Cardiac Flashcards
Automaticity
The ability to spontaneously initiate an electrical impulse
Causes of dysthymia’s
Acid, autonomic nervous system, electrolyte imbalances, ischemia, injury, hypoxia, unhealthy heart, drugs
Excitability
The ability to respond to an electrical impulse
Conductivity
The ability to transmit the impulse to another cardiac cell
Contractility
The ability to contract after receiving a stimulus
What cells in the heart can spontaneously initiate an electrical impulse
Any cell
What move in cells when ventricles contract
Sodium and calcium
What enters the cells when ventricles repolarize
Potassium
Depolarization
Contraction or systole
Repolarization
Relaxation or diastole
What is the primary pacemaker
SA node
SA node
Primary pacemaker, located in right atrium, 60-100 bpm
AV node
Located in lower right atrium, delays conduction, gatekeeper so it allows time for the atria to contract and the ventricles to fill
Bundle of HIS
2 branches (left and right bundle), 30-40 bpm
Purkinje fibers
Where the bundle branches terminate in a network of fibers, 20-40 bpm
can the electrical system exist without the mechanical contraction
yes
can the mechanical exist without the electrical activity
no
what does the autonomic nervous system control
rate of impulse formation
speed of conduction
strength of contraction
what does the parasympathetic nervous system control
vagus nerve: decreaes rate, slows impulse conduction, decreases force of contraction
what does the sympathetic nervous system control
incrase rate incrases force of contraction
absolute refractory period
heart cells cant respond to stimulus, starts at Q wave to 1st 1/3rd of the T wave
relative refractory period
cardiac cells respond to a strong stimulus usually with a unorganized response, later 2/3 rds of the T wave
supernormal period
cardiac cells can respond to a weaker tan normal stimulus, @ the end of the T wave
refractory period
period between depolarizations
isoelectric line
base line of te EKG
P Wave
SA node firing, the right and left atria are contracting/systole/deplarization, it is a positive defelectino in lead II
PR interval
time from the begining of the P wave to the begining of the Q wave, duration is 0.12-0.2 seconds, represents the electrical impulse spread through the atria, AV node, bundle of HIS, BB, purkinje
QRS complex
contraction/systole/depolarization of the ventricles, duration is less than 0.10, measure from the begining of the Q to the end of the S wave, a positive deflection in lead I is normal, a negative deflection is normal in lead V1
ST segment
ventricular walls relax/diastole/repolarization, measure from end of S wave to begining of T wave
elevation of 2mm or higher or depression
ST segment depression or elevation is a sign of
MI, pericarditis, pulmonary emboli, electrolyte imbalance
T wave
ventricular repolarization/relaxation/diastole, follows the QRS wave and ST segment, typically rounded and smooth
an inverted T wave coud represent what
ischemia
a peaked T wave respresents what
hyperkalemia
QT interval
represents the time required for ventricular depolarizationand repoalrization to occur, starts at begining of Q to the end of the T wave
length of the QT interval
less than alf the distance between consecutive R waves (R-R interval) when the rhythm is regular
normal PR interval
0.12-0.2 seconds
normal QRS complex
less than 0.1 seconds
normal QT interval
half of the R-R interval
sinus rhythm
60-100 bpm, regular, pacemaker site is SA node, PR interval is 0.12-0.2 seconds, QRS is less than 0.1 seconds
sinus bradycardia
less than 60 bpm,
what can cause bradycardia
acute MI, CAD, SA node disease, CCB, BB, hyperkalemia, digitalis
clinical Sz of bradycardia
hypotension, pale, cool skin, weakness, angina, dizziness, confusion, shortness of breath
Tx for bradycardia
atropine, pacemaker, dopamine if BP is decreased
sinus tachycardia
100 bpm or more, pacemaker sire is SA node, p wave usually normal but may be slightly taller can be buried in the preceding T wave
causes of tachycardia
