MS Exam #1

Normal ABGs

• PH         7.35--7.45 

• PaCo2   35-45 mmHg 

• PaO2     80-100 mmHg 

• HCO3     22-26 mEq/ L 

• SaO2 95%-100%

rule of 5s

O2 being given to pt x 5 = PaO2

terminology

• Hypoxia- Inadequate oxygenation of the tissue 

• Hypoxemia- A low oxygen content of arterial blood, short of anoxia 

• Hypercarbia/hypercapnia- High carbon dioxide in the blood 

• Acidemia- Too much acid in the blood 

• Alkalemia- Too many base 

ABG 5 basic components

• 1- Percentage of hemoglobin saturated with oxygen in arterial blood (SaO2) 

• 2- Partial pressure of oxygen dissolved in arterial blood (PaO2) 

• 3- arterial blood acidity or alkalinity (pH) 

• 4- Partial pressure of carbon dioxide in arterial blood (PaCO2) 

• Inverse relationship with pH 

• 5- Concentration of bicarbonate ions in arterial blood (HCO3) 

• Increases or decreases the pH depending on if it rises or falls 

30-60-90 rule

• When the PaO2 is 30 the SaO2 is usually 60 

• When the PaO2 is 60 the SaO2 is usually 90 

the body’s ability to adjust

• If the PaCO2 is elevated, the body can adjust the level of PaCO2 in a matter of minutes by increasing the respiratory rate and the volume 

• The renal system is unlike the respiratory system.  A person with normal kidney function may take several hours to alter the HCO3 levels 

• In the elderly or decreased renal function the process could take days 

causes of respiratory acidosis

• Increased PaCO2 and Decreased pH

  • Over-sedation

  • Opiates and benzos

  • Head Trauma 

  • COPD 

  • Paralytics  

  • Respiratory failure 

  • Respiratory muscle failure 

causes of respiratory alkalosis

• Decreased PaCO2 and Increases pH

  • Hyperventilation

  • Pain

  • Early Pneumothorax

  • Anxiety

  • Fear

  • Atelectasis 

  • Anemia

compensation

• Uncompensated- The body systems (Renal and Respiratory) have made no attempt to compensate for pH changes 

• Partially Compensated- The opposing body system is attempting to compensate, but has not changed enough to normalize the pH 

  • Indicator that matches the pH is the primary disturbance 

• Fully Compensated- The pH is within normal limits but the values for the respiratory and metabolic components are outside normal ranges 

systematic approach to ABGs

• Step #1 Examine the PaO2 and the SaO2 levels to determine hypoxemia 

  • If they are low, intervene immediately with oxygen and monitor 

• Step # 2 Examine the pH and decide if the pH is acidotic or alkalotic 

  • (7.35-7.45 is normal) 

  • 7.34 and lower is acidosis

  • 7.46 and higher is alkalosis 

• Step #3 Examine the PaCo2 

  • Determine if this lab is normal, acidotic, or alkalotic

  • Normal range is 35-45 

• Step #4 Examine the HCO3 and determine in this is normal, acidosis, or alkalosis 

  • Normal range is 22-26 mEg/ Liter 

• Step #5 Identify the origin of the Acid-Base disturbance.   

  • Which component matches the pH disturbance. 

  • Now determine if the patient is compensated 

    • Is the pH within normal limits? 

    • Look at the opposite value, is it normal or outside the normal range to the opposite value causing the shift in pH

PaCO2

• PaCO2 is the partial pressure of dissolved Carbon dioxide 

• Directly relates to the amount of carbon dioxide produced by the cells 

• The value is inversely related to the rate of alveolar ventilation.   

• Increase the ventilation- decrease the PaCO2 

• Decrease the ventilation-increase the PaCO2 

HCO3

• HCO3 is the bicarbonate ion 

• This is the acid base component regulated by the kidneys 

• Metabolic acidosis in renal failure because it cannot secrete HCO3 into the vessels 

• The kidney’s retain or excrete bicarbonate as needed.   

• Metabolic acidosis is a level below 22 

• Metabolic alkalosis is a level above 26 

Acute Respiratory Failure

• The inability of the lungs to maintain adequate oxygenation of the blood with or without carbon dioxide retention 

• Impairment of gas exchange is the major factor. 

• PaO2 < 60 mm Hg on room air or a PaCO2 > 50 mm Hg and a pH < 7.35 

• Could be 

  • Pulmonary edema 

  • Pulmonary contusion

  • ARDS (worst case) 

  • CF 

• Pathophysiology

  • Hypoxemia 

    • V/Q mismatch 

    • Impaired Gas diffusion 

  • Hypoxemia & Hypercapnia 

    • V/Q mismatch 

    • Impaired gas diffusion 

    • Hypoventilation 

      • Could be OD 

types of respiratory failure

Primary Hypoxemic Respiratory Failure 

• PaO2 < 60 mm Hg 

• Oxygen saturations < 90% 

• Can be treated with oxygen 

• PaO2 will come up if no mechanical problems 

Combination of Hypercarbia & Hypoxemia 

• Hypoxemia is present and an elevated PaCO2 (PaCO2 > 50 mm Hg) 

  • Raise HOB and give O2 (call once you get up to 6L) 

• Hypercapnia: insufficient CO2 removal 

• Requires mechanical ventilation 

ARDS

• Fulminant form of respiratory failure 

  • Clinical syndrome of acute hypoxemic respiratory failure due to acute lung inflammation and diffuse alveolar-capillary membrane disruption. No cardiac pulmonary edema 

