shock

Cardiac Output (CO) X Systemic Vascular Resistance (SVR) =

Arterial BP

Cardiac output

Stroke Volume X Heart Rate

Stroke Volume

Preload, Afterload and contractility

Preload (PL)

stretching of ventricles related to cover cardiac blood volume

Afterload same as SVR need for ventricular filling and needs to be overcome by the heart

Contractility factors

calcium, epi, o2

CO/CI (cardiac output) – 4-8L/min

PVR

(<250 dynes*sec/cm5) pulmonary VR

SVR

900-1400 dynes/sec/cm

SVO2

(60-75%) mixed venous oxygen saturation how oxygenated is the blood before the lungs (how much oxygen was use in the body)

MAP

60-80 mmHg (constant perfusion pressure)

CVP Central Venus pressure + SVC

2-6 mmHg (preload of R side)

PA (pulmonary artery)

25/10 mmHg (quarter over dime) (Left heart preload indirect)

PCWP (PAOP)

6-12 mmHg

Continuous monitoring

CVP and PA

General Poor perfusion signs

mental status change, weak pulses, SOB, lactic acidosis, High K

Poor perfusion volume depleted

dry mucus membrane and poor skin turgor with general signs

Poor perfusion with volume overload

edema, JVD, hepatomegaly splenomegaly with general sings

Ways to assess the variables of blood pressure/perfusion

Continuous BP monitoring with an arterial line, Central venous pressure monitoring, Pulmonary artery catheter

Continuous BP monitoring with

an arterial line (usually radial can also draw labs)

Central venous pressure monitoring

(through any central line) sits in SVC (2-4 no HCP wants it that low even though its technically normal)

Pulmonary artery catheter

(swan cath, goes through cordis usually subclavian, thread it thought the cordis (like Large IV) floated all the way to Pulmonary Artery

Hemodynamic Monitoring Systems

Readings displayed as waveforms on a monitor. Transducer is the “synapse” between the patient and monitor, Leveled to the phlebostatic axis. Pressurized tubing system to maintain patency

Leveled to the phlebostatic axis.

phlebostatic axis.

Right atria of the heart bc it’s the place where pressure is the closes to 0

phlebostatic axis. Anatomic landmarks

forth IC mid axially

Significance of leveling to the phlebostatic axis.?

Helps make other number accurate

When the patient is repositioned, the transducer is repositioned.

Transducer too high, values will be falsely low. Transducer too low, values will be falsely high

Hemodynamic Monitoring Pressurized tubing system to

maintain patency. (atrial pressure is a bit high 300

Hemodynamic Monitoring Infection and safety concerns

Can bleed most artery

Obtain values from central line or PA catheter at

end expiration. The pressure from thorax can cause inaccurate values

Arterial line care & SAFETY

Arterial line Always keep

the line in view. Not under blankets (sutured?)

Arterial line Routinely assess

perfusion of distal extremity RT are supposed to do the Allens test shouldn’t (make sure ulnar is fully function b4 occulting the other))

Arterial line Maintain

pressurized system.

Arterial line Compare

to non-invasive BP values.

Arterial line NEVER

turn off alarms and administer meds or fluids through (goes through capillary hand first cant handle)

Arterial line If discontinuing the line, hold pressure

3-5 minutes routinely, 10 minutes or more if the patient is receiving anti-coagulants.

Only qualified health care providers should place/advance the PA catheter because risk for

arrythmias, misplacement, knotting of Cather, MI, vessel or valve rupture

PA catheter Rn can

inflate ballon and wedge the catchers (with HCP orders) not commonly done anymore – similar of PA diastolic values Left side preload)

PA catheter Secure the catheter and document the catheter position

at the beginning of the shift.

Usually 50-60 cm Want to make sure it hasn’t moved, changes values, can cause ectopic beats etc.

