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Pathophysiology > cardio > Flashcards

cardio Flashcards

1
Q

Left and right atria

A

Chambers that receive blood returning from your body through your veins

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2
Q

Left and right ventricles

A

Chambers where blood is pumped to your body through your arteries

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3
Q

Mitral valve

A

The mitral valve controls the flow of oxygen-rich blood from the left atrium to the left ventricle

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4
Q

Tricuspid valve

A

The tricuspid valve controls the flow of oxygen-poor blood from the right atrium to the right ventricle

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5
Q

Aortic valve

A

The aortic valve controls flow of oxygen-rich blood from the left ventricle to the body

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6
Q

Pulmonary valve

A

The pulmonary valve controls flow of oxygen-poor blood from the right ventricle to the lungs

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7
Q

heart wall

A
  • pericardium - outer layer of the heart.
  • parietal layer and visceral layer with space between
  • Myocardium - muscle layer in middle
  • endocardium - inner lining
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8
Q

heart chambers

A
  • right atrium - collects oxygen poor blood returning from your body
  • left atrium - chamber that collects oxygen rich blood returning from the lungs
  • right ventricle - pumps oxygen poor blood through pulmonary valve and into lungs
  • left ventricle - largest and strongest chamber of the heart. pumps o2 rich blood through aortic valve. extra myocardium muscle
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9
Q

heart valves

A
  • atrioventricular valves:
    1. tricuspid valve: The tricuspid valve controls the flow of oxygen-poor blood from the right atrium to the right ventricle
    2. mitral valve: The mitral valve controls the flow of oxygen-rich blood from the left atrium to the left ventricle
  • semilunar valves:
    1. pulmonic semiulnar valve: The pulmonary valve controls flow of oxygen-poor blood from the right ventricle to the lungs
    2. aortic semiulnar valve: The aortic valve controls flow of oxygen-rich blood from the left ventricle to the body
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10
Q

heart vessels

A
  • Superior/Inferior Vena Cava (SVC, IVC) = into rt atrium
  • Pulmonary Trunk to Pulmonary Arteries = out rt vent to lungs
  • Only deoxy arteries in body
  • Pulmonary Veins = into lt atrium
  • Only oxy veins in body
  • Aorta = out lt vent to all tissues of body
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11
Q

SinoAtrial Node

A
  • pacemaker of the body
  • starts the first contraction of the heart
  • keeps HR consistent and constant
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12
Q

AtriVentricular Node

A
  • sends impulse through ventricles to contract
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13
Q

Systole and Distole

A
  • Systole = contraction, Diastole = relaxation
  • We can say atrial systole occurs during ventricular diastole, and atrial diastole
    occurs during ventricular systole
  • when you just hear “systole” that refers to ventricular systole (ventricles are contracting while the atria are relaxed, atrial diastole)
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14
Q

Pulmonary vs. Systemic circulation

A

pulmonary - heart and lungs

  • recycles blood
  • takes up co2 and puts o2 into blood

systemic - heart and rest of body organs and tissues
- distribute o2 to tissues and organs and pick up CO2 and recycle it through pulmonary circulation

  1. brain picked up 02 from systemic blood and giving back co2
  2. blood travels through vena cava - to right atrium - through tricuspid valve - to rt ventricle - to semilunar valve - pulmonary after - lungs - gas exchange vis diffusion co2 into lungs and o2 into blood - blood leaves lungs with o2 - pulmonary vein - to lt atrium - bicuspid valve - lt ventricle - semilunar valve - aorta - to body tissues and organs - tissues pick up 02, give back co2
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15
Q

cardiac circulation

A

heart’s blood supply

  • myocardium - left main corononary (left descending and circumflex) and right main coronary after
  • intramyocardial arteries
  • perfusion to myocardium
  • changes in aortic pressure and compression of myocardial vessles during systole
  • during heart contractions it affects coronary blood supply
  • during systole - pressure on myocardial vessels and reduces myocardial blood flow
  • during stress cardiac arteries dilate. ischemia happens when these arteries cannot dilate
  • cardiac veins drain into cardiac sinus = collects deoxy blood from coronary heart circulation and sends back to rt atrium to get o2