• Mortality rate 

  • ~35-45% 

• Most survivors have almost normal lung function 1 year post illness 

• Predisposing Factors 

  • Pneumonia – most common 

  • Sepsis (non-pulmonary) – most common 

  • Aspiration of gastric contents 

  • Non-cardiogenic shock 

  • Pancreatitis 

  • Severe trauma

    • Leads to shock 

  • Drug overdose 

  • Ischemia-reperfusion injury 

VQ Mismatch

C: V/Q MATCH 

B: Ventilation imbalance (V/ventilation) 

• Bronchospasms 

• Mild atelectasis 

• Pneumonia (pus in alveoli) 

D: Perfusion imbalance (Q/perfusion) 

• Could be mild PE 

• Anything that decreases CO 

  • HF

  • Pulmonary hypertension 

E: Perfusion 

• PE  

• Creates deadspace because no gas exchange 

A: ARDS  

• Shunt  

• No oxygen in alveoli/inflammation/atelectasis 

ARDS Patho

• Neutrophils releasing leukotrienes and proteases  

• Inactivated surfactant 

  • Alveoli will collapse 

• Gap formation 

  • Breakdown in alveolar pathway preventing oxygen from crossing the membrane and reaching the RBCs 

• Have normal, diseased, and collapsed alveoli 

• Disease throughout the lung and affecting the alveoli 

  • Have pockets where alveoli works  

  • Adding more PEEP can fix the collapsed alveoli  

  • “recruit alveoli” 

R → L Shunting

venous blood returning to the heart bypasses the lungs as in an intracardiac shunt (cyanotic heart disease) or intrapulmonary shunt (heart is pumping unoxygenated blood)

• symptoms

  • shortness of breath

  • cyanosis

  • exercise intolerance

ARDS symptoms

• R -> L shunting (intrapulmonary) 

• Hypoxemia 

  • Causes pulmonary hypertension 

  • Causes vasoconstriction 

  • Leads to R sided HF 

• Microvascular obstruction 

  • Leads to pulmonary hypertension 

  • V/Q mismatch 

  • Increased in dead space and minute ventilation  

Present with: 

• Dyspnea, cyanosis (hypoxemia) (78-80%), and diffuse crackles. 

• Respiratory distress: 

  • Tachypnea (PIV increases because more pressure is needed to open lung), tachycardia, diaphoresis and use of accessory muscles. 

  • May also complain of cough & chest pain 

• Decrease in lung compliance 

• Hypoxemia unresponsive to O2 therapy (Refractory Hypoxemia) 

• Diffuse alveolar infiltrates seen on C-Xray or CT scan without evidence of cardiac disease 

ARDS Mechanical Ventilation

Low Tidal volume 

• 6 ml/kg 

• Increase RR to 20-30 bpm 

Permissive Hypercapnia 

• Decrease in tidal volume with normal RR 

• Correct acidosis with Bicarb drip 

  • Never treat respiratory acidosis with bicarb only metabolic 

  • Unless purposefully inducing it to regulate pH 

• Low TV and lung protective is more frequently used  

• Increase in epi and norepi release 

  • Mild HF can be exacerbated with this 

• Contraindicated with increased ICP 

  • CO2 vasodilates in brain  

PEEP (Positive End Expiratory Pressure) 

Pressure Control Ventilation 

• Preset pressure 

  • 30-35 

• Tidal volumes vary 

  • NEED TO MONITOR 

Inverse Ratio Ventilation 

• Reverses the normal I:E ratio 

  • 2:1 

  • Inspire over 2 seconds then exhale 1 

  • Stack breaths -> auto PEEP 

High-Frequency Jet or Oscillatory Ventilation 

• Very high respiratory rates with small tidal volumes 

• RR 50-100 

proning in ARDS

• front part of the lungs is down 

  • Gravity will have the blood flowing to the front  

  • Less diseased area 

  • Perfusing the less damaged part of the lung 

• NO PRONING IN INCREASED ICP 

• NO PRONINNG WITH SPINAL CORD INJURY 

• NO PRONING WITH TRAUMA WITH OPEN ABDOMEN OR ADBOMINAL COMPARTMENT SYNDROME 

• If PaO2 improves by 30% then its successful 

ARDS assessment and interventions

• Monitor for increasing respiratory distress 

• Monitor for decreasing SpO2 with increasing FIO2 

• Monitor for decreased cardiac output 

• Monitor for fluid overload/deficit 

• Assure nutritional support early 

• Monitor for infectious processes 

• Hematest all stools and body fluids 

• Psychosocial support 

ACLS Airway

• Asynchronous ventilations at a rate of 10 breaths per minute (1 every 6 seconds) 

• Waveform capnography is the gold standard 

• No significant evidence that advanced airways promote higher resuscitation results over a bvm in the first 10 minutes of a cardiac arrest 

systematic approach to ekgs

• Fast or slow 

• Regular or irregular 

• P before every QRS? 

