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cardiac output
amount of blood pumped out by either ventricle
5-6L/min
stroke volume SV
amount of blood pumped out by either ventricle in a single contraction
60-100ml
heart rate HR
number of cardiac contractions per minute
60-100 bpm
cardiac output formula
cardiac output = stroke volume x heart rate
preload
the pressure under which a ventricle fills.
influenced by:
volume of blood returned by veins to heart
afterload
the load or pressure against which the heart contracts to eject blood
rise in systemic vascular resistance increases after load
when after load is high, cardiac output falls or heart works harder to overcome increased pressure
contractility/inotropy
strength of the hearts contraction
influenced by mediations that have inotropic effect
regulated by nervous system
sinoatrial node
dominant pacemaker of heart located in right atrium
receives blood from right coronary artery
impulses travel btwn atria via internodial pathways
impulse is delayed by 0.12s here to allow atria to empty
AV junction: contains AV node and surrounding tissue along with bundle of his
impulses travel via AV node to bundle of his, into right and left bundle branches, into purkinje fibres which contract ventricles simultaneously
depolarization
when muscle fibers are stimulated to contract
sodium ions rush into cell making it positive » calcium enters to maintain depolarization and supply calcium ions for contraction
repolarization
sodium and calcium channels close » potassium channels open » potassium rushes out » sodium potassium pump restores proper balance
refractory period
absolute refractory period: cell is highly depolarized » new action potential cannot be initiated
from q wave to peak of t wave
relative refractory period: partially depolarized » new action potential inhibited but not impossible
second half of T wave
secondary pacemakers
SA node is damaged » any other component of conduction system takes over
the farther the conduction tissue is from the SA node, the slower its intrinsic rate of firing
SA node: 6-100 bpm » AV junction: 40-60 bpm » purkinje fibres: 20-40 bpm
electrolytes function in cardiac
sodium: flows into cell to initiate depolarization
potassium: flows out of cell to initiate repolarization
hypokalemia: increased myocardial irritability
hyperkalemia: decreased atomicity/conduction
calcium: maintains depolarization, contracts heart tissue
hypocalcemia: decreased contractility and increased myocardial irritability
hypercalcemia: increased myocardial contractility
magnesium: stabilizes cell membrane, opposes actions of calcium, acts in concert with potassium
hypomagnesemia: decreased conduction
hypermagnesemia: increased myocardial irritability
P wave
caused by depolarization of the atria » followed by pause as conduction is slowed by AV junction
are the P waves regular?
is there one P for every QRS?
is the P wave in front of the QRS or behind?
is the P wave normal and upright in lead I?
are there more P waves than QRS
do all the P waves look alike?
are the irregular P waves associated with ectopic beats
measure from first positive deflection from baseline to where wave returns to baseline
<0.10s, 0.5 - 2.5mm
QRS complex
caused by depolarization of the ventricles
a QRS less than 0.12s means the impulse was supra ventricular
amplitude 5 - 15 mm
are all the QRS complexes of equal duration?
what is the measurement?
within normal limits?
do they all look alike?
are the irregular QRS complexes associated with ectopic beats
wide QRS can be caused by:
supra ventricular impulse that reaches obstruction in bundle branches
supra ventricular impulse that cannot be conducted normally via ventricles because they are in refractory
irritable focus on the ventricles assumes pacemaking responsibility
T wave
caused by the repolarization of the atria and ventricles
atrial repolarization wave is not visible
ventricular wave follows the QRS complex
deep symmetrically inverted T waves may suggest cardiac ischemia
elevated more than half the height of QRS complex may indicate new onset of myocardial ischemia or hyperkalemia
leads
a lead provides an electrical image of a certain vantage point of the heart
electricity moving away from SA node towards lead causes a positive line (upwards)
PR interval (PRI)
distance from beginning of the P wave to the beginning of the QRS complex
time required for impulse to traverse atria and AV junction
usually 0.12-0.20s (3-5 squares)
includes all atrial and nodal activity
are all the PRIs constant?
is the measurement within normal range?
is there a pattern to the changing measurements?
