Hemodynamic Stability

hemodynamic stability

refers to the heart pumping blood through the vessels at a sufficient force that maintains a steady state of blood to all tissues and organs

hemodynamic instability

a clinical state of perfusion failure. It may be caused by circulatory shock (e.g., hypovolemia), heart failure, or other pathologic conditions. Clinical signs of acute circulatory failure include hypotension, abnormal HR, cold extremities, peripheral cyanosis, increased right-sided filling pressure, and decreased urine output

What Does Hemodynamic Instability Mean for My Patient?

Increased confusion, inability to follow basic commands
Fatigue with poor activity tolerance
Dyspnea
Diaphoresis, inability to regulate body temperature
Decreased blood pressure, syncope
Loss of consciousness

*Overall reduced ability to tolerate any type of physical activity

causes of hemodynamic instability

• Within the hospital setting, postoperative complication can lead to hemodynamic instability

• May occur in the post anesthesia care unit (PACU) and could be caused by anything listed below...

• Other events outside of the hospital can lead to an ED visit...MVA, MI, critical illness, etc, leading to one of the conditions below...

• Critical loss of blood volume (hypovolemic shock)
  ◦ External blood/fluid loss or internal bleeding

• Obstruction of blood flow (obstructive shock)
  ◦ PE, dissecting AAA

• Heart pump failure (cardiogenic shock)
  ◦ MI

• Loss of blood distribution (distributive shock)
  ◦ Systemic vasodilation caused by sepsis, SIRS, anaphylaxis, severe burns

sepsis

• A life-threatening organ dysfunction due to a dysregulated host response to an infection

• Risk factors: age, frailty, multiple comorbidities, indwelling lines or catheters, invasive procedures, breach in skin integrity, and immunosuppression

• High mortality rate increases with age, 5x higher among adults aged 85 and older

• Leading cause of hospitalization and most expensive inpatient condition

• Sepsis differentiated from infection by a dysregulated host response that results in organ dysfunction

• Loss of adaptive homeostasis in response to infection
  

sepsis clinical considerations

• Early activity and minimization of sedatives can help prevent critical illness acquired weakness/ myopathy and critical illness polyneuropathy
  ◦ These are forms of ICU-acquired weakness (ICUAW)

• Warrants close monitoring of all vital signs

• MAP is the primary clinical target during medical treatment for sepsis
  ◦ MAP Goal: > 65 mmHg
  ◦ ECG, temperature, oxygenation (PaO2/ FiO2 ratio), electrolytes, glucose, and arterial blood gas (ABGs) are closely monitored

• Older adults as well as individuals undergoing cancer treatments are less likely to develop an ↑ temperature with sepsis

role of vasoactive drugs

• Inotropic, vasopressor, or vasodilator agents provide temporary hemodynamic support to assist in the recovery of hemodynamically unstable patients

• Used to improve SVR and blood pressure

• Patients be on one or more agents
  ◦ Categorized into either low, moderate, or high level of support

• Vasoactive drugs are an independent risk factor for the development of ICU-acquired weakness
  ◦ Can be minimized by early mobilization

• May be barrier to mobilizing patient
  ◦ Hospitals may have protocols (ie, patients on >2 agents are not mobilized

My Patient is on Vasoactive Agents and is Hemodynamically Stable-Now What?

the important component that influences the clinical decision to initiate mobilization was the hemodynamic stability of the patient, not the dosage, or the number of vasoactive drugs

use of sedatives in ICU

• Sedation is commonly used in ICU and sedation protocols are in widespread use and are considered best practice

• Purpose:
  • allows patients to tolerate painful/distressing procedures (e.g. endotracheal intubation, invasive lines)
  • optimize mechanical ventilation (e.g. tolerate permissive hypercapnia)
  • used to decrease O2 consumption (e.g. sepsis)
  • decrease ICP in neurosurgical patients
  • facilitate cooling (e.g. therapeutic hypothermia)
  • control agitation

• Sedation is a common reason why Rehab (PT, OT, SLP) cannot proceed with patient evaluations

common AE - sedatives

• hypotension

• respiratory depression

• arrhythmias

• drug specific effects

• sleep disturbance

• withdrawal\

• delirium

Richmond Agitation-Sedation Score

• assess depth of sedation

• Most patients titrated to a RASS score of -2 or higher (no more than light sedation); very ill or agitated patients (e.g., severe ARDS, raised ICP) may “rarely” require RASS -3 or -4

at what RASS level do you think patients can participate w/ PT?

