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Critical Care > Exam I > Flashcards

Exam I Flashcards

1
Q

hypernatremia: causes

A
  • excess sodium intake (IV, PO)
  • decreased water intake
  • sodium retention r/t Cushing’s, hyperaldosteronism, renal failure
  • excessive free body water loss r/t DI, osmotic diuresis (Mannitol), burns, dehydration, fever/infection, diarrhea
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2
Q

hypoatremia: causes

A
  • decreased sodium intake (IV, PO. dextrose)
  • increased sodium loss r/t Addison’s, diuretics, vomiting, diaphoresis, wounds, decreased aldosterone secretion
  • excessive free body water r/t SIADH, HF, polydipsia/hyperglycemia, excess intake
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3
Q

sodium imbalances: s/s, treatment

A 
s/s: patient dependent
- neuro changes
- mucous membranes/thirt (sticky mucous, white membranes)
treatment
- fluid replacement
- stabilize s/s
- treat cause
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4
Q

hyperkalemia: causes

A
  • excessive intake
  • renal failure
  • medications: K sparing diuretics, ACE/ARBs
  • burn injuries (due to initial cell lysis)
  • acidosis: metabolic (renal failure(
  • adrenal insufficiency
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5
Q

hyperkalemia: ECG changes

A
  • tall, peaked T waves
  • widened QRS
  • flat P wave
  • ectopic beats &/or abnormal rhythms
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6
Q

hyperkalemia: treatment

A
  • D50 & insulin IV
  • kayexelate
  • diuretics
  • dialysis
    heart protection:
  • calcium chloride/Ca gluconate
  • albuterol
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7
Q

hypokalemia: causes

A
  • deficient intake (IV, PO, NPO status)
  • burns (after initial fluid restrictions)
  • GI loss: vomiting/diarrhea, prolonged GI suction
  • diuretics
  • renal artery stenosis
  • Cushing’s syndrome/Corticosteroids
  • Alkalosis
  • hyperinsulinemia
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8
Q

hyperkalemia: s/s

A
  • ECG changes
  • muscle cramps & paresthesias: progresses to weakness, flaccidity
  • diarrhea, GI symptoms
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9
Q

hypokalemia: s/s

A
  • ECG changes
  • weakness, lethargy
  • hyporeflexia; possible paralysis
  • constipation/ileus
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10
Q

hypokalemia: treatment

A 
IV repletion for K < 3.0
- 25mEq/h
- burns if infused too quickly (try and give through central line. works better PO)
PO
- less expensive
- better absorption
- common with loop diuretics
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11
Q

Alteration in Carbon Dioxide

A
  • serum CO2 roughly equal to Arterial HCO3
  • increased CO2–>metabolic alkalosis
  • decreased CO2–>metabolic acidosis
    (if it doesn’t say “paCO2 it’s a venous blood draw)
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12
Q

BUN: levels

A

10-20 mg/dL

  • increased BUN= azotemia. pre, intra, postrenal
  • decreased BUN= hepatic dysfunction, protein catabolism alterations
  • increased BUN + Normal Cr= dehydration
  • BUN:Cr ratio 15.5:1 is optimal
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13
Q

Creatinine: levels

A
  1. 5-1.1mg/dL (F)
  2. 6-1.2 mg/dL (M)
    - increased Cr indicates renal damage
    - rise indicates chronicity of renal disease
    - doubling of Cr= 50% renal loss of fx
    - decreased Cr reflection of decreased muscle mass
    - above 1.2 indicates damage
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14
Q

serum osmolality

A
  • 275-295 mOsm/kg h2o
  • concentration of dissolved particles in blood
  • quick formula: 2 x Na
  • formula: 2(Na)+K+(BUN/3)+(Glucose/18)
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15
Q

reasons for increased serum osmolality

A
  • dehydration
  • DKA/HHNK
  • DI
  • hypernatremia
  • metabolic acidosis
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16
Q