• QRS wide or narrow 

• Positive or negative 

• Check leads 

epinephrine

• FIRST LINE IN PTS W/O A PULSE 

• Alpha & beta receptor agonist 

• Increases perfusion to coronary arteries and brain 

• Can help restore blood flow post defibrillation 

• Dose – 1 mg 1:10,000 iv/io push q 3-5 minutes 

• ALWAYS DILUTED WHEN GIVEN IV 

  • Not necessary when IM 

Hs & Ts

PEA

• Some variation in EKG 

• Typically, in trauma 

• Massive volume loss d/t trauma -> no volume in atria -> heart is pumping (creates rhythm) -> no blood ejecting -> no pulse = PEA 

• CPR then Epi

Vfib

• No discernible waves or complexes 

• Rhythm causing ‘all’ sudden cardiac arrest 

• Useless quivering heart – no blood flow 

• Treatment – defibrillation 

• Defibrillation success chances drop with every minute 

• Can be scratching chest, seizing (always check patient first)

VTach

• Fast, no P wave, Regular, Wide QRS, Negative deflection 

• Compression and epi IF no pulse 

amiodarone

• Calcium/potassium sodium channel blocker 

• May assist in terminating 

• FIRST LINE V-fib/pulseless v-tach in refractory ventricular rhythms 

• Dose – 300 mg iv/io push, 150 mg iv/io push

lidocaine

• Sodium channel blocker 

• ONLY WORKS IN VENTRICULAR ARRHYTHMIAS 

• Can be used to increase ventricular threshold 

• Dose – 1 mg/kg iv/io push 

synchronized cardioversion vs defibrillation

SVT

• Phrase used to describe a rapid, regular supraventricular arrhythmia when more accurate identification is impossible because P waves aren’t visible and rate is common to other arrhythmias 

• SVTs with Overlapping Rate Ranges: 

  • Sinus Tachycardia 100-160 beats/min 

  • Atrial Tachycardia 150-250 beats/min 

  • Atrial Flutter 150-250 beats/min 

  • Junctional Tachycardia 100-180 beats/min 

• Fast, Regular, narrow QRS, no p wave, Upright 

• Make them vagal 

  • Bear down, ice water in face, lift legs up 

adenosine

• Antiarrhythmic used secondary to vagal maneuvers to lower heart rate in narrow complex tachycardias 

• Dose – 6 mg rapid iv/io push then 12 mg rapid iv/io push 

• FIRST LINE FOR SVT 

  • SVT -> Asystole -> NSR 

  • Doesnt bottom out BP like other meds

verapamil/cardizem

• Calcium channel blockers used to reduced heart rate with atrial fibrillation and atrial flutter with rapid ventricular response 

• VERAPAMIL DOSE – 2.5 MG 

• CARDIZEM DOSE – 0.25 MG/KG 

atropine

• anticholinergic 

• Medication that affects stimulation of the vagus nerve 

• Recommended for symptomatic bradycardia 

• Dose – 1 mg iv/io push (max 3 mg) 

atrial arrhythmias

• Treatment Considerations 

• Treat unstable patients 

• Control rate 

• Convert rhythm 

• Anticoagulation if indicated 

MI Tx

• MONA 

  • Oxygen at 4 L/min – if needed (O2 Sats < 92%) 

    • Not perfusing heart 

  • Aspirin 160 to 325 mg 

    • Antiplatelet  

  • Nitroglycerin SL or spray 

    • vasodilate 

  • Morphine IV (if pain not relieved with nitroglycerin) 

    • Can be fentanyl (prehospital just due to stocking) 

• Is patient stable or unstable? 

• Patient has serious signs or symptoms? Look for 

  • Chest pain (ischemic? possible ACS?) 

  • Shortness of breath (lungs getting ‘wet’? possible CHF?) 

  • Low blood pressure (orthostatic? dizzy? lightheaded?) 

  • Decreased level of consciousness (poor cerebral perfusion?) 

  • Clinical shock (cool and clammy? peripheral vasoconstriction?) 

• Can the symptoms be attributed to their heart rhythm? 

  • Know the Rhythm 

  • Prepare for the Rhythm 

  • Treat the Patient

mechanical ventialtion indications

• Apnea 

• Inadequate oxygen uptake 

• Inadequate CO2 elimination 

• Control of ventilation 

• Need for positive pressure therapy 

• Can use CPAP 

• Respiratory weakness due to disease or muscle relaxant or anesthetic drugs

negative pressure vs positive pressure

• Negative pressure ventilators require patient's spontaneous airway and ability to protect airway 

  • iron lung

•  Positive pressure ventilators require a closed airway system between the patient and the ventilator (endotracheal tube, tracheostomy tube or sealed mask unit) 

  • Bag Valve Mask 

  • Positive pressure 

  • Mechanical Ventilators 

  • Transport Ventilators 

volume cycled ventilation

• Certain volume of gas (oxygen) in a set period of time 

• Average of 7cc of air volume per Kg 

• Air is delivered until certain volume is reached 

• Tidal volume at 400 and RR at 10 

  • 4L/min Minute ventilation 

  • Breath every 6 seconds 

• Peak inspiratory pressure 

  • Amount of pressure to achieve breath 

  • Normal 15-20 

• Pressure increases as lungs become less compliant 

  • 45-50 

  • NEED TO MONITOR 

  • Can pop a lung 

  • Tidal volume is decreasing because pressure monitor will cut off the breath 

• More comfortable for patient

pressure controlled ventilation

• The amount of pressure needed to get the volume of air to a certain pressure (30 mmHg) 

• More protective to the lung 

• NEED TO MONITOR VOLUME 

• 10 of PEEP and 25 Peak Expiratory Pressure 

  • Tidal volume will be only about 200cc 

    • Stops when you reach the pressure 

    • If volume keeps increasing at same pressure, then lungs are more compliant and healing 

