Transcript Alterations In Homeostasis

Alterations In Homeostasis
Shock
Homeostasis
• What is homeostasis?????
• Homeostasis is an (ideal or virtual) state of equilibrium, in which
all body systems are working and interacting in an appropriate
way to fulfill all the needs of the person and/or the body. When
homeostasis is interrupted (e.g. by response to a stressor), the
body tries to restore it by adjusting one or more physiological
processes. This stress-adaption mechanism includes activation
of the Hypothalamic-Pitauitary-Andrenal Axis (HPA Axis) with the
autonomous nervous system and endocrine reactions of the
body.
• Severe stressors or long lasting adjustment demands can cause
severe imbalance of this steady state. This might cause not only
psychological distress but also psycho-somatic disorders.
Shock
• Can occur when any part of the cardiovascular
system does not function properly for any reason
• Begins with abnormal cellular metabolism that
occurs when too little oxygen is delivered to
tissues
• Shock is a condition in which a systemic
decrease in perfusion to tissue and organs leads
to poor gas and nutrient exchange. Delays in
recognition and treatment can lead to irreversible
shock, multisystem organ failure, and death.
• Types of shock and their causes vary because
shock is a manifestation of a pathologic condition
rather than a disease state. More then one type
of shock can be present at one timie
Process of Shock
• Initial stage (early shock)
• Nonprogressive stage
(compensatory stage)
• Progressive stage (intermediate
stage)
• Refractory stage (irreversible stage)
Initial stage (early
shock) Reversible
• Pathophysiology
Nonprogressive Stage
(Compensatory)
• Pathophysiology
Progressive Stage
(Intermediate Stage)
• Pathophysiology
Refractory stage
(Irreversible Stage)
• Pathophysiology
Multiple Organ
Dysfunction Syndrome
• Pathophysiology
Effects of Shock on Body
Systems
• Cardiovascular System
Effects of Shock on Body
Systems
• Respiratory System
Effects of Shock on Body
Systems
• GI System/Renal
Effects of Shock on Body
Systems
• Neurologic System
Effects of Shock on Body
Systems
• Skin, Temperature, and Thirst
Collaboration
Diagnostic test
Pharmacologic
Therapies
Oxygen Therapy
Endotrachial Tube
Vented Patient
Inline Sterile Suction
Ventilator
Nutrition/Fluid Therapy
Pain and Comfort
Clinical Therapies
Central Venous Catheter
CVP
Normal CVP: 0-6mm Hg
Increased CVP:
• Aggressive fluid resuscitation
• right-sided heart failure with venoconstriction
• renal failure
• tricuspid or pulmonic valvular disorders
• right ventricular infarction
• COPD
• pulmonary embolis
• pulmonary hypertension.
What does the patient look like? dyspnea, crackles,
distended neck veins
CVP
Decreased CVP
• Hypovolemia-relative or actual
• Hemmorhage
• Vasodilitation
• Diuretics
• Fliud shifts-sepsis
What does the patient look like?
Tachycardia
CVP will fall before the patient becomes
hypotensive.
Complication of CVP
Catheters
• Infection
• Thrombosis
• Hemorrhage
• Arrhythmia
• Pneumothorax
• Cardiac Tamponade
Pulmonary Artery Catheter
• Used to continuously monitor right
atrium (RA) and pulmonary artery
(PA) pressures.
• Swan-Ganz Catheter
• Insertion sites: subclavian, internal
or external jugular, femoral, brachial.
PA Catheter
PA Catheter in the RA
PA Catheter in the RV
PA Catheter in the PA
PA Catheter in a Pulmonary
Arteriole
Left Heart Preload/PCWP
PAOP=PCWP=LVEDP=left heart preload
Measures filling pressures in the left heart
Normal: 5-12mmHg
PAD=PCWP in the absence of pulmonary hypertension
PCWP
PCWP normally correlates with
volume
Low PCWP indicates hypovolemia
(Volume expanders, packed RBC)
High PCWP indicates hypervolemia
(diuretics, venodilators)
Cardiac Output/Cardiac Index
Normals: CO: 4-8L/min; CI:2.5-4.0L/min/m2
What can cause Low CO/CI:
• HR: Fast or slow
• Preload: decreased from diuresis, dehydration, fluid
shifts, hypovolemia, vasodilitation
• Afterload: Increased from vasoconstriction secondary
to HTN, compensatory vasoconstriction
• Contractility: Decreased from MI, HF, cardiomyopathy,
cardiogenic shock, cardiac tamponade
Cardiac Output/Cardiac Index
High CO/CI:
• Anxiety
• Compensatory response in pulmonary edema
• Increased metabolic states (fever, hyperthyroid)
• sepsis
Right Heart Afterload
• Right heart afterload=pulmonary
vascular resistance (PVR)
• Normal: 50-250 dynes/sec/cm2
• Increased in acute lung injury
Left Heart Afterload
• Left heart afterload=systemic vascular
resistance (SVR)
• Normal: 800-1200 dynes/sec/cm2
Increased Afterload (SVR)
• Use of vasopressors
• Aortic stanosis
• hypothermia
• hypertension
Increased Afterload (SVR)
• Treatment
– Vasodilators (nipride, NTG)
– Ace Inhibitors (captopril, enalapril)
– Calcium channel blockers (verapamil
nifedipine)
Decreased Afterload (SVR)
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Sepsis/septic shock
Anaphylactic Shock
Neurogenic Shock
Treatment
– Levophed
– Neosynephrine
– Dopamine
– Vasopressin
Arterial line
Indication for an A-line
• Critically ill patients with intra-aortic
balloon pumps
• Monitor the effects of potent
vasodilators and vasopressors
• Frequent ABG testing
• Morbid obesity
• Burn patients
Nursing Process
• Assessment
– Health History
– Physical Examination
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Nursing Diagnosis
Plan
Implantation
Evaluation