cardiac patho Flashcards
ischemic heart disease
CAD, stable angina, unstable angina
CAD
atherosclerosis of CA
cardiac artery branches from aorta, give heart cells oxygenated blood
become clogged due to atherosclerosis - cant feed heart cells and they die
L anterior descending artery (widow maker), feeds LV (powerhouse)
increased risk of MI but they arent the same
stable angina = lumen is smaller bc of plaque buildup so blood cant flow as freely
problems with heart
electrical (conduction)
plumbing (artery blockage, spasm, valve issues)
pump (heart muscle)
CAD: rf - non modifiable
age (oa)
fam hx (shared env exposure)
gender (m younger, F same after menopause - estrogen protects)
ethnicity (AA, hispanic, native), also death disparity
genetics
CAD: rf - modifiable
htn
smoking - endothelial function of cells in CA, nicotine stim catecholamines to increase hld and htn risks
DM - damage increases inflam
obesity/inactivity - abd (android), increase inflam, adipokines - hormone
diet - salt, high fat, trans fat, high carb, DASH is protective
hld - high TG and LDL, low HDL (big pharm target - statins)
dep/stress and anx - systemic inflam
patho of ischemic heart problems
plumbing issue
atherosclerosis in arteries supplying myocardium = artery blockage = decreased perfusion, endothelial dysF, heart works harder to pump
endothelial dysF: vessels arent blocked but they narrow when suppose to dilate bc inappropriate hormones and chm (DM, htn, hld, smoking); worse when combined with plaque filled arteries
angina
main S of CAD
may be asymp
as they continue to narrow, decreased BF may cause angina
MI = complete occlusion
associate s: dizzy, heart burn, irregular HR (palpitations), weakness, anx, n, cold sweat, burning sensation (chest, shoulder, abd)
stable angina
coronary BF is decreased but not completely blocked
imbalance btw O2 supply and demand
occurs on exertion and is relieved by rest (2-5 min) - mistaken for indigestion esp with large meal
nitrate
chest pain
L arm, jaw, L shoulder, diaphoresis, pallor
exclude heart as cause before exploring non heart causes
chest pain - cardiac causes
pressure or tightness, diffuse/poorly localized, associated with phys exertion or other stress, relieved with rest w/n mins, prolonged s may indicate acute MI
chest pain - non cardiac causes
sharp, stabbing, focal, well localized; may be positional, spont, at rest
no predictable relation to phys exertion
may last from sec to days at a time
atypical angina in women
discomfort - hot/burn, tender
location - not always chest
other s: indigestion, heart burn, n, fatigue/weak, lightheaded, dyspnea
angina pectoris and pain with MI
arteries completely blocked
pain not brought on by exertion
radiate to neck, jaw, upper abd, shoulders, arm
not bc exertion, not relieved in 2-5 minutes, often accompanied by n/v, SOA, diaphoresis
increased r/o MI
stable angina: nc
educate - rest and relax, decrease O2 demand on heart
nitrates
prevent/treat further atherosclerosis
teach about MI (dif btw stable and unstable) -> call 911 if pain not better after 5 min of rest and nitrates
heart failure: cardiomyopathy
disease that affects myocardium - heart muscle, L/R/both ventricles
usually idiopathic or - ischemia d/t cardiac disease, htn, inherited disorders, infections, toxins, myocarditis, autoimmune
lead to HF
heart failure: cardiomyopathy - types
dilated, hypertrophia, restrictive
heart failure: cardiomyopathy - dilated
ischemic, valve disease, OH and drugs, poster peripartum HF issues, infection
genetic link
leads to HF with decreased ejection fraction
heart failure: cardiomyopathy - hypertrophia
htn
increased risk of deadly arrythmias, sudden cardiac death
