EKG Lecture Flashcards
What 4 ions determine the electro-chemical gradient in cardiac cells?
K+
Na+
Ca++
Cl-
Resting membrane potential
- 90 mV
Quick Review of Cardiac Action Potential
1) Simple two molecule systemwith semi-permeable membrane
2) Ion pump (Na-K ATPase) alters theconcentration of ions across membrane
3) An open K+ ion channel allows + charges to move out of the Compartment on the left, leaving behind relatively more negative charges
The resting membrane potential of cardiac muscle is primarily due to what ?
K+ equilibrium potential
Cardiac Muscle Action Potential
- Wave of depolarization
- Initially, only the K+ channels are open, so RMP = -90 mV
- Depolarization of one part of the membrane (movement of + charge
into the cell) spreads in a wave, causing voltage-gated Na+ ion channels in the adjacent membrane to spring open
What does the cardiac action potential depend on?
time-varying membrane conductance
What is QRS primarily caused by?
myocardial Na+ movement
T wave is the result of what?
myocardial K+ ion movement
What does ST segment mean as far as ion movement
no net movement
caused by Ca++
Refractory Period
- During the Plateau phase (Phase 2 of the
action potential) and during the first part of Phase 3, the
myocardium cannot be stimulated again - During the later part of phase 3 and hyperpolarization, the
myocardium can only be stimulated under abnormal conditions or with an extra impulse (ischemia, re-entrant currents, altered electrolytes
What is the state of the channels at rest
– K+ channels are open
– Na+ channels are closed
– eq potential = -90 mV
What is the state of the channels during depolarization
– K+ channels stay open
– Na+ channels open
– membrane potential= +30 mV
Is V4 positive or negative deflection
Depolarization is moving toward the electrode, producing a + deflection
Little block of ECG
1 vertical mm = 0.1 mV.
1 horizontal mm = 0.04 sec. (paper speed = 25 mm/sec)
Big Block of ECG
= 0.5 mV high
= 0.2 seconds long
Normal P-R Interval Time
0.12 - 0.2 s
normal QRS time
0.04- 0.1 s
normal Q-T time
0.32 - 0.40
Einthoven’s Triangle
- Leads I, II, and III are bipolar with a + and - pole
- Limb leads AVR (RA), AVL (LA), and AVF (LF)
Chest Leads
- V1: 4th IC space R
- V2: 4th IC space L
- V3 : 1/2 way between V2 and V4
- V4 : 5th IC space
midclavicular line - V5 : 1/2 way between
V4 and V6 - V6: 5th IC space ant. axillary line
EKG Set up
- first column: bipolar leads I, II, III
- second column: unipolar limb leads avL, avR, avF
- third column: unipolar chest leads
Conductions Path of Heart
- From SA node, depolarization spreads to R and L atrium via inter- and intra- atrial tracts (Bachman’s bundle).
- At AV node, conduction slows (P-R interval).
- From AV node, depolarization spreads via the Bundle of His to the R & L Bundle branches (L anterior and posterior fascicles).
- L & R bundles carry depolarization to Purkinje fibers.
- Purkinje fibers spread depolarization to myocytes
what does Duration of P-R interval depend on?
- Conduction velocity at AV node
What does QRS Complex Reflect?
- Conduction through myocardium
- Extensive branching
and expansion of the
wave of depolarization occurs via
Purkinje’s fibers
What does the T wave represent?
left ventricle repolarizing in an organized manner
In what areas can a 12 lead EKG detect problems?
– heart rate
– heart rhythm
– hypertrophy (must be calibrated)
– infarction/ischemia (must be calibrated)
what do single lead EKGs detect?
rhythm and rate abnormalities
What cant telemetry detect?
hypertrophy or ischemia because it cant be calibrated
Systematic Evaluation of the EKG
1) P-wave: upright, before every QRS, always same
2) P-R interval: is it 0.12-0.2 s
3) QRS: all same, is it 0.06-0.10 s
4) T-wave: upright, normal
5) R-R interval: is it regular
6) HR: is it 60-100 bpm
7) Observe patient: does pt’s response to exercise
correlate with EKG?
Sinus Bradycardia
HR < 60 bpm.
– Normal in athletes (inc. SV)
– may occur with beta-blockers, Ca2+-channel blockers,
antiarrhythmic drugs or with vagal stimulation (vomiting or
suctioning)
Consequences of Sinus Bradycardia
dizziness, syncope, angina, diaphoresis
Sinus Tachycardia
HR > 100 bpm.
