Test 1 Week 1-4 Flashcards
How is the renal system a buffer system
kidneys excrete or retain bicarbonate, blood pH decreases - then kidney retain HCO3, if pH rises, kidneys will excrete HCO3 through urine
System can take hours or days to compensate
How is the respiratory system a buffer
CO2 is a by-product of metabolism, CO2 is carried from blood into lungs - excess CO2 binds with H20 - to create carbonic acid
the level of H2CO3 triggers lungs to either increase or decrease rate of respriatrion - compensation begins in 1-3 minutes
how long is a large box and small box on ECG paper
1 large box has 25 small boxes
large box is .20 seconds
small box 0.04 seconds
how long is normal PR interval
what does it measure
0.12-0.20 seconds (3-5 small boxes)
Time from SA node to AV node, delay represents a block in atrial conduction
How long should QRS interval be what does it represent
0.06 - 0.12 (1.5 to 3 small boxes)
time from AV node to bundle of His and purkinjie fibres
Delay - block in ventricualr conduction
narrow - pulse originated in atria, wide pulse originated in ventricles
How to manage/avoid the complication of unexplained extubation
Signs, prevention, what to do
**Signs **
* patient vocalization, low-pressure alarm, diminished/absent breath sounds, respiratory distress, gastric distension
**Prevent **
* adequate securment of ET tube
* support ET tube during reposition/procedure
* soft wrist restraints
* sedation/analegsia
**Managment **
* stay with patient, call for help, manully ventialte patient with 100% O2, psychological support
How to treat sinus bradycardia if symptomatic
- pulse oximetry
- give O2 if needed
- IV access
- 12-lead ECG
- Atropine - blocks vagus nerve- more sympathetic activity - SA note rate will increase - can use until temp pacemaker availble (if unstable or needed)
How to treat sinus tachycardia
what symptoms are seen
treat undelrying cause
* fluid replacment, reflief of pain, removal of offending mechanisms, reducing fever or anxiety
dizziness, dyspnea, hypotension
If someone comes in unconcious, with respiratory problems, with no knoweldge of why - what will you give
D50 (hypoglycemia), B12 (alcoholic), & nalaxone
Important steps for after ET intubation
- inflate cuff and confirm placement, will manually ventalting pt with 100% O2
- CO2 detected (usually 30-40)
- ascultate lung bases and bilaterally (bc right lobe is less of an angle so tube might go into right lung so might not hear breath sounds in L lung - need 2 cm above fork)
- bilateral chest movment
- Chest x-ray will confirm placment
- measure - mark and document distance form edge of the lip to end of tube and monitor
Oral care needed for patients with ET intubation
- brush teeth BID
- every 2-4hours and PRN suction oral/pharyngeal cavity
- reposition and retake ET tube every 24 hours
*chlorhexidine mouth swabs to prevetn infection - gums, mouth should be moistned with slaine or water swabs
Respiratory Distress VS Failure
Distress - increased WOB in the presence of normal state & oxygenation abilities - increase resp rate and effort. - trying to maintain homeostasis
Failure - inability of the respiratory system to fulfil gas exchange needs of the patient - hypoxemia - abnormal PO2 and PCO2
Types of mechnical ventilation - what is volume, pressure, time
volume - delivers precise volume of air for each cycle regardless of pressure
Pressure - generates flow until pressure is reached - need to monitor closely - if pt breathd out of synchrony with machine, pressure limit may be reached quickly- dont get enough air
Time - generates flow for preset amt of time
what are 4 types of disorder of impulse formation
**Enhanced Automaticity ** - cardiac cells depolarize sponatenously OR pacemaker site other then SA increases its firing rate beyond normal
**Abornal electrical impulses **during repolarization requires a stimulus
**Conduction blocks ** partial (slowed, intermittent) and complete (no impulses are conducted)
Reentry impulse returns to stimualte tissue that was previosuly depolarized - closed loop (wolf parkinson white syndrome)
what are causes of hypoxemic respiraotry failure
- ventilation - perfusion mismatch (COPD/asthma)
- shunting (anatomical or intrapulmonary)
- diffusion limitation (decrease gas exchange)
- alveolar hypoventialtion
often it is combination of things
What are complications of ET suction
Complications
* hypoxemia (preoxygenate)
* bonrchospasm
* ICP
* Dysrrhythmias (may be result of hypoxemia).
