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62 Cards in this Set
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- Back
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**some arrhythmias are
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normal**
not always a result of disease |
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examples of normal arrhythmias:
(4) |
1. exercise => sinus tachycardia
2. vagal stim. => sinus brady 3. long-term aerobic exercise => lower resting HR 4. breathing in and out (slight) |
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the lower resting HR of athletes is mostly due to:
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increased vagal tone
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inspiration stimulates the cp, expiration **inc. thoracic pressure**:
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inc. HR, dec. HR respectively
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"sinus" ~
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driven by the SA node
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First-degree heart block = defects in Na+ or Ca2+ conductance due to
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tissue damage
=> decreased conduction velocity |
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decreased conduction velocity =>
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**prolonged P-R interval**
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what's the sign of first-degree HB on the EKG?
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prolonged P-R interval
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first-degree HB is usually caused by:
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ischemia
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2nd-degree HB is also called
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Mobitz HB
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Mobitz Type 1 EKG:
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progressively-increasing PR interval => missing QRST every 3rd or 4th beat => normal PQRST=> repeat
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Mobitz Type 2 EKG:
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every other beat, QRST is missing
called a 2 to 1 block |
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less common Mobitz Type 2's:
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3 to 1,
4 to 1 blocks |
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both Type 1 and Type 2 are:
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intermittent blocks
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another intermittent block =
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Rate-dependent block
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in a Rate-dependent block, one Bundle of His is compromised (via ischemia), such that it doesn't:
only a problem at: |
**repolarize** fast enough;
*very high* heart beats |
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effect of Rate-dependent block / EKG manifestation:
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***slower*** conductance => *enlarged/widened QRS*
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3rd-degree HB =
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a type of **AV nodal escape**
(atria being driven by SA node, ventricles driven by AV node) |
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in 3rd-degree, P-wave occurs the normal 0.8 seconds apart, while
QRS occurs every 1.2 second => 3rd degree ~ to: |
**no conductance** between SA and AV nodes
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EKG of 3rd-degree:
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occasional superposition of QRS and P - random
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one can live with 3rd-degree, but can't exert too much, due to reduced
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CO
(50 bpm versus normal 72) (EDV also decreases by 10% in 3rd degree) |
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to fix 3rd-degree:
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get a pacemaker that stimulates the AV node like normal
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Unidirectional block =>
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circular excitation:
continuous, *premature depolarization* |
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circular excitation =>
(1) |
**fibrillation**
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what causes Unidirectional blocks?
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ischemia
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EKG of unidirectional blocks:
(2) |
1. **no discernible P wave**,
2. occasional random QRST as atrial signal reaches ventricles |
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fibrillation typically occurs b/c there are several
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broken circuits in the heart
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broken circuits / circular excitation are typically caused by
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ischemia
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defibrillation =
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shock that **depolarizes** ALL of the heart at once, so that hopefully it repolarizes at once
will NEED medicine/pacemaker to follow |
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ischemia causes some NON-pacemakers to:
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fire spontaneously
(called ectopic focus of excitation) |
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what causes 1st degree HB?
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tissue damage, from ischemia
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WPW syndrome:
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an extra bundle (of Kent) exists near the AV node
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effect of WPW syndrome =
(term) |
signal can bypass AV and go through Kent instead
=> "pre-excitation" |
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pre-excitation manifests itself as a ______ and ____________ on the EKG
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delta wave;
*shortened* P-R interval |
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when is WPW syndrome actually detrimental?
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when you have ischemia
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WPW + ischemia =>
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bifurcation of pathway, between AV and Kent, =>
danger for recurring signal |
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digitalis toxicity =>
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abnormal Ca2+ channels' opening patterns ==> afterdepolarizations
=> palpitations => abnormal ventricle contraction patterns |
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uni-block below the AV node => ventricular fibrillation, =
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multiple, recurring circuits; =>
irregular heart beat **an emergency condition** |
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Rheumatic heart disease is caused by
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strep
|
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strep => pharyngitis and secretes a
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toxin
|
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before penicillin, people would harbor this toxin, non-symptomatically, for
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10-30 years
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when the toxin manifests itself, it affects
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the heart, specifically;
valves become misshapen or thicken or don't close properly or stick together |
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which valve is most commonly affected by Rheumatic heart disease?
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the mitral valve
then the aortic valve |
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the heart responds to valve pressure in two ways:
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1. concentric hypertrophy
2. eccentric hypertrophy |
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concentric hypertrophy is a result of too much ___________; =>
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pressure;
inc. in thickness of walls to reduce wall stress but walls become stiff, can't expand |
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concentric hypertrophy occurs in both:
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atria and ventricles
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with concentric hypertrophy, the wall is less ___________, may actually _____________
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compliant;
increase Pressure |
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eccentric hypertrophy is a result of an increase in Volume; result =
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increase in chamber size
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in eccentric hypertrophy, the chamber
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increases in size;
walls don't - they stay compliant will ultimately be unable to pump out blood |
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mitral stenosis =
usually in the form of: |
narrowing;
**sticking** |
|
increase in pressure due to stenosis =>
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pulmonary hypertentension
|
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pulmonary hypertension =
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>16 mmHG in **pulm. caps**
|
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pulm. hypertension =>
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edema in the lungs, dyspnea, congestation
|
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untreated mitral stenosis/pulm. hypertension => back pressure =>
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inability to pump blood into **veins** from the Right heart, due to great afterload
(e.g. in head, jug. vein pops out) |
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effect of being unable to pump blood into veins =
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liver edema, ascites (edema of abdomen), swelling of legs,
as blood backs up into the system form the Right heart |
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on ventricular side of stenosis:
(1) |
low EDV
|
|
low EDV =>
(3) |
low BP, low SV, low CO => listlessness
|
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EKG for mitral stenosis:
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higher-than-normal v-wave in LA
|
|
sound that ~ to mitral stenosis =
|
diastolic murmur
|
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to treat rheumatic heart disease:
(3) |
1. Beta-blockers to *slow HR* so that **ventricle can fill**
2. percutaneous balloon to try and break up sticking commissure 3. new valve |
|
sinus arrhythmia =
|
compromise of SA node
OR normal change in heart rhythm by way of SA node |
|
atrial fibrillation =>
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***ventricular tachycardia***
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