ejection fraction eventually decreases
heart failure: cardiomyopathy - restrictive
ventricles become resistant to filling, muscles harden - rigid and non compliant
R sided HF, systemic congestion
amyloid disease
heart failure
problems with heart pump (muscle)
chronic progressive condition where heart muscle is unable to pump enough blood to meet body’s needs for blood and O2
basically, heart cant keep up with workload because the muscle doesnt work or is weak
heart failure and CO: HR and SV factors
HR: only affective at increasing or changing CO btw 60-120
SV:
preload = FV, amount in LV before it squeezes, increases with HF
afterload = BP, P that heart squeezes against when contracting, increases with HF
myocardial contractility = pump muscle, decreases with HF
heart failure: patho
volume overload - fluid backup bc heart not pumping enough out
impaired ventricular filling -> ventricular filling during diastole
weak ventricular muscle
decreased ventricular contractile function -> during systole
heart failure: etiology
repeated ischemic episodes -> ischemic cardiomyopathy (unstable angina, MI, etc)
myocardial infarction +/- papillary muscle rupture
chronic htn
COPD -> pulm back up alters RV filling (RVF)
dysR -> can decrease CO, decrease perfusion to CA
valve disorders: mitral insufficiency, aortic stenosis
pulm emboli -> pulm back up alters RVF
heart failure: rf
htn! - DM bc of inflam and endothelial dysF
w/n 6 mo MI, M before menopause, AA (htn), genetics, fam hx, OA >65, obesity, smoking, sedentary, COPD, severe anemia, congenital heart defects, ischemic heart disease, viruses that cause myocarditis (weaken), OH, drugs (crack/cocaine)
kidney conditions: excess BV, edema, htn, accumulation of nitrogenous waste, which can weaken heart
stable angina is NOT a rf
HF classifications: L
blood backs up in pulm circ
congestion in L chambers, LV increase in size (LVH - to compensate), backflow into pulm veins, congestion in lungs -> pulm symptoms
related to htn!
cough, crackles, wheeze, confusion, tachy, exertional dyspnea, fatigue, cyanosis, tachypnea, elevated pulmonary vascular wedge pressure
frothy sputum - may be blood tinged
paroxysmla nocturnal dyspnea (PND) - feel smothered in middle of night
orthopnea - cant breathe laying flat, tripod
pulmonary edema
pts present with both L and R as disease progresses
HF classifications: R
blood backs up in systemic circ
usually due to COPD (severe) with cor pulmonale, congestion in R chambers, RVH, backflow into vena cava, decreased in lungs, congestion in jugular veins, liver, LE
related to COPD!
JVD, dependent edema (LE), weight increase, hepatosplenomegaly, fatigue, anorexia and GI distress, ascites
pts present with both L and R as disease progresses
HF: ejection fraction
continuum with distinct features
amount of blood pumped out with LV with each squeeze
55-65% normal
HF: ejection fraction - reduced
HFrEF, systolic HF
younger, male, CAD, DM, valve disease
<40% -> via echocardiogram (transthoracic or TEE)
caused by impaired contractile function (heart muscle cant squeeze effectively), increased afterload, cardiomyopathy, mechanical problems
LV loses ability to generate P to eject blood
weakened muscle cannot generate SV -> low CO
LV fails, blood backs up, causes fluid backup and accumulation (pulm, then systemic)
HF: ejection fraction - preserved
HFpEF, diastolic HF
inability of ventricles to relax and fill during diastole -> too big, restriction
htn!, F, OA, DM, obesity
LV is stiff and noncompliant (muscle present but not effective), leads to increased filling P -> decreased SV and CO -> fluid congestion
EF normal or moderately decreased (40-45%)
HF: chronic v acute
