Mf1 Cardio Vocab

Front 1

Fetal Circulatory system overview

Back 1

- O2blood from placenta enters fetus thru umbilical vein
- bypasses liver via ductus venosus, combines with deO2blood in IVC
- joins deO2blood in SVC
- empties into RA
- shunted through to LA via foramen ovale
- some blood to RV to pulmonary trunk shunted to aorta via ductus arteriosus
- deO2 blood returns to placenta via umbilical arteries from internal iliacs near bladder

Front 2

Postnatal circulatory system changes

Back 2

1) 1st breath = increased alveolar PO2 = vasodilation pulm. vessels
2) obstetrical clamping = constriction = ligamentum venosum (umbilical vein to ligamentum teres; arteries to medial umbilical ligaments)
3)10-15 hours = ductus arteriosus constricts = ligamentum arteriosum
4) increased LA pressure = closure foramen ovale = fossa ovalis
5)ductus venosus = ligamentum venosum

Front 3

P

Back 3

Atrial depolarization

corresponds to atrial contraction, although continues past p wave

Front 4

QRS complex

Back 4

ventricular depolarization

represents ventricular contraction, although lasts longer than QRS

Q wave often missing on EKG

Front 5

ST segment

Back 5

Slow start of ventricular repolarization

followed by T wave - rapid ventricular repolarization

ventricular systole persists until end of T wave

Front 6

QT interval

Back 6

includes QRS complex, ST segment, T wave

represents ventricular systole

important clinical implications

QT interval normal when it is less than half of the R - R interval at normal rates

Front 7

cardiac cycle

Back 7

P wave - atrial depol
pause - ventricular filling
QRS complex - ventricular depol
ST segement - plateau phase, slow vent repol
T wave - rapid phase vent repol
baseline until next P wave

Front 8

EKG deflection

Back 8

wave direction

positive = upward
negative = downward

Front 9

EKG amplitude

Back 9

magnitude in mm of upward or downward deflection

measure of voltage

10mm = 1 mV

reflects how parallel the electrical force is to the axis of the lead being examined

Front 10

EKG time measure

Back 10

horizontal axis

bw heavy black lines = 0.2 sec
bw light black lines = 0.04 sec

Front 11

AVF

Back 11

Augmented Voltage left Foot

L foot has 2 positive leads, arms as a common negative ground

Front 12

augmented limb leads

Back 12

aka unipolar limb leads

AVR - Right arm positive
AVL - Left arm positive
AVF - Left Foot positive

intersect at different angles than the bipolar limb leads (split the angles)

Front 13

lateral leads

Back 13

I and AVL

have positive electrode positioned laterally on left arm

Front 14

inferior leads

Back 14

II
III
AVF

positive electrode positioned inferiorly on L foot

Front 15

chest leads

Back 15

aka precordial leads
6
numbered and placed successively from R to L side of chest, following normal anatomical position of heart within chest

orientated through the AV node, projects thru back which is negative

horizontal plane

Front 16

Limb leads

Back 16

I, II, III
AVR, AVL, AVF

frontal plane

Front 17

cardiac excitatory effects

Back 17

increases:
rate SA Node pacing
rate conduction
force of contraction
irritability of foci

via beta-1 adrenergic receptors stim by NE (Epinepherine even more potent stimulator) - sympathetic nerves distributed to ALL parts of heart, esp V muscle

Front 18

Cardiac inhibitory effects of parasymp

Back 18

decreased:
rate of SA node pacing***
rate of conduction
force of contraction
irritability of atrial and junctional foci**

vagus nerve, ACh activates cholinergic receptors (mostly within SA and AV nodes, some atrial muscle, v little to V muscle)

Front 19

autonomic receptors on systemic arteries

Back 19

Sympathetic : alpha1 adrenergic = vasoconstriction (more responsive to NE than Epi)

Parasymp: cholinergic = vasodilation

Front 20

merciful syncope

Back 20

severe pain or bleeding

parasympathetic reflex

slows SA node pacing = bradycardia

dilates systemic arteries = hypotension

reduces brain's blood supply to point of syncope

type of vaso-vagal syncope

Front 21

autonomic response to standing

Back 21

compensatory sympathetic response to standing since blood wants to move to pool in legs, but vasoconstriction of peripheral arteries plus stimulation of sinus pacing prevents this

in response to pressure changes sensed by cardiovascular baroreceptors

orthostatic hypotension is failure of these compensatory mechanisms

syncope results if impaired response

Front 22

neuro-cardiogenic syncope

Back 22

normal sympathetic response to standing fails over prolonged standing in certain elderly patients - vasoconstriction fails, but still tachcardic

tachycardia with poor cardiac volume stimulates left ventricular stretch receptors (parasymp mechanoreceptors) initiating parasymp reflex=

slow SA node
reduce blood pressure
reduced blood flow to brain
syncope

test with Head Up Tilt (HUT)

Front 23

Proper Interpretation of EKG requires consideration of

Back 23

Rate
Rhythm
Axis
Hypertrophy
Infarction

Front 24

Layers of heart

Back 24

interior
Endocardium - single layer endothelial cells

subendocarial tissue - fibroblasts, veins, nerves, branches conducting system

myocardium - thickest layer, cardiac muscle cell bundles

layer connective and adipose tissue

epicardium - outermost, aka visceral pericardium

Front 25

R vs L ventricle

Back 25

R > L trabeculae carneae
L thinner trabeculae carneae

L>R thickness (~3 times)

L 2 papillary muscles (thicker chordae tendineae, less numerous); R 3

Front 26

S1 heart sound

Back 26

pressure in ventricles rapidly builds at beginning of systole and tricuspid and mitral valves close quickly = noise

two nearly superimposed components because mitral valve closes first due to earlier electrical activation of L ventricle (0.01 sec difference - audibly split because of delayed RV contraction and late closure of tricuspid valve - right bundle branch block)

