Critical Care Nursing: Hemodynamic Monitoring PDF

CRITICAL CARE NURSING: HEMODYNAMIC MONITORING Critical care nursing Concerned with human responses to life threatening problems (such as in trauma , comoborbid conditions) Focus of nurses: pt. and family responses to illness involves prevention and cure C...

CRITICAL CARE NURSING: HEMODYNAMIC MONITORING Critical care nursing Concerned with human responses to life threatening problems (such as in trauma , comoborbid conditions) Focus of nurses: pt. and family responses to illness involves prevention and cure Competencies of nurses caring for the critically ill Clinical judgement and clinical reasoning skills. Advocacy and moral agency in identifying and resolving ethical issues.( refer for financial aids ( PCSO or social workers ) Caring practices that are tailored to the uniqueness of the patient and family.( Transcultural theory by Madeleine Leininger) Collaboration with patients, family,family members , and health care team members. Systems thinking that promotes holistic nursing care Response to diversity Facilitator of learning for patients and family members,team members, and the community. Clinical inquiry and innovation to promote the best patient outcome. CARDIOVASCULAR SYSTEM  1. Pulomonary artery : an only artery that carries de oxygenated blood 2. RIGHT SIDE : volume oriented: increase in volume will reflect on the right side 3. LEFT SIDE: pressure oriented: PMI SHOULD BE ON 4th to 5th if its in 6th to 7th ( it means it is enlarged( heart enlargement /cardiomegaly), since the pt. has hypertension, the pressure increases leading to the hypertrophy ) LAYERS OF THE HEART 1. Endocardium 2. Myocardiom 3. Pericardial space 4. Pericardiom If there is fluid accumulation on the percardial space (pericardial effusion ): Cardiac tamponade What makes your heart beats: Electrical signals Conduction System of the heart ELECTRICAL PRECEDES MECHANICAL Contraction-relaxation ( mechanical activity of the heart ( structural based )) Depolarization- repolarization( electrical impulses) IF THE AV NODE HAS NO ELECTRICAL IMPULSE leading to no ventricular contractions (mechanical activity); can be seen on the QRS  The heart does not simultaneously ( if it pumps simultaneously it indicates heart failure) TWO MAIN: Right (supply the right side inferior and posterior)and left coronary artery (circumflex supplies lateral and posterior ; left anterior supplies anterior) POSTERIOR MI RARE TO HAPPENED - IT HAS TWO SUPPLIERS ( circumflex and right coronary artery ) Hemodynamic monitoring-use of pressure monitoring devices to directly measure cardiovascular function.  NEGLIGENCE- you did what u needed to do but it is not right MALPRACTICE- neglect of the nursing standards Blood Pressure (BP= CO X SVR) Cardiac Output (CO= HR x SV)( N:48 per liter ) amount of blood pumped by each ventricle in liters per minute Pulse pressure (PP= SBP - DBP) ( N:40-60 mmhg) Mean Arterial Pressure (SBP +DBP (2) divided by 3) average mean arterial pressure (N: 80-100 mmhg) (decreased MAP indicates organ/brain perfusion leading to ischemia , necrosis, and failure ) Stroke volume is primarily determined by three factors: preload, afterload, and contractility. 