CHF, MI, pericarditis, cardiogenic shock, anxiety exercise, fever, infection, pain, hemorrhage, pulmonary embolis, hypovolemia, ingestion of stimulus, pharmacologics: atropine, caffeine, cocaine, nicotine….-ine
Sx of tachycardia
dizziness, hypotension
sinus tachycardia is frequently a COMPENSATORY MECHANISM
what does sinus tachycardia do the the oxygen demands
it increases the oxygen demands,
Tx for sinus tachycardia
Tx underlying cause
*if hypovolemic give fluids
sinus arrhythmia
60-100 bpm, may increase during inspiration and decrease during expiration, regularly irregular (R-R interval greater than or = to squars difference
what Tx is there for sinus arrhythima
none
premature atrial contraction (PAC)
contraction originating from ectopic (abnormal position) focus in atrium in location other than SA node, represents irritable atrial tissue
PAC can lead to what
a flutter or a fib
Tx for PAC
Tx underlying cause (emotional stress, COPD, electrolyte imblances), beta blockers are used
atrial tachycardia
140-250 bpm, pacemaker site is ectopic (not SA node), P wave may be hidden in T wave,
paroxsymal atrial tachycardia
atrial tachycardia that starts and dtops suddenly
supraventricular tachycardia (SVT)
umbrella term that can mean a fib or a flutter or atrial tach
what rhythm do you have if you have more than 3 PACs in a row
PAT paroxsymal atrial tachycardia
causes of atrial tachycardia
stress, anxiety, caffeine, alcohol, stimulants, chronic lung disease, dig toxicity
Tx of atrial tachycardia
depends on the pt tolerance of the rhythm
* stable: O2, diltiazem or BB or amiodarone
*unstable: O2, amiodarone or diltiazem
12 lead EKG
a flutter
recurring, regular sawtooth shaped flutter waves, originates from a single ectopic focus, atrial HR 250-400, ventricular HR 60-150
what keeps the ventricles from increasing HR although the atria are beating 250-400 bpm
AV node (gatekeeper)
Cause of a flutter
CAD, HTn, mitral valve disorders, pulmonary embolis, cardiomyopathy, digoxin, quinidine,epi
what are you at risk for after a flutter
stroke because of a possible thrombus formation in the atria
Tx of a flutter
slow ventricular responses by increasing AV block (CCB, BB), electrocardioversion, cardiozem, if there is no thrombi, to be put on a heparin drip to prevent clots then cardiozem, if the Rxs dont work, cardioversion is needed
what will be done if a pt has multiple episodes of flutter
they will get an ablation
a fib
atrial HR of 400 or more, ventricle HR greater than 100 is uncontrolled, less than 100 is controlled, PR interval is unable to be measured, pacemaker has multiple ectopic sites in the atira
cause of a fib
heart disease (rheumatic), CAD, cardiomyopathy, HF, pericarditits
what can happen if a fib is not tx
thrombi can form in the atria as a result from blood stasis, embolus may develop and travel to the brain, cauing a stroke
Tx of a fib
goal: decrease ventricular response, prevent embolic stroke
give CCb, CBB, digoxin
long term coumadin
what do you do if the duration of the arrhythmia has lasted longer than 48 hours
begin heparin, TEE, cardioversion, anticoag
junctional dysrhytmia
originates in the area of the AV node, SA node has failed to fire or has been blocked by the AV node, P wave may be absent, or premature with negative deflection
cause of premature junctional contraction (PJC)
acute inferior myocaridal infarction, rheumatic heart disease, valvular disease, excessive caffeine intake
Tx of premature junctional contractions
tx the cause
hold digoxin, restrict caffeine intake
junctional rhythum
HR 40-60, pacemaker is Av node, negative deflection of P wave
Tx for junctional dysrhythmias
is symptomatic (brady): atropine
tachy: BB, CCB, amiodarone used for rate control (when not caused by dig toxicity
CARDIOVERSION IS CONTRAINDICATED
first degree AV block
PR interval is prolonged greater than 0.2 seconds
Tx for first degree block
check medications, continue to monitor, usually no Tx
second degree AV block Type 1
gradual lengthening of PR interval then a QRS complex that is blocked (missing), more p waves than R waves
Tx for sencond degree AV block type 1
usually no Tx, if symptomatic: atropine or a temporary pacemaker
