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ICU Final Exam

Terms in this set (99)

Positive inotrope (increase HR and BP), vasopressor

What is normal p-wave duration?

<0.12 seconds (3 small boxes)

What is a normal PR interval?

<0.20 seconds (5 boxes)

What is a normal QRS duration?

<0.12 seconds (3 small boxes)

HR < 60 bpm
-Maintain patent airway, assist breathing as needed
-Give oxygen
-Monitor ECG (identify rhythm), BP, oximetry
-Establish IV access

How do you treat symptomatic bradycardia?

1. Prepare for transcutaneous pacing
2. Atropine 0.5 mg IV (may repeat to a total dose of 3 mg)
3. Consider Ephedrine or Dopamine
4. Transvenous pacing

How is SVT treated?

6mg Adenosine IV push (can give 12mg if you need a second dose). Cardioversion if unstable.

Treated with Defibrillation (shock) x 2 --> CPR 2 min/5 cycles (obtain IV/IO access) --> Shock --> CPR 2 min/5 cycles (Epinephrine 1 mg every 3-5 minutes) --> Shock --> CPR 2 min/5 cycles (Amiodarone and Lidocaine) --> Shock

Pulseless V-tach/V-Fib

Treated with CPR 2 min/5 cycles (obtain IV/IO access) --> Epinephrine every 3-5 minutes --> Shock if shockable rhythm --> CPR 2 min/5 cycles

-PR interval is prolonged > 0.20 seconds (1 box)
-Causes: beta blockers, CCBs, hyperkalemia, getting older and heart changes
-Treatment: Monitor

First degree heart block

-Longer, longer, longer, drop
-P-R intervals should be fairly consistent
-Causes: CAD, beta blockers, CCBs, digoxin, inferior wall MI
-Symptoms: lightheadedness, hypotension
-Treatment: Monitor cardiac rhythm, may need temporary pacemaker

Second degree type 1 heart block (Wenckebach)

-HR usually slow
-2, 3, or 4 before each QRS, identical
-PR interval 0.12-0.20
-QRS <0.12 depends
-QRS complex is dropped but PR interval stays the same
-Causes: Anterior wall MI, CAD
-Symptoms: Dyspnea, fatigue, hypotension, slow pulse
-Treatment: Reduce myocardial demands (MONA), Transvenous pacemaker, IV 0.5 mg Atropine (max 3mg), epi for symptomatic bradycardia

Second degree type 2 heart block (Mobitz 2)

-No association between atria and ventricles
-P waves and R waves are regular but there will be P waves with no QRS because they will fall at a random time
-Causes: Toxic effects of digoxin, propranolol
-Symptoms: Diaphoresis, chest pain, dyspnea, pallor, slow pulse, change in LOC, hypotension
-Treatment: Transcutaneous/Transvenous pacing, IV atropine, epinephrine, dopamine

Third degree heart block

-Not synchronized
-For cardiac arrest: V-Fib/V-Tach without pulse
-Higher energy joules (360J) immediately, not escalating

-Synchronized on R wave
-For persistent tachyarrythmias (unstable): A fib, A flutter, SVT, V-tach with pulse
-Lower energy joules
-Escalate for next shock (100-200-300-360)

If the atria is paced, where will you see the pacer spike?

If the ventricle is paced, where will you see the pacer spike?

If we hear audible gurgling and they have an ET tube, then what do we need to do?

Check cuff pressure (cuff is not fully inflated)

How do we assess ET tube placement?

Bilateral breath sounds, end tidal CO2, chest x-ray

______ pressure alarm on vent indicates disconnection or opening in the circuit (ET tube disconnected from ventilator-pop it back on)

_________ pressure alarm means there is some kind of obstruction or opening in the circuit (kink in tubing, biting ET tube, suctioning needed)

If the vent is alarming and you can't figure out why, what do you do?

Bag the patient

S/S:
-Muffled or distant heart tones
-Tachycardia
-JVD
-Narrow pulse pressure
-PA and CVP will be high

Cardiac tamponade

-Inserted for cariogenic shock
-Improves coronary artery perfusion and oxygenation to muscle
-Check peripheral pulses (occludes femoral or renal arteries-check for urine output too)

What things indicate that IABP is placement is effective?