reasons for decreased serum osmolality

A
  • overhydration

- SIADH

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17
Q

anion gap

A
  • difference between anions and cations
  • normal range: 8-16mEq/L
  • formula: Na- (Cl+CO2)= anion gap
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18
Q

increased anion gap

A 
MUDPILES
M: methanol
U: uremia
D: DKA
P: paraldehyde
I: isoniazid/iron 
L: lactic acid
E: ethylene glycol
S: salicylates
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19
Q

decreased anion gap

A
  • hypercalcemia
  • hypermagnesemia
  • hyperkalemia
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20
Q

reasons for increased WBCs

A

leukocytosis: excess
- infection
- inflammation
- tissue necrosis

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21
Q

reasons for decreased WBCs

A

leukopenia: absence
- immunosuppression (we want this in transplant patients)
- autoimmune diseases

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22
Q

granulocytes

A 
Neutrophils: bacterial infections
- immature neutrophils "bands"
- increased bands--> shift to the left
Eosinophils: allergic reactions
- parasitic infections
Basophils: allergic reactions
- no response to bacterial/viral infections
People with seasonal allergies/asthma have inherent increase in eosinophils and basophils
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23
Q

alterations in H&H

A 
decreased:
- hemorrhage
- anemia
- menses
increased:
- severe dehydration
- malnutrition
usually do a transfusion if lower than 7 & 21
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24
Q

hematologic studies

A 
RBC
- increased (dehydration)
- decreased (heorrhage, anemia)
RDW: red cell distribution width
- used to classify anemia
- increased with increased erythropoiesis 
MPV:
- useful in diagnosing thrombocytopenia
- immature platelets larger
- decreased bone marrow production
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25
Q

coagulation studies

A 
APTT: 30-40 seconds
- increased (hepatic disease, hemophilia)
- Heparin gtt monitoring
PT: 11.0-12.5 seconds
INR: 1.0
- Increased: hepatitis, cirrhosis
- warfarin therapy monitoring
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26
Q

sinus bradycardia: possible causes

A
  • decreased metabolic rate- sleep, hypothermia
  • ICP
  • increased vagal tone: gagging, vomiting, straining, carotid massage, tracheal suctioning
  • drugs: digitalis, B blockers
  • diseases that have a depressive effect on the SA node: hypopituitarism, myxedema, obstructive jaundice
  • damage to SA node from MI (esp inferior since right coronary artery supplies the SA)
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27
Q

sinus bradycardia: clinical significance

A
  • may be normal in some adults
  • may lead to an inadequate stroke volume, result in tiredness, hypotension, lightheadedness, altered LOC, angina/ischemia, PVCs, syncope
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28
Q

sinus bradycardia: treatment

A
  • if asymptomatic, no treatment
  • atropine, dopamine, epinephrine, isoproterenol
  • if severe, pacer
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29
Q

sinus tachycardia: possible causes

A
  • increased metabolic demands or decreased nutrients: exercise, hypoxia, hyperthyroidism, fever (est increase 8bpm for every degree rise in body temp)
  • increased sympathetic tone
  • stimulants
  • compensatory mechanism for decreased blood flow or volume
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30
Q

sinus tachycardia: clinical significance

A
  • shortened diastolic period–>less time for ventricular filling–>hypotension, angina, palpitations, dizziness, lightheadedness
  • produces increased workload–>more O2 consumption–>greater concern for MI patient
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31
Q

sinus tachycardia: treatment

A
  • mild sedation
  • fluids for dehydration
  • B blockers
  • Ca channel blockers: verapamil, amiodarone, digoxin
  • diuretics in the case of CHF
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32
Q

PACs: possible causes

A
  • periods of stress or fatigue
  • increased consumption of alcohol, caffeine, nicotine
  • increased catecholamine levels associated with hyperthyroidism
  • coronary or valvular heart disease
  • atrial hypertrophy and atrial hypoxia
  • digitalis, quinidine, procainamide
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33
Q