second degree AV block type 2
have 2 or 3 p waves before each QRS complex, PR interval remains constant (may be normal or prolonged),
what is the clinical significance of a sencond degree AV block type 2
can progress to third degree AV block and isassociated with a poor prognosis
Tx for second degree AV block type 2
if symptomatic: (hypotension, angina), temporary pacemaker, epi for HR, dopamine for BP permanent pacemaker
tird degree AV block
HR 20-40, no association between atria and ventricles, PT interval varies greatly
Tx of third degree AV block
if symptomatic (syncope, bradycardia): pacemaker, epiniphrine, atropine
premature ventricular contractions (PVC)
contraction originating in ectopic areas of the ventricles, wide distorted QRS complex (greater than 0.12), R opposite T reflection, PR interval is not measureable
Tx for PVC
usually not treated when isolated/infrequent, oxygen therapy for hypoxia, electrolyte replacement, BB, CCB, amiodarone
ventricular tachycardia
run of 3 or more PVCs, HR 140-250, no p waves associated with V tach, non measureable PR interval, QRS complex is wide ( 0.12 seconds or greater), considered life threatening because of the decreased CO and the possibility of deterioration ventricular fibrillation
a pt who has v tach with a pulse what is the tx
cardioversion with sedation (versed), if BP is stable
a pt who has v tach without a pulse what is the tx
CPR and rapid defibrillation, epi if defibrillation is unsuccessful
PTorsades de pointes
give IV magnesium
if v tach is not tx what will happen
turn into v fib then asystole
ventricular fibrillation (v fib)
severe derangement of the heart rythm characterized by irregular undulations of varying contour and amplitude
Tx of v fib
CPR, ACLS, defibrillation
asystole
represents total absence of ventricular electrical activity, no CO occurs because no depolarization occurs, may have occasional P
pulsesless electrical activity (PEA)
electrical activity can be observed on the EKG but there is no mechanical activity of the ventricles and the pt has no pulse
tx for PEA
CPR followed by intubation and IV epi, defibrillation
defibrillation
passage of electrical shock through the heart to depoalrize the cells of the myocardium to allow the SA node to resume the role of pacemaker
what do we defibrillate
V fib and pulseless V tach
biphasic defibrillators
deliver succeful shocks at lower energies and with fewer post shock EKG abnormalities
synchronized cardioversion
synchronized circuit delivers a countershock on the R wave of the QRS complex
what do we cardiovert
rapid a fib, rapid a flutter, PAT, V tach with pulse
sodium
135-145, stimulates reactions within nerve and muscle tissue, important for depolarization
SE of sodium
hyponatremia: HA, N/V, anxiety, weak, confused, anorexia
hypernatremia: dry mucous membranes, fatigue, restlessness, agitation, convulsions
potassium
3.5-5, regulates cardiac electrical activity, important for replarization and stable polarized state,
hypokalemia
ventricular arhythmias (PVCs), muscle weakness, U ave, lef cramps, anorexia, N/V
hyperkalemia
confusion, diarrhea, peasked T wave, blocks, asystole
hyponatremia
HA, N/V, anxiety, weakness, confused, anorexia
hypernatremia
dry MM, fatigue, restlessness, weakness, agitation, convulsions
calcium
8.5-10.5, transmits electrical impulses in the heart, important for initiation and propagation of electrical impulse for myocardial contraction
pulsesless electrical activity (PEA)
electrical activity can be observed on the EKG but there is no mechanical activity of the ventricles and the pt has no pulse
tx for PEA
CPR followed by intubation and IV epi, defibrillation
defibrillation
passage of electrical shock through the heart to depoalrize the cells of the myocardium to allow the SA node to resume the role of pacemaker
what do we defibrillate
V fib and pulseless V tach
biphasic defibrillators
deliver succeful shocks at lower energies and with fewer post shock EKG abnormalities
synchronized cardioversion
synchronized circuit delivers a countershock on the R wave of the QRS complex