Coronary arteries
§ Come off the aorta (=fresh O2!) either on the LEFT or RIGHT side of the Pulm. Trunk
§ Left Coronary Artery; branches into:
• Left Anterior Descending (LAD) or Anterior interventricular
o “Widow maker” because its blockage leads to sudden and deadly MI (heart attack)
• Circumflex Artery
§ Right Coronary Artery; branches into:
• Right Marginal
• Posterior Descending (PDA) or Posterior interventricular

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16
Q

conduction system

A

SA node - wall of atrium - AV node - atria contracts - atrioventricular bundle - right and left bundle branches - action potential goes to apex - ventricular walls - perking fibers - contraction in unison

  • SA node
  • AV node
  • Bundle of His
  • Right and left bundle branches
  • Perkinje fibers
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17
Q

EKG

A

Know how to draw and label!
o Measures ELECTRICITY of heart (not heartbeat!) o Pwave
- Atrial Depo o QRS Complex
- Vent. Depo and Atrial Repo (Atr. repo is hidden by big vent. depo) o Twave Vent. Repo
o Flat segment between P-Q = Atr. contraction o Flat segment between S-T = Vent. contraction

  1. rt atrium signal from SA node (pacemaker)
  2. signal spreads across both atria and tell muscle cells to depolarize and contract = atrial systole = p wave
  3. period of conduction between atrial systole and ventricle contraction = PR segment = AV node releases signal to ventricles
  4. enters bundle of his and spreads through bundle branches and perkinge fibers along ventricle walls = ventricle systole = contraction of ventricles = QRS = rapid ventricle depolarization
  5. signal passes out of ventricles, vertical walls relax and recover = ventricle diastole = ST period = ventricle depolarization
  6. T wave = ventricle depolarization
  7. QT period = depolarization and depolarization of ventricles
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18
Q

heart sounds

A

Heart sounds (“lub/dub”) = sounds made of the valves closing
o S1 –“lub”
- AV’s closing = vents. start to contract
o S2–“dub”
- Semi’s closing = vents. relax

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19
Q

Cardiac Innervation from Brain

A 
o Sympathetic nerves
- increase heart rate (norepi/epi)
-  increase blood pressure
o Parasympathetic nerves (Vagus nerve)
-  decrease heart rate (AcH)
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20
Q

Arteries

A

o Greatest velocity of blood

o Highest pressure

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21
Q

Arterioles

A

o Greatest resistance (due to push of narrower vessel walls on blood flow)
o Resistance leads to many pathos!

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22
Q

Capillaries

A

o Lowest resistance

o allows for fluid/gas/nutrient exchange with tissues

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23
Q

Venules

A

o drain out of caps

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24
Q

Veins

A

o Lowest pressure

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25
Q

Vessel Anatomy

A

o Lumen = open center of the tube o Tunica intima = endothelium
- smooth epithelial lining for good blood flow
- need to keep intact or PATHOs!
- veins have added valves made from this endothelium
• =prevents backflow and ensure 1-way flow back to heart
• aided with skeletal muscle contractions and respiration to move
deoxy blood back to heart
o Tunica media
- smooth muscle = vasoconstriction and vasodilation!
- arteries have thicker muscle and have added elastic layers due to high
pressure!
o Tunica externa = adventitia
- outer connective tissue of vessel

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26
Q

Blood Pressure (BP)

A

o = force of blood on vessel walls

o Resistance = blood vessel walls’ push back on blood

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27
Q

Measurement BP

A

o BP = CO x PR (cardiac output times peripheral resistance)
- CO = HR x SV (heart rate times stroke volume)
- Cardiac Output is the amount of blood pumped out of the heart per
minute – we multiply the heart rate (beats/min) times the stroke
volume (amt of blood pumped per beat (mL/beat))
- You will not have to actually calculate any of these
o Cardiac output is affected by the preload and afterload
- Preload – how much did ventricle fill = STRECTH
- Afterload – pressure needed to eject this blood out of heart
• Myocardial contractility = the heart muscles’ ability to contract
• more contractility = more force of contraction = increase BP

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28
Q

Control of BP

A

o nervous system measure with baro’s (pressure) and chemo’s (CO2) to modify
cardiac function and BP
o vasodilation/vasoconstriction of vessels