  • Increase RR if not enough ventilation 

  • 12 or 14 to increase volume

time cycled ventilation

• amount of time before a breath is terminated 

• Sometimes in the NICU 

flow

Based on the patient’s respiratory effort 

trigger

• The variable that initiates the change from exhalation to inspiration 

• All is based on the settings of the patient’s sensitivity setting 

• Inspiratory effort 

• Time of each breath 

• Rate of breaths per minute 

Continuous Mandatory Ventilation (CMV)/Assist Control (AC) 

• Not adjusted (CMV) 

• AC 

  • The ventilator is set at specific rate and TV 

  • 10 (RR) and 400 (TV) = MV of 4000 (4L)

  • Patient begins to wake up but still weak and sick 

    • Try to breath on their own (5ccs) 

  • Ventilator senses inspiratory effort and triggers a breath with full TV  

  • More breaths per minute 

  • Can be too much once hitting MV of 6000 (6L) -> pop a lung 

• assist control = any extra breaths you take vent will give full tidal volume that vent is

VC modes

• Continuous Mandatory Ventilation (CMV)/Assist Control (AC) 

•  Intermittent Mandatory (IMV)/Synchronized Intermittent Mandatory Ventilation (SIMV) 

Intermittent Mandatory (IMV)/Synchronized Intermittent Mandatory Ventilation (SIMV) 

• Senses when a patient breath and holds the breath until the patient exhales 

• Patient sets the tidal volume  

• Whatever they take that's what they get 

• TV will be whatever they take in 

pressure support trigger

• Method to decrease the work of breathing by giving a “boost” with each breath.  All of the breaths are initiated by the patients.  An apnea alarms must be set  

• Delivers a preset tidal volume using lowest possible airway pressure.  Airway pressure will not exceed a maximum pressure limit 

  • 15  

• Use Pressure support for weaning towards extubating 

Other Ventilation methods

Continuous Positive Airway Pressure (CPAP) 

• Keeps alveoli popped open (prevent atelectasis) 

• With apneic period alveoli are still open to facilitate gas exchange 

Bi-Level Positive Airway Pressure (Bi-PAP) 

• Pressure support with PEEP 

• Support getting the air in and keeping alveoli open 

PEEP

• Naturally occurs  

  • About 5 

  • ET tubes prevent naturally occurring PEEP bc the glottis is stuck open 

• May need when lungs are less elastic 

  • Can increase but it increases the pressure in the chest 

• Can reduce trauma to the alveolus 

• Helps keep the alveoli open for gas exchange 

  • 12.5 is high 

Vent settings

• f -Respiratory rate set 

• Vt-Tidal Volume 

• FiO2-Fraction of inspired oxygen 

• PEEP- Positive End Expiratory Pressure 

• PS- Pressure Support 

High Pressure limit 

• Regulates the amount of pressure the ventilator can generate to deliver the breath 

• RT will set it (usually starts around 30) 

  • 10-15 higher than whatever the first breath is 

• Kinks in tubing can disturb the pressure 

  • Bite block to prevent biting tube 

• Secretions  

• If none of the above 

  • Lungs are becoming more non-compliant 

I:E Ratio

• Represent Inspiratory time and expiration 

• Usually set 1:2 (normal for normal lungs) 

• Will set 1:3 for patients who have Chronic Obstructive Pulmonary Disease 

whats lost with intubation

• Lost the ability to moisturize the air 

• Cannot clear our secretions 

  • Requires suctioning (This is a sterile procedure!!) 

  • Considerations for suctioning- Hypoxemia, atelectasis, bronchospasms, dysrhythmias, increased intracranial pressure 

  • DO NOT INJECT SALINE BULLET DOWN ET TUBE NO MATTER THE ORDER NOT CORRCET PRACTICE 

    • Use it to clean catheter NOT IN TUBE 

• Cannot communicate 

  • Very frustrating for the patient and staff 

  • Passy-muir valve for patients who have a tracheostomy   

  • NEED a cuff 

    • More likely in an LTACH 

• Difficult to clear normal mouth secretions 

  • Brush the teeth every shift with mouth care every 2 hours 

  • Need MD order to clean w/ CHG 

Vent-induced Lung Injury

• Barotrauma- excessive pressure in the alveoli 

• Volutrauma- excessive volume in the alveoli 

• Atelectrauma- shearing due to repeated opening and closing of the alveoli 

  • Inflammatory process 

• Air leaks- are the result of all the above that causes damage and air leaks into the hilum 

• Air in the 

  • Mediastinum- pneumomediastinum 

  • Pleural space- pneumothorax 

  • Subcutaneous tissue-Subcutaneous emphysema 

    • Can knock a trach out 

  • Pericardium- pneumopericardium 

  • Can be benign to potentially lethal 

    • Most lethal-  Pneumothorax (tension) and Pneumopericardium (cardiac tamponade) 

• Biotrauma- The results of barotraumas, volutrauma and atelectrauma causes release of the initiation of the inflammatory-immune response 

• Can develop into acute lung injury which carries a 40% mortality 

CV compromise

• Negative pressure creates venous return 

• Positive-Pressure Ventilation  

  • Decrease in cardiac output due to the increase in intrathoracic pressure  

  • Leads to decrease venous return 

  • Decrease preload 

    • Decrease in SV 

  • Decrease cardiac output 

    • Could lead to renal and hepatic failure 

    • Could cause an increase in intracranial pressure 

  • Higher O2 sat 

  • Increase risk of pneumothorax and decrease in CO 

ABCDEF Bundle

• Assess, prevent, & manage pain 

• Both SAT & SBT 

• Choice of analgesia and sedation 

  • Do not need fentanyl if not in pain  

    • Propofol or versed 

    • Can administer and titrate propofol ONLY if patient is intubated 

• Delirium: assess, prevent & manage 

• Early mobility and exercise 

• Family engagement and empowerment 

hemodynamics

The study of forces that aid in circulating blood throughout the body 

• Monitored by frequent assessments of: 