progressive
chronic: episodes of decompensated HF - new or worse s/s, freq ER visits (d/t s/s from FVE), hospitalization, less common - new onset HF
HF: ventricular remodeling
weakened heart muscle -> secretes things that are supposed to help: A2, aldosterone, endothelin, TNF alpha, catecholamines, insulin like growth factor, growth hormone
provoke genetic change in heart cells - apoptosis, hypertrophy of cardiac myocytes, and collagen deposits and myocardial fibrosis
changes cause enlargement and dilation of LV -> worsens HF
HF: S3 gallop
low pitch sound heard after S2
during rapid filing of ventricle in early part of diastole
increased ventricular end diastolic V -> fluid still in ventricle after contraciton
increased P in ventricles
when >40 y/o, S3 is abn and indicates HF
cardiac muscle cells
automaticity: ability to generate electrical impulse
excitability: ability to respond to outside impulse (chm, mech, elec)
conductivity: ability to receive electrical impulse and conduct it
contractility: pump, ability of myocardial cells to shorten in response to impulse
cardiac conduction
Action potential - Na/K pump
depolarization = contract (atria and ventricle), systole
atria = P wave, generated by SA node
ventricle = bigger hill bc they are bigger -> QRS complex from AV node
repolarize = heart ramping back up, cant see atrial only ventricular (bc atrial is during QRS) = T wave
flat line = isoelectric
E impulse travels down bundle of His and Purkinje fibers so (L) vent contracts
cardiac conduction - normal E conduction
SINUS rhythm - originates from SA node
rate 60 -100, rhythm regular -> same amount of time btw each repolarization and depolarization
P: upright and rounded, one before each QRS, reg rhythm, even
PR interval = 0.12 - 0.2 seconds, beginning of P to tip of R
QRS <0.12 s -> narrow
each box = 0.04s
sinus arrythmia
still considered normal
degree of variability in HR
originates from SA still, but fluctuation in rate and initiation
rate still btw 60 - 100
no change to CO
PR still btw 12 - 20, QRS still narrow
common in young people
HR fluctuates with resp or autonomic NS
dysrhythmias
problem with impulsse generation or conduction
significant bc altering rhythm affects CO -> mostly HR but sometimes SV
causes: inappropriate automaticity, triggered activity, re entry
dysrhythmias: inappropriate automaticity
cell initiates AP when not supposed to, in atria mostly
d/t MI or e imbalance (K)
dysrhythmias: triggered activity
extra impulse generated during or just after repolarization, cells think they are supposed to contract
digoxin tox, SNS stim, genetics
dysrhythmias: re entry
cardiac impulse in 1 part of heart continues to depolarize after main impulse has finished
MI, e imbalance
dysrhythmias: sinus brady
SA, regular, <60, normal rhythm, normal PR and QRS
causes: hyperK (slow depolarization), vagal stim, digoxin tox, late hypoxia, meds (BB, CCB, amiodarone), MI (ischemia around SA node)
dysrhythmias: sinus brady - cm
d/t decreased CO and lack of O2 to certain cells
lightheaded/dizzy esp with exertion, syncope, dyspnea, chest pain or discomfort, confusion
dysrhythmias: sinus brady - tm
treat symptomatic only - some people are fine, always assess for S!
atropine: anticholinergic
pacemaker if drug not effective
dysrhythmias: sinus tachy
SA, 100 - 150, reg rhythm, P waves similar (may be partially hidden), normal PR and QRS
causes:
catecholamines - exercise, pain, strong emotions (anx, happy, grief)
fever - decreased met rate
FVD - 1st S is tachy
meds - epi, albuterol, Beta agonists
substances - caffeine, nicotine, cocaine
hypoxia - early
dysrhythmias: sinus tachy - tm
only if symptomatic
based on cause!