Front 27

S2 heart sounds

Back 27

aortic and pulmonary valve closing

A2 normally precedes P2 because diastolic pressure gradient between aorta and L ventricle is greater and shuts more readily

physiological splitting during inspiration (expiration hear as one sound)

Front 28

atrial pressure curve

Back 28

a wave = final bolus of blood propelled into venrticles from atria

c wave = small rise in atrial pressure as AV valves close and bulge into respective atria

v wave = passive filling of atria during systole from systemic and pulmonary veins b/c AV valves closed

Front 29

jugular venous pulse

Back 29

representative of right atrial pressure (bc no structure impeding blood flow bw SVC, internal jugular veins and RA)

matches atrial pressure curve (a, c, v) with two descents = x and y

measured as max vertical height of internal jugular vein in cm above centre of R atrium
normal <9cm (add 5cm to measure above sternal angle)

right easier to visualize bc extends directly above RA and SVC

Front 30

factors determining intensity of S1

Back 30

1) distance separating leaflets of open valves at onset of ventricular contraction

2) mobility of leaflets (normal or rigid bc of stenosis)

3) rate of rise of ventricular pressure

Front 31

causes of accentuated S1 sound

Back 31

1) shortened PR interval
2) mild mitral stenosis
3) high cardiac output states or tachycardia (eg exercise, anemia)

Front 32

causes of diminished S1 sound

Back 32

1) lengthened PR interval: first degree AV nodal block
2) mitral regurgitation
3) severe mitral stenosis
4) "Stiff" left ventricle (eg systemic hypertension)

Front 33

physiologic splitting

Back 33

A2 and P2 become audibly separated during inspiration

chest expansion = negative interthoracic pressure transiently increases capacitance (reducing impedance) of interthoracic pulm vessels = temporary delay in back pressure of pulm artery closing pulmonic valve - P2 delayed

increase of pulm vessel capacity during inspiration= decrease venous return to LA and LV temporarily = diminished stroke volume = shortened time for LV emptying = earlier A2 closure

high frequency sounds

Front 34

Position of EKG chest electrodes

Back 34

V1: 4th ICS, 2cm R sternum
V2: 4th ICS, 2cm L sternum
V3: midway between V2 and V4
V4: 5th ICS, L midclavicular line
V5: 5th ICS L anterior axillary line
V6: 5th ICS L midaxillary line

Front 35

bipolar limb leads

Back 35

one limb electrode is positive, another single electrode provides negative reference

lead I - Left arm (+) to right arm
lead II - Left Leg (+) to right arm
lead III - Left Leg (+) to Left arm

Front 36

R wave progression

Back 36

R wave becomes progressively taller from lead V1 to lead V6; s wave also becomes less deep

Front 37

transition lead

Back 37

V3 or V4
When height of R wave becomes greater than depth of S wave

Front 38

sequence of EKG analysis

Back 38

1) check voltage calibration
2) heart rhythm
3) heart rate
4) intervals (PR, QRS, QT)
5) Mean QRS axis
6) abnormalities of P wave
7) abnormalities of QRS (hypertrophy, bundle branch block, infarction)
8) abnormalities of the ST segment and T wave

Front 39

sinus rhythm

Back 39

normal cardiac rhythm as initiated by depolarization of sinus node

present if:
1) every P wave is followed by QRS
2) every QRS is preceded by a P wave
3) the P wave is upright in leads I, II, III
4) the PR interval is greater than 0.12 sec (3 small boxes)

between 60 - 100 bpm

Front 40

count off method for determining heart rate

Back 40

300- 150 -100 - 75 - 60 - 50

Front 41

arrhythmia

Back 41

any disturbance in the rate, regularity, site of origin, or conduction of the cardiac electrical impulse

can be a single aberrant beat (or even a prolonged pause between beats) or a sustained rhythm disturbance that can persist for the lifetime of the patient

Front 42

clinical manifestations of arrhythmia

Back 42

palpatations
symptoms of decreased CO (syncope, lightheadedness)
angina
congestive heart failure
sudden death

prolonged QT segments

Front 43

palpatations

Back 43

awareness of own heart beat

intermittent accelerations or decelerations of their heartbeat, or a sustained rapid heartbeat that may be regular or irregular

Front 44

causes of arrhythmias

Back 44

HIS DEBS
Hypoxia
Ischemia and Irritability
Sympathetic Stimulation
Drugs
Electrolyte Disturbance (Hypokalemia, Ca2+, Mg)
Bradycardia
Stretch (enlargement and hypertrophy)

Front 45

rhythm strip

Back 45

long tracing of single lead of EKG when suspect arrhythmia to identify irregularities

Front 46

Holter monitor

Back 46

essentially portable EKG machine with a memory, worn 24-48 hours to get complete record of heart rhythm

compare with patient diary of symptoms while wearing

aka ambulatory monitor

compare with event monitor that only records when pt is feeling symptoms

Front 47

5 basic types of arrhythmias

Back 47

1) arrhythmias of sinus origin: follows usual conduction, but too fast, slow or irreg

2) ectopic rhythms: electrical activity originates at foci other than SA node

3) reentrant arrhythmias: electrical activity trapped in area of heart

4) conduction blocks: originates in SA node, follows normal path BUT blocks and delays

5) preexcitation syndromes: follows accessory conduction pathways that bypass normal ones = short circuit

Front 48

escape beats

Back 48

rescuing beats during sinus arrest , originating from pacemaking of other myocardial cells

beats originating outside of sinus node

Front 49

intrinsic rhythms of potential pacemaker cells

Back 49

SA node: 60 - 100 bpm
atrial pacemakers: 60-75
junctional pacemaker: 40-60
ventricular pacemakers: 30-45