PACs: clinical significance and treatment

A 
CS:
- infrequently: no CS
- frequent: atrial arrhythmias ie. flutter or fib
Treatment:
- based on severity
- remove stimulus, administer O2
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34
Q

SVT: possible causes

A
  • digitalis toxicity
  • chronic ishemic heart disease
  • hyperthyroidism
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35
Q

SVT: clinical significance and treatment

A

CS:
- may increase area of infarction size
- s/s may include dizziness, SOB, hypotension, syncope
Treatment:
- attempt therapeutic diagnostic maneuver: vagal maneuver, adenosine
- AV nodal blockade w/BB, CCB: diltiazem, amiodarone, digoxin
- synchronized cardioversion
- antiarrhythmics: procainamide, amiodarone, sotalol

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36
Q

atrial flutter: possible causes

A
  • chronic and acute heart disease
  • complication of MI
  • usually due to organic heart disease: rheumatic, valvular, sick sinus, heart surgery, cor pulmonale, atrial hypertrophy, pericarditis
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37
Q

atrial flutter: clinical significance and treatment

A

CS:
- possible compromised ventricular filling, coronary artery blood flow
- experience syncope, lightheadedness, etc.
- inadequate perfusion
Treatment:
- remove underlying cause
- control ventricular rate and/or convert to NSR
- drug therapy
- synchronized cardioversion

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38
Q

atrial fibrillation: possible causes

A
  • rheumatic mitral valve disease
  • congestive heart failure
  • coronary artery disease
  • occurs as a result of digitalis toxicity
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39
Q

a. fib: clinical significance and treatment

A

CS:
- inefficient heart pumping–>decreased ventricular filling, coronary blood flow
- contribution of atrial contraction to vent. filling (atrial kick) is eliminated
- prone to clot formation
Treatment:
- conversion
- drugs

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40
Q

PVC: possible causes

A
  • ischemic heart disease
  • drugs such as digitalis, quinidine, procainamide
  • electrolyte disturbances, esp. potassium
  • hypoxia
  • acid-base imbalance
  • ventricular aneurysms
  • valvular diseases
  • mechanical irritation of the myocardium by catheters or wires
  • anesthesia
  • caffeine, alcohol, nicotine
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41
Q

PVC: clinical significance

A

occasionally occur in healthy individuals
of concern when:
- occur at a rate of more than 6 per minute, originate from more than 1 ectopic foci (multifocal), two in a row or more occur
- when bigeminy, trigeminy, or quadrigeminy
- occur near the preceding T wave: R on T
- patient is symptomatic

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42
Q

PVC: treatment

A
  • drugs that suppress ventricular irritability: IV lidocaine, oral antiarrhythmic
  • if result of severe bradycardia: atropine administered to increase HR, improve cardiac output
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43
Q

V. tach: possible cause

A
  • ischemia heart disease
  • electrolyte imbalance
  • hypoxia
  • anesthesia
  • myocarditis
  • mechanical irritation or the myocardium
  • R on T
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44
Q

V. tach: clinical significane, treatment

A 
CS:
- life threatening arrhythmia: compromised ventricular filling = decreased CO.
Treatment: 
- CPR
- electrical defibrillation
- antiarrhythmics: procainamide IV
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45
Q

V. fib: possible causes

A
  • Acute MI (very high incidence in first 2 hours post MI)
  • hypoxia
  • anesthesia
  • myocarditis
  • mechanical irritation of the myocardium by catheters or wires
  • R on T phenomenon
46
Q

V. fib: clinical significance, treatment

A

CS:
- life threatening arrhythmia: no coordinated ventricular contraction.
- loss of pulse, bp, consciousness
- irreversible brain damage may develop
Treatment:
- defibrillation- good prognosis if defib in 1-3min
- CPR
- epi IVP or vasopressin IV
- IV amiodarone, lidocaine, magnesiu, procainamide
- defibrillate 200j-300j-360j in quick succession

