406 patho - wk 1 Flashcards
myocarditis
an inflammatory disease of the myocardium that be mild to lethal and can cause degeneration & necrosis of cardiac myocytes
conduction disruption is common
what is the most common cause of myocarditis
viruses
coxsackie A & B
treatment of myocarditis
-anti inflammatories
-anti virals
-heart transplant (severe)
pericarditis
when the pericardium undergoes inflammation, fluid accumulates in the pericardial space -> the fluid is called pericardial effusion and it surrounds the heart
edema of pericardial space
when fluid around the heart accumulates to 200ml or greater and the heart becomes compressed, this is called
a cardiac tamponade
cardiac tamponade
the heart chamber are restricted by the surrounding pericardial fluid so they cannot stretch or fill with blood
a cardiac tamponade is a
medical emergency -> the fluid needs to be drained very quickly
pericardiocentesis
signs of acute pericarditis
-sharp chest pain that worsens w/ a deep breath
-fever
-dyspnea
-pericardial friction rub (scratching sound)
-ECG finds of ST elevations
-hyoptension/JVD/muffled heart sounds/confused/dizzy d/t tamponade
-pulsus paradoxus
pulsus paradoxus
a decrease in systolic blood pressure of 10 mmHg or more w/ inspiration (seen best w/ an ART line)
systolic should increase slightly w/ inspiration
treatment for pericarditis
-nsaids
-asa
-corticosteroids
-colchicine
aneurysms usually occur w/ what
high blood pressure -> the pressure weakens the arterial walls which causes bulges in the arterial wall (aka the aneurysm itself)
aneurysm facts
-cause turbulent blood flow
-susceptible to rupture
-bruits may be heard over them
-most common areas are aorta & cerebral arteries
risk factors for aneurysm
atherosclerosis, hypertension, diseases of blood vessels, trauma, tobacco use, >65yrs
aortic aneurysm
-abdominal aortic aneurysm (triple A)
-thoracic
-dissecting aortic aneurysm
cerebral aneurysm
anywhere in the brain
saccular aneurysm
-balloon shaped
-involves only one part of circumference
-wide neck
Berry aneurysm
subtype of saccular
-small neck
-located at bifurcation (commonly circle of willis)
how to dx a berry aneurysm
-angiography
-hx & clinical manifestations
treatment of a berry aneurysms
-medical control of HTN & vasospasm
-surgical: drain, clipping, or coiling
where is the circle of willis located
base of brain
so vessels off of it supply majority of blood to the brain
fusiform aneurysm
-entire circumference of vessel
-gradual/progressive dilation
-potentially extensive involvement or can only be monitored
related to diffuse of anterior sclerotic changes
false (pseudo) aneurysm
-localized dissection or tear in inner artery wall
-type of hematoma
-complication of vascular interventional procedures
-can be self limiting
leakage in between vascular graft and natural artery
abdominal aortic aneurysm (AAA)
-auscultation of a bruit over the abdominal aorta suggests presence
-if a pulsatile mass is evident in the abdomen during inspection or light palpation -> deep palpation should not be performed until the possibility a AAA is ruled out
-if ruptured, pt can bleed out very quickly
dissection aneurysm
layers of the wall of the artery are separated & blood enters the region
can be a medical emergency
aortic dissection clinical manifestations
-sudden severe, tearing pain
-elevated BP (early)
-later stages: BP unobtainable, syncope, hemiplegia, paralysis of lower extremities
-cardiovascular collapse -> shock -> death
emergency, minutes count
aneurysm can be “” where dissections will have “”
asymptomatic ; severe sudden pain
aortic dissection dx
CT scan or MRA (angiogram)
emergency pharmacotherapy for aortic dissection
beta blockers
nitrates
aneurysms are
dilation or out pouching of a vessel wall
true aneurysm involve all 3 layers of the arterial wall
acute coronary syndrome (ACS)
umbrella term for situations where the blood supply to the heart muscle is suddenly blocked or compromised -> blockage can be sudden and complete or come & go (either way, tissue is dying)