Front 50

junctional escape

Back 50

most common escape beat during sinus arrest

usual atrial depolarization doesn't occur (abnormal P wave, or absent: usually retrograde bc moving backward thru atrium)

Front 51

pacemaker cell

Back 51

small cells (5-10micrometers long)
- able to depolarize spontaneously over and over again
- rate determined by innate electrical characteristics of cell and by neurohormonal input
- AP slightly different - no resting potential

Front 52

Bachman's bundle

Back 52

fibers at top of inter-atrial septum

allows for rapid activation of L atrium from R

Front 53

excitation-contraction coupling

Back 53

wave of depolarization reaches myocardial cell
= Ca2+ released
= contraction

Front 54

myocardial cell

Back 54

50-100 micrometers (10X pacemaker cells)

can transmit electrical current, but far less efficiently

excitation-contraction coupling occurs

Front 55

segment vs interval

Back 55

straight line connecting 2 waves
vs
encompasses one wave plus connecting straight line

Front 56

Major categories of bradyarrhythmias

Back 56

Sinus bradycardia, including sinoatrial block

Atrioventricular (AV) junctional (nodal) escape rhythm

AV heart block (second or third degree) or AV dissociation

Atrial fibrillation or flutter with a slow ventricular response

Idioventricular escape rhythm

Front 57

indications SA node is pacemaker

Back 57

P wave is:
negative in lead aVR and
positive in lead II

Front 58

things to consider in bradycardia

Back 58

drugs: beta-blockers, calcium channel blockers, lithium carbonate, digitalis

hyperkalemia

obstructive sleep apnea if at night

Front 59

sick sinus syndrome

Back 59

patients with sinoatrial node dysfunction who have a marked sinus bradycardia, sometimes with sinus arrest or slow junctional rhythms that causes light-headedness or syncope

elderly get SA node degeneration
periods of tachycardia alternating with the bradycardia
(brady-tachy syndrome)

Treatment: permanent pacemaker to prevent sinus arrest and radiofrequency ablation therapy or antiarrhythmic drugs to control the tachycardias after the pacemaker has been inserted

Front 60

pacemaker

Back 60

battery-powered device, stimulates heart electrically

usually used in bradyarrhythmias

temporary or permanent (implanted)

wire usually threaded thru vein into RV so can stim endocardium of RV
- dual-chamber has wire into RA and RV

Front 61

specialized uses of pacemakers:

Back 61

treating tachycardia

improving ventricular fn in patients with congestive heart failure (cardiac resychronization therapy, biventricular pacing)

Front 62

modes of pacemaker function

Back 62

fixed rate: fires at specific preset rate, regardless of pt HR

demand: functions only when pt HR falls below a certain preset value
- sensing mechanism (pacemaker inhibited when pt HR adequate)
- pacing mechanism

Front 63

dual chamber pacing

Back 63

helpful in maintaining physiologic timing between atrial and ventricular systole (AV delay)

significant improvement in cardiac performance when CO is reduced with typical pacemakers

Front 64

pacemaker programmable parameters

Back 64

rate
voltage of discharge
sensitivity to intrinsic beats
refractory period
duration of pacemaker spike

Front 65

temporary pacemakers

Back 65

transvenous: battery connected to pacing electrode threaded thru vein into R ventricle

transcutaneous: specially designed electrodes pasted on chest wall (may cause discomfort, can't use on all pts)

use in cardiac emergencies (eg, MI); after open heart surgery; during cardiac arrest when not responding to tx; digitalis or other drug toxicity

Front 66

syncope

Back 66

transient loss of consciousness due to transient global cerebral hypoperfusion characterized by
- rapid onset,
- short duration,
- spontaneous recovery

reduction of blood flow to the reticular activating system located in the brainstem (LOC with 10 sec of no perfusion)

Front 67

importance of syncope clinically

Back 67

- common
- costly
- may cause injury
- often disabling
- may be only sign before sudden cardiac death

Front 68

distinguishing syncope from other transient loss of conciousness

Back 68

yes to:
- transient
- rapid in onset
- short duration
- followed by spontaneous recovery
(yes and did not result from head trauma)

Front 69

Vascular causes of syncope

Back 69

Anatomic = Vascular steal syndromes (subclavian steal syndrome)
Orthostatic =
- Autonomic insufficiency
- Idiopathic
- Volume depletion
- Drug and alcohol induced
Reflex mediated
- Carotid sinus hypersensitivity
- Neurally mediated syncope (common faint, vasodepressor, neurocardiogenic, vasovagal)
- Glossopharyngeal syncope
- Situational (acute hemorrhage, cough, defecation, laugh, micturition, sneeze, swallow, postprandial)

Front 70

Cardiac causes of syncope

Back 70

Anatomic=
- Obstructive cardiac valve disease
- Aortic dissection
- Atrial myxoma
- Pericardial disease, tamponade
- Hypertrophic obstructive cardiomyopathy
- Myocardial ischemia, infarction
- Pulmonary embolism
- Pulmonary hypertension
Arrhythmias=
- Bradyarrhythmias: (Atrioventricular block; Sinus node dysfunction, bradycardia)
- Tachyarrhythmias: Supraventricular tachycardia;
(Atrial fibrillation= Paroxysmal supraventricular tachycardia (AVNRT, WPW))
(Ventricular tachycardia: Structural heart disease; Inherited syndromes (ARVD, HCM, Brugada syndrome, long-QT syndrome); Drug-induced proarrhythmia);
Implanted pacemaker or ICD malfunction)

Front 71

Causes of Real or Apparent Transient Loss of Consciousness

Back 71

1)Syncope
2)Neurologic or cerebrovascular disease
- Epilepsy
- Vertebrobasilar transient ischemic attack
3) Metabolic syndromes and coma
- Hyperventilation with hypocapnia
- Hypoglycemia
- Hypoxemia
- Intoxication with drugs or alcohol
- Coma
4) Psychogenic syncope
- Anxiety, panic disorder
- Somatization disorders