47
Q

asystole: treatment

A
  • primary survey: ABC(check another lead)D(defibrillate)
  • secondary survey: airway, intubate, IV access
  • interventions: transcutaneous pacing, epinephrine, atropine
48
Q

PJC: possible causes, clinical significance, treatment

A 
Possible causes:
- digitalis toxicity
- enhanced automaticity of the junction
- increased vagal tone on the SA node
- excessive dose of quinidine or procainamide
CS:
- rarely significant
Tx:
- rarely needed
49
Q

1st degree AVB: possible causes, cs, tx

A

PC:
- MI, ishemia, infection, valvular heart disease, rheumatic fever, dig toxicity
CS:
- usually benign
- if associated with MI, monitor carefully for progression of higher degrees of block
Tx:
- none if asymptomatic
- atropine if associated with bradycardia

50
Q

2nd degree AVB Type I: possible causes, cs, tx

A

PC:
- MI, cardiac surgery involving area of AV node, ischemia, dig tox.
CS:
- often transient, disappears as underlying cause is removed
- if brady, may experience effects of decreased CO
- risk of progressing to complete HB
Tx:
- monitor for further development
- administer atropine if rate not providing adequate output.
- temporary transvenous pacing may be used.

51
Q

2nd degree AVB Type II: possible causes, cs, tx

A 
PC:
- MI, ischemia, dig tox
CS: 
- tolerance depends on ventricular rate
- hypotension, decreased CO, angina CHF, shock
- risk of progression
TX:
- monitor for further development
- administer drugs with caution
- symptomatic: temporary cardiac pacing
52
Q

3rd degree AVB: possible causes, cs, tx

A 
PC:
- MI, ischemia, dig tox, atherosclerosis of conduction system, surgical injury/trauma to AV
CS:
- slow ventricular rate symptoms
- danger that ventricular ectopic focus will either cease to function or initiate v. fib
- atria and ventricles not working in synchrony= hemodynamic compromise
Tx:
- immediate management
- ventricular ectopic pacemaker
- drugs to increase ventricular rate
- CPR if indicated
- when stable: pacemaker
53
Q

bundle branch block: possible causes, cs, tx

A

PC:
- MI, ischemia, myocarditis, valvular heart disease, idiopathic degenerative disease of electrical conduction system, cardiomyopathy, severe left ventricular hypertrophy
CS:
- underlying cause may need treatment
- left BBB: obscures ECG signs of AMI, right does not
- acute BBB generally reflects extensive ischemic damage secondary to AMI
- chronic BBB results from chronic degeneration or fibrotic scarring of conduction system
Tx:
- chronic: none
- acute: temporary pacer

54
Q

PEA: possible causes, cs, tx

A

PC:
- hypovolemia, hypoxia, acidosis hyper/hypokalemia, hypothermia, tablets (BB, CC, dig), tamponade, tension pnemo, thrombosis
CS: complete loss of cardiac output and requires immediate intervention
Tx:
- primary and secondary ABCs
- high concentration O2
- epi followed by fluid flush, repeat 3-5x
- if brady, atropine

55
Q

hemodynamic monitoring

A
  • invasive method
  • monitor cardiac function
  • aid in diagnosis of cardiac dysfunction
  • guide (not give) therapeutic interventions (don’t put meds in it!)
56
Q

arterial pressure monitoring: purpose and indications

A

Purpose:
- provide continuous measurement of blood pressure
- sample arterial blood
Indications:
- monitor BP of patients receiving vasoactive agents or for those with an unstable bp
- for frequent ABGs
- NOT for administration of meds or IV solutions