-1 → +1

richmond sedation scale

+4 Combative
+3 Very agitated
+2 Agitated
+1 Restless
0 Alert and calm
-1 Drowsy
-2 Light sedation
-3 Moderate sedation
-4 Deep sedation
-5 Unrousable

pulmonary measures - lack of readiness for PT

• SpO2: <88% or patient experiences a 10% oxygen desaturation below resting SpO2

• Respiratory rate: >50 breaths/min

• PEEP: >10 cm H2O

• FiO2: ≥0.6 (60%

lab values- lack of readiness for PT

◦ HCT <20%: May need to hold PT
◦ HGB <8 g/dl: May need to hold PT
◦ Platelets <20,000: No exercise
◦ Platelets Anticoag INR >4: High risk for bleeding, Hold

CV measures - lack of readiness for PT

◦ MAP: <65 or >120 mm Hg or ≥10 mm Hg lower than normal systolic or diastolic blood pressure for patients receiving renal dialysis
◦ Resting HR: <50 or >140 bpm
◦ Systolic blood pressure: <80 or >180 mm Hg
◦ New arrhythmia developed (including frequent ventricular ectopic beats or new onset atrial fibrillation)
◦ New onset angina-type chest pain

metabolic measure- lack of readiness for PT

◦ Fasting glucose levels <70 or >240 mg/dL

implications for PT

• Patients who are hemodynamically stable can safely response to increased vascular and oxygen demands of physical exam and treatment

• Patient status can fluctuate daily, hourly, and by the minute
  • “Response-dependent management”

• Requires moment-to-moment interpretation of patient response
  • Delivery of oxygen must match consumption of oxygen!

OH complications

• Orthostatic hypotension can occur within 3 weeks of bed rest– sooner for elderly

• Excessive pooling of blood in LEs, decreased circulating blood volume, rapid HR = diminished diastolic ventricular filling and decline in cerebral perfusion

• Characterized by drop in BP during a change in position (supinesittingstanding)

• Drop of more than 20 mm Hg systolic and 10 mm Hg diastolic accompanied by 10-20% increased HR

OH tx

• Early mobilization!

• LE exercises to increase blood circulation

• Compression stockings (TED hose)

• Slowly increasing head of bed height

• Patient may only tolerate sitting upright in bed before being able to sit EOB

• Tilt table for very prolonged immobilization or profound ANS issues (SCI)

• These tables are usually found in inpatient rehab hospitals rather than acute/ICU

Decreased FRC (blue+tan)

◦ Less alveolar tension pulling airways open, narrowing airway results in increased airway resistance
◦ Can cause shunts and atelectasis

Decreased RV and TV (tan+green)

◦ Causes decreased ventilation and minute ventilator volume
◦ Results in increased resting respiratory rate

immobility cardiopulm effects

increased risk for atelectasis and pneumonia: impaired ability to clear airway

hematologic effects

• RBC mass reduction by 5% to 25%

• Decreased total blood volume, red blood cell mass, and plasma volume

• Elevated HCT due to decreased plasma volume → DVT

• Reduced capillarization of muscle beds

Hematologic Effects: DVTs

• Venous thromboembolism: Virchow

• Triad
  ◦ Venous stasis
  ◦ Hypercoagulability
  ◦ Blood vessel damage

• Primary site: calf and soleus sinus

• Length of bed rest directly related to frequency of DVT

• Often no clinical signs of DVT
  ◦ Clinical signs usually unreliable
  ◦ Pain and calf tenderness, swelling, redness, positive Homan’s sign

• Doppler US, contrast venography (gold standard)

Hematologic Effects: DVTs treatment

• Treatment
  ◦ Early mobility, LE exercise
  ◦ Compression stockings
  ◦ Leg elevation

• Prophylactic methods
  ◦ Low-dose heparin,
  ◦ Sequential compression device (SCD)

• Pharmacology
  ◦ Unfractionated heparin (UFH)
  ◦ heparin: IV
  ◦ warfarin (Coumadin): PO
  ◦ Low Molecular Weight Heparin (LMWH)
  ◦ enoxaparin (Lovenox), dalteparin (Fragmin)
  ◦ Novel oral anticoagulants (NOACs)
  ◦ rivaroxaban (Xarelto), apixaban (Eliquis)

MSK effects

• Key elements of bedrest contributing to musculoskeletal changes:
  ◦ Lack of LE weight-bearing forces
  ◦ Decreased number/magnitude of muscle contractions

• Adaptations to decreased loading occurs WITHIN DAYS of immobility

• Aerobic metabolism enzymes decreased while anaerobic pathway enzymes spared

• Loss of aerobic capability and spared glycolytic pathway leads to early fatigue

• Fiber atrophy also leads to reduced total mitochondria content → impaired endurance capacity
  • Rate of recovery: SLOW!

changes in muscle fibers

• Decrease in size

• Type IIB (fast twitch) more affected than type I (slow twitch) and type IIA (intermediate fibers)