  • BP *  

  • Cardiac Output 

  • HR *  

  • Urinary Output 

  • Mental Status  

• Helps RNs evaluation effectiveness of patients’ cardiac function  

• Patient symptoms that indicate compromised hemodynamic status: 

  • hypotension  

  • *Chest pain

  • SOB  

  • decreased U.O.  

  • *Altered LOC  

  • *CHF 

  • diaphoresis  

  • * Syncope  

  • *palpitation

CO

Equal to the heart rate multiplied by stroke volume (the amount of blood ejected with each heartbeat) 

• Normal is 4-8 liters per minute 

• Does not take into account body size 

  • Cardiac Index is body size adjusted cardiac output 

  • 2.5 – 4.0 L/min/m2 

  • (CO/BSA) 

• In ICU setting, CO/CI measured by Swan-Ganz (PA catheter) or an attachment to an arterial line (e.g., Flotrac) 

obtaining

• Thermodilution method 

  • Intermittent Bolus 

  • Closed System 

  • Technique 

    • iced or room temperature injection rapidly instilled through proximal port of PA catheter 

    • thermistor notes change in temperature 

    • calculation of blood flow determines CO 

• Continuous (CCO) 

  • Hemosphere (Sickest patients)

SV

• depends on three major factors 

  • Preload 

  • Contractility 

  • Afterload 

preload

• Filling pressure/stretch on ventricles 

• Determined by volume in ventricles  

• Central venous pressure (CVP): 2-6 mmHg  

  • Clinical indicator of increased preload= JVD  

• Factors affecting preload= volume, vessel status, pumping ability of heart 

  • remember If we increase preload, we increase the volume in the ventricles at the end of diastole 

afterload

• Resistance the ventricle has to overcome during each heartbeat to eject blood from the ventricle during systole 

  • AS, PH, HTN- hypotension, sepsis 

  • Meds 

• Systemic vascular resistance “SVR” 

  • Clinical indicator of afterload 

  • Increased: Vasoconstriction, vasopressors, cold 

  • Decreased: Vasodilation, sepsis, fever 

what affects CO

Inadequate LV Filling 

• Tachycardia 

• Hypovolemia 

• Valvular stenosis 

• Pericarditis 

• Tamponade 

• Cardiomyopathy 

• Arrhythmia 

• CAD 

• HTN 

• Mitral regurgitation 

• Negative inotropes 

• Metabolic disorders

preload vs afterload

preload 

• Amount of blood returning to the heart via the vena cava 

• Amount of blood received by the heart 

• Increased in hypervolemia, heart failure, regurgitation of heart valves 

Afterload 

• Resistance the LV must overcome to circulate blood to the body. 

• Increased afterload= increased cardiac workload 

 

effects of preload and afterload

Increased preload 

• *Caused by:  

  • *increasing fluid volume (giving IV fluids)  

  • Vasoconstriction  

• Effects on heart:  

  • Increases stroke volume, ventricular work, myocardial o2 requirements 

Decreased Preload 

• Caused by: 

  • Hypovolemia 

  • vasodilation 

• Effects on heart: 

  • Decreases stroke volume, ventricular work, and myocardial o2 requirement 

Increased afterload 

• Caused by: 

  • Hypovolemia 

  • Vasoconstriction 

• Effects on heart: 

  • Decreases stroke volume 

  • Increases ventricular work and myocardial o2 requirement 

Decreased afterload  

• Caused by: 

  • Vasodilation 

• Effects on heart: 

  • Increases stroke volume 

  • Decreases ventricular work and myocardial o2 requirements 

contractility

• Squeeze 

• Ability of cardiac muscle to pump 

  • r/t intracellular Ca 

• Force with which heart contracts 

• If too high, heart squeezing harder than necessary 

• Also known as ”inotropy” 

  • Positive inotropes – increase contractility (increase intracellular Ca) 

    • Dig, norepinephrine, dopamine, phenylephrine 

  • Negative inotropes – decrease contractility (decrease the force of cardiac contraction) 

    • Beta blockers, antiarrhythmics, calcium channel blockers (metoprolol, Amio, diltiazem) 

 Measured by

• Ejection Fraction

  • % of blood ejected with each beat 

  • Normal 

    • 60 – 75% 

• Cardiac Output is indirect measurement

advantages vs disadvantages

Advantages 

• Used for high-risk patients 

• continuous monitoring of minute-to-minute changes 

• Accurate titration of drugs and administration of fluid volumes 

• Diagnostic of 

• cardiac vs non-cardiac failure 

• cardiac tamponade 

• hypovolemia vs septic shock 

• Hypervolemia 

 

Disadvantages 

• Increased risk of infection 

• Endocarditis 

• Restrictive to patient movement and positioning 

• Possible damage to other structures during insertion or removal 

• Pneumothorax 

• Pulmonary infarction (Swan-Ganz catheters) 

• PA rupture 

• Dysrhythmias 

• Anxiety-producing to patient and family members 

types of invasive monitoring

3 most common ways to invasively monitor hemodynamics in ICU 

• 1) Central Venous Pressures (CVP) 

  • via central venous catheter or Swan-Ganz Catheter 

• 2) Arterial Catheters/Lines (“Art lines” or “A-Lines”) 

  • continuous blood pressure monitoring via soft catheter in artery 

• 3) Swan-Ganz Catheter (Pulmonary Artery or “PA catheter”) 

  • Monitors cardiac output, cardiac index, CVP, PVR, SVR, PCWP 

components of monitoring

• Pressure transducer: senses pressure changes that are transmitted from the intravascular space or cardiac chamber to the fluid in the pressure tubing in the patient to the transducer then transmitted to the monitor. 