PA catheter Marking

thick 50 cm thin 10 cm. Estimate the distance to the tip

PA catheter Monitor for

inappropriate balloon inflation/prolonged wedge!

How would you recognize inappropriate balloon inflation

wedged wave form

inappropriate balloon inflation Why is it a problem?

Occultation of forward blood flow from pulmonary arteries

inappropriate balloon inflation prevention? How to respond?

Look if ballon inflated, position of catheter, suction the patient, Cough, turn patient from side to side , If it doesn’t resolve, call HCP

PA catheter Notify the health care provider (HCP)for

development of ventricular ectopic beats (PVCs). Could be that the catheters in Right ventricle , check the placement, , If many PVC  V tach

PA catheter what to do if development of ventricular ectopic beats (PVCs).

Check placement check wave form notify may need to withdraw with ballon down deflated, RN is qualified to pull it out , don’t move it forward call HCP

Shock

Circulatory system unable to supply adequate amount of oxygen to the tissues to meet basic metabolic requirements “poor perfusion”

ALL types of shock have in common

Poor perfusion / hypotension , potential for Lactic Acidosis, Hyper Kalema

Types of Shock

Hypovolemic, Cardiogenic, obstructive , Distributive (anaphylaxis, neurogenic, septic)

Shock Compensatory Systems

RAAS, SNS, ADH Together they – vasoconstriction (gut mainly), and volume retention

Hypovolemic Common Causes

Hemorrhagic Shock, Extracellular Fluid or Plasma Loss (Gi, burns)

Hypovolemic Hemodynamic Changes

CVP down , PAOP or (PA diastolic) criticality low, CO low , SVR increase - compensation / vasoconstriction

Cardiogenic Common Causes

Myocardial Damage (MI) Valvular Heart disease, Sustained Arrhythmia

Cardiogenic Hemodynamic Changes

CVP up , PAOP up, CO down (critically), SVR up

Obstructive Common Causes

Obstructed systole (PE), Obstructed Diastole (Cardiac Tamponade), Obstructed venous flow (tension pneumothorax or asthma)

Obstructive Hemodynamic Changes

CVP up, PAOP up, CO down, SVR up

Neurogenic common causes

Spinal cord injury above T6 (blocks SNS from going down)

Neurogenic shock

CVP low, PAOP low , CO – low (bradycardia can’t compensate), SVR – low (no SNS response) below injury level dilated

Anaphylactic shock

CVP - Low, PAOP – low, CO – low, SVR – low (vasodilated)

Septic Shock early

warm, hyperdynamic, vasodilation, High HR, CO, BP not low, fever, flushed, restlessness

Septic Shock late

Cold vasoconstriction, High HR, low CO, high RR, low BP, Map < 65, Oliguria, cold clammy skin, metalstsi change, Lactate >4 mm

Inflammatory medicators make

adrenergic receptors less receptive to hormones (epi and norepi)

High RR in late septic shock because

Compastions low perfusion, and get rid of CO2 (acid base balancing, acidic from lactate)

Sepsis is

“life threatening organ dysfunction caused by a dysregulated/deregulated host response to an infection.”

Septic shock occurs when

“circulatory and metabolic abnormalities are profound, greatly increasing mortality.”

Sepsis Pathophysiology

Activation of innate immune response, Aggressive inflammatory response (SIRS), Endothelial damage (vasodilation, loss of tone, increased permeability). Activation of clotting (DIC Potential), Myocardial suppression, Activation of compensatory systems (RAAS, SNS), Acute respiratory distress syndrome (ARDS) potential, Multiple organ dysfunction syndrome (MODS)

Sepsis Pathophysiology Endothelial damage

vasodilation, loss of tone, increased permeability causing low preload and volume

