cardiac ischemia, failure, shock Flashcards by Alicen Honner

what are the 3 components of myocardial O2 supply?

coronary artery vessel patency

ventricular wall compression

diastolic filling time (HR)

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what are the 3 components of myocardial O2 demand?

myocardial contractility

wall stress (pre and afterload)

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CORONARY ARTERY DISEASE:
risk factors: (8)

etiology: (2)

manifestations: (3)

RF: smoking (nicotine leads to vasocon), hypertension, high LDL, low HDL, DM, age, obesity, inactivity

E: atherosclerosis (plaque formation) = impaired coronary blood flow (slow/progressive)

M: asymptomatic = d/t collateral channels, seen as chronic ischemic heart disease or Acute Coronary Syndrome

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what are the 2 CAD classifications

acute coronary syndrome (ACS)
Chronic ischemic heart disease

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what is ACS and what are 3 examples

sudden and severe reduction of BF to heart (plaque rupture = partial/full blockage of coronary a)

unstable angina, STEMI, NSTEMI

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what is chronic ischemic heart disease (IHD)?
and one example:

long term condition (stable), heart gradually recieves ;ess blood supply d/t atherosclerosis (progressive narrowing of coronary a)

stable angina

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what is a stable plaque?
composition:
inflammation + risk of rupture:
causes:
blood flow:
progression:

thick fibrous cap, less lipid
low
stable angina
partial obstruction
gradual narrowing

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plaque types are associated with:
ACS:
IHD:

ACS: unstable
IHD: stable

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what is a unstable plaque?
composition:
inflammation + risk of rupture:
causes:
blood flow:
progression:

thin fibrous, large lipid core
high
ACS: unstable angina, N/STEMI
rupture = clot = full/partial blockage
sudden rupture

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what are the 2 contributing factors to plaque disruption?

vessel tension
sudden surge of SNS (inc BP, HR, contraction, coronary blood flow)

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what is stable angina?
manifestations: (3)

when there is a fixed or stable plaque that obstructs blood flow = demand > supply/availability of blood

M: CP (with exertion/inc demand)

constricting, squeezing, suffocating

precordial or substernal area (Left shoulder, arm, jaw)

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what is unstable angina? (4 parts)
Manifestations:

unstable plaque (plt aggregation) =
narrowing coronary lumen =
inflammation=
ischemia!

M: CP that is persistent (20+ mins) and severe (new or longer than other times)
NO SERUM BIOMARKERS

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what is the main differences between unstable and stable angina?

unstable angina is not relieved by rest, lasts for a long time, unpredictable

stable angina is relieved by rest and short

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what is an NSTEMI?
manifestations:

unstable plaque = partial occlusion = INFARCTION = cardiac cells are dying but not full thickness

CP that is persistent (20+ mins) and severe (new or longer than other times) + SERUM BIOMARKERS (troponin I and T, CK-MB)

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troponin I and T

released when cardiomyocytes are damaged (troponin protein is only present in heart m cells)

most sensitive, peaks at 12 h and returns to normal @ 14 days

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CK-MB (creatine kinase- MB)

released when cardiac and/or skeletal muscle is destroyed

less sensitive, peaks at 18-34 hours and returns by 3 - 6 days

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what is a STEMI?
Cause: (2 parts)
Manifestations: (5)

complete coronary artery occlusion = cardiac cell necrosis (full thickness of myocardium)

sudden, crushing CP (not relieved by rest of nitroglycerin)
epigastric pain
N and V
ST elevation on EKG
troponin and CK-MB released

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what heart issue: Predictable, relieved with rest or nitroglycerin, low risk for immediate heart damage.

stable angina

what heart issue: Unpredictable, often occurs at rest, a precursor to MI

unstable angina

what heart issue: Partial blockage of coronary artery, heart muscle damage occurs, troponin elevated

NSTEMI

what heart issue: Complete blockage of coronary artery, severe heart muscle damage, ST elevation on ECG

STEMI

HEART FAILURE: a complex syndrome that results from _______ or _________ disorder that leads to ______ CO and/or pulmonary/systemic ________

functional, structural
low
congestion

HEART FAILURE: patho
muscle _______ = reduced _________ = cardiac output _______ = _________ of the heart

weakness
contractility
declines
overload

HEART FAILURE: causes (4)