• Flush device: manually flush the system 

• IV fluid: continuous infusion of normal saline in a pressure bag that is inflated and maintains constant pressure to prevent backflow of blood and to allow for accurate pressure transmissions 

• Pressure monitor: converts the transducers electrical signals into a pressure waveform and value 

• Three-way stopcock: controls the flow of iv solution through system 

• Pressure tube: connecting from the catheter in the patient to the flush device and transducer system. It should be rigid and nonpliable. 

• Transducer cable: connects pressure transducer to monitor 

zeroing

• Atmospheric pressure of the air around us exerts 760 mm Hg pressure on any object on the earth’s surface (at sea level) 

Zero technique: 

• Open system to air to establish atmospheric pressure as zero 

• Turn stopcock off to the patient (open to air and transducer) 

• Press the “zero” button on the monitor system, a straight line and zero number will appear 

• Return the stopcock off to the air position 

• Re-zero every 8 hours and with any change in position 

leveling

• All circulatory measurements of pressure are referenced from the mid chest position at the 4th intercostal space known as the phlebostatic axis. 

• Determine phlebostatic axis: level of patient's atria is the zero-referencing point for the pressure monitoring system. 

• This position is chosen since the left ventricle and aorta are usually located at the mid chest position 

• For every inch, the transducer is below the phlebostatic axis, 2mmHG is added – needs to stay level! 

• *If level too high= BP reads false low 

• *If level too low= BP reads false high 

dampened waveform

check pressure bag

art line

• Hemodynamically unstable patients for a continuous read out of SBP, DBP, & MAP 

• Frequent blood draws or ABGs 

• Patients in hypertensive crisis 

• Patients whose condition results in severe vasoconstriction or vasodilation requiring vasoactive medications (e.g., nitroprusside, norepinephrine) 

• Sites include- radial, brachial, femoral, axillary 

  • CANNOT MANUALY FLUSH A BRACHIAL 

• Radial Artery Allen Test: Ulnar circulation should resolve blanching within 5 seconds. Inadequate circulation if hand is pale >10 seconds 

• *The purpose is to assess adequate blood flow in the radial and ulnar arteries

  • patients can lose digits

• Caring for a lines: dressing, immobilizing, assessing (transparent dressing, circulation) 

Aline considerations

• NEVER GIVE MEDS THROUGH AN ALINE 

• Only red waveform on monitor 

  • Matches EKG 

• Art lines are monitoring/access devices ONLY – meds never to be given in arterial line 

• Dampened waveform causes:  

  • Catheter lodged against the vessel wall  

  • Clot formation at the tip of the catheter 

  • Air in the transducer  

  • Kinks in the tubing system  

  • Failures to zero at the air-fluid interface  

  • Pressure bag <300mm Hg 

  • Make sure the patient is not becoming acutely hypotensive!!! 

central venous pressure

• Ultrasound-guided insertion is a standard of care- evidence based 

• Vein is compressible - Accessed under direct visualization 

  • Can be IJ, Subclavian or femoral 

  • Femoral last resort d/t infection risk 

    • Often used in emergency 

• Major complication of central venous lines is infection 

CVP Catheters

• Percutaneous insertion of a central venous (CV) or pulmonary artery (PA) catheter include IJ, SC, femoral. 

• Risk of insertion- pneumothorax 

• Sterile procedure- catheter is flow directed, allowing venous circulation to carry it through to a position in or near the right atrium for CV catheters, or through the right atrium and ventricle. 

• To the PA for PA catheters. 

• Watch for ectopy on monitor when provider is placing central line! Beware of migration and arrythmias 

• Single-lumen, large gauge catheters (introducer) 

• Multi-lumen (CVC) to infuse multiple medications, medications that will damage peripheral tissues, TPN, rapidly infuse blood products or fluid, 

• May connect pressure tubing to monitor CVP 

• Tip of central line should be in superior vena cava (SVC) 

• CXR to confirm proper placement 

CVP and PA Cath indications

• Useful to evaluate volume status in patients who are acutely ill. 

• Useful in determining whether the patient has fluid volume status changes and left ventricular heart dysfunction 

• The PA catheter can specifically provide continuous monitoring of the PA pressure and cand be used to obtain cardiac output. 

• Pressure monitoring of the CVP or PA catheter can be useful in guiding theuse of fluid therapy and or vasoactive medication titration 

PA Cath (Swan Ganz)

NEVER INJECT IN YELLOW PORT

• gold standard” in evaluating cardiac output/cardiac index, CVP, and SVR 

• In the correct position, the tip of the PA catheter sits in the pulmonary artery 

  • never infuse anything through the PA port, the PA port is a monitoring device only 

• Waveform- 

  • Produced by the PAP monitoring is similar to the arterial pressure waveform, except the pressures are lower because of the lower pressures in the pulmonary arteries when compared to pressures in systemic arteries. 