-Cardiac output increased
-Chest pain decreases or resolves
-Improved mental status
-MAP should improved

What medications are used in hypertensive crisis/urgency?

-Cardene
-Nitroprusside (Nipry)
-Beta Blockers

What should you monitor for in a patient with hypertensive crisis/urgency?

-Ventricles are quivering and not contracting
-No cardiac output (check patient)
-No pulse in this rhythm ever
-They are unconscious

-Acute onset
-Predisposing condition
-Bilateral infiltrates
-PaO2/FiO2 < 200mmHg
-PCWP < 18

S/S:
-Restlessness, disorientation, change in LOC
-CXR studies are usually normal in normal initial stage (basilar infiltrates begin to appear in about 24 hours)
-Respiratory distress with dyspnea, tachycardia, and hypoxia that does not respond to O2 therapy and PEEP
-Intervostal/suprasternal retractions
-Metabolic acidosis caused by lactic acid build-up - elevated serum lactate levels
-Crackles/rhonchi/bronchial breath sounds audible as fluid moves into the airways
-Low PaO2 despite increases in supplemental O2 administration-refractory hypoxemia
-Initial increase in blood pH (respiratory alkalosis)
-As ARDS worsens-become acidotic
-Thick frothy sputum-indicative of pulmonary edema
-CXR may worsen as ARDS progresses-"White out"
-Vent may show a rise in PIP-indicating a decrease in compliance
-Skin cool and cyanotic/mottled
-Labs may indicate multiple body system dysfunction
-Pulmonary function tests may reveal decreasing lung compliance
-Hypotension

Vent management for ________:
-TV between 4-6 ml/kg
-End-Inspiratory Plateau Pressure < 30
-Keep FiO2 < 60
-PEEP at 5-15
-Permissive hypercapnia (PaCO2 60-100)
-Maintain SaO2 between 88-95%

Nursing Management for __________?
-Treat underlying cause of the inflammation
-Provide oxygenation (keep HOB 30-45, PEEP, 4-6mL/kg/ideal body weight)
-Monitor ABGs
-Decrease O2 consumption (treat fever/pain/decrease use of accessory respiratory muscles)
-Maintain HgB > 7 to improve oxygenation-carrying capacity
-Early nutrition
-Bronchodilators
-Administration of exogenous surfactant
-Sedation/neuromuscular blocking agents
-Nutritional support
-Monitor vitals and urine output
-Fluid therapy
-DVT prophylaxis
-Peptic ulcer prophylaxis
-Chest physiotherapy
-Monitor end tidal CO2
-Prevent infection (high incidence of ventilator-induced pneumonia, loss of skin integrity from invasive devices/lines)
-Prone position

-Best if done in best 36 hours
-Adequately sedate them
-Improved oxygenation by increasing ventilation and perfusion and decreasing shunt. Decreased pleural pressures in this position that result in improvement in the regional lung inflation. Early in the disease process seems to have more benefit than when used as last resort.
-Maintain for 18-20 consecutive hours
-Considered when P/F ratio is less than 100

Prone positioning

What is normal tidal volume?

6-8 mL/kg (ideal weight)

What is normal PEEP?

-Continuous positive airway pressure throughout respiratory cycle to patient who is spontaneously breathing
-They get PEEP and oxygen
-May facilitate weaning
-Patient initiates all of their breaths and their own tidal volumes
-Stop sedative so patient can wake up and breathe on their own.

CPAP (vent weaning)

What is the vasopressor of choice for hypotensive septic patient?

Norepinephrine (Levophed)

What 4 things should you do in the 1 hour bundle?

-Check lactic acid
-Give fluids
-Blood cultures
-Antibiotics

Why do they monitor PA waveforms while placing a PA catheter?

They can tell where they are at in the heart based on the waveforms

What is the normal CVP range?