* hyper/hypotension
* mucosal damage, bleeding
* pain infection
what are important guidelines for suctioing ET tubes
How to avoid complication
- suctioning should not be regular
- assess pt b4, during and after
- if performing CST - hyperoxygenate
- limit suction pressure to 120mm Hg
- provide adequate hydration - saline - manage thick secretions
*
What are interventions for B-breathing
- Position (high fowlers chest can expand more, ^ gas exchange, if fatigue semi-fowlers & tripod (COPD))
- Coached breathing ( pursed lip breathing causes PEEP )
- Oxygen - NP (2L (21%) 6L(40%)) - face mask (5-10L to get out CO2), Venturi mask 24-50% O2 Non-rebreather & partial rebreather
- Bronchodilators (ventolin)
- Bipap - help keep lung open
- Intubation
- ventilation - ambu bag
PEEP -limit air that comes in, max exhalation - keep alveloi open longer
what are interventions in respiratory failure ( include drugs )
- oxygen
- mobilization of secretions
- effective coughing/positing
- hydration/humidification
- chest physiotherpay
- airway suctioning
- positive-pressure venitaltion (BiPAP)
- DRUGS - bronchodilators, corticosteriods, dieuretic, antibiotics, opiod, sedative, muscle relaxant
What are interventions to maintain A- Airway
- Open airway (head tilt chin lift & jaw thurst if spinal injury)
- Suction - yankauer
- Oropharygeal tube (no gag reflex)
- nasopharyngeal airway (if trauma to mouth, or still conscious)
- HOB FLAT no pillows
What are nursing considerations/assessments with mechanical ventilation
- assess cardiopulmonary status q2h-q4h (VS, breaht sounds, SpO2, ETCO2, I/O)
- assess for complications (decrease CO, pneumothorax, O2 toxicity, ulcerations VAP, atelactasis)
- HOB elevated 30 degree - turn pt every 1-2 hours to help lung expansion/remove secretions
- active/passive ROM, call bell
- sedative/neuromuscular blocking agents as required
- be ready to give manual respiration (ambu bag)
what are nursing implications for ventialtor associated pneumonia
- elevate head of bed - 45 degrees when possible, otherwise 30 (enteral nutrtion, protein to fight infection)
- avoid routine chanigng of circuit tubing
- daily evaluation for extubation
- use ET tubes with subglottic secretion drainage
- oral care and use of chlorhexidine BID
- intiation of safe enteral nutrion 24-48 h of ICU admission
- hand hygiene
- VTE prophylaxis
What are patterns/types of positive pressure ventilattion
CV, AC, SIMV, PEEP
CV - controlled ventilation, prederminted rate/volume independent of pts resps
AC - assist-control - client may initaite cycle with inspriation
SIMV - synchronised intermittent mandaotry respiration - deleiver preset tidal volume, pressure, rate alllows for spontaneous breaths between - synchronize with client - weaning
PEEP - pt unable to intiate spontaneous breaths - maintain positive pressure in alveloi at end of expiration, facilitate O2 diffusion (WILL increase intrathoracic pressure - decreased return- decrease BP - will give fluid, intropes)
What are possible complications of ET intubation
- bronchospasm/laryngospasm
- aspiration during procedure
- tooth damage
- injury to lips, mouth, pharynx, vocal cords
- hypoxemia
- tracheal stenosis, erosion, necrosis (often with cuff too inflated- pressure)
What are predisposing factors to respiratory failure
- ARDS - acute respiratory distress syndrome
- direct lung injury (aspiration, infection, near-drowning, toxins)
- indirect airway injury (sepsis, shock, bypass)
- asthma, COPD
- CF
- opiod overdose
- brainstem infarction, head injury
- obesity, scoliosis, rib fracture
- ALS
What are S/S of sinus bradycardia
pale, cool skin, hypotension, weakness, angina, dizziness, syncope, confusion disorientation, SOB
what are the 3 things to specify when interpreting a rhythm
specify site of origin
specify mehcanism (brady, tachy)
specify ventricular rate
What are the important aspects of nursing managment in terms of ET intubation
- maintaing proper cuff inflation (20-25mm HG)
- monitoring oxygen (signs of hypoxemia & change in mental status)