ST segment
line from end of QRS complex to the start of the T wave
should be at same level as baseline
elevated or depressed could mean myocardial ischemia, injury or infarction
findings are significant if viewed in 2 or more leads looking at the same or adjacent area of heart
indicates refractory phase
RR interval
time between two successive QRS complexes
interval between two ventricular depolarizations
gives indication of HR
parasympathetic slowing heart
brain senses heart should slow » electrical impulse travels down vagus nerve to SA node » ACh is released » heart rate slows
sympathetic increasing heart
muscles send signal to brain » brain sends message via sympathetic nerves to SA node » norepinephrine is released » heart speeds up increasing cardiac output
blood pressure formula
BP = cardiac output x systemic vascular resistance
alpha beta receptors
alpha:
arteries: constriction
lungs: mild bronchoconstriction
beta 1:
heart: increased dromotropy, inotropy, chronotropy
beta 2:
lungs: smooth bronchial muscle dilation
arteries: dilation
blood pressure formula
blood pressure = cardiac output x systemic vascular resistance
alterations in one variable bring about compensatory changes in the other to restore BP
cardiac dysrhythmia
disturbance in normal cardiac rhythm
can be caused by ischemia, electrolyte imbalances or disturbances/damage in electrical conduction system
resulting in escape beats, circus reentry, or enhanced automaticity
develop after AMI for 2 reasons
irritability of ischemic heart muscle surrounding an infarct may cause damaged muscle to generate abnormal electrical impulses
infarct damages conduction tissues
very slow HR <50bpm lead to inadequate cardiac output and often precede electrical instability of the heart
produces escape beats to assist in maintaining cardiac output
very rapid HR >140bpm lead to decreased cardiac output and decreased stroke volume since ventricles have less time to fill
hypoxia, hypokalemia, metabolic alkalosis, hypocalcemia can lead to electrical instability causing cells that usually do not have automaticity to fire
causes potential for tachycardias, flutters and fibrillations in the atria or ventricles, heralding grave rhythms (VT and VF)
impulses get stuck in a pattern of repetition causing multiple ectopic beats or VF
ECG leads placement
white: right upper chest near shoulder (arm for 12 lead)
black: left upper chest near the shoulder (arm for 12 lead)
red: left lower abdomen (leg for 12 lead)
green: right lower abdomen (leg for 12 lead)
left leg (red) is positive terminal
lead 1 is formed between left and right arm electrodes
lead 2 is formed between right arm and left leg
lead 3 is formed between left arm and left leg
bipolar leads
contain leads 1,2,3
leads that contain a positive and negative pole
impulses moving toward positive terminal make positive deflection on ECG
impulses moving toward negative electrode causes negative deflection
perpendicular to lead causes isoelectric tracing or very little inflection in any direction
which segment for isoelectric line (0 mV)
TP segment since PR depression can occur with pericarditis and ST depression, and elevation can occur with cardiac ischemia, infarction and other causes.
two types of cells
electrical (conductive) cell: initiate electrical activity and conduct it through heart
mechanical (contracting) cell: respond to electrical stimulus and contract to pump blood
automaticity
the ability of cardiac cells to initiate electrical impulses on their own
primary electrolytes involved in creating hearts electrical stimulus
sodium (Na) and potassium (K)
both have positive charge
Na outweighs K making K relatively negative to Na
difference in potential allows electrolytes to move through cell membrane
movement of electrolytes through the cell membrane generates electrical impulse
electrical conduction through heart
sinoatrial node »inrernodal and intraatrial pathways » AV junction » bundle of His » left and right bundle branches » purjinje fibers
inherent rate ranges
SA node: 60-100 bpm
AV junction: 40-60 bpm
ventricle: 20-40 bpm
parasympathetic vs sympathetic effect on heart
sympathetic: effects both atrium and ventricles
increased rate
increased conduction via AV node
increased irritability
parasympathetic: effects only atrium
decreases rate
decreases irritability
slows conduction via AV node
height of deflection indicates
voltage or amplitude
how much distance between one vertical line
.04 sec
between thick lines: 0.20 sec
sodium role in cardiac function
flows into the cell to initiate depolarization
potassium role in cardiac function
flows out of the cell to initiate repolarozation
hypokalemia» increased myocardial irritability
hyperkalemia» decreased myocardial contractility
calcium role in cardiac function
major role in depolarization of pacemaker cells (maintains depolarization) and in myocardial contractility (contraction of heart muscle tissue)
hypocalcemia » decreased contractility and increased myocardial irritability
hypercalcemia » increased contractility
magnesium role in cardiac function
stabilizes cell membrane
acts in concert with K
acts in opposition with Ca
hypomagnesemia » decreased conduction
hypermagnesemia » increased myocardial irritability
PR segment
indicates the delay of the impulse as it travels through the SA node
Q wave
first negative deflection following the P wave but before the R wave
represents depolarization of the interventricular septum
R wave
the first positive deflection following the Q wave
indicates ventricular depolarization
should correspond to the patients pulse
S wave
second negative deflection following the P and R waves
R and S waves represent the sum of electrical forces from depolarization of L and R ventricles
T wave
positive deflection following S wave
represents ventricular repolarization
QRS segment
normal range: 0.06s - 0.11s or <0.12s
indicates ventricular depolarization
analyzing regularity and rate
looking at the R-R interval
is it regular?
is it irregular?
are there any patterns to the irregularity?
are there any ectopic beats? early or late?
determine the rate
what is the exact rate?
is the atrial rate the same as the ventricular rate?
normal sinus rhythm
pacemaker impulse originates from the sinus node and travels through normal conduction pathways within normal time frames
uniform, upright, P waves; one in front of every QRS
60-100bpm
PR interval 0.12-0.20s and consistant
QRS less than 0.12s
sinus bradycardia
rate lower than 60bpm with impulse originating from the sinus node
normal upright P wave in front of every QRS
normal PRI and QRS
regular
fits all rules for NSR except for HR>60bpm
sinus tachycardia
rhythm that fits all the rules for NSR except for HR<100
regular, uniform P wave in front of every QRS
normal and constant PRI and QRS
rate > 100bpm
indications for ECG
risk for dysrhythmias
suspected cardiac patients
suspected OD
electrical injuries
syncope
elderly patients feeling unwell
issues concerning sympathetic NS
everybody
horizontal plane leads
v1: forth intercostal space, right sternal border
v2: forth intercostal space, left sternal border
v3: midway between v2 and v4
v4: fifth intercostal, left midclavicular line
v5: fifth intercostal, left anterior axillary line
v6: fifth intercostal, left midaxillary line
3 lead what nodes for each lead
lead 1: RA is negative, LA is positive
lead 2: RA is negative, LL positive
lead 3: LA is negative, LL is positive
QT interval
period from beginning of ventricular depolarization (QRS) until the end of ventricular repolarization (end of T)