57
Q

arterial line insertion

A
  • radial artery most common
  • femoral, ulnar, dorsalis pedis are alternatives but not ideal
  • perform Allen’s Test PRIOR to assure there is adequate blood supply to the hand if the radial artery becomes occluded by the catheter
  • catheter is inserted into artery
  • then connected to special system used for monitoring
58
Q

monitoring system components

A
  • non-distensible tubing: needed to generate positive pressure to prevent back flow (should not be blood in here). only used for this purpose.
  • transducer: senses “blips” in the catheter, transforms them to electical signal, which displays on the monitor
  • cardiac monitor: displays waveform. values are assigned by the monitor to the waveform.
  • pressurized fluid: maintains patency & positive pressure, prevents backflow, needs 300mmHg. use NS or heparinized saline
  • sampling port: used for sampling blood, maintains sterility, maintain tight connections throughout system!!
59
Q

preparing monitoring system

A
  • level transducer at phlebostatic axis (axillary level)- above could indicate low pressure, below;high.
  • zero the system: open it to air
  • calibrate the system: tells the monitor that atmospheric pressure is zero
  • re-zero when turning patient, document.
60
Q

arterial waveform: upstroke

A
  • rapid upstroke represents rapid ejection of blood from the ventricle
  • at the peak of he upstroke, systolic BP is measured
  • QRS complex precedes upstroke
61
Q

arterial waveform: dicrotic notch

A
  • represents a slight back flow of blood toward the heart, therefore closure of the aortic valve
  • corresponds with the T wave on the ECG
  • marks beginning of ventricular diastole
62
Q

arterial waveform: end diastolic

A
  • as blood flows away from the heart, the pressure in the arterial system decreases
  • the lowest point of the waveform marks the diastolic pressure
63
Q

MAP

A

Normal: 70-105

  • 70 minimum amt required to perfuse brain/kidneys
  • set alarms at 75 and 65 to tell you when to do interventions
  • formula 2(Diastolic)+Systolic/3
  • diastole 2/3 longer than systole
64
Q

indirect vs. direct arterial line

A
  • arterial line SBP will be HIGHER than indirect SBP by 5-20mmHg
  • a.line DBP will be LOWER than indirect SBP by 5-10
  • a. line and indirect MAP’s will be about +/- 5mmHg
65
Q

arterial line complications

A 
Infection
- sterile dressing
- stopcocks covered with sterile caps
- assess your patient for s/s infection
Blood loss
- tight connections
- q1h checks
- immobilize extremity
- remember it's arterial blood- loss will happen FAST
Impaired circulation
- assess color, temperature, sensation, movement frequently
- at least q4h
- hand assessment, cap refill
66
Q

pulmonary artery pressure: description and purpose

A

Description
- pulmonary catheter is a balloon-tipped catheter inserted into the heart
- can measure right heart pressures directly and indirectly measure left heart pressures
Purpose
- aid in establishment of diagnosis, guide and optimize therapy, provide prognostic information
- assess fx of right and left side of the heart
- for patients who are really sick

67
Q

the pulmonary artery catheter

A

At minimum, has 4 lumens with 4 ports:
- proximal: in right atrium, attached to a transducer and continuous flush.
- distal: in pulmonary artery, also attached to a transducer and flush.
- balloon inflation port (for PAWP)
- thermisor port: connected to bedside monitor to calculate CO, also great way to measure temp.
DO NOT use distal port to infuse medications
The catheter is passes through an introducer which is placed in one of the great veins (subclavian and internal jugular veins)

68
Q

measures obtained by pulmonary artery catheter

A
  • right atrial pressure (=CVP)
  • right ventricular pressure (RVP)
  • pulmonary artery pressure (PAP)
  • pulmonary artery wedge pressure (PAWP)
  • cardiac output
  • many more calculated values
  • oxygenation information
69
Q

Preload

A
  • mostly left ventricle
  • the amount of stretch placed on cardiac chamber muscle just before systole
  • stretch is usually proportional to the volume of blood in the chamber at the end of diastole
  • volume stretches the ventricular wall, exerting a pressure, measured by the catheter
70
Q

right-sided preload

A
  • the right atrial pressure reflects preload of the right side of the heart
  • also use Central Venous Pressure to reflect this
  • normal is 0-8mmHg
71
Q