what do we cardiovert
rapid a fib, rapid a flutter, PAT, V tach with pulse
sodium
135-145, stimulates reactions within nerve and muscle tissue, important for depolarization
SE of sodium
hyponatremia: HA, N/V, anxiety, weak, confused, anorexia
hypernatremia: dry mucous membranes, fatigue, restlessness, agitation, convulsions
potassium
3.5-5, regulates cardiac electrical activity, important for replarization and stable polarized state,
hypokalemia
ventricular arhythmias (PVCs), muscle weakness, U ave, lef cramps, anorexia, N/V
hyperkalemia
confusion, diarrhea, peasked T wave, blocks, asystole
hyponatremia
HA, N/V, anxiety, weakness, confused, anorexia
hypernatremia
dry MM, fatigue, restlessness, weakness, agitation, convulsions
calcium
transmits electrical impulses in the heart
hypocalcemia
prolonged QT interval, numbness, tingling, tetany, bleeding
hypercalcemia
AV block, weak, abdominal cramps, confused
magnesium
1.2-2.5, transmission of electrical activity in the heart, a decrease in Mg will increase intracellular K which increases cellular membrane excitability
hypomagnesemia
prolonged QT interval, ventricular arrhythimas
hypermagnesemia
tremors, vasodilation, bradycardia, weak, impaired respirations, heart block, arrest
lidocaine/rythmol
NA channel blocker, slow down depolarization, suppress conduction of electrical impulse, CLASS 1
Se of lidocaine/rythmol
dissiness, confusion, altered mental status, seizure, arrythmias, hypotension
Na channel blockers treat what
PVC, V tach, V fib
* NOT used for MI
Atenolol, metoprolol
Beta adrenegic receptor blockers, CLASS 2, reduce SA node automaticity and conduction through AV node, decrease renin secretion by kidney, prevents remodeling
SE of BB
decrease HR, BP, fatigue, weakness, depression, bronchospasm, AV node block, 2nd degree heart block
BB tx what
SVTs (PSVT, PAT, AT), a flutter, a fib, ischemia, ACS (MI & unstable angina), PVCs
amiodarone
CALSS 3, lengthen refractory period, prolong or delay repolarization (relaxation), inhibit Na channels
SE of amiodarone
decrease Hr, BP, arrhthimas, heart failure, pulmonary fibrosis, weakness, prolongs QT interval, angioedema
what does amiodarone tx
atrial and ventricular arrhytmias
*need glass bottle or polyolefin bag and special tubing
cardizem, verapamil
CLASS 4, CCB, inhibit Ca channels within SA & AV nodes, decreases automaticity of SA node, decrease HR, BP, and contractility
Se of cardizem and verapamil
decrease BP, HR, arrhythimas, fatigue, HA, edema, nausea
what does cardizem and verapmil tx
SVT (PSVT, AT, PAT), a fib, a flutter
verapimil also txs PVC
adenosine
CLASS 5, decreases SA node automaticity and ACV node conduction, slows conduction through AV node and interrupts AV node pathways
SE of adenosine
flushing, dyspnea, HA, heart block, transient asystole (common), use caution in asthma pts
adenosine is used to Tx
primarily for Dx of underlying rhythm, SVTs, and Wolff parkinson white syndrome
atropine
CLASS 5, increases sinus rate, accelerates AV conduction by blocking vagus nerve (effects acetylcholine)
SE of atropine
tachycardia, dry mouth, urinary hesitancy, drowsiness
wat is atropine used to Tx
symptomatic sinus bradycardia
digoxin
CLASS 5, antiarrhythmic, postive inotropic agent, increases CO, decreases HR, increases force of contraction, decreases conduction through SA & AV nodes
SE of digoxin
anorexia, N/V, visual halos, decrease HR, prolongs PRI, AV block (dont give if pt has any type of AV block)
digoxin is used for Tx of
SVTs, atrial arrhythmias
epinephrine
alpha and beta adrenergic receptor stimulation, increases HR (facilitates automaticity), increase blood flow to myocardium, vasoconstriction, increase myocardial O2 consumptionand lactate production
Se of epinephrine
arrhythmias, increase of BP and HR, palpatations, tremor, restlessness
what is epinephrine used to Tx
V fib, pulseless v tach, asystole, PEA, symptomatic bradycardia after atropine, pacing
*used to initiate a heart beat
dopamine
stimulates dopaminergic , beta and alpha receptors, positive inotropic effect, increae BRP, increase CO, increases cardiac contractility
