Cardiovascular (Heart) Flashcards
(25 cards)
Cardiovascular Diseases
Coronary Artery disease:
•Myocardial Ischemia: O2 content cannot meet metabolic demands of myocardium
•Acute coronary syndromes: plaque blockage, coronary spasm causing sudden reduced blood flow to heart
Angina
Myocardial infarct
Heart failure: left and right HF
Shock: hypovolemia, cardiogenic, neurogenic, septic, anaphylactic
Congenital heart defects
4 Main Coronary Arteries
•Right coronary artery
•Left main coronary artery (widow maker)
•Left anterior descending (widow maker)
•Left circumflex artery
Blockage of these arteries is common cause of angina, heart disease, heart attacks and heart failure
Cardiac Output Formula
HR (beats/min) x Stroke Volume (ml/beat) = CO
Stroke Volume
volume of blood pumped out by left ventricle during systole
60-100 mL/beat
Normal Cardiac Output
Normal stroke = 60-100 ml/min
Normal HR = 70 BPM
Cardiac output = HR x Stroke
70 x 60 ml = 4200
70 x 100 ml = 7000
Normal cardiac output = 4.2 - 7 L/min
Ejection Fraction
Volume pumped out of left ventricle divided by volume in the left ventricle at end of diastole
Stroke volume / End diastolic volume
Normal: 75 ml/120ml = 62%
Frank-Starling Law
States that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to myocyte stretch causing a more forceful systolic contraction
Heart Failure
Decreased contractility. Decreased ability for muscle to snap back
Preload
Stretching of cardiac muscle at end of diastole, right before contraction
Decreased preload = decreased stretch = decreased contractility = decreased cardiac output
Afterload
The pressure the heart works against to eject blood during systole (ventricular contraction)
High afterload = decreased CO
High afterload is caused by a high pressure in arteries
Stable angina
Chronic coronary obstruction
Gradual narrowing
Activated by physical exertion or stress
Symptoms: Pressure, heaviness, radiate to left neck or jaw, arm, shoulder. Pallor, diaphoresis, dyspnea.
Causes:
Stable plaques
Uncontrolled diabetes
Hypertension
Increased LDLs
Decreased HDLs
Sedentary lifestyle
High BMI
Genes
Prinzmetal angina
Not from blockage, but rather from spasms.
Unstable, unpredictable, can occur at rest.
With or without atherosclerosis .
Occurs at night.
Hyperactivity of SNS
Can cause dysrhythmias
Treated with longterm meds
Silent Ischemia
Mental stress induced ischemia
Asymptomatic. Doesn’t present as typical ischemia.
If symptomatic: fatigue, dyspnea, feeling of unease
Can occur on their own or when individuals have angina
Increased risk for cardiac event
Causes: Diabetes mellitus, cardiac transplant, previous MI (nerve injury), Mental stress
Angina causes
Vessel spasm
Atherosclerosis: Stable plaques
Atherosclerosis: Unstable complicated plaques
Hypotension
Anemia
Hypoxemia
Increased O2 demand
Unstable Plaques
Unstable plaques can rupture and lift off the artery wall, leading to an acute event such as heart attack, stroke or death. Unstable plaques are potentially more dangerous than stable plaques because of their propensity to rupture and cause complete obstruction to blood flow.
considerations for female patients
Atypical symptoms of MI and angina: palpitations, anxiety, weakness, fatigue
42% of women do not have chest pain. Women present with more fatigue and right sided chest pain.
Heart disease and stroke leading cause of death in women
Microvascular changes
Acute Coronary Syndrome
refers to a group of conditions that include ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina.
Stable vs Unstable Angina
Stable: Increased O2 demand in setting of a stable atherosclerotic plaque. Vessel unable to dilate enough to allow proper blood flow
Unstable: Plaque ruptures and thrombus forms around the ruptured plaque, causing partial occlusion of the vessel. Angina pain at rest or progresses rapidly over short period
NSTEMI
Plaque ruptures and thrombus causes partial occlusion. Damage limited to myocardium below endocardium.
ST wave depression, T wave inversion
STEMI
Complete occlusion of blood vessel. Damage extends frim endocardium to epicardium
ST elevation
How long can cardiac cells withstand ischemic conditions
20 minutes
Myocardial stunning
Temporary loss of contractile function persists hours to days after perfusion is restored
Hibernating myocardium
Tissue persistently ischemic and undergoes metabolic adaptation to prolong myocyte survival until perfusion can be restored
Valve dysfunction: Stenosis
Valve opening becomes narrow, doesn’t open all the way. blood has hard time getting through
“Doorway isn’t all the way open so it is hard to get blood past”
Aortic stenosis most common (valve between left ventricle and aorta)
Mitral stenosis also common (valve between left atria and left ventricle)