1.Preload (filling pressure) -represents degree of ventricular stretch at the end of diastole and influenced by volume of blood in the ventricles ; preload in the right and left; the higher the volume , the greater the stretch by starling's law DETERMINANTS: 1. Circulating blood volume 2. Atrial contraction ATRIAL FIBRILLATION: ATRIA is fibrillating ( not contracting adequately) 2. Afterload-resistance against which the R (PA)or L(SC) ventricle has to pump Pulmonary vascular resistance (PVR)- the resistance against blood flow from the 4 pulmonary veins of the lung to the left atrium. increased pressure in the pulmonary system = increased PVR (r ventricle pumping blood should be greater in the pulmonary) Systemic vascular resistance (SVR)-the resistance against the systemic circulation; (L ventricle pump blood should overcome the pressure against aorta and systemic)  PLEURAL EFFUSION - HAS HIGH PVR due to the accumulation of fluid to the pleural space leading to high pressure. HYPERTENSION- HAS HIGH SVR AORTIC STENOSIS ( narrowing ) - HAS HIGH SVR NITROGLYCERIN OVER DOSE (nitrate base medication a vasodilator)- HAS LOW SVR ELEVATED PRELOAD (RIGHT VENTRICLE ) 1. FLUID OVERLOAD 2. PULMONARY STENOSIS 3. PULMONARY INSUFFICIENCY 4. PERICARDIAL TAMPONADE- accumulation of fluid in the pericardial space(drowning of the heart) leading compression of the heart which decreases the stretch of the heart making the heart not to pump effectively 5. CONSTRICTIVE PERICARDITIS DECREASED PRELOAD (RIGHT) HYPOVOLEMIA VASODILATION -SEPTIC SHOCK (LEADS TO THE RELEASE OF INFLAMMATORY CYTOKINES AND BACTERIAL ENDOTOXINS WHICH CAUSES VASODILATION AND INCREASED CAPILLARY PERMEABILITY ) ELEVATED PRELOAD (LEFT) LEFT SIDED HEART FAILURE VOLUME OVERLOAD CARDIOMYOPATHY MYOCARDITIS PERICARDIAL TAMPONADE DECREASED PRELOAD (left) HYPOVOLEMIA - (trauma and surgery ) ELEVATED SVR (AFTERLOAD) 1. Hypertension 2. Vasopressor use  3. Aortic stenosis 4. hypothermia - vasoconstriction ELEVATED PVR (Afterload) 1. Pulmonary hypertension 2. Hypoxia 3. Pulmonary embolism - obstruction of the pulmonary artery it increases PVR 4. Pulmonary stenosis DECREASED SVR (AFTERLOAD) 1. SEPTIC SHOCK 2. ANAPHYLACTIC SHOCK 3. NEUROGENIC SHOCK 4. USE OF VASODILATOR(NITROGLYCERIN) - BEFORE ADMINISTERING, ASK IF HE TOOK NITROGLYCERIN BASED MED. SUCH AS VIAGRA AND ASSESS BLOOD PRESSURE. IN IV NITROGLY. USED AN INFUSION PUMP DECREASED PVR (AFTERLOAD) 1. USE OF VASODILATORS CONTRACTILITY(force) influenced by: 1. electrolyte abnormality- 2. Acid-based abnormality-m 3. Myocardial oxygen demand/supply abnormalities  HYPOCALCEMIA- widened QRS complex NON-INVASIVE HEMODYNAMIC MONITORING 1. Non-invasive blood pressure (NIBP) Check size of cuff Arm at the level of the heart 2. Jugular venous pressure Supine Head of bed at 30-45 degrees Have patient turn head slightly to the left( in order to expose the right side of the the neck to note pulsation) Observe the highest point of pulsation in the internal jugular vein at end exhalation Measure the vertical distance between the pulsation and angle of Louis (in cm) 2nd ICS Add 5 cm to estimate CVP ( added estimation Normal: 7-9 cm low cvp- fluid deficit , right sided heart failure High CVP- fluid overload ,right sided heart failure 3.LACTATE Normal arterial lactate: 0.5-1.6 mEq/L Determines tissue hypoperfusion  higher lactate higher the perfusion INVASIVE HEMODYNAMIC MONITORING (AT RISK FOR INFECTION) other TEST TO ASSESS FLUID STATUS CBC : HEMATOCRIT (for men is 40 to 54%; for women it is 36 to 48%) AND UA: SPECIFIC GRAVITY 1.005 to 1.030. 