CAD
HTN
dilated cardiomyopathies
valvular heart disease

HEART FAILURE: associated with (3)

increased preload (inc venous return to heart) increased afterload (d/t inc force to pump against is greater = less ejection) decreased contractility (dec efficiency of heart to pump)

right heart failure = congestion of __________ tissues = dependent ________ and ascites AND GI tract __________ (anorexia, GI distress, weight loss) AND liver ________

peripheral edema congestion congestion

left heart failure = ________ CO (activity intolerance and ________) AND ________ congestion = impaired ______ exchange (cyanosis and _______) AND pulmonary _______ (cough with _______, difficulty breathing at night/laying down)

decreased hypoperfusion Pulmonary gas hypoxia edema sputum

right-sided heart failure PATHO (2)

increase in RV afterload RV dilates or becomes hypertrophic

right-sided heart failure CAUSES (7)

1.LV heart failure 2. pulmonary hypertension (aortic/mitral stenosis) 3. cor pulmonale (chronic pulmonary disease) 4. tricuspid/pulmonic valve stenosis/regurgitation 5.RV infarction 6. cardiomyopathy 7. congenital heart diseases (TOF/VSD)

right-sided heart failure MANIFESTATIONS (

fatigue inc peripheral venous pressure ascites enlarged liver/spleen dependent edema weight gain anorexia/GI distress JVD secondary to chronic pulm. problem

left-sided heart failure PATHO (4)

impaired movement of blood from low pulmonary pressure to high arterial circulation = increased LV afterload = LV hypertrophy = LV ischemia

left-sided heart failure CAUSES (3)

HTN acute MI valve stenosis/regurgitation

left-sided heart failure MANIFESTATIONS (14)

dyspnea at night elevated pulmonary pressure restlessness confusion orthnopnea tachycardia exertional dyspnea fatigue cyanosis pulmonary congestion: cough crackles wheezes blood-tinged sputum tachypnea

cardiogenic shock PATHO (3 parts)

altered cardiac function d/t extensive damage to heart = decrease in SV = decrease in CO

cardiogenic shock CAUSES (4)

MI myocardial contusion sustained arrhythmias cardiac surgeries

what are the 3 stages of cardiogenic shock

compensatory (early/reversible) progressive (decompensated) refractory (irreversible)

CARDIOGENIC SHOCK: compensatory phase description: manifestations: (5)

D: body tries to compensate low CO by activated SNS and RAAS M: tachy cool clammy skin mild hypotension reduced urine output anxiety/restlessness

CARDIOGENIC SHOCK: progressive phase description: manifestations: (6)

D: compensaotry mechanisms fail = severe hypoperfusion = organ dysfunction M: severe hypotension weak, thread pulse pulmonary congestion (crackles, SOB) metabolic acidosis altered mental status oliguira

CARDIOGENIC SHOCK: refractory phase description: manifestations: (5)

D: prolonged hypoperfusion = multi-organ failure + severe acidosis = death M: profound hypotension (MAP <50) bradycardia and arrhythmias cyanosis, cold mottled skin anuria coma/death

what are the causes of cardiogenic shock?

myocardial damage (MI or contusion) sustained arrythmias acute valve damage, ventricular septal defect cardiac surgery

what are the 4 types of shock?

cardiogenic hypovolemic obstructive distributive

COMPENSATORY MECHANISMS FOR SHOCK: maintain cardiovascular function (2)

increased HR and contractility vasoconstriction, so the blood goes to vital organs

COMPENSATORY MECHANISMS FOR SHOCK: maintain blood volume (

hypothalamus release ADH = kidney keeps Na/H2O = dec urine output RAAS = aldosterone = keep H2O = dec urine output liver veins constrict = mobilization of stored blood

cardiac ischemia, failure, shock Flashcards

Discuss the causes and manifestations of coronary artery disease. Differentiate between coronary artery disease, stable angina, and the stages of acute coronary syndrome. Discuss causes and manifestations of heart failure. Discuss the phases and manifestations of cardiogenic shock.