Front 72

symptoms of orthostatic intolerence

Back 72

- syncope
- lightheadedness
- presyncope
- tremulousness
- weakness
- fatigue
- palipitations
- diaphoresis
- blurred/tunnel vision

Front 73

Echocardiographic findings considered diagnostic of the cause of syncope

Back 73

- severe aortic stenosis,
- pericardial tamponade,
- aortic dissection,
- congenital abnormalities of the coronary arteries,
- obstructive atrial myxomas or thrombi

Front 74

refractory period cardiac muscle

Back 74

ventricle:
refractory: 0.25 - 0.30 s (same as plateau)
relative refractory: 0.05

artial:
refractory: 0.15

Front 75

duration of atrial and ventricular contraction

Back 75

function of duration of action potential - begins to contract few ms after start AP, and continues few ms after AP

ventricular muscle - 0.3 s
atrial muscle - 0.2 s

Front 76

changes in cardiac cycle when HR increases

Back 76

duration of each portion decreases, but relaxation phase (diastole) decreases the most

means don't get complete filling of cardiac chambers before next contraction when v. rapid HR

Front 77

isovolumic/ isometric contraction

Back 77

tension is increasing in muscle but little or no shortening of muscle fiber is occuring

cardiac: 0.02 - 0.03 sec when pressure building in ventricles to push open semilunar valves
(LV above 80mmHg, RV above 8mmHg)

also get isovolumic/ isometric relaxation b4 atrial contraction

Front 78

ventricular blood volumes

Back 78

end-diastolyic= 110-120mL
end-systolic = 40-50mL
therefore stroke volume output ~ 70mL

can increase stroke volume by increasing end-diastolic and decreasing end-systolic

Front 79

ejection fraction

Back 79

fraction end-diastolic volume that is ejected
(longer filling, stronger contraction)

usually equal to 60%

Front 80

function of papillary muscles

Back 80

NOT to help valves close

pull vanes of valves inward during ventricular contraction to prevent their bulging too far backward into atria

if rupture chordae tendineae or paralyze papillary muscle, get leakage

Front 81

types of membrane ion channels of cardiac muscle

Back 81

1) fast sodium = rapid upstroke spike
2) slow sodium-calcium = plateau (0.3s)
3) potassium = repolarization to RMP

* in SA node, RMP less negative (-55 vs -90mV) so 1) is permenantly closed, therefore slower de- and repol

Front 82

Cause of self-excitation of SA node fibers

Back 82

leaky membrane to Na+

influx Na+ causes "RMP" changes - -55mV to -40mV

at -40mV, slow Na-Ca channels open = AP

100-150 ms after opening, Na-Ca close, K+ open = repol

K+ stay open a bit longer = hyperpolarization to -60 to -55mV

Front 83

anterior interatrial band

Back 83

small band atrial fibers
passes from RA to LA
conduction faster than mycardial (1m/sec vs 0.3m/s)

transmits conduction to LA for contraction

Front 84

internodal conducting pathways

Back 84

anterior, middle and posterior
converge on AV node
create delay of 0.03s of conduction from SA to AV node

*AV node adds 0.09s to delay,
AV bundle adds 0.04s, total 0.16s delay from SA to ventricular myocytes

due to diminished # gap junctions bw cells

Front 85

delays in conduction pathway

Back 85

SA-AV node = 0.03 (via internodal pathways)

AV node = 0.09s

AV bundle = 0.04s

total delay 0.16s

due to diminished # gap junctions bw successive cells in conduction system

Front 86

Purkinje cell transmission

Back 86

1.5 - 4.0 m/s = instantaneous transmission cardiac impulse thru remainder ventricular system

due to high level permeability of gab junctions at intercalated discs

Front 87

ectopic pacemaker

Back 87

an area of heart other than SA node due to abnormal excitation of this area. can be AV, purkinje, or A or V muscle (rare)

abnormal sequence of contraction of diff parts of heart = significant debility of heart pumping

could also be block

Front 88

Stokes-Adams syndrome

Back 88

total AV block comes and goes
* hearts w borderline ischemia of conductive system
delayed pickup of heart beat

after sudden AV block, Purkinje system doesnt emit intrinsic impulses for 5-20s b/c previously overdriven by rapid sinus impulses = overdrive suppression, eventual ventricular escape
- ventricles fail to pump
- faint in 4-7 sec
tx = pacemaker

Front 89

ventricular escape

Back 89

Strong vagi stimulation = stop SA node or block conduction from AV node

ventricles stop beating for 5-20 sec

Purkinje fibers pick up rhythm (15-40 bpm)

Front 90

mechanism of parasympathetic effects on heart

Back 90

causes increased permeability of fibers to K+
- rapid leakage out of conductive fibers
= more negative "RMP" (hyperpolarization)
= less excitable

Front 91

normal mean QRS vector

Back 91

+59-degree
(avg vector during spread of depolarization thru ventricles)

aka mean electrical axis of the ventricles

in normal heart can swing 20 to 100 degrees
(mainly anatomical diff Purkinje system or musculature)

Front 92

hexagonal reference system

Back 92

Lead I = 0*
Lead II = +60*
aVF = +90*
Lead III = +120*
aVR = +210*
aVL = -30*

Front 93

Q wave

Back 93

initial depolarization of left side of septum before right side
= weak vector from L to R for fraction of second before usual base to apex vector occurs

Front 94

conditions causing axis deviation

Back 94

change in position of heart in chest:
- end deep exp (L)
- supine position (L)
- obese (L)
- end deep insp (R)
- when stand up (R)
- tall lanky person w hanging heart (R)
Hypertrophy of one ventricle
- to side of hypertophy (due to increase quantity of muscle and time required for depol)
Bundle Branch Block
- LBBB (L)
- RBBB (R)