-Pressure created by volume in the right side of the heart. When the tricuspid valve is open, the CVP reflects filling pressures in the right ventricle. Clinically, the CVP is often used as a guid to overall fluid balance.
-Can be monitored via the distal port of a CVL or with a PA catheter
-Used to determine fluid volume status. Tells us all the blood returning to right side of the heart
-Refers to preload (volume of blood that is preloading or filling the heart so the heart can pump it)

Would hemorrhagic shock have low or high CVP? Give fluid or blood depending on what was lost

Volume of blood in ventricles at end of diastole (end diastolic pressure). Referred to as "filling pressures."

Resistance left ventricle must overcome to circulate blood. AKA SVR

Represents the resistance against which the left ventricle must pump to eject its volume.

What is normal SVR range?

Amount of blood ejected by the ventricle with each heartbeat, expressed in mL.

What is normal stroke volume range?

The heart's contractile force. Also know as isotropy. Can be positive or negative. Inotropes increase strength of the heart. Heart failure patients, cardiogenic shock need help with the heart pump. Ex: Dobutamine is a positive inotrope drug

Amount of blood pumped out by a ventricle over 1 minute. Equals HR x SV

What is the normal cardiac output?

Considered more accurate than CO since it is individualized to height and weight. Equals CO/BSA

What is a normal cardiac index?

What does the basic set-up of hemodynamic monitoring consist of?

-Invasive catheter (A-line, CVL, swan)
-High pressure-tubing with transducer
-Transducer holder
-Transducer cable
-Bag of NS
-Pressure bag inflated to 300mmHg

-Maintain under pressure to prevent back flow and assure continuous forward flow
-No air bubbles!
-Level transducer at the phlebostatic axis (4th ICS, midaxillary line)
-Zero (eliminates effect of atmospheric pressure
-Calibrate

Hemodynamic monitoring set up

Where is the phlebostatic axis?

4th ICS, mid-axillary line, about the level of the atrium

Major advantage of the radial artery is the supply of _____________ _____________ to the hand provided by the ulnar artery.

Collateral circulation

-Radial and ulnar arteries are compressed simultaneously
-The patient is asked to clench and unclench hand until it blanches.
-One of the arteries is then released, and the hand should immediately flush from that side
-If there is adequate collateral flow, there should be rapid return of color to the hand upon release of the ulnar artery

-Can simultaneously assess PA systolic and diastolic pressures, PA mean pressure, and PAOP (wedge pressure).
-Used to measure CO, determine mixed venous oxygen saturation, and calculate additional hemodynamic parameters.
-Placed centrally, sits in pulmonary artery
-Distal tip monitors PA pressure and sits in pulmonary artery.
-Determines if there is increased pressure in the left side of the heart.

What is the normal PA systolic pressure?

What is the normal PA diastolic pressure?

What is the normal wedge pressure?

What needs to be done post intubation before giving any oral meds/food?

How do you change the vent setting for a patient who has respiratory acidosis?

Increase the rate to blow off CO2

How do you change the vent setting for a patient who has respiratory alkalosis?

Decrease the rate

If a patient has an MVA and absent breath sounds, what would you expect?

What do you use to treat an pneumothorax?

What do super tall T waves indicate?

What do T wave inversion and ST segment depression indicate?

What does ST segment elevation indicate?

Injury to cardiac cells

What do Q waves represent?

Cell death (complete infarction)

ST segment elevation in lead II, III, AVF

What vessel does an inferior MI affect?

Right coronary artery

ST segment elevation in leads V1-V4

Anterior or anteroseptal MI

What vessel does an anterior or anteroseptal MI affect?

Left anterior descending artery (LADA)

ST segment elevation in leads V5-V5, lead I, AVL

What vessel is affected by lateral MI?

Left circumflex artery

ST depression in V1, V2

What vessels are affected by posterior MI?

