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: L/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: dynes/sec/cm2 Increased in acute lung injury

Left Heart Afterload Left heart afterload=systemic vascular resistance (SVR) Normal: 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) 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 Nursing Diagnosis Plan Implantation Evaluation