- monitoring ventilation (PaCO2)
- maintaing tube patency (suction when needed - not routinely - closed suction )
What are the methods of determining rate off of ECG strip
6 second, large, small
Six-Second - count number of QRS complexes within 6 seconds (30 big box) - multiply by 10 (good for irregular rhythm)
Large Box method - count number of large boxes between two waveforms (r-r or p-p) and divide into 300 (ex if you have 4 boxes between 75bpm)
Small box method - count number of small boxes between two waveforms and dvidie into 1500 (ex 18 small boxes 83 bpm)
What are the risk factors for aspriation with ET tube, what can we do to prevent that
Risk factors
* imporper cuff inflation, patient positiong, tracheoesophgeal fistula
* the ET tube cuff cannot totally prevent trickle of oral/gastric secretions into the trachea
prevention
* patient always be 30 degree - often have NG tube as well
* suction oral cavity frequently
What are the S/S of decreased CO
- SOB
- Altered LOC
- Syncope/presyncope
- weakness
- chest pain
- hypotension
What are the steps needed before ET intubation
and positioning for oral/nasal
- Pre-oxygenate with 100% O2 for 3-5 minutes
- limit each intubation attempt to less then 30 seconds
- ORAL - place patient supine with head extended and neck flexed
- Nasal - spray nasal passage with local anesthetic and vasoconstriction (maybe)
what are the three lethal rhythms
pulseless Vtach, Vfib, asystole
What are these rhythms, what causes, what do you do about it, what are complications
A - Unifocal PVC
B - multiform PVC
PVC - is a contraction originating in an ectopic foscs in ventricles - preamture QRS that is wide/distored. 0.12 sec or greater
Rhythm regular with preamture beats, rate usually normal, p waves usuall absent, PR none, QRS longer with bizarre T in opposite direction
CAUSE - acid-base, Acute conroary syndrom, digitialis toxicity, elecotrlyte imabalnce, exercise, HF, hypoxia, medications, stimulants
Treatment based on cause - infrequent PVC not typically treated - Assess ABC- S/S decrease CO - can give amniodarone or lidocaine
what are vagal manoeuvers
carotid sinus massage
application of a cold sitmulus to the face
valsalva manoeuvre
bear down
What can cause sinus tachycarida
**Fear, anxeity, fever,pain **
MI, caffeine, hypovolemia, cannabis, exercise, HF, hypoxia, medications, nicotine, PE, shock
Things that increase sympathetic stimulation
what is r-r used for
used to determine ventricular rate and regularity
More important then P-P as it contributes more to CO
What is the P wave, PR interval, QRS, ST segment and T wave
what is the rhyhm, what causes it, what can you do
asystole
absence of ventricular electrical activity
5H/5T reversible causes -Hypoxia, Hypovolemia, Hydrogen ions (acidosis), Hyper/Hypo-kalemia, Hypothermia; Tension pneumothorax, Tamponade-cardiac, Toxins, Thrombosis-coronary (MI), Thrombosis-pulmonary(PE).
treatment - CPR, ACLS
- IV, IO, epineprhine, advanced airway, capnograph
What is the rhyhm, what causes it, what do you do
**Third Degree AV Block **
WORST - affects CO the most - comp;ete block of impulses between the atria and ventricles - a cell in the ventricles becomes pacemaker for ventricles
QRS wider
CAUSES - MI, myocarditis, heard disease, Drug (amnio, BB, CC, digoxin) fibrosis, **increased parasymapthic tone **
If symptomatic bc slow heart rate
- pulse oximetry, O2, IV, 12-lead, Atropine, Epi, dopamine, isoproterenol IV, temp/permaent pacing - Frequent reassessment
What is the rhyhm, what causes it, what do you do about it
Ventricular Fibrilation
NO CO - CPR/DEFIB ASAP
the ventricle is quivering and no effecitve contraction - no CO.
Occurs with acute MI, myocaridal ischemia, CAD, cardiomyopathy. dysrhythmias, electrlyte imbalance, electrocution, hypertrophy, increase SNS, severe HF, vagal stimulation, medications
Puslessness - defibrialte - CPR - epinephrine amniodarone
What is the rhythm, what causes it, what do you
second degree AV block Type II
delay occurs in his&purkinjie system - less common then type I and more serious.