Sepsis Pathophysiology Activation of compensatory systems

RAAS, SNS causes gut neglect watch for ileus and gut death

Sepsis Pathophysiology Acute respiratory distress syndrome (ARDS) potential

because of fluids leaking to lungs and alveoli

Sepsis Pathophysiology Multiple organ dysfunction syndrome (MODS)

low CO means low perfusion, low function and death of organs

Risk factors for sepsis

ICU Admission, Bacteremia (+ cultures), Advanced age (65 or older), Immunosuppression, Diabetes and obesity, Cancer, Community acquired PNA, Previous hospitalization, Genetic factors

Clinical recognition of Sepsis qSOFA

Resp Rate ≥ 22, Altered LOC, Systolic BP ≤ 100 mm Hg (Score of >2 criteria suggests a greater risk of a poor outcome )

Sepsis Early Stage

(hyperdynamic, warm),Tachycardia with bounding pulses, Warm, flushed skin and fever, Blood pressure may be OK due to compensatory efforts, Initial signs of decreased organ perfusion possible—confusion, decreased UOP, Increased CO as long as there is adequate fluid administration

Confusion in elderly always think

infection

Sepsis Late Stage

(Hypodynamic, cold) Cool, pale skin, decreased temp, Tachycardia, weak/thready pulses, Hypotension, Signs of hypoperfusion—decreasing LOC, anuria

Sepsis Late Stage decreased temp because

hypothallus no longer responding

Sepsis Additional potential manifestations

Symptoms and signs specific to an infection, pain increase, Tachypnea, Delayed capillary refill(slows down before BP), Hypoactive or absent bowel sounds (ileus potential), Cyanosis, or mottling of skin in late stages.

pain increase with sepsis because

same mediators for inflammation are the ones for pain

If the patient has hemodynamic lines

respond to what the numbers are telling you, CO low CVP low PA diastolic low (fluids), if SVR low vasopressors

Essential Diagnostic Criteria for Septic Shock

Confirmed or suspected infection, MAP, Serum lactate

Diagnostic Criteria for Septic Shock MAP

less than/equal to 65 mm Hg even after fluid resuscitation—vasopressors needed to keep BP up.

Diagnostic Criteria for Septic Shock Serum lactate

remains elevated even after fluid resuscitation.

Surviving Sepsis Campaign Bundle

(within 1 hour of sepsis dx—see table), Lactate level, Blood cultures (before Abx), Broad spectrum Abx, Fluid resuscitation (30 ml/kg bolus), Vasopressors for BP that doesn’t respond to fluids

Sepsis Fluid resuscitation (30 ml/kg bolus) if

Hypotension OR Lactate 4 mmol/L or greater

Vasopressors for BP that doesn’t respond to fluids.

(maintain MAP ≥ 65 mm Hg)

Sepsis Additional helpful labs

increased WBC count, Pan culture, Procalcitonin, increased Blood glucose, C-reactive protein, Serum creatinine, Bilirubin and liver enzymes, Electrolytes (K), ABG changes

Procalcitonin

inflammatory markers for specially bacterial infections

Sepsis ABG changes

metabolic acidosis (low HCO₃⁻, low Co2), respiratory acidosis (high CO2 ARDS) to MIXED acidosis (low HCO₃⁻, high CO2)

DIC lab assessment

low Platelet count, Fibrinogen, Protein C & S, high D Dimer , Pt/INR, PTT

DIC treatment

replace plasma and platelets, may give crypto precipitate (just clotting factors), may give heparin

Sepsis Additional Patient Care Concerns

Oxygenation, Fluid Resuscitation, Possible corticosteroids, Possible blood products, Insulin, Nutrition, Skin care, DVT prevention, Vitamin C

Sepsis Fluid Resuscitation

Crystalloid (NS or LR (more balance), Colloid (protein) albumin

Sepsis Assessing response to fluid

increased blood pressure (1st), UOP,

Sepsis Treatment Possible corticosteroids

controversial, decrease inflammation (can help adrenal fatigue)

Sepsis Treatment Possible blood products

PRBCs, FFP, Platelets (DIC)