Exam I Flashcards
hypernatremia: causes
- 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
hypoatremia: causes
- 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
sodium imbalances: s/s, treatment
s/s: patient dependent - neuro changes - mucous membranes/thirt (sticky mucous, white membranes) treatment - fluid replacement - stabilize s/s - treat cause
hyperkalemia: causes
- excessive intake
- renal failure
- medications: K sparing diuretics, ACE/ARBs
- burn injuries (due to initial cell lysis)
- acidosis: metabolic (renal failure(
- adrenal insufficiency
hyperkalemia: ECG changes
- tall, peaked T waves
- widened QRS
- flat P wave
- ectopic beats &/or abnormal rhythms
hyperkalemia: treatment
- D50 & insulin IV
- kayexelate
- diuretics
- dialysis
heart protection: - calcium chloride/Ca gluconate
- albuterol
hypokalemia: causes
- 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
hyperkalemia: s/s
- ECG changes
- muscle cramps & paresthesias: progresses to weakness, flaccidity
- diarrhea, GI symptoms
hypokalemia: s/s
- ECG changes
- weakness, lethargy
- hyporeflexia; possible paralysis
- constipation/ileus
hypokalemia: treatment
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
Alteration in Carbon Dioxide
- 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)
BUN: levels
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
Creatinine: levels
- 5-1.1mg/dL (F)
- 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
serum osmolality
- 275-295 mOsm/kg h2o
- concentration of dissolved particles in blood
- quick formula: 2 x Na
- formula: 2(Na)+K+(BUN/3)+(Glucose/18)
reasons for increased serum osmolality
- dehydration
- DKA/HHNK
- DI
- hypernatremia
- metabolic acidosis
reasons for decreased serum osmolality
- overhydration
- SIADH
anion gap
- difference between anions and cations
- normal range: 8-16mEq/L
- formula: Na- (Cl+CO2)= anion gap
increased anion gap
MUDPILES M: methanol U: uremia D: DKA P: paraldehyde I: isoniazid/iron L: lactic acid E: ethylene glycol S: salicylates
decreased anion gap
- hypercalcemia
- hypermagnesemia
- hyperkalemia
reasons for increased WBCs
leukocytosis: excess
- infection
- inflammation
- tissue necrosis
reasons for decreased WBCs
leukopenia: absence
- immunosuppression (we want this in transplant patients)
- autoimmune diseases
granulocytes
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
alterations in H&H
decreased: - hemorrhage - anemia - menses increased: - severe dehydration - malnutrition usually do a transfusion if lower than 7 & 21
hematologic studies
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
coagulation studies
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
sinus bradycardia: possible causes
- 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)
sinus bradycardia: clinical significance
- may be normal in some adults
- may lead to an inadequate stroke volume, result in tiredness, hypotension, lightheadedness, altered LOC, angina/ischemia, PVCs, syncope
sinus bradycardia: treatment
- if asymptomatic, no treatment
- atropine, dopamine, epinephrine, isoproterenol
- if severe, pacer
sinus tachycardia: possible causes
- 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
sinus tachycardia: clinical significance
- shortened diastolic period–>less time for ventricular filling–>hypotension, angina, palpitations, dizziness, lightheadedness
- produces increased workload–>more O2 consumption–>greater concern for MI patient
sinus tachycardia: treatment
- mild sedation
- fluids for dehydration
- B blockers
- Ca channel blockers: verapamil, amiodarone, digoxin
- diuretics in the case of CHF
PACs: possible causes
- 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
PACs: clinical significance and treatment
CS: - infrequently: no CS - frequent: atrial arrhythmias ie. flutter or fib Treatment: - based on severity - remove stimulus, administer O2
SVT: possible causes
- digitalis toxicity
- chronic ishemic heart disease
- hyperthyroidism
SVT: clinical significance and treatment
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
atrial flutter: possible causes
- 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
atrial flutter: clinical significance and treatment
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
atrial fibrillation: possible causes
- rheumatic mitral valve disease
- congestive heart failure
- coronary artery disease
- occurs as a result of digitalis toxicity
a. fib: clinical significance and treatment
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
PVC: possible causes
- 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
PVC: clinical significance
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
PVC: treatment
- drugs that suppress ventricular irritability: IV lidocaine, oral antiarrhythmic
- if result of severe bradycardia: atropine administered to increase HR, improve cardiac output
V. tach: possible cause
- ischemia heart disease
- electrolyte imbalance
- hypoxia
- anesthesia
- myocarditis
- mechanical irritation or the myocardium
- R on T
V. tach: clinical significane, treatment
CS: - life threatening arrhythmia: compromised ventricular filling = decreased CO. Treatment: - CPR - electrical defibrillation - antiarrhythmics: procainamide IV
V. fib: possible causes
- 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
V. fib: clinical significance, treatment
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
asystole: treatment
- primary survey: ABC(check another lead)D(defibrillate)
- secondary survey: airway, intubate, IV access
- interventions: transcutaneous pacing, epinephrine, atropine
PJC: possible causes, clinical significance, treatment
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
1st degree AVB: possible causes, cs, tx
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
2nd degree AVB Type I: possible causes, cs, tx
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.