• Normal PAP parameters 

• Right ventricular pressure- systolic 20-30mm Hg diastolic 0-5 mm Hg 

• Pulmonary artery pressure- systolic 20-30 mm Hg diastolic 6-12 mm Hg 

• Pulmonary artery wedge pressure- 4-12mm Hg

key info from PA Cath

• Cardiac output (CO): The amount of blood the heart pumps per minute. 

• Right-sided heart pressures: The filling pressures in the right atrium (central venous pressure) and right ventricle. 

• Left-sided heart pressures: The catheter can indirectly estimate the pressure in the left atrium and left ventricle through the pulmonary artery wedge pressure measurement. 

• Pulmonary artery pressure: The blood pressure in the arteries leading to the lungs. 

• Mixed venous oxygen saturation (SvO2): The amount of oxygen in the blood returning to the heart, which indicates the balance between oxygen supply and demand. 

• Pulmonary artery wedge pressure (PAWP): reflects left atrial and left ventricular pressures. 

  • Obtained by inflating balloon on PA catheter tip and floats downstream with venous blood flow to smaller branch of the PA. Catheter wedges, causing occlusion and reflects the backpressure from the left side of the heart 

• Cardiac output 

• Preload 

nursing care/considerations PA cath

• Observation of the waveforms  

• Sutures in place!  

• Document length of catheter at skin  

• Level & Zero - at the phlebostatic axis  

• PCWP/PAOP at end of expiration  

• Infection risk  

• Dysrhythmias - irritation to the endocardium during insertion, migration back into the right ventricle

• Pulmonary artery rupture or infarction**  

• Over-inflation of the balloon or migration  

• We no longer wedge as nurses 

pacemaker indication

• Any slow rate where the patient is symptomatic 

The slow rate could be: 

• Sinus Bradycardia 

• 2nd degree heart block 

• 3rd degree heart block 

• Junctional rhythm 

• Idioventricular rhythm 

• Tachy-arrythmias 

• Prolonged QT interval 

• SVT 

• A fib/a flutter 

pacemaker types

• Single-lead pacemakers use one lead, usually placed in the right ventricle (the lower right chamber of your heart). 

• Dual-lead pacemakers use one lead in the right atrium and one lead in the right ventricle. 

• Biventricular pacemakers (also called cardiac resynchronization therapy or CRT) use three leads. They are placed in the right atrium, right ventricle and left ventricle. 

• Determined by cardiologist/EP specialist 

 

types of temporary pacing

• 1. Transcutaneous pacing via multifunction pads attached to our Philips Defib machines set on Pacer Mode.  

• 2. Transvenous pacing via a pacing wire that is inserted thru an introducer in a central large vein into the right ventricle, then attached to a pacer box (pulse generator box) via a pacing cable.  

• 3. Epicardial pacing (post cardiac surgery) via epicardial pacing wires inserted into the endocardium during cardiac surgery that are attached to a pacer box (pulse generator box) via a pacing cable 

It is done when the patients own “intrinsic‟ or built in ability to pace fails or to cause a more effective depolarization 

how pacemakers work

• The sinus node is the heart’s natural pacemaker. It’s a small mass of specialized cells in the top of the right atrium- It produces the electrical impulses that cause your heart to beat. 

• A chamber of the heart contracts when an electrical impulse or signal moves across it

• When the heart’s natural pacemaker is defective, the heartbeat may be too fast, too slow or irregular. Rhythm problems also can occur because of a blockage or abnormality of your heart’s electrical pathways. 

  • =PACEMAKER IS NEEDED 

  • An artificial pacemaker replaces the heart’s defective natural pacemaker functions. 

• Most pacemakers work only when they’re needed (demand pacemakers). 

  • Demand pacemakers have a sensing device. It shuts the pacemaker off if the heartbeat is above a certain rate. 

• When the heartbeat is slower than the pacemaker rate, the sensing device turns the pacemaker on again. 

• The sensors (electrodes) at the end of the wires (leads) detect abnormal heartbeats and deliver electrical impulses to return your heart to its normal rhythm 

pacemaker modes

• First letter is which chamber(s) is/are paced 

• Second is the chamber where the pacemaker senses intrinsic activity 

• Third shows the response to sensed event 

• Fourth describes rate modulation aka rate responsiveness or rate adaptive pacing 

• Fifth rarely used but specifies the location or absence of multisite pacing 

• V= ventricle 

• A= atrium 

• D= double/dual (both A & V) 

• O= none 

• I= inhibits pacing 

• T= triggers pacing 

common pacemaker modes

• VVI= paces and senses in the ventricle. A sensed beat inhibits pacing (V demand) 

• AAI= paces and senses in the atrium. A sensed beat inhibits the pacing stimulus (A demand) 

• DDD= paces and senses in both chambers. A sensed beat in the ventricle inhibits both ventricle and the atrium. A sensed beat in the atrium inhibits atrial pacing but stimulates ventricular pacing after a programmed A-V interval. 

• Demand (synchronous)- pacer is set at appropriate sensitivity that intrinsic rhythm will inhibit pacing. Delivers electrical stimulus only when needed 

• Asynchronous- fixed rate- pacer will not sense intrinsic rhythm. Delivers electrical stimuli at a selected rate. Used only in emergency such as with asystole or idioventricular rhythms 

epicardial pacing

• Epicardial pacing wires are temporary electrodes attached directly to the heart's surface during open-heart surgery to manage or prevent post-operative arrhythmias, such as abnormal heart rhythms. 