Front 95

common causes of cardiac arrhythmias

Back 95

1) Abnormal rhythmicity of pacemaker
2) Shift of pacemaker from SA node to other
3) Blocks at different points
4) Abnormal pathways of impulse transmission
5) Spontaneous generation of spurious impulses (ectopic pacemaker)

Front 96

heart rate changes with body temperature

Back 96

HR increases about 10 beats/min for each degree F increase

18 bpm / degree C

up to 105* F/40.5* C
beyond may decrease bc of debility of heart muscle to fever

due to increase rate of metab of SA node and therefore increase excitability

Front 97

sinus arrythmias

Back 97

result of many different circulatory conditions altering the strengths of symp and parasymp nerve signals to heart

Front 98

Sinoatrial block

Back 98

conduction not transmitted away from SA node to atria

loss of P wave
ventricles pick up new rhythm so QRS slow but normal

Front 99

conditions causing AV block

Back 99

1) ischemia of AV node or bundle (coronary insufficiency)

2) Compression of AV bundle (scar, calcification)

3) Inflammation of AV node or bundle (myocarditis)

4) Extreme stimulation of heart by vagus nerve (ie carotid sinus syndrome)

Front 100

carotid sinus syndrome

Back 100

people have extremely sensitive baroreceptors in carotid sinus region of carotid artery

mild external pressure elicits barorecpetor reflex, extreme bradycardia

Front 101

First degree block

Back 101

incomplete AV block
Prolonged P-R interval >0.20s (normal 0.16s)
delay of conduction from A to V
* wont be above 0.35-0.45s bc means so depressed conduction usually stops entirely

Front 102

Second degree block

Back 102

incomplete AV block

conduction thru AV bundle slowed enough to increase PR interval 0.25 to 0.45

start to see dropped QRS-T because not always getting strong enough AP to pass thru

can sometimes determine rhythm ie) 2:1 dropped

Front 103

third degree block

Back 103

complete AV block

ventricles will spontaneously establish own signal

P waves dissociate with QRS-T

different rates of rhythms of A and V

Front 104

electrical alternans

Back 104

incomplete block of intraventricular system (sometime in peripheral ventricular Purkinje system)

partial intraventricular block every other heartbeat

possible causes:
tachycardia (not enough refractory time)
ischemia
myocardiis
digitalis toxicity

Front 105

Conditions commonly associated with sinus tachycardia

Back 105

- Anxiety, excitement, exertion, and pain
- Drugs that increase sympathetic tone (e.g., epinephrine, dopamine, tricyclic antidepressants, isoproterenol, and cocaine)
- Drugs that block vagal tone (e.g., atropine and other anticholinergic agents)
- Fever, many infections, and septic shock
- Congestive heart failure (CHF)
- Pulmonary embolism
- Acute myocardial infarction (MI), which may produce virtually any arrhythmia
- Hyperthyroidism
- Pheochromocytoma
- Intravascular volume loss because of bleeding, vomiting, diarrhea, acute pancreatitis, dehydration, and related conditions
- Alcohol intoxication or withdrawal

Front 106

Common conditions causing bradycardia

Back 106

- Normal variant
- Drugs that increase vagal tone (e.g., digitalis or edrophonium) or that decrease sympathetic tone (e.g., beta blockers)
- Hypothyroidism
- Hyperkalemia
- Sick sinus syndrome
- Sleep apnea syndromes
- Carotid sinus hypersensitivity syndrome
- Vasovagal reactions

Front 107

Respiratory sinus arrhythmia

Back 107

normal finding
HR increases with inspiration,
decreases with expiration

can be quite marked, up to 10 - 20 bpm
particularly in children and young adults

due to changes in vagal tone

Front 108

conditions causing sinus arrest or SA block

Back 108

**acute
- Hypoxemia
- Myocardial ischemia or infarction
- Hyperkalemia
- Digitalis toxicity
- Toxic responses to drugs such as beta blockers and calcium channel blockers (e.g., diltiazem and verapamil)
- Vagal hyperreactivity (e.g., severe vasovagal episode)

Front 109

possible causes of ectopic foci

Back 109

1) local areas of ischemia
2) small calcified plaques, pressing against cardiac muscle and irritating fibers (also irritation during cardiac catheterization)
3) toxic irritation of AV node, Purkinje, myocardium by
-drugs
-caffeine
-nicotine

Front 110

premature atrial contractions

Back 110

P wave beat occuring too soon
PR interval shortened
compensatory pause - bw premature contraction and subsequent contraction

freq in otherwise healthy ppl

Front 111

pulse deficit

Back 111

deficit in number radial pulses felt when compared with actual # heart contractions

heart contracting ahead of schedule leads to incomplete ventricular filling, low SV

Front 112

AV nodal or AV bundle premature contractions

Back 112

wave travels thru ventricles and backwards to atria at same time

P wave superimposed onto QRS-T complex = slight distortion

Front 113

premature ventricular contractions

Back 113

QRS prolonged (impulse conducted thru muscles vs Purkinje)

QRS has high voltage (both sides do not depol at same time)

T wave polarity opposite to QRS - slow depol means also slow repol in same direction

dont take PVCs lightly - can be from toxicity, emotional, etc, but also can be serious, higher chance developing V fib.