1. Central Venous Pressure (CVP) Volume status(BURNS) Pulmonary status(PLEURAL EFFUSION) Right sided cardiac function Medication effects(NITROGLYCERIN IV ) INSERTION AND MEASUREMENT Sites:Right jugular vein, Subclavian vein CVP value :Pressure monitoring System: ; Manometer (MANUAL TYPE) MAJOR DISADVANTAGES Infection ( clean it with chlorhexidine gluconate) Daily flushing Routine sterile dressing changes Restrictions on activities (FLAT ON BED ) EQUIPMENT CVP CATHETER IV LINE - FLUSH SYSTEM TRANSDUCER- SENSOR SYSTEM Zero & level the Pressure Monitoring System Level of Left Atrium (supine) 4th ICS halfway between the AP diameter of chest RESULTS: NORMAL : 2-6 mmHG ( PRESSURE MONITORING SYSTEM) (2 below) decrease : fluid deficit- low: pressure , (6 beyond) increase: fluid overload-high pressure 3-8 cm H20 ( MANOMETER) DECREASED Reduced RV preload Shock Dehydration INCREASED: increased RV preload Hypovolemia Heart failure- the heart fails to contract effectively, which fills that heart Cardiac Tamonade Pleural Effusion- COMPLICATIONS Infection Pneumothorax/hemothorax (exposure of pleural space(negative pressure ) to the atmospheric pressure )- punctured pleural space or the jugular vein which atmospheric pressure enters Laceration of major vessels Catheter malposition Thrombus formation (pt. with high viscosity of blood, high concentrated(sluggish and slow) , and endothelial injury which leads to inflammation - flush it or catheter reinsertion Air embulos-the tube is full of air 1. signs: chest pain and difficulty breathing 2. Intervention:left lateral because the atrium is on the right 2. Pulmonary Artery Pressure (PAP) Monitoring 1. Determine heart failure 2. Guide therapy 3. Monitor cardiac function 4. Assess determinants of 02 delivery Pressures measured: 1. CVP 2. Pulmonary artery systolic and diastolic pressure 3. Mean pulmonary artery pressure 4. Pulmonary artery wedge pressure- an estimation of the stroke volume (if the PAWP is high the stroke volume is high vice versa) Complications:  1. Infection 2. Pulmonary artery rupture 3. thromboembolism 4. Catheter kinking 5. Dysrrhythmias 6. Air embolism- if 50 ml and above of air introduced to the patient NURSING RESPONSIBILITIES: 1. Ensure that chest x ray is done 2. Prevent infection 3.ATERIAL PRESSURE MONITORING Continous BP monitoring Frequent ABG measurements Insertion & Measurement Most common site: Radial artery ( less risk for infection and accessible) Others: a. Femoral b. Brachial c. Dorsalis Pedis COMPLICATIONS 1. Hemorrhage 2. Thrombosis 3. Tissue ischemia 4. Infection PRIOR INSERTION 1. ALLEN TEST 2. DUPPLER NR: 1. Check connections 2. Pressure bag: 300 mmHg 3. Neurovascular assessment ( 6 p’s) 4. Activate monitor pressure alarm  5. Record hourly or as ordered 6. Observe signs of infection ( rubor, pallor, dolor, loss of function) 7. Dressing changes, flush tubing and solution changes PREVENT CENTRAL LINE INFECTION 1. Hand hygiene 2. Barrier precautions 3. Chlorhexidine skin asepsis 4. Daily review of line necessity 3. Intra-arterial BP UNIT 2 : ACUTE RESPIRATORY DISTRESS SYNDROME Basic unit of the respiratory system- ALVEOLI Gas exchange- DIFFUSION The alveolar capillary membrane is destroyed or damaged resulting to have a problem in Co2 and o2 exchange which will lead to have low levels of oxygen, which will now result to hypoxia or hypoxemia and elevated Co2 indicating hypercarbia Hypoxemia is low oxygen levels in your blood and hypoxia is low oxygen levels in your tissues. ARDS-occurs when lung swelling causes fluid to build up in the tiny elastic air sacs in the lungs ARDS- Severe , acute lung injury involving: 1. Diffuse alveolar damage- 2. Increased microvascular permeability- damaged capillary membrane which allows the fluid to enter the alveolus( POOR O2 and HIGH Co2) 3. Non-cardiogenic pulmonary edema? ( no problem of the contraction of the L ventricle) -