Left circumflex artery or right coronary artery

Intubate if GCS < _______

-Simple fracture, not depressed, like a hairline fracture
-S/S: headache, decreased LOC

Linear fracture

-Depression in skull, you truly have a break, risk of infection
-S/S: decreased LOC, headache, palpable defect over fracture site

Depressed fracture

-Way more complex and compound because they carry more of an increased r/o seizure and intracranial infection, involves more bones
-Fracture involving bones of skull base
-S/S: headache, altered LOC, periorbital ecchymosis, hemotympanum, CSF otorrhea or rhinorrhea, facial nerve palsy, do not place NGT, should consider oral gastric tube

Three goal of treatment for ______ ________:
-Restore and maintain brain function
-Prevent and treat complications
-Maintain and enhance the injured person's cognitive, psychosocial, and emotional processes

-Prehospital and when they get to the ER, worry about ABC
-Airway potency: loss of cough and gag reflexes vs. stimulation, chin-lift and jaw-thrust, no NGT for basilar skull fracture, intubate if GCS < *
-Supplemental oxygen/adequate ventilation: PaO2 < 50 correlated with adverse outcomes, monitor for abnormal breathing, avoid hypercarbia, preoxygenate before suctioning
-Adequate systemic and cerebral perfusion: systolic BP < 90 strongly correlated with poor outcomes (avoid hypotonic fluids like D5W bc it exacerbates cerebral edema)
-Clinical assessment: establish baseline assessment, reassess to guide interventions, obtain CT scan
-Sedation and analgesia: pain and agitation increase ICP

Resuscitation phase

-Prevent or treat hypoxia or hypercapnia
-Respiratory care: suctioning, positioning, chest PT, ventilator settings, aspiration precautions
-BP: goal is MAP 70-90, CPP at least 70
-Control ICP
-Mannitol: goal serum osmolality less than 320 (hypertonic fluid decreases swelling and will increase serum osmolality, above 300 means we have cell dehydration and we don't want to dehydrate anymore)
-Hypertonic saline (3% NS): watch sodium and expect an elevation
-Steroids
-Decrease stimulation and metabolic demand: normothermia, sedation and analgesia, barbiturate coma, paralysis
-Avoid neurological complications: vasospasm, seizure, intracranial infection
-Avoid fluids and electrolyte imbalance: DI, SIADH, cerebral salt wasting, feed them

Critical Care Phase

-Maintain patent airway
-Effects of immobility: spasticity, bowel and bladder function, cognitive rehabilitation

Intermediate and rehabilitation phase

-Reflects three volumes: brain, CSF, blood
-Monro-Kellie Law
-Compensatory mechanisms: displace CSF, vasoconstrictor blood vessels and these can only be done for a short period of time

What is normal ICP?

__________ signs of increased ICP:
-Head
-N/V
-Amnesia
-Altered LOC
-Restlessness, drowsiness
-Changes in speech
-Loss of judgement

_________ signs of increased ICP:
-Dilated, non-reactive pupils
-Unresponsiveness to verbal or painful stimuli
-Abnormal motor posturing
-Changes in respiratory rate pattern

An attempt to increase cerebral blood flow to try to help the body (a little more vasoconstriction with the widening pulse pressure and increased systolic BP, decreased HR and RR)

Cushing's response

-Clinical manifestations r/t widespread vasodilation
-Metabolic acidosis
-Acute encephalopathy
-Oliguria
-Hypoxemia
-Coagulation disorders
-Hypotension
-Decreased skin perfusion/mottling
-Petechiae
-Edema and hypotension, tachycardia , inflammation
-Elevated AST, ALT
-Relative hypovolemia

What kind/how much fluid should be administered within 3 hours for a septic patient?

30 mL/kg of IV crystalloid fluid (LR instead of NS because hyperchloremic metabolic acidosis)

S/S:
-Loss of consciousness (agitation)
-Skin cool and pale (delayed capillary refill)
-Tachycardia
-Decreased urinary output
-Narrow pulse pressure
-Decreased BP (later sign)

Hypovolemic shock

What should you monitor for a patient in DKA?

Potassium (insulin decreases potassium)

When is ICP monitoring appropriate for patients?

GCS of 3-8 with abnormal CT scan

ICP treatment should be initiated at an upper threshold of _____-______.

How can you test for CSF?

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