Front 114

Long QT Syndromes and causes

Back 114

disorders that delay repolarization of the ventricles

increases susceptibility to developing 'torsades de pointes'

inherited:
- mutations Na or K channel genes
aquired: more common
- plasma electrolyte disturbances (hypoK, hypoCa. hypoMg)
-antiarrhythmic drugs (quinidine)
- Antibiotics (fluoroquinolones, erythromycin)

Front 115

LQTS tx

Back 115

acute:
Magnesium sulfate

lont-term:
antiarrhythmia meds (beta-adrenergic blocker)
implantation cardiac defib

Front 116

atrial bigeminy

Back 116

each sinus beat is followed by an APB

Front 117

Paroxysmal supraventricular tachycardia types

Back 117

1) atrial tachycardia

2) atrioventricular nodal reentrant tachycardia

3) AV reentrant tachycardia

Front 118

atrial tachycardia

Back 118

3+ consecutive APBs
most due to ectopic foci in atrium

+30 sec may cause light-headedness or syncope, induce angina or CHF

longer issues = antiarrhythmic drugs or radiofrequency catheter ablation

also can have multifocal atrial tachycardia

Front 119

Valslava maneuver

Back 119

patient instructed to strain against a closed glottis by bearing down, as for a bowel movement

can increase vagal tone, similar to carotid sinus massage

Front 120

frog sign

Back 120

prominant jugular venous a waves due to atrial contraction against closed tricuspid valve

Front 121

adenosine treatment for tachycardias

Back 121

6mg terminated 60-80%
12mg terminated 90-95%

causes transient AV node block

requires EKG monitoring and resucitation equipment

ineffective and potentially deliterious in pts with ventricular tachycardia

Front 122

bpm for tachyarrhythmia categories

Back 122

PSVT = 140-250 bpm
Atrial flutter = 250-350 (ventricular 150, 100, 75)
Atrial fibrillation = 350-600 bpm (ventricular 110-180)

Front 123

conditions for atrial flutter

Back 123

rarely see in normal heart
not specific for any particular type of heart disease
- valvular (especially mitral) disease,
- chronic ischemic heart disease,
- cardiomyopathy,
- hypertensive heart disease,
-acute myocardial infarction (MI),
-chronic obstructive lung disease
-pulmonary emboli

Front 124

atrial flutter tx

Back 124

-drugs (beta blockers, Ca channel blockers, digitalis), some antiarrhythmics
- synchronized DC shock
- rapid atrial pacing
- RF ablation therapy

Front 125

symptoms atrial flutter

Back 125

symptoms due to loss of normal atrial contraction and fast/irreg heart beat

-palpitations
- light headedness
- syncope
- angina from rapid HR (esp in coronary disease or symptoms of CHF: SOB, fatigue)

Front 126

EKG characteristics of atrial fibrillation

Back 126

1) An irregular wavy baseline produced by the rapid f waves

2) A ventricular (QRS) rate that is usually quite irregular

When the ventricular rate is very fast, the f waves may be difficult to distinguish. In such cases, the diagnosis of AF can usually be suspected by finding a very irregular ventricular rate in the absence of distinct P waves

Front 127

classification of atrial fibrillation patterns

Back 127

Paroxysmal - stops spontaneously within 7 days, usually within 48hrs

Persistant - Last more than 7 days and usually requires cardioversion

Permenant - lasts indefinitely, fails to terminate or reoccurs even with cardioversion

Front 128

symptoms of atrial fibrillation

Back 128

**May be Asymptomatic!

- palpitations
- chest discomfort
- dyspnea
- weakness
- lightheadedness

Front 129

AV dissociation

Back 129

associated w >75% ventricular tachycardia

A and V beat independently

AV node constantly refractory due to bombardment from above and below

occasionally atria contract against closed AV valves (simultaneous V contraction) = sudden back flow into jugular veins = CANNON A WAVES

Front 130

cannon A waves

Back 130

sudden back flow of blood from atria into jugular vein = large A wave of jugular venous pressure

due to AV dissociation

Front 131

Progress of Endothelial dysfunction in atherosclerosis

Back 131

Foam cells
Fatty Streak
Intermediate Lesion
Atheroma
Fibrous plaque
Complicated lesions/rupture

Front 132

Angina symptoms

Back 132

Symptoms include chest pain or discomfort, shortness of breath, palpitations, faster heart rate, dizziness, nausea, extreme weakness and sweating.

last just a few minutes and are usually relieved by rest and/or medications

Front 133

Symptoms of MI

Back 133

Symptoms usually last more than a few minutes and include chest pain or discomfort that lasts for more than a few minutes or goes away and comes back; pain or discomfort in other areas of the upper body; difficulty breathing or shortness of breath; sweating or “cold” sweat; fullness, indigestion or choking feeling; nausea or vomiting; light-headedness; extreme weakness; anxiety; rapid or irregular heartbeats

Front 134

Stable angina

Back 134

type of angina brought on by an imbalance between the heart’s need for oxygen-rich blood and the amount available.

It is "stable," which means the same activities bring it on; it feels the same way each time; and is relieved by rest and/or oral medications.

Stable angina is a warning sign of heart disease

Front 135

Unstable angina

Back 135

considered an acute coronary syndrome.

It may be a new symptom or a change from stable angina. The angina may occur more frequently, occur more easily at rest, feel more severe, or last longer.
Although this angina can often be relieved with oral medications, it is unstable and may progress to a heart attack.

Usually more intense medical treatment or a procedure is required.
Unstable angina is an acute coronary syndrome and should be treated as an emergency.

