etiology:  pulm dz, congenital heart dz

-RAD lead 1:  negative AVF:  positive

in RVH the electrical activity flows predominantly towards the V1 lead and not the V6 lead.

-R wave larger than S wave in V1

-S wave larger than R wave in V6

in a heart without RVH, in the V1 lead you would expect the R wave to be smaller than the S wave since most of the electrical activity would be flowing away from the lead.  

whereas in the V6 lead you would normally see a larger R than S wave since the electrical activity would be flowing towards the lead

etiology:  systemic HTN, valve dz

-R wave amp in V5/V6 + S wave amp in V1/V2 >35mm

-R wave amplitude in lead V6 exceeds R wave amplitude in lead V5

-R wave amplitude in lead aVL >13mm

-R wave amplitude in lead 1 >14mm

-crushing, squeezing, pressure, burning w/w out radiation to arms, neck, jaw

-chronic, stable angina precipitated by exertion and relieved by rest, NTG

-unstable angina, MI pain similar but more severe, longer lasting, unrelenting despite rest/NTG

-may not have any signs/sxs

-other sxs:  SOB, nausea, vomiting, diaphoresis, doomed feeling

-palpitations:  awareness of one's own beat

-light-headedness/syncope (sudden faint):  sxs of decreased CO, which happens when

arrhythmia compromises cardiac function

-angina:  caused by increased O2 demands of myocardium during rapid arrhythmias

-sudden death

delays RV depolarization resulting in:

-QRS >0.12sec

-RSR' complex in leads V1 and V2

-ST segment depression and T wave inversion in these leads as well

-presence of deep S waves in left lateral leads (I, aVL, V5, and V6)

left ventricular depolarization is delayed resulting in:

-QRS complex width >0.12sec

-broad, notched R waves in left lateral leads (I, aVL, V5, V6)

-ST segment depression and T wave inversion in these leads as well

-broad, deep S waves in leads overlying RV (V1, V2)

pt presents with signs and symptoms of CAD and has ST elevation on EKG

stemi, nonstemi, usa?

pt presents with signs and symptoms of an MI, however the EKG looks normal

stemi, nonstemi, usa

must wait for cardiac enzymes (troponin, CPK-MB isoenzymes)

positive enzymes indicate NSTEMI (actual damage)

negative enzymes indicate Unstable Angina (no damage but still high risk)

coronary heart dz

rheumatic heart dz

1:  prolonged pr 0.20

2,1:  gradually longer pr, followed by dropped qrs

2,2:  normal pr, sudden drop of qrs

3:  dissociation btwn qrs and p waves

onset:  T-wave peaking ("hyperacute T")--->T-wave inversion..... ischemia

ST segment elevation...........injury

significant Q waves (wider and deeper).................infarction

conditions with possible ST elevations

ST depressions

T-wave inversions

MIs (specific leads indicate portion of heart)

pericarditis (diffuse ST elevations)

depressions:

positive stress tests (down-sloping or horizontal- not up-sloping)

ventricular hypertrophy

BBB

inversions:

LBBB (1, aVL, V5, V6)

RBBB (V1, V2)

MI onsets start off as hyperacute T waves but progress to T wave inversion

ventricular hypertrophy

pericarditis (after ST elevation returns to baseline)

left anterior hemiblock

Q waves of inferior MI

artificial pacing

emphysema

hyperkalaemia

WPW (right sided access)

tricuspid atresia

ostium primum atrial septal defect

injection of contrast into left coronary artery

normal finding in children and tall thin adults

riight ventricular hypertrophy

chronic lung dz even w/out HTN

anterolateral MI

left posterior hemiblock

pulmonary embolus

WPW (Left sided acce)

atrial septal defect

ventricular septal defect

causes of NW axis

"no mans land"

emphysmea

hyperkalaemia

lead transposition

artificial cardiac pacing

ventricular tachycardia

pathophysiology of both L and R ventricular hypertrophy

and then causes of each

increased pressure and/or volume

RVH:  pulm valve stenosis COPD status asthmaticus pulm embolus mitral valve stenosis or insufficiency

LVH:   mitral insufficiency systemic HTN acute MI aortic stenosis or insuffciency hypertrophic cardiomyopathy

dilated- doesn't work well as a pump

hypertrophic- thickened heart muscle (usu septum and LV)

restrictive-STIFF 

dilated

etiology:  most often idiopathic

post viral, EtOH (other toxins too), cocaine, famililial

-inflam:  myocarditis

-metabolic-nutrient and electrolyte deficiencies

-post partum

-sustained rapid a fib

-may overlap with restrictive

CO OUTPUT MAYY BE NORMAL but may not increase as should with exertion

EF,30%

elarged ventricle

risk for tachy, sudden death

non-specific non ischemic CP

syncope:  arrhythmias, emboli

sxs of HF

cardiomegaly-PMI, LV lift

signs LHF:  rales, wheezes

signs RHF:  edema, HJR, LHF

hypertrophic cardiomyopathy

etiology

age

sxs

genetic etiology

LV and septum thickened

ages 20-40

sxs:  dyspnea on exertion, CP, syncope, palpitations

EF >60%

LV volume decreased

inc risk for v. tach and a. fib

may be cause of sudden death in atheletes

what test establishes diagnosis in hypertrophic cardiomyopathy

and 

what to look for on EKG

echocardiogram

look for LVH (R of V5, V6 + S of V1, V2) and Q waves

syncope during exercise? -->sign of heart dz

any cardiac murmur

further eval with EKG, ECHO, and stress text with positive results to exertion syncope and murmurs

prominent LV impulse

S4 gallop

murmur along LSB

-DEC ON INSPIRATION (RETURNS more blood)

-inc on expiration

-increases from squatting to standing and valsalva because more blood to heart

restrictive- stiff heart wall does contract well, can stretch out but doesn't snap back

infiltrative dz:  amyloidosis, sarcoidosis

storage dz

metabolic ddz

radiation

restrcitive pericarditits

chemotherapy

endomyocardial fiborsis:  Africans, children, and young adults

idiopathic

systolic HF

diastolic HF

heart doesn't contract well, strongly enough to supply blood to periphery

*primary abn in dilated cardiomyopathy

abn relaxation of myocardium, reduced filling of ventricle

*common result of hypertrophic and restrictive cardiomyopathy

-although other causes that increase LV stiffness:  CAD, DM, HTN, valve heart dz, age