– caused by: fear, pain, exercise, caffeine, amphetamines,
nicotine, atropine, hyperthyroidism, hypoxia, CHF, fever
Consequences of Sinus Tachycardia
usually benign
What is Sinus Arrhythmia?
- irregularity caused by SA node
- often due to altered vagal stimulation
- can be respiratory or non respiratory
Respiratory Sinus Arrhythmia
increased heart rate with inspiration, decreased heart rate with expiration
Causes of Non-Respiratory Sinus Arrhythmia
- fever
- infection
- drug side effect or toxicity (digitalis and morphine)
What do the chest leads indicated?
the axis of the heart (anatomic orientation of heart)
What does left axis deviation suggest?
LV hypertrophy
What does right axis shift suggest?
- RV hypertrophy or MI
What do you see on an EKG for RV hypertrophy
an increased R in V1
What do you see on an EKG for LV hypertrophy?
Increased S wave in V1, increased R wave in V5
How can ischemia be detected on an EKG
- ST segment elevation
- An inverted T wave or ST segment depression indicates acute ischemia
What is happening in the heart between T and next cycles P wave?
passive ventricular filling
What is occurring during the PR interval
atrial ejection
what is occurring during QRS wave
isovolumic ventricular contraction
what occurs during the ST segment
ventricular ejection
Review Wiggers Diagram
3 important determinants of CO
- Preload
- Afterload
- Contractility
Preload
- volume with which ventricle is loaded
what is preload determined by?
venous return and atrial kick
Starling Law of the Heart
Greater stretch = greater force
Afterload
resistance to blood flow
what is the primary determinant of after load?
diastolic BP
contractility
state of the cardiac muscle with regard to ability to generate force
what happens to contractility with heart failure?
goes down
what happens to contractility during acute and chronic exercise?
goes up
how is contractility often measured?
- with ejection fraction
- Normal EF =50-75% (AHA, 2020), HF ≤ 40%
What does the contractile state of the heart depend on?
intrinsic factors, the autonomic nervous system and hormonal states
– Intrinsic factors: training, disease, structure
– ANS: ACh (Vagus N.), Norepi. (Cardiac N’s)
– Hormonal factors: Epinephrine, Angiotensin and
other hormones
What determines the level of activation of cardiac muscle?
Ca2+ influx
what do drugs like calcium channel blockers, beta blockers, digitalis, etc affect
contractility by altering Ca delivery
Effect of beta Adrenergic Stimulation
increased force, increased HR, increased relaxation rate
Baroreceptor (cardiac reflexes)
– Carotid body sense increase in BP and alters vasodilatation, HR & contractility to normalize BP
Bainbridge Reflex
R atrium senses increases in blood volume and modulates
HR (responsible for respiratory ECG rhythm)
Chemoreceptor reflex
Brain stem senses CO2, H+ and O2 levels and alters HR, BP, contractility and respiration
where is the primary sit of resistance
arterioles
- varies, depending on arterial vasomotor state
Poiseuille’s Law
R= 8hl/pier4
For all practical purposes, R ~ 1 / r 4
what are the two types of resistance in the body?
-Series: RT = R1+R2+R3 …
-Parallel: 1/RT = 1/R1+1/R2 +1/R3
for the most part, what type of resistance is in the body?
parallel, so taking
away a R (such as in amputation of a limb) increases the total peripheral resistance (RT)
what is radius of a blood vessel determined by?
– Local metabolic needs
– Vasoactive substances (adenosine, K+, H+, etc..)
– CNS (Sympathetic nervous system)
– Hormones: epinephrine (a1 receptors in vessels), angiotensin, antidiuretic H
where does nutrient and waste exchange occur?
capillaries and venules
two mechanisms of nutrient and waste exchange
- Diffusion and Filtration
– diffusion is most important for nutrient/waste
– movement in to and out of tissues
– filtration is most important for fluid balance
Starling’s Hypothesis
depending of these forces, net filtration or absorption will occur
What occurs to contractility and heart rate and resistance during acute exercise
- HR and contractility increase
- Resistance decreases
what is the net effect of acute exercise on BP
SBP rises
Normal response: SBP increases to 130 or greater at max
what occurs to BP if larger mutuel groups are exercised?
DBP either remains constant or decreases
what occurs to BP if smaller mutuel groups are exercised?
DBP may increase slightly
What does resistive exercise do to BP?
increases both SBP and DBP
Abnormal responses of exercise on HR
– very rapid rise in HR:
* deconditioning or CV problem limiting SV
– little rise in HR:
* cardiac meds or heart disease
– decreased HR:
* severe disease and/or arrhythmia