Ventricular rate irregular, atiral regular, ventricular rate often slow, P waves normal, missing QRS complexes, PR normal and constant
CAUSE - left CAD, MI, mycocaridits, aortic valve disease, cardiomyopathy, fibrosis, heart disease
IF PT symptomatic bc slow HR
- pulse oxumetry, O2, IV access, 12-lead ECG, IV atropine (pacemaking may be necessary) reassess
What is this rhythm
Sinus arrhythmia- When SA node fires irregularly
Respiraotry - associated with the changes in intrathroacic pressure with breathing
**Nonrespiraotry - **not realted to breathing, seen with heart disease, after MI, increased ICP, medications
Usually 60-100bpm - IF bpm is less then 60 or above 100 then sinus brady-arrhythmia /tachy-arrythmia
Rhythm/interval - NOT normal - rate, p wave, PR, QRS normal
What is this rhythm & What are you going to do about it
**Atrial Tachycardia **
* rapid atrial rate overdies the SA node and becomes pacemaker
* rhythm regular, rate 100-250bpm p and t waves may blend together, p wave not normal shape, QRS normal length
Assess S/S - decrease CO
If Stable
- pusle oxumetry, oxygen, VS, IV access, caridac monitor, 12-lead ECG, vagal manoeuvers, adenosine
Unstable
- pulse oximtry, O2, IV access, sedation - synchroized cardioversion
May give BB/ calcium, channel based on heart
what is this rhythm, what causes it, what do you do about it
Ventricular tachycardia - ventricle takes control as the pacemaker - multiple PVC at rate higher then 100 bpm
- nonsustained - short run lasting less then 30 seconds, and sustained lasts for more then 30 seconds
Rhythm regular, ventricular ratre 101-250 bpm, p wave not seen, no PR, cant really see QRS/t wave
CAUSE - acid/base imbalance, ACS, cardiomyopathy, cocaine, digitlais toxciity, elecotrlyte imbalance, mitral valve prolapse, trauma
PULSE OR NO PULSE
Pulse & Stable - O2, IV, ventricular antiarrhythmics (lidocaine, amniodarone)
Pulse & Unstable - O2, IV, sedation, synchronized cardioversion
NO PULSE - defibirilate immediately CPR
what rhyhm is this, what causes it, what do you do
**First Degree AV Block ** delayed impulse conduction
rate regular, usually normal bpm, p wave normal, PR prolonged, QRS normal
CAUSES - MI, heart infection, cardiomyopathy, degenrative fibrosis, drug, Hyperkalemia, vagal tone, ischemia, heart disease
Usually no symptoms - if acute MI monitor pt closely
What rhythm is this
Sinus bradycardia
Interval normal, **Rate is less then 60 ** P wave normal, PR normal, QRS normal
what rhythm is this
Sinus tachycardia
Intervals regular, 101-180 bpm, usually not higher then 150 as that gets into atrial tachycarida P waves normal, QRS normla, PR normal
What rhythm is this, what causes it, what do you do about it
Atrial Flutter - an irritable site within the atria fires reguallry an rapid rate - sawtooth flutter - closed loop - not every beat is converted to ventricles
Rhythm regular or irregular, Rate less then 180 bpm, no identifiable p waves, QRS may or may not be burrie
CAUSES : paroxysmal rhythm, caridac surgery, cardiomyopathy, MI, digitlais or quindine toxicity, hypethyroidism, heard disease, regurgitation, infection of heart, PE - NOTE no stress/pain = pathological causes only
IF rapid ventricular rate - control rate
IF rapid rate with S/S - syncrhonized cardioversion, (prophyalxis, warfarin potentially)
What rhythm is this, what causes it, what do you do about it
Atrial Fibrilation - disorganization of atrial electrical activity cause by multiple ectopic foci - loose effective atrial contraction
Rhythm - irregular, atria rate 400-600bpm, ventrical varries, no P waves, QRS normal
CAUSES - MI, heart infection, age, caridac surgery, cardiomyopathy, lung dieases, chest trauma, HF, heard disease, PE, wolf-white – STROKE RISK bc turbulence
TREAT - if rapid ventrucalr rate. control - BB, Calcium channel, digoxin, amiodarone
- if rapid ventricular and S/S - synchronized cardioversion
IF more then 48 hours - give anticoagulants
What rhythm is this, what causes what do you do about it
Second Degree AV block Type I
Progressive increase in length of PR until drop in QRS,
Atrial rate regular, ventricular rate irregular, p wave normal, PR inconsistent, QRS complexes periodically dropped
CAUSES - block in RCA, athletes bc of vagl tone, during sleep, aortic valve disease, medications (BB, CC, digxin ) heart disease
PT usually asymptomatic - fix underlying cause (structural)
If symptomatic bc low HR
- pulse oxumetry, O2, TV, 12-lead ECG, IV atropine (maybe), monitor
What rhythm is this, what do you do about it what causes it
**AV Nodal Reentrant Tachycardia (AVNRT) **
Most common type of SVT, closed loop - signal keeps firing, narrow QRS so orignated above AV.
Rhythm usually regular, rate 150-250bpm, p waves often hidden in QRS
Causes : hypoxia, stress, anxiety, caffeine, smoking, sleep deprivation, medications, COPD, heart disease, HR, digitialis toxicity
ASSESS S/S
Stable - PO2, O2, VS, IV, caridac monitor, 12-lead ECG, vagal manoeuver, adensoine
Unstable - PO2, O2, IV, sedation - synchronized cardioversion
what types of aciodsis/alkalosis can you have in terms of compensation
