Neuro/Cardiac Section Flashcards
Midline structures affected with stroke
Medial lemniscus
Motor pathway (corticospinal)
Motor aspects of CN
Medial longitudinal fasciculus
Lateral structures affected with stroke
Spinothalamic
Spinocerebellar
Sympathetic - Hoerner’s
Sensory sections of CN V
Signs and symptoms of uncal herniation
Dilation of pupil on side of hernitation (CN III paresis), hemiparesis, coma, homonymous hemianopsia
S/S of central hernitation
Decrebrate rigidity and coma
S/S of tonsilar herniation
Neck pain and stiffness, flaccidity, coma, alteration of vital signs
Branches of right coronary artery
Sinus node artery (right atrium)
Right marginal artery (right ventricle)
Posterior descending (inferior walls of ventricles)
Branches of left coronary artery
Circumflex artery (left atrium and ventricle) Left anterior descending (IV septum)
ABI normal
1.0-1.3
ABI mild
0.99-0.80 (beginning of PAD)
ABI moderate
0.40-0.79 (intermittent claudication)
ABI severe
<0.40 (claudication at rest)
Bronchophony
Increased vocal resonance with greater clarity and loudness of spoken word
Egophony
Spoken long “E” changes to nasal “A”
Whispered pectoriloquy
Recognition of whispered word
Infant HR
100-130
Child HR
80-100
Adult HR
60-100
Newborn RR
33-45
1 yr RR
25-35
10 yr RR
15-20
Adult RR
12-20
PR interval
Time for atrial depolarization and conduction from SA node to AV node
0.12-.20
QRS compex
Ventricular depolarization and atrial repolarization
0.06-1.0
QT interval
Time for both ventricular depolarization and repolarization
0.20-0.40
Submax training RPE
Initial 12-13
Final 15-16
Mobitz I
General prolongation of PR interval until QRS is dropped
Mobitz II
Dropped QRS, PR interval remains unchanged
Hypermagenesemia
Calcium channel blocker so can lead to arrhythmias or cardiac arrest
Hypomagenesemia
Ventricular arrhythmias, coronary artery vasospasm, sudden death
Hyperkalemia
Decreases the rate and force of contraction, widened PR interval and QRS, tall T waves
Hypokalemia
Flattened T waves, prolonged PR and QT intervals, produces a U wave
Hypothermia effects on ECG
Elevates ST segment; slows rhythm
Digitalis effects on ECG
Depresses ST segment, flattens T wave, QT shortens
Quinidine effects on ECG
QT lengthens, T wave flattens, QRS lengthens
Beta blockers
Decrease HR, blunts HR response to exercise
Nitrates
Increase HR
Normal BP
120-129/80-84
High Normal BP
130-139/85-89
Grade I HTN
140-159/90-99
Grade II HTN
160-179/100-109
Grade III HTN
> 180/>110
Levine’s sign
Pt clenches fist over sternum
Inferior MI
Right coronary artery (upper conduction system)
Lateral MI
Circumflex artery
Anterior MI
L anterior descending (lower conduction system)
Tinetti high risk for falls
<18
Berg high risk for falls
<20
TUG high risk for falls
> 30
Functional reach risk for falls
<10 in
DGI prediction of falls
<19/24
Berg moderate risk for falls
21-40
Tinetti moderate risk for falls
19-24
Normal adult TUG
<10
Normal elderly TUG
11-20
Mild TBI criteria
LOC <30 min, PTA <1 day, GCS 13-15
Moderate TBI criteria
LOC >30 min <1 day, PTA >1 day, <7 days, GCS 9-12
Severe TBI criteria
LOC >24 hrs, PTA > 7 days, GCS <9
MOA Alpha adrenergic agents
Cause vasodilation of arterioles and veins to decrease BP
MOA of ACE inhibitors
Suppress conversion of angiotensin I to angiotensin II to decrease BP and afterload
MOA Sodium channel blockers
Control cardiac excitation and conduction
MOA Beta blockers
Inhibit sympathetic activity which decreases HR and contractility
MOA of statins
Inhibit enzyme action in cholesterol synthesis, break down LDLs, decrease triglycerides, and increase HDL levels
MOA calcium channel blockers
Decrease entry of calcium into vascular smooth tissue resulting in diminished myocardial contraction, vasodilation, and decreased oxygen demand
MOA nitrates
Decrease ischemia through smooth muscle relaxation and dilation of peripheral vessels
MOA positive inotropic agents
Increase the force and velocity of myocardial contraction, slow HR, decrease conduction velocity thru AV node, and decrease activation of SNS