Front 136

inotropy

Back 136

increased contractility of heart

increases SV for same LVedv

shift of Frank Starling Curve up and L

any change in SV for same LVedv means different contractile state

Front 137

heart as functional syncytium

Back 137

every myocardial fiber mechanically activated during each wave of depolarization

compare to skeletal muscle that can recruit more fibers as needed to increase its force of contraction

therefore heart needs to increase force and velocity of contraction in order to create psve inotropic state

Front 138

afterload of heart

Back 138

determinant of stroke volume

total load born by V myocardium throughout systole

LV systolic tension development X LV volume

practical purposes, ~ as mean aortic pressure mmHg

normal heart can withstand high afterload without sig decrease in SV

Front 139

preload of heart

Back 139

volume of blood at end diastole

Front 140

pressures of various heart chambers

Back 140

RA 0-8 (only diastolic)
RV 15-25/ 0-8
PA 15-25/5-10 (pulm valve closes b4 reaches lower diastolic)
Aorta = 100-140/60-80 (systemic BP)
LV = 100-140/5-12
LA = 5-12 (measured via wedge point)

Front 141

coronary reserve

Back 141

the ability to increase flow above resting values in response to pharmacologic vasodilation

reduced when diastolic time for subendocardial filling is reduced (tachycardia) or compressive determinants of preload are increased

diminished by anything that increases resting flow, including increases in the hemodynamic determinants of oxygen consumption (systolic pressure, heart rate, contractility) and reductions in arterial oxygen supply (anemia, hypoxia

Front 142

resting cardiac blood flow

Back 142

0.7 - 1.0 mL/min/g

can increase 4-5 fold during vasodilation

Front 143

autoregulation

Back 143

normal heart keeps coronary blood flow constant as regional coronary pressure varies over wide range

below autoreg pressure limit (40mmHg) subendocardial vessels are maximally vasodilated and develop myocardial ischemia; subepicardial flow maintained until pressure falls below 25mmHg)

Front 144

upper reference limit

Back 144

99th percentile of a normal reference control group

Front 145

Testing types and features of MI identified

Back 145

Pathology - myocyte cell death

Biochemistry - markers of myocyte cell death in blood sample

EKG - evidence of myocardial ischemia (ST and T wave abn); evidence of loss of electrically f'ning cardiac tissue (Q waves)

Imaging: reduction or loss tissue perfusion, cardiac wall movement abnormalities

Front 146

Criteria for acute, evolving or recent MI

Back 146

1) Typical rise/fall biochem markers of myocardial necrosis plus one of:
a) ischemic symptoms
b) development of pathological Q waves in EKG
c) EKG changes indicative of ischemia
d) imaging evidence of new loss viable myocardium or new regional wall motion abn

2) pathologic findings of acute MI

Front 147

Class 1 MI

Back 147

Spontaeous MI related to ischemia caused by 1* coronary event such as plaque erosion and/or rupture, fissuring, or dissection

Front 148

Class 2 MI

Back 148

MI 2* to ischemia caused by increased O2 demand, or decreased supply

eg coronary artery spasm
coronary embolism
anemia
arrhythmias
HTN
Hypotension

Front 149

Class 3 MI

Back 149

Sudden unexpected cardiac death, including cardiac arrest, often w symptoms of myocardial ischemia, accompanied by new ST-seg elevation, or new LBBB, or new obstruction, but death occuring b4 blood samples could be obtained, or b4 appearance of biomarkers

Front 150

Class 4 MI

Back 150

a) MI associated with PCI

b) MI associated with stent thrombosis, as documented by angiography or autopsy

Front 151

Class 5 MI

Back 151

MI associated with CABG

Front 152

STEMI Epi

Back 152

rate rises for both men and women with age

occurs more often in black people regardless of age

rising in developing countries

1 mill pts/ year in US

Front 153

Causes of MI

Back 153

Almost all from coronary atherosclerosis, generally w superimposed coronary thrombosis

CAD other than atherosclerosis:
- Arteritis
- Trauma to coronary arteries
- Coronary mural thickening
- Luminal narrowing by other mechs
Emboli to Coronary arteries
Congenital coronary artery abn
Myocardial O2 supply-demand disproportion
Hematologic (In Situ Thrombosis)
Miscellaneous (Cocaine...)

Front 154

factors influencing plaque disruption

Back 154

stresses induced by
- intraluminal pressure,
- coronary vasomotor tone,
- tachycardia (cyclic stretching and compression),
- disruption of nutrient vessels combine to produce plaque disruption esp at shoulder region

- systolic blood pressure,
- heart rate,
- blood viscosity,
- endogenous tissue plasminogen activator (t-PA) activity,
- plasminogen activator inhibitor type 1 (PAI-1) levels,
- plasma cortisol levels,
- plasma epinephrine levels exhibit circadian and seasonal variations and increase at times of stress (early morning, winter, after natural disasters)

Front 155

Q-wave infarction

Back 155

get Q wave evolution in areas overlying the infarct zone; most characteristic change in most pts initially presenting with STEMI

other abnormalities could be smaller R wave height, notching/splintering of QRS

Front 156

transmural infarcts

Back 156

myocardial necrosis involves the full thickness (or nearly full thickness) of the ventricular wall

occlusive coronary thrombosis appears to be far more common when the infarction is transmural and localized to the distribution of a single coronary artery

Front 157

subendocardial infarcts

Back 157

(nontransmural)

necrosis involves the subendocardium, the intramural myocardium, or both without extending all the way through the ventricular wall to the epicardium

frequently occur in the presence of severely narrowed but still patent coronary arteries

Front 158

factors affecting viability of myocardial cells distal to occusion

Back 158

- collateral artery blood flow
- level metabolism
- presence and location stenosis in other arteries
- rate of development of obstruction
- quantity of myocardium supplied

Front 159

Anteroseptal cardiac region on EKG

Back 159

V1
V2

Supplied by LAD

Front 160

Anteroapical cardiac region on EKG

Back 160

V3
V4

Supplied by LAD (distal)

Front 161

Anterolateral cardiac region on EKG

Back 161

I
AVL
V5
V6

Supplied by CFX

Front 162

Inferior cardiac region on EKG

Back 162

II
III
AVF

Supplied by RCA

Front 163

Anterior cardiac region on EKG

Back 163

V1-V6

Front 164

Posterior cardiac site on EKG for MI

Back 164

V1
V2
Tall R wave, not Q wave

Supplied by RCA

Front 165

Myocardial cell structure

Back 165

Cell
= numerous myofibrils
= chains of sarcomeres
= actin, myosin, titin
35% mitochondria
Membrane = sarcolemma, t-tubule system

