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25 Cards in this Set

  • Front
  • Back
Flow of Blood in the Heart
*Inferior Vena Cava → Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Valve → Pulmonary Arteries to Lungs → Blood is then oxygenated and sent to the Pulmonary Veins → Left Atrium → Mitral Valve → Left Ventricle → Aortic Valve → Aorta → Oxygenated blood is sent throughout the body
Coronary Circulation
*Coronary arteries ensure that enough blood goes to the heart
*A patient who has a clog, due to arteriosclerosis, it is known as Coronary Artery Disease (CAD)
*More CAD, the more risk for an M.I.
Cardiac Conduction
* SA Node sends a signal → Causes R and L Atrium to contract and push blood into the lower ventricles → AV node receives the signal and sends it to → AV Bundles and is sent into the Left and Right Bundles Branches around the ventricles → Purkinje Fibers send signals to ventricular walls → Causes contraction of ventricles and blood to be pushed to the lungs and body.
Atrial Fibrillation
*Most common cardiac arrhythmia
*SA nodes signals rapid atrial contraction, which does not allow the atria enough time to completely contract.
*This causes blood to pool in the atria, leading to clots, and if they are released can cause a CVA
*Causes an irregular heart rate, increased risk for stroke
Atrial Fibrillation Continued...
*Increased risk with age, hypertension, hyperthyroidism and some cancers
*Symptoms: Asymptomatic, though some have palpitations, edema, activity intolerance or dsypnea
*Treatment: Control heart rate, under 100, using medications. Or to give coumadin, blood thinner, to prevent clotting ( Dangerous if patient falls, they can bleed out, so High Risk for Falls after A Fib)
Relationship of EKG to Cardiac Cycle
*P Wave: Atrial Depolarization
*QRS Wave: Ventricular Depolarization and Atrial Repolarization
*T Wave: Ventricular Repolarization
Cardiac Output
*Cardiac Out: Amount of blood being pumped by the heart over 1 min. *Affected by 2 Things:
1. HR: # of times the heart contracts over 1 min
2. Stroke Volume: Amount of blood pushed out of the L ventricle during Systole
*Normal Cardiac Output :5 liters/min
*Ejection Fraction:Amount of blood in the left ventricle after contraction. Usually 60-75%. AKA end of diastolic volume
3 Things Affect Stroke Volume:

1. Preload
* Volume and pressure generated in the ventricle at the end of diastole
*Affected by 2 things
a. Amount of venous return to the ventricle
b. Blood left in the ventricles after systole
3 Things Affect Stroke Volume:

2. Afterload
*Resistance or impedance to ejection of blood from the Left Ventricle
*Decreased after load enables the heart to contract more rapidly
*Increased afterload slows the contraction and causes higher workloads to eject the blood
*Can be effected by aortic valve dysfunction
*Hypertension is the major cause of increased afterload
3 Things Affect Stroke Volume:

3. Contractillity
*Amount the heart contracts to push blood out of the Left Ventricle during systole
*Effected by many diseases and conditions:
a. M.I.: Causes tissue scarring and death of cardiac tissue
b. L Vent Hypertrophy: L Vent is enlarged and thickened, due to M.I. or increased afterload
*Can be increased by athletes who work out hard
*Thicking and hardening of the artery walls caused by accumulation of lipid-laden macrophaces in the arterial wall
*Plaque development
*It is the leading cause of CAD and CVA
*Pathology is chronic inflammation and irritation of the lining of BV
Atherosclerosis Continued...
*Atherosclerosis develops as we age, but it can be maintained at a non harmful level in the body through diet and exercise
*Genetics plays a role
*This disease can also increase risk of DB, HTN, renal failure, high cholesterol or triglycerides
3 Lesions Associated with Atherosclerosis:

1. Fatty Streaks
*Thin, flat, yellow areas of fat that progressively enlarge and become thicker
*Made up of machrophages and smooth muscles that have become distended with lipids
*Develops within the 1 yr of life
3 Lesions Associated with Atherosclerosis:

2. Fibrous Plaque
*Accumulation of intracellular and extracellular lipids, mainly cholesterol, proliferation of vascular smooth muscle cells and formation of scar tissue with calcifies.
*As plaque increases in size it causes significant narrowing and even occlusion of vessels
*Can also cause thrombus formation
3 Lesions Associated with Atherosclerosis:

3. Complicated Lesion
*Contains hemorrage, ulceration and scar tissue deposits
*Thrombosis often occurs from these types of lesions
Vulnerable Plaque
*Large lipid core and thin fibrous cap
*Can open up and allow the lipid core, which contains collagen and other materials, to be released, creating a blood clot
*3 Things can occur after this happens:
1. Clot dissolves and no harm is done
2. Clot causes partial blockage that over time is cleared or solidified within the vessel becoming permanent and restricting blood flow. If in coronary artery, it leads to Stable Agina, where a patient experiences chest pain when exerting themselves
3. Clot can move to a smaller coronary artery and caused Unstable Agina, where the patient experience chest pain at rest. If not relieved after a nitroglycerin or removed with PCI, it can lead to M.I.
Risk Factors of Atherosclerosis
*Age, family history, diabetes, smoking, hypertension, cholesterol, sedentary lifestyle, obesity, peripheral vascular disease, stroke, heart failure, sudden cardiac death, M.I., stable and unstable angina and gender
Primary Hypertension (HTN)
* No medical cause, genetic and environmental factors
*Affects 92-95% of people with hypertension
a. Normal: 120/80
b. Pre Hypertension: 121-139/81-89
c. Stage I: 140-159/90-99
d. Stage II: >160/>100
*Patients are staged by the higher BP... 120/90 is stage I bc of the 90, even tho the 120 is normal
Causes of Primary HTN:

1. Sympathetic Nervous System
*Smooth muscle of the BV contract and dilates based on what the SNS tells it to do
*Sometimes it tells the BV to constrict too much, causing BP to go up
*SNS controls BP
Causes of Primary HTN:

2. Netriuertic Hormones
*Tells BV to constrict, so their overproduction can lead HTN
Causes of Primary HTN:

3. Antidiueretic Hormones
*ADH, also known as vasopressin, is released by the posterior pituitary gland and causes water to be reabsorbed in the kidney, causing an increased in BP
*Also causes increased peripheral vascular resistance by signaling constriction to occur in the SNS
Causes of Primary HTN:

4. Inflammation
*Causes vasodilation, but can also signal for salt and water to be retained causing an increased BP
Causes of Primary HTN:

5. Renin
*Renin is secreted whenever a drop in BP or NaCl occurs in the kidneys
*When renin is released it causes angiotensionogen, which is an inactive enzyme created by the liver, to cleave to Angiotensin I.
*Angiostension I is then converted into Angiotension II by Angiotension Converting Enzyme (ACE), and becomes activated.
*Angiotension II signals 2 process which cause an increased in BP
Two Processes Signaled by Angiotension II that Cause an Increased BP
*1.Signals SNS to release vasopressin (ADH), causing vasoconstriction and thus an increased BP
*2. Signals the renal cortex to release aldesterone, which then works on the kidney to retain sodium. When sodium is retained, water is also retained, and thus a higher BP
ACE Inhibitors and ARB's
*ACE Inhibitors: Work by preventing Angiotension I from converting to Angiotension II thus preventing the release of aldesterone and vasoconstriction
*ARB's: Angiontension Receptor Blockers, work by blocking Angiotension receptors in the SNS and the adrenal glands, preventing the release of aldostrone and vasopressin (ADH)