2nd degree AVB Type II: possible causes, cs, tx
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
3rd degree AVB: possible causes, cs, tx
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
bundle branch block: possible causes, cs, tx
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
PEA: possible causes, cs, tx
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
hemodynamic monitoring
- invasive method
- monitor cardiac function
- aid in diagnosis of cardiac dysfunction
- guide (not give) therapeutic interventions (don’t put meds in it!)
arterial pressure monitoring: purpose and indications
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
arterial line insertion
- 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
monitoring system components
- 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!!
preparing monitoring system
- 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.
arterial waveform: upstroke
- rapid upstroke represents rapid ejection of blood from the ventricle
- at the peak of he upstroke, systolic BP is measured
- QRS complex precedes upstroke
arterial waveform: dicrotic notch
- 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
arterial waveform: end diastolic
- as blood flows away from the heart, the pressure in the arterial system decreases
- the lowest point of the waveform marks the diastolic pressure
MAP
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
indirect vs. direct arterial line
- 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
arterial line complications
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
pulmonary artery pressure: description and purpose
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
the pulmonary artery catheter
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)
measures obtained by pulmonary artery catheter
- 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
Preload
- 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
right-sided preload
- 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
Increased right/left sided preload: causes and treatment
Causes: - fluid overload - right/left sided HF - right/left side MI - pericardial effusion or cardiac tampnade Treatment - diuretics - inotropes (increase force of contraction)
Decreased right and left sided preload: causes and treatment
Causes: - dehydration Treatment: - fluids - blood if anemic (if under 10/30) - treat cause of fluid loss
left-sided preload
- the pulmonary artery occlusion pressure (PAOP) reflects the preload on the left side of the heart
- normal PAWP= 8-12mmHg
afterload
- 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
increased right sided afterload: causes and treatment
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
increased left sided afterload (SVR): causes and treatment
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
decreased left sided afterload (SVR): causes and treatment
Causes: - septic shock - excessive administration of afterload reducers Treatment: - bring bp up - dopamine - epi - norepi - phenylephrine
contractility (elasticity)
- 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
cardiac output
- 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
right ventricular pressure
- need a special catheter to assess this on a regular basis
- otherwise it is assessed upon insertion only
- normal: 20-30/0-8
pulmonary artery pressure
- 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
relationship of PAWP to left ventricular preload
- 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.
Measures and ports used
RAP–>proximal port in R atrium
PAWP–>distal port with balloon occluded
PAP–>distal port with balloon down
RVP–>distal port during insertion
waveforms
- 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
complications of pulmonary artery catheters
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
echocardiogram: uses
Assess cardiac structure and mobility
- cardiomyopathy
- ventricular aneurysms
- valvular disorders
- cardiac tumors
- LV function
- pericardial effusion
echo: types
- transthoracic: non invasive
- transesophageal: invasive
- use sound waves
transthoracic echo procedure
- 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).
esophageal echocardiogram
- 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.
cardiac catheterization: definition
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
cardiac catheterization: indications
- 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
cardiac catheterization: pre procedure
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.
cardiac catheterization: pre procedure concerns
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.
cardiac cath: same day nursing role
- 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
cardiac cath: sequence of procedure
- 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
cardiac catheterization: intra procedure nursing role
in the lab - orient patient to lab - prep access areas (groin) during procedure - administer medications/sedation: Fentanyl/Morphine/Demerol, Midazolam - pass equipment
PTCA
- balloon tip catheter
- stent acts as “scaffolding”
- complications: dye reaction (might feel flushing sensation), coronary vessel rupture/aneurysm
cardiac cath: post procedure arterial closure
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
cardiac cath: post procedure nursing role
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
electrophysiologic studies: definition
an invasive procedure i which intracardiac electrocardiograms are recorded for the purpose of diagnosing an arrhythmia and determining appropriate treatment
electrophysiologic studies: purpose
- 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
electrophysiologic studies: indications
- ventricular arrhythmias
- SVTs
- syncope evaluation
- unexplained sudden death
- SA Node dysfunction
- AV nodal rhythms
applications of EPS
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
EPS procedure
- venous access: inferior vena cave
- multipolar catheters: monitor, introduce electricity
- mapping: find where SA node is
- electical stimulation
complications of EPS
- death
- arrythmias
- hemorrhage: holes in vasculature
- thromboembolism
- cardiac perforation/tamponade
- hemo or pneumo thorax
ablation: definintion
- used for treatment of dysrhythmias
- intervention developed in the 1980s
- application of energy/radiofrequency
- destruction of arrythmic circuit
re-entry circuit (tachycardias)
abnormal conduction circuit electrical impulse: circular pattern heart muscle: contracts in response locations - a. fib - AV nodal - accessory pathway - v. tach
abnormal slow heart rhythms
sick sinus syndrome - SA node malfunctions - bradycardia (pacemaker malfunction) - brady-tachy syndrome - sinus pause heart block - slow ventricular rate - lack of CO, perfusion
indication for ablation
- a.fib
- a. flutter (lose atrial kick)
- Wolff-Parkinson-White syndrome
- v. tach
complications of ablation
arrhythmias - intraprocedure defibrillation damage to conduction system - pacemaker may be needed - hemorrhage - cardiac perforation/tamponade
ablation procedure
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
cardiac cath: contraindications
absolute: inadequate facility/equipment relative: - uncontrolled BP/arrhythmias/HF - pregnancy - coagulopathy/anticoags: esp thrombolytics - renal failure (Cr>1.5) - recent CVA (<1 month)