Increased right/left sided preload: causes and treatment

A 
Causes:
- fluid overload
- right/left sided HF
- right/left side MI
- pericardial effusion or cardiac tampnade
Treatment
- diuretics
- inotropes (increase force of contraction)
72
Q

Decreased right and left sided preload: causes and treatment

A 
Causes:
- dehydration
Treatment:
- fluids
- blood if anemic (if under 10/30)
- treat cause of fluid loss
73
Q

left-sided preload

A
  • the pulmonary artery occlusion pressure (PAOP) reflects the preload on the left side of the heart
  • normal PAWP= 8-12mmHg
74
Q

afterload

A
  • the force or pressure against which a cardiac chamber must eject blood during systole
  • the amount of resistance the chamber has to overcome to eject blood during systole
  • a calculated value
  • formulas look at the gradient difference between inflow of the circuit and the outflow
  • what the ventricles need to push against
75
Q

increased right sided afterload: causes and treatment

A

Causes:
- primary pulmonary hypertension
- COPD
- ARDS (massive fluid shift. alveoli drowning)
- pulmonic valve stenosis
Treatments:
- treat underlying cause of pulmonary failure
- the pulmonary vasculature reacts poorly to neural and pharmacological therapy

76
Q

increased left sided afterload (SVR): causes and treatment

A

Causes:
- systemic hypertension (diastolic)
- aortic stenosis: valve doesn’t open all the way
- stress: cortisol
Treatment:
- lower BP with vasodilators (i.e. Nitroglycerin, Nitroprusside, Dobutamine)
- surgery for AS

77
Q

decreased left sided afterload (SVR): causes and treatment

A 
Causes:
- septic shock
- excessive administration of afterload reducers
Treatment:
- bring bp up
- dopamine
- epi
- norepi
- phenylephrine
78
Q

contractility (elasticity)

A
  • defined as the ability to shorten and develop tension
  • a calculated value
  • estimates the work of the heart
  • low contractility can be the result of a failing heart
79
Q

cardiac output

A
  • normal CO is 4-8L/min
  • this can be individualized to the patient’s size by dividing the CO by the body surface area: cardiac index
  • normal cardiac index is 2/4-4L/min/m2
    causes decreased or increased:
  • things affecting stroke volume: uppers, anything increasing HR
80
Q

right ventricular pressure

A
  • need a special catheter to assess this on a regular basis
  • otherwise it is assessed upon insertion only
  • normal: 20-30/0-8
81
Q

pulmonary artery pressure

A
  • normal systolic: 20-30mmHg
  • normal diastolic: 8-15 (wedge pressure)
  • normal PA mean: 10-20
  • PA diastolic pressure is an indirect measure of the pressure in the left ventricle
82
Q

relationship of PAWP to left ventricular preload

A
  • the balloon at the tip of the catheter is inflated and occludes forward blood flow
  • during diastole, the mitral valve is open. at this time, there are not other obstructions between the tip of the catheter and the left ventricle
  • a static column of blood is created on the left side and the pressure obtained reflects end-diastolic pressure.
83
Q

Measures and ports used

A

RAP–>proximal port in R atrium
PAWP–>distal port with balloon occluded
PAP–>distal port with balloon down
RVP–>distal port during insertion