• Type IIA transition to type IIX and type IIB

effects of positioning

• Immobilization in shortened position → enhances atrophy

• Immobilization in lengthened/stretched position → may decrease loss of muscle fiber proteins

Musculoskeletal Connective Tissue and Joint Contractures

• In areas of little or no motion  collagen fibers laid down in dense, mesh sheets

• Collagen becomes shortened when immobilized

Musculoskeletal: Disuse Osteoporosis

• Healthy bone density depends on normal forces placed on bone: action of tendons pulling on bone, weight bearing

• Hypercalciuria and negative calcium balance results from immobilization

• Loss of bone mass is the result of increased bone resorption (parathyroid hormone not suppressed)

• Within one week of bedrest:
  ◦ Negative calcium balance

• Bone loss greater in LEs than UEs

• Calcaneus, femoral neck, spine

Integumentary: Decubitus Ulcer

• Lesion caused by unrelieved pressure resulting in damage to underlying tissue

• Usually occur over bony prominences that contact surface (sacrum, heels, ischial tuberosity, greater trochanter)

• PREVENTION is key
  ◦ Bed positioning with bed-bound patients
  (reposition high-risk patient at least every 2 hours)

GI effects

• Constipation
  ◦ From immobility, medications, disease process, medical procedures
  ◦ Movement helps, especially walking

• Ileus
  ◦ Reduced gastrointestinal propulsion without obstruction
  ◦ Most often caused by surgery but other causes include meds, trauma, illness

• Early mobilization is key to address these problems

neurologic effects

• Sensory and sleep deprivation

• Depression, restlessness, insomnia

• Decreased balance, coordination, visual acuity

• Increased risk compression neuropathy

• Reduced pain threshold

*delirium significant problem

Psychiatric/Cognitive Effects

• More than 50% of patients of all ages experience mood alterations during prolonged hospitalizations
  ◦ Anxiety
  ◦ Agitation
  ◦ Delirium
  ◦ Depression

• Reduced psych functioning leads to increased morbidity and mortality

• Intellectual and perceptual deficits result from altered sleep patterns, circadian rhythms, presence of noxious stimuli (noise, lights, etc)

delirium

• ICU Triad: Pain, Agitation and Delirium

• Syndrome
  ◦ Abrupt onset of inattention and other cognitive symptoms
  ◦ Inattention: inability to direct, sustain, and shift attention
  ◦ Decreased awareness
  ◦ Change in cognition and/or perception

• Delirium accelerates cognitive impairment!

Psychological Effects

• 1 in 3 patients who survive ICU stay and required mechanical ventilation have PTSD

• Hospital demoralization

• Vastly undertreated both in patients and their caregivers

ICU-Acquired Weakness

• Muscle weakness that develops as a secondary disorder during an ICU stay

• Typically generalized, symmetrical, affects limbs (proximal > distal), and respiratory muscles (especially diaphragm)

• Characterized by:
  ◦ Reduced muscle tone
  ◦ DTRs may be normal or may be reduced
  ◦ Greatly reduced muscle mass
  ◦ can exceed 10% over 1st week in ICU
  ◦ Electrophysiological exam shows abnormal patterns

• Manifest in 1 of 3 ways: polyneuropathy, myopathy, or muscle atrophy

Who Gets ICU-Acquired Weakness

• Patients in the ICU who have a critical illness (like sepsis or acute respiratory distress syndrome)

• Patients at risk for multiple organ failure (an outcome of sepsis)

• Critical illness combined with mobility restrictions, hyperglycemia, use of glucorticoids, and/or neuromuscular blocking agents (NMBA)
  ◦ NMBAs: used to facilitate endotracheal intubation through sedation
  ◦ As a result, patients mechanically vented have higher incidences

• Up to 70% of elderly patients have muscle atrophy complications

ICU weakness meaning for clinical presentation

• Rapid onset of muscle weakness

• Significantly reduced functional mobility

• Significantly increased risk of complications (see slides 53+54)

• Modified PT evaluation to accommodate patient’s poor strength and endurance

• Use strategies to promote early mobility
  ◦ Use shorter, lower-intensity PT sessions
  ◦ Start in bed with head raised and progress to edge of bed then to bedside chair
  ◦ If available, use mechanical lift to get patient into bedside chair to start short periods (< 2hrs) OOB

What Increases the Risk for ICUAW?

• Higher severity of illness, especially persistent critical illness

• Sepsis high lactate level

• Multiple organ failure

• Longer duration on mechanical ventilation

• Longer length of stay in the ICU

• Consider this:
  ◦ Prolonged ventilation increases risk for ICUAW and diaphragmatic dysfunction
  ◦ ICUAW increases the risk of prolonged ventilation and failed weaning