• These wires are either unipolar or bipolar, allowing the surgeon to connect them to an external pulse generator for temporary pacing. 

  • Need to know if they are atrial or ventricularly paced 

• After the risk of complications has passed, typically, a few days post-surgery, the wires are removed through gentle traction 

transvenous wires

• Transvenous wires are inserted thru an introducer placed in a large central vessel such as the jugular or femoral veins 

  • (try and stay away from subclavian because the EP might need it for access for a permanent pacer). 

• More reliable and involves threading an electrode catheter through a vein into the patient's right atrium or ventricle 

• Connected to pulse generator that provides electrical stimulus directly to the endocardium 

• Be careful moving the patient! 

  • Best advice is to always move the patient with extreme care, watching the monitor and always be prepared for the worse case scenario 

pulse genertors/boxes

• Pulse generators/pacer boxes 

• Pulse generators are small, battery-powered medical devices designed to electrically stimulate the heart muscle in an effort to restore a heart rhythm or increase the rate of a heart rhythm. 

• They are used with either transvenous or epicardial pacing wires 

• With these pacer boxes you can choose and adjust: 

  • Asynchronous or demand pacing. 

  • The rate at which you pace the patient’s heart. 

  • The amount of energy in milliamps (mA) required for to cause a depolarization in the myocyte, referred to as “capture‟. 

  • How sensitive you want the pacer box to be to the intrinsic activity of the heart. 

Common mode practice

• AAI: Paces the atrium, senses the atrium, and inhibits itself when a native atrial beat is detected. Not suitable for heart block as the ventricle isn't monitored. 

• VVI: Paces the ventricle, senses the ventricle, and inhibits itself when a native ventricular beat (QRS complex) is detected. Lacks atrioventricular synchrony, which can affect cardiac output in a compromised heart. 

• DDD: Paces both the atria and ventricles, senses both chambers, and can trigger ventricular pacing based on atrial activity. It can inhibit pacing if native activity is sensed or pace both chambers if needed to maintain a proper heart rhythm 

determination of pacing

• Transcutaneous patches are quick to apply, noninvasive, but should only be used for a short time. 

• Transvenous pacing should be provided when available: easiest route is right internal jugular or left subclavian; fluoroscopy should be used but it can be attempted without it in an emergency 

• If the patient has epicardial wires post cardiac surgery then this is the primary method of pacing 

sensing

What it is:

• A pacemaker's ability to sense your heart's intrinsic electrical activity. 

How it's set:

• Sensitivity is set in millivolts (mV). 

• Lower mV = More Sensitive: A lower mV setting makes the pacemaker more sensitive to even small electrical signals from the heart, allowing it to correctly recognize and allow the heart's natural rhythm. 

• Higher mV = Less Sensitive: A higher mV setting means the pacemaker requires a larger electrical signal to trigger, making it less sensitive. 

• Why it matters: Setting the sensitivity too high can cause the pacemaker to "miss" native beats, while setting it too low can lead it to "over sense" other electrical signals (like T-waves) and inhibit pacing inappropriately 

capture

What it is: 

• The mechanical contraction (or heartbeat) of the heart muscle in response to the pacemaker's electrical stimulus. 

How it's set: 

• Capture is related to the pacemaker's energy output, measured in milliamps (mA). 

How to achieve it: 

• Find the threshold: Slowly decrease the pacemaker's mA output until the heart no longer responds to the stimulus, which is the point of "loss of capture". 

• Increase output for safety: Increase the mA output to 2-3 times that stimulation threshold to ensure consistent capture. 

Confirming capture: 

• A successful capture is indicated by a visible QRS complex on the ECG monitor that is different from the patient's intrinsic QRS 

failure to capture and sense

• Failure to sense- pacemaker doesn’t detect the hearts natural electrical activity, leading to inappropriate pacing and potentially too many spikes on EKG. 

• Failure to capture- the pacemaker sends an electrical impulse, but it doesn’t make the heart muscle contract, visible on an EKG as a pacing spike not followed by a QRS complex 

failure to capture (spike w no QRS)

what is wrong with this strip

ICD indications

• Experiencing cardiac arrest caused by ventricular fibrillation (VF) or ventricular tachycardia (VT) 

• Spontaneous sustained VT not responsive to drug therapy 

• Syncope with hemodynamically compromising VT or VF during EP study. 

• Occasionally atrial tachyarrhythmias 

• At high risk for Vtach or prolonged QT interval -> Torsades 

• R wave is on the T wave 

ICD care

ICD Monitoring

Potential complication 

• Bleeding or severe Bruising 

• Pneumothorax 

• Myocardial puncture 

• Infection 

 
Interventions 

• OR- routine post-operative management. 

• Will need to keep arm in a sling for at least 24 hours 

  • Lifting arm can pull wires 

• Transvenous approach 

  • Recovery similar to post-cardiac catheterization 

  • Shorter hospital stay 

• Make sure you know: 

  • the type of ICD implanted 

  • how the device functions 

  • whether or not it is activated 

tiered therapy

• First line of treatment – Tachycardia pacing 

  • Burst pacing 

  • May only feel palpitations 

  • If successful then thats it 

• If pacing is unsuccessful – cardioversion or defibrillation. 

• Asystole or idioventricular rhythm – brady back-up pacing