SE of dopamine
arrhythmias, HTN
what is dopamine used as a Tx for
hypotension, unless caused by hypovolemia
magnesium sulfate
necessary for cellular reactions
SE of magnesium sulfate
ventricular arrhythimas, tremors, bradycardia, impaired respirations, arrest, heart block
Magnesium sulfate is used to Tx
ventricular arrhythmias (torsades) and PVCs
Vasopressin
alternative to epinephrine for refractory VF, only used one time, potent vasoconstrictor
what medications need to be given via ET tube
NAVEL Narcan Atropine Vasopressin Epinephrine Lidocaine
What is the Tx for sinus bradycardia
O2, atropine, epinephrine, dopamine, pacing (rare)
What is the Tx for SVT (AT, PAT, PSVT)
vagal stimulation, adenosine, CCB, BB, digoxin (for EF less than 40% after cardioversion), Cardioversion when hemodynamically unstable (cool clammy, increase HR), amiodarone,
What is the Tx for a flutter and a fib
rate control (CCb, BB, digoxin, sotalol {long term rate control})
rhythm control (amiodarone, propafenone)
less than 48 hours: cardioversion after TEE, convert rhythm after control rate
more than 48 hours: heparin drip, amiodarone, diltiazem or CCB, BB, digoxin
if hemodynamically unstable : cardioversion immediatelyregardless of duration of rhythm
what is the Tx for second degree AV block
transcutaneous pacemaker
epi
dopamine if hypotension
permanent pacemaker
what is the Tx for 3rd degree AV block
transcutaneous pacemaker, epi, atropine, dopamine, permanent pacemaker
what is the Tx for PVCs
treat the cause, BB, amiodarone, lidocaine, rythmol
what is the Tx for Stable V tachwith a pulse
amiodarone, lidocaine, cardioversion if TRx doesnt convert
unstable v tach with a pulse
sedate, cardiovert, IV meds as for PVCs, O2
what is the Tx for v fib or v tach without a pulse
check pulse, call for help, CPR, defibrillate, CPR (5 cycles/2 minutes), IV, intubate, epi orvasopression…etc
what is the Tx for ventricular irritability
Mg or K supplement
what is the Tx for asystole and PEA
epi, vasopression, treat underlying cause
what are the 2 most common and easily reversible causes of PEA
hypovolemia and hypoxia
what PVCs are dangerous
more than 6 a minute, run of 3, bifocal, multifocal, cuplet
Cardiac conduction
SA node internodal pathways AV node Bundle of HIS Bundle branches purkinje fibers
a standardized performance measure that provides a way to rate the performance of Beebe in comparision to other hospitals
quality measure
adult CPR
30:2
sinus rhythm
reqular PQRST, rate 60-100
sinus bradycardia
regular PQRST, rate less than 60
sinus tachycardia
regular PQRST, rate more than 100
sinus arrhythmia
irregular PQRST (3 or more squares difference 0.12), rate less than 100
P wave may be in previous T wave, PR shortened, PQRST came too soon, no compensatory pause
PAC
3 or more PACs in a row with rate of greater than 140, PQRST all look the same
AT
sudden start and end of AT, sudden doubling or tripling of HR
PAT
saw tooth pattern variable conduction to ventricle, QRS look same
a flutter
R-R-R intervals are off, wavy baseline, no P wave, irregular irregularity, QRS look the same
a fib
may refer to AT, PAT, PSVT, junctional tachycardia, rate over 100
SVT
inverted P before or after QRS, or no P with a QRS, beat came too soon, QRS looks normal, regular rhythm, no compensatory pause
PJC
QRS greater than 0.12, R opposite T wave, wide bizarre, beat came too soon, complete compensatory pause
PVC
3 or more PVCs in a row, uniform pattern wide and bizarre
V tach
irregular waves, chaotic, no pattern no PQRST
v fib
Stable PR greater than 0.2 seconds
first degree AV block
gradual prolongation of PR interval until QRS is dropped
second degree AV block type 1 (Wenckebach)
stable PR when present, Ps without QRS
PR is constant
second degree AV block type 2
no stable PR interval, atria and ventricles beat independently, HR 20-40
third degree AV block
blood flow through heart
superior/inferior vena cava right atrium tricuspid valve right ventricle pulmonary vavle pulmonary artery lungs aveoli (gas exchange) pulmonary vein left atrium mitral valve left ventricle aortic valve aorta body