medical emergency
what 3 conditions do we think about w/ ACS
1) unstable angina -> most blood is able to get through
2) a non ST segment elevation MI (non stemi) -> reduced blood flow
3) a ST elevate segment elevated MI (stemi) -> blood flow is completely blocked
unstable angina
new or unchanging chest pain caused by ischemia
what do we do to differentiate between is causing the ACS
ECG
variant / vasospastic angina
prinzemtal angina
-causes: coronary artery spasm d/t endothelial dysfunction
-may or may not have CAD
-sx occur usually at rest & at night
-possible elevated ST segment
treatment for variant / vasospastic angina
nitrate
unstable plaque characteristics that lead to ACS
-large lipid core
-active inflammation
-smooth muscle cells proliferate into intima (middle lining of blood vessel)
unstable angina
1) chest pain occurring for the first time (myocardial ischemia)
2) chest pain more severe than usual w/ chronic angina (new regions of the heart myocardial ischemia)
emergency situation
what is our main concern w/ unstable angina
plaque rupture & the thrombus formation bc size of clot & blockage determines how much blood gets through
if a clot ruptures w/ unstable angina but no infraction occurs, what could be the reason
1) occlusion is partial
2) thrombus dissolved
cardiac enzymes will not be elevated
what factors contribute to increasing SNS activity
-psychological stress
-exercise
-circadian rhythms
theory of plaque rupture (look more in depth, basic overview)
increased SNS activity -> plaque rupture -> thrombus formation
difference between ACS and stable angina + pt teaching
-severity & duration (stable should last 5 min & be gone within 15, ACS is longer than 15)
-ACS pt get no relief from nitrates, stable will
-stable “my chest is tight”, ACS “an elephant is sitting on my chest”
-ACS will have more diaphoresis, SOA, n/v, feeling of impending doom
ACS signs in men
-discomfort or tingling in arms, back, neck, shoulder or jaw
-chest pain
-SOB
ACS signs in women
-sudden dizziness
-heartburn like feeling
-cold sweat
-unuasal tiredness
-N/v
S/s of an MI
diaphoresis, dyspnea, extreme anxiety, levine’s sign (fist to chest), pallor, retrosternal crushing chest pain that radiate to should, arm, jaw or back
-weak pulses
what is an acute myocardial infarction
ruptured plaque + thrombus w/ an infarction d/t prolonged blow flow disruption or total blood flow disruption
will see ECG changes & an increase in cardiac enzymes
is acute MI damage reversible
no -> it is prolonged ischemia w/o recovery & the myocardial cells suffer irreversible ischemic necrosis
ischemia defined
“when the oxygen supplied does not meet the heart’s metabolic demands”
infarction defined
“actual irreversible tissue death”
can myocardial cells make ATP
no -> cells need a continuous supple of oxygen to make ATP so if oxygen levels go down so does the cells main source of energy
what is the relationship between acute ischemia & ATP
when you have acute ischemia, ATP goes down instantly followed by decreased ability to contract
irreversible injury w/ MI occurs within
30 mins - 4 hrs then tissue necrosis begins
when is necrotic tissue cleared after an MI
in 1-2 weeks then the myocardium is very weak and susceptible to rupture
by 6 weeks, completely replaced by scar tissue
three zones of damage w/ an MI
1) infarction = necrosis
2) injury = some recovery possible
3) ischemia = full recovery possible
to avoid infarction, increase oxygen & decrease demand on the heart
what does the extent of damage depend on w/ an MI
-location or level of occlusion in the coronary artery
-length of time that the coronary artery has been occluded
-heart’s availability of collateral circulation
STEMi: ST seg, QRS, T wave, Troponin, size, outcomes
ST seg: elevated
QRS: pathologic (wide), develops over hours
T wave: peaked then inverted
Troponin: elevated
size: larger
outcomes: poor
NSTERMI: ST seg, QRS, T wave, Troponin, size, outcomes
ST seg: depression or normal
QRS: normal
T wave: inverted
Troponin: elevated
size: smaller
outcomes: better