Sarcoplasmic reticulum also surrounds sarcomeres (R angle w T tubules @ terminal cisternae sacs of Ca2+)

Front 166

Resting myocardial cell membrane internal and external ion concentrations

Back 166

Internal:
Na 15mM
K 150mM
Cl 5mM
Ca 10-7 M

External:
Na 145mM
K 5mM
Cl 120mM
Ca 2mM

Front 167

Functional properties ion channels

Back 167

Selectivity: specific ion, manifestation size and structure of pore

Gating: ion can pass thru only at specific times; voltage sensitive

Front 168

Cardiac fast sodium channels

Back 168

At -90mV, closed resting state, able for conversion

Open with depolarization, only briefly, then close to inactive state

Can't be converted back to open until cell repolarozes and get resting state again

*at chronically less negative RMP, channels stay inactivated w/o opening (important in pacemaker cells that stay at -70mV)

Front 169

Determinants of resting potential

Back 169

Concentration gradients of ions

Relative permeability of ion channels that are open at rest
- cardiac have K+ inward rectifier channels open at rest: balance achieved be concentration and electrical gradients: -91mV (slight leak due of Na+ into cell makes RMP slightly less neg)

Front 170

Na+K+-ATPase

Back 170

Pumps 3Na+ out for 2K+ in

(more psve out than in)

Front 171

Phase 4 of cardiac AP

Back 171

Resting at -90mV,
Stable

Front 172

Phase 0 of cardiac AP

Back 172

Prominent influx Na+
rapid upstroke

Front 173

Threshold potential cardiac cells

Back 173

Approximately -70mV
Enough fast Na+ channels open to generate self sustaining inward Na+ current

Front 174

Phase 1 of cardiac AP

Back 174

Brief repol to bring membrane current back to 0mV

Mostly outward flow K+ (transiently activated channels)

Front 175

Phase 2 of cardiac AP

Back 175

Relatively long phase

Balance of outward K+ (delayed rectifier channels) and inward Ca++ (L-type channels, start opening phase 0, at approximate -40mV)
No net current! PLATEAU

Ca++ channels begin to inactivate, K movement > Ca

Front 176

Phase 3 of cardiac AP

Back 176

Final phase repolarization
Returns to RMP

Due to continued K+ movement out

Front 177

Return of cellular concentrations after AP

Back 177

Ca++ removed by sarcolemmal Na-Ca exchanger and sarcolemmal Ca-ATPase pump

Na-K ATPase pump

Front 178

Phase 1 of cardiac AP

Back 178

Brief repol to bring membrane current back to 0mV

Mostly outward flow K+ (transiently activated channels)

Front 179

Phase 2 of cardiac AP

Back 179

Relatively long phase

Balance of outward K+ (delayed rectifier channels) and inward Ca++ (L-type channels, start opening phase 0, at approximate -40mV)
No net current! PLATEAU

Ca++ channels begin to inactivate, K movement > Ca

Front 180

Phase 3 of cardiac AP

Back 180

Final phase repolarization
Returns to RMP

Due to continued K+ movement out

Front 181

Return of cellular concentrations after AP

Back 181

Ca++ removed by sarcolemmal Na-Ca exchanger and sarcolemmal Ca-ATPase pump

Na-K ATPase pump

Front 182

Diff bw pacemaker and myocyte AP

Back 182

1) max negative voltage pacemaker -70mV, myocyte -90mV

2) phase 4 pacemaker not flat (spontaneous gradual depol= pacemaker current If; due to Na+ channels that open during repol)

3) phase 0 less rapid, less amplitude than myocyte (upstroke relies on relatively slow Ca++)

Front 183

Degree of refractoriness of cardiac AP

Back 183

Primarily reflects number fast Na+ channels that have reactivated

Absolute: completely inexcusable to new stimulus

Effective: includes absolute, but extends beyond to part of phase 3, can get localized AP but not enough to propagate AP

Relative: stim triggers AP , but slower rate of rise

Short supra normal: less-than-norm stimuli will cause AP

Atria has shorter refractory periods than ventricles

Front 184

Factors affecting speed of impulse conduction

Back 184

Number Na+ channels

RMP (affects # Na channels open to begin with)

Eg Purkinjie cells have high concentration Na+ channels

Pacemaker cells have less negative RMP

Front 185

Titin

Back 185

Aka connectin

Protein

Feathers myosin to z line of sarcomere

Provides elasticity

Front 186

Troponin subunits and fns

Back 186

TnT: links troponin complex to actin and tropomyosin

TnI: inhibits ATPase activity of actin-myosin interaction

TnC: responsible for binding Ca++; activated TnC inhibits TnI

Front 187

Ryanodine receptors

Back 187

Ca++ release receptors on SR
Ca++ binds and causes release of much more Ca++ from terminal cisternae

CICR

Front 188

ANS effects on myocyte contraction

Back 188

Symp: Beta1-adrenergic
- coupled to and activates stim G protien system
- adenylate cyclase increases production cAMP
- P L-type Ca++ Channels and PL (phospholamban- inhibits Ca++ uptake by SERCA until P, faster relaxation)

PNS: cholinergic on M2 R
- inhibitory G protein
- negative effect on adenylate cyclase
- deP, counteracts B2-R stim effects
- ventricular cells less sensitive to

Front 189

Heart failure definition

Back 189

Clinical syndrome of symptoms (dyspnea and fatigue) in medical hx and signs (edema and rales) on exam

Doesn't include cardiomyopathies of LV dysfunction causes

Usually LV Myocardial fn impairment

4 stages complementary to NYHA