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29
Q

Factors that affect blood flow

A

o Velocity of blood = speed
o Laminar flow = from smooth, dilated vessels § =good straight flow
o Tubular flow = from constriction that causes turbulence in blood flow § =pushes against endothelium (=may cause damage)
o Vascular compliance = vessel’s ability to stretch

30
Q

Peripheral Artery Disease (PAD)

A
  • Obstruction (occlusion) or narrowing (stenosis) of peripheral vessels (not heart or brain)
  • Usually do to atherosclerosis (fatty plaque buildup)
31
Q

Coronary Artery Disease (CAD)

A
  • Occlusion and stenosis of coronary arteries
  • Most common cause is atherosclerosis
  • Myocardial Infarction (MI)
  • permanent myocardial muscle necrosis from ischemia
  • STEMI – S-T segment Elevation Myocardial Infarction (on EKG) = ischemia is happening NOW! = relieve blockage ASAP!
  • Non-STEMI – S-T segment is not elevated = past ischemia
  • Most common symptom of coronary ischemia is Angina = chest pain
  • Treatment for coronary blockage
  • Angioplasty
    ballooning to widen the lumen of occluded vessel = compresses plaque to wall
    can also place a stent to hold the vessel open longer term
  • Coronary Artery Bypass Graft (CABG) = bypass surgery
    connecting new blood supply to areas suffering ischemia
32
Q

Pericarditis

A
  • inflammation of pericardium
  • usually due to infection
  • constrictive = squeezes heart because of inflammation
  • pericardial effusion = increase/accumulation of pericardial fluid in sac
  • tamponade = pressure on heart due to excess fluid = limits heart function
33
Q

Cardiomyopathies

A
  • pathologies to the heart muscle

we’ll define in class =)

34
Q

Valve Dysfunctions

A
  • valve stenosis = opening is too narrow for good blood flow
  • valve regurgitation = not closing due to prolapse = swishy flow and backflow
    most common is mitral valve prolapse
  • rheumatic heart disease = autoimmune disease from previous strep throat infection that produces Abs that attack heart valves
35
Q

Dysrhythmias

A

-changes to heart rhythm

though you already know most, we’ll define these in class, too =)

36
Q

Heart Failure

A
  • heart is not effectively pumping blood out
  • *Left Heart Failure
  • not able to pump blood to systemic tissues
  • most often from systemic HTN = can’t force blood out = ventricular - hypertrophy/less volume for pumping
  • if left can’t force blood out to tissues, backs up blood in lungs = pulm HTN/pulm edema
  • *Right Heart Failure
  • not able to pump blood to lungs
  • mostly due to pulmonary HTN = can’t force blood out = hypertrophy/less volume
  • if right can’t force blood out to lungs, backs up blood in veins
  • (notice if left fails due to systemic HTN, and causes back up into lungs, this can then lead to right failure!!)
  • *High Output Failure = heart working fine, just not getting the “goods” from blood (O2, glucose, etc)
  • brain thinks heart is not working because tissues are starving and makes heart work harder = overwork/hypertrophy/failure
37
Q

Shock

A
  • response and loss of function in tissue cells after what comes from cardiovascular failure to get good O2 or glucose
  • We’ll again define in class =)
38
Q

vessel endothelium damage

A

1 cause of heart attack

39
Q

hormonal effects on BP

A
  1. ADH: stores and releases water to help maintain blood pressure
  2. Naturetic Hormones/ ANH: opposite of aldosterone. generates sodium loss. lowers BP , increases urine production
  3. RAAS: Renin –> aldosterone: aldosterone: increases BP and decreases urine production
40
Q

vessels of blood flow

A
  1. arteries: greatest pressure
  2. arterioles: greatest resistance. most pathologies
  3. capillaries: gas exchange. Lease resistance
  4. venules: small vessels
  5. Veins: larges. Lowest pressure.
41
Q

vascular anatomy

A
  • lumen - open part of vessel where blood flows
  • tunica intima (endothelium) - increase risk of cardio pathologies
  • tunica media - muscle. thicker in arteries
  • tunica externa (adventitia) - connective tissue
42
Q