hypovolemia = fluids
fever = antipyretics (acetaminophen)
pain = analgesics
BB (-lol) to decrease HR and myocardial O2 consumption -> for cardiac disease state
dysrhythmias: paroxysmal supraventricular tachy
PSVT -> tachycardia originating above ventricle
paroxysmal = intermittent/occasional
supraventricular - above ventricle
150 - 250, AV node (maybe - just know originating point is above ventricles), usually no P wave (if present, they look abn), QRS normal
usually caused by re-entry phenomenon, typically begins and ends suddenly, described as racing heart
dysrhythmias: paroxysmal supraventricular tachy - causes
over exertion, emotional stress, stimulants, digoxin tox, rheumatic cardiac disease, CAD, wolff parkinson white, R sided HF
dysrhythmias: paroxysmal supraventricular tachy - cm
palpitations, chest pain, fatigue, lightheaded/dizzy (d/t decreased CO bc too fast), dyspnea
dysrhythmias: premature atrial contractions (PACs)
early P waves that usually look a little different (morphological change - sad looking)
normal PR, QRS follows PAC
usually no consequences, but if freq = indicates pt at increase risk for another dysR (usually afib)
check electrolytes!
make sure pt in safe env, dont d/c
may need O2, rule out issues of perfussion
atrial dysrhythmias: atrial flutter
originate in AV - overrides SA
re-entry impulse - repetitive and cyclic
reg atrial rhythm with atrial rate >250 - atria contracting moral than ventricles -> slower, fewer QRS and P - 2:1, 3:1, 4:1, (QRS usually narrow)
P wave = saw tooth appearance
atrial dysrhythmias: atrial flutter - causes
coronary heart disease, cardiomyopathy, heart valve disease, congenital heart disease, inflam of heart (myocarditis), htn, other conditions such as any lung disease or overactive thyroid, electrolytes, heart sx
atrial dysrhythmias: atrial fib
is it rate controlled? higher HR = decreased CO -> lots of s/s, rhythm important but so is rate!
multiple irritable spots in atria
irregularly irregular -> atrial and vent not communicating
100 - 175, not identifiable P wave (could be <100)
“fibrilation” waves -> all over the place
atrial dysrhythmias: atrial flutter + atrail fib - cm
A fib usually more s bc flutter more consistent CO
palpitations, racing, prolonged fatigue, dizzy, chest discomfort, SOB, may be asymp (some never know)
depends on cardiac status (how sick?) and CO
complications: decreased CO, HF, embolus - in atria bc blood just jiggling around in there; stroke
atrial dysrhythmias: atrial flutter + atrail fib - causes
electrolytes, hypoxia - first thoughts if no CV hx
all CV diseases
atrial dysrhythmias: atrial flutter + atrail fib - tm
most commonly treated dysR
pahrm:
rate control = BB, CCB, digoxin, amiodarone
stroke prevent = anticoags, antiplts
non pharm:
ablation, cardioversion
ventricular dysrhythmias: premature ventricular contractions
PVCs
contraction coming from ectopic focus in ventricles, it comes earlier than QRS should and doesnt follow normal rhythm or P wave
wide and distorted in shape compared to normal QRS
causes: stimulants (caffeine, nicotine), electrolytes, hypoxia, fever, exercise, emotional stress, CVD
treat cause - esp if s/s
bigeminy, tigeminy, quadrigeminy
if they occur regularly -> probably progressing to something worse
+ or -
ventricular dysrhythmias: ventricular tachy
deadly rhythm!
3+ PVCs together
ectopic focus w/n ventricles takes control and fires repeatedly -> no atrial contractions occurring
seriously decrease CO and cause lots of damage to heart -> immediate intervention
associated with MI, CAD, significant electrolyte abn, HF, drug tox and other bad things
150-200, usually regular, will eventually become pulseless
no P wave evident, PR not measurable
treat ACLS -> depend on pulse, pt will be symptomatic v quickly unless converts back to other rhythm (12 run of VTACH), may need antidysR med -> BB, CCB; electrolyte replacement
1st Q: pulse or pulseless (CPR)
ventricular dysrhythmias: ventricular fibrillation
deadly rhythm!
irregular waveforms of varying shapes and sizes
ventricles are quivering
not effective contractions = no CO
pulse or pulseless -> CPR