84
Q

waveforms

A
  • for the RAP and PAOP: a,v, and sometimes c can be seen
  • the “a” wave is caused by atrial contraction
  • the “c” wave is caused by ventricular contraction and bulging of the AV valves
  • the “v” wave is cause by the slow flow of blood into the atria from the veins while the AV valves are closed during ventricular contraction
85
Q

complications of pulmonary artery catheters

A

Pneumothorax
- patient must have chest xray post insertion
Infection
- contamination of PA catheter, insertion site, pressure monitoring system
- assess patient, use sterile technique
Dysrhythmias
- common during insertion, stop once positioned in PA
- if appears suddenly, catheter might have migrated back into the RV. Check PA waveform.
Pulmonary artery rupture or perforation
- balloon over-inflation
- do not inflate with more than 1.5cc air
Pulmonary infarction
- prolonged balloon inflation
- leave balloon up long enough to get measurement then let it deflate passively

86
Q

echocardiogram: uses

A

Assess cardiac structure and mobility

  • cardiomyopathy
  • ventricular aneurysms
  • valvular disorders
  • cardiac tumors
  • LV function
  • pericardial effusion
87
Q

echo: types

A
  • transthoracic: non invasive
  • transesophageal: invasive
  • use sound waves
88
Q

transthoracic echo procedure

A
  • no special preparation
  • bedside or in lab
  • 30-60 minutes
  • HOB 15-20 degrees
  • supine and left side
  • lubricated transducer
  • 3rd or 4th intercostal space
  • videotaped
  • measurements: chamber size (smaller in LVH), wall thickness, ejection fraction, flow gradient (retrograde flow- leaky mitral valve).
89
Q

esophageal echocardiogram

A
  • posterior view: left atrium, mitral valve, aortic arch
  • body habitus: extra adipose, breasts
  • bite blocks: prevent from biting tube
  • conscious sedation: separate consent. Versed.
  • less interference
    NPO after midnight.
90
Q

cardiac catheterization: definition

A 
invasive procedure
diagnostic:
- fluoroscopic mapping of coronary arteries
- measure pressures in the heart
interventional
- percutaneous transluminal coronary angioplasty
- valvuloplasty
Left side: femoral artery
Right side: femoral vein or jugular
91
Q

cardiac catheterization: indications

A
  • myocardial infarction
  • abnormal stress test
  • pre surgical evaluation
  • valvular heart disease
  • endomyocardial biopsy: transplant. see if pt is rejecting.
  • pre CABG surgery assessment: L internal mammary artery- checking for patency.
  • hemodynamic assessment: left and right heart pressures
92
Q

cardiac catheterization: pre procedure

A

days prior
- Labs: CBC, chemistries, coags- Cr, PTT. Need a baseline.
- phone call 24-48 hours prior to procedure
medication changes
- Metformin held 48 hours prior
- half normal insulin dose in AM
- hold diuretics in AM. don’t want patient to need to urinate while having procedure.

93
Q

cardiac catheterization: pre procedure concerns

A 
diabetic patient:
- blood sugar upon arrival
- NPH/Protamine reaction
renal failure
- Cr >1.5
- treatment: hydration
allergies
- iodine/shellfish (give Diphenhydramine, steroids, Ranitidine)
- narcotics/benzos
anticoag therapy
- ASA/Clopidogrel
- Warfarin (PTT day of procedure). stop taking a couple days beforehand.
94
Q

cardiac cath: same day nursing role

A
  • v/s, H&P
  • PIV started, fluids @ KVO. have 20g in case of need for blood product infusion.
  • witness consent: procedure, conscious sedation
  • answer questions
  • advance directives
95
Q

cardiac cath: sequence of procedure

A
  • prep in same day area
  • prep in lab
  • femoral artery approach: introducer sheath, catheter to coronary sinus, dye injection (diagnostic), passing of balloon catheters/stents
96
Q

cardiac catheterization: intra procedure nursing role

A 
in the lab
- orient patient to lab
- prep access areas (groin)
during procedure
- administer medications/sedation: Fentanyl/Morphine/Demerol, Midazolam
- pass equipment
97
Q

PTCA

A
  • balloon tip catheter
  • stent acts as “scaffolding”
  • complications: dye reaction (might feel flushing sensation), coronary vessel rupture/aneurysm
98
Q

cardiac cath: post procedure arterial closure

A 
sheath in place
- pressure for ~15 minutes post sheath removal
- 4 hours in recovery prior to discharge
angioseal
- collagen plug; dissolves
- discharge in 2 hours
perclose
- suture device: criss cross
- discharge in 2 hours
99
Q

cardiac cath: post procedure nursing role

A 
monitor v/s
- q15x4, q30x2, q60x2
- q3min during sheath removal
- distal pulses
observe access site
- bleeding
- hematoma
food & hydration
- Fowler's position 1 hour post sheath removal
- leg straight
- hold groin when coughing
monitor for dysrhythmias 
lab work PRN
- hypoglycemic reaction
education
- new medications
- follow up appointments: cardiologist
discharge instructions
- no driving for 72 hours
- limited use of stairs: no lifting more than 5lbs x 2 days
100
Q

electrophysiologic studies: definition

A

an invasive procedure i which intracardiac electrocardiograms are recorded for the purpose of diagnosing an arrhythmia and determining appropriate treatment

101
Q

electrophysiologic studies: purpose

A
  • record activities of the conducting system
  • localize the source of an arrhythmia
  • differentiate types of rhythms
  • guide in the selection of therapy
  • evaluate effectiveness of therapy
102
Q

electrophysiologic studies: indications

A
  • ventricular arrhythmias
  • SVTs
  • syncope evaluation
  • unexplained sudden death
  • SA Node dysfunction
  • AV nodal rhythms
103
Q

applications of EPS

A 
diagnostic
- nodal dysfunction
- mechanism of ST/VT
- cause of unexplained syncope
therapeutic
- drug therapy
- determine AICD appropriateness
- test efficacy of ablative techniques
interventional
- AV nodal ablation
- ablation for atrial dysrhythmias
- VT ablation
prognostic
- risk post MI
- risk for asymptomatic WPW
- risk for nonsustained VT
104
Q

EPS procedure

A
  • venous access: inferior vena cave
  • multipolar catheters: monitor, introduce electricity
  • mapping: find where SA node is
  • electical stimulation
105
Q

complications of EPS

A
  • death
  • arrythmias
  • hemorrhage: holes in vasculature
  • thromboembolism
  • cardiac perforation/tamponade
  • hemo or pneumo thorax
106
Q

ablation: definintion

A
  • used for treatment of dysrhythmias
  • intervention developed in the 1980s
  • application of energy/radiofrequency
  • destruction of arrythmic circuit
107
Q

re-entry circuit (tachycardias)

A 
abnormal conduction circuit
electrical impulse: circular pattern
heart muscle: contracts in response
locations
- a. fib
- AV nodal
- accessory pathway
- v. tach
108
Q

abnormal slow heart rhythms

A 
sick sinus syndrome
- SA node malfunctions
- bradycardia (pacemaker malfunction)
- brady-tachy syndrome
- sinus pause
heart block
- slow ventricular rate
- lack of CO, perfusion
109
Q

indication for ablation

A
  • a.fib
  • a. flutter (lose atrial kick)
  • Wolff-Parkinson-White syndrome
  • v. tach
110
Q

complications of ablation

A 
arrhythmias
- intraprocedure defibrillation
damage to conduction system
- pacemaker may be needed
- hemorrhage
- cardiac perforation/tamponade
111
Q

ablation procedure

A 
usually performed at time of EPS
a. fib
- AV node destroyed
- permanent pacer required
- AV nodal modification experimental
a. flutter
- reentry circuit
- posterior RA septum 
v.tach
- variety of locations
- transseptal approach
success based on location
112
Q

cardiac cath: contraindications

A 
absolute: inadequate facility/equipment
relative:
- uncontrolled BP/arrhythmias/HF
- pregnancy
- coagulopathy/anticoags: esp thrombolytics
- renal failure (Cr>1.5)
- recent CVA (<1 month)

Critical Care (3 decks)

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