factors affecting blood flow

A
  1. pressure: force exerted on a liquid per unit area
  2. resistence: opposition to force. diameter and length of the blood vessels contribute to resistance
  3. Velocity
  4. laminar vs. turbulent flow: turbulent = vasoconstriction = damaged endothelium
  5. vascular compliance - stretch
    * baroreceptors = pressure
    * chemoreceptors = co2
43
Q

equations

A

BP = Cardiac Ooutput X Peripheral Resistence

CO = Heart Rate X Stroke Volume = ml/min

  • PR = amount of force from vessel wall back onto blood (resistance_
  • CO = amount of blood pumpted out of heart in given time
44
Q

preload vs afterload

A
  • preload- left ventricle end- diastolic volume (how much blood can fit into ventricle pre-systole
  • afterload - pressure of contraction to send the blood around the body
  • hypertension = increased after load
45
Q

inotripic agents

A

increase heart rate

46
Q

varicose veins

A

vein in which blood has pooled

  • distened, tortuous, palpable veins
  • caused by trauma or gradual venous distention
  • vein valves malfunction
47
Q

chronic venous insufficiency

A

lack of venous blood flow to heart

  • inadequate venous return over a long period of time due to vericose veins or valvular incompetence
  • venous status ulcers: blood not moving, ulceration of tissue and necrosis
48
Q

deep venous thrombosis

A
  • clot in arms and legs
  • obstruction of venous flow leading to increased venous pressure
  • factors: venous stasis, venous endothelial damange, hyper coagulable states

VIRCHOW’S TRIAD:
circulator stasis - lack of blood flow
hyper coagulable state - too much clotting
endothelial injury - damage to endothelium, clots athrosclerosis

49
Q

Thrombus formation

A

blood clot that remains attached to the vessel wall

  • thromboembolus - dislodged and moving
  • thrombophlebitis - inflammation of vessel walls = increased clots
  • arterial thrombi - ischemic stroke. coronary artery and cerebral arteries. Athrosclerosis and clot
  • venous thrombi
  • *obstruction –> ischemia –> hypoxia –> necrosis –> MI**
50
Q

Embolism

A

traveling air, fat, plaque, blood clot, tumor, foreign matter traveling through circulation
- obstuction
-

51
Q

aneurysm

A

local instability of vessel wall - distention

  • arterial = increased pressure
  • arterioles = more at risk for aneurysm
  • fusiform cirumforential - on both sides
  • fusiform saccular - big bulge on one side
  • false - plaque grows on outside of vessel and damages it
  • dissecting saccular - breaks through endothelium but flows through outer layer instead. damage to endothelium wall
52
Q

Hypertension

A

most common causes = target organ diseases

  • heart - cardiac remodeling (hypertrophy)
  • brain - cerebrovascular disease
  • vasculature - peripheral vascular disease
  • kidneys - nephrosclerosis (volume exchange)
  • eyes - retinopathies
53
Q

primary vs secondary hypertension

A
  • primary: no other root cause. essential or idiopathic
  • genes, diet, exercise
  • secondary: systemic disease that raises peripheral vascular resistence
  • isolated systolic hypertension: elevations of systolic pressure are caused by increases in cardiac output
  • Complicated hypertension: endothelial damage
  • malignant hypertension: rapidly progressive hypertension. > 140 diastolic
54
Q

hypOtension

A
  • orthostatic/postural hypotension: not enough volume to pump
    *
55
Q

peripheral artery disease

A

atherosclerotic disease of the arteries

  • exclusive of coronary, aortic, and brain
  • hardening/thickening of arteries
56
Q

arteriosclerosis vs atherosclerosis

A
  • arteriosclerosis: thickening, hardening or artery. chronic disease of arterial system. scarring
  • thromboangitis obliterates: burger disease. –> inflammatory disease of peripheral arteries resulting in non-atherosclerotic lesions - hard vessels
  • young men smokers and drinkers
  • atherosclerosis: due to fatty plaque build up
  • occlusion of coronary blood vessels
  • thickening and hardening due to FATTY deposits
  • leading cause of CAD and MI
57
Q

atherosclerosis progresson

A
  1. endothelium inflammation/damage - smoking, virus, LDL leak, hypertension, displace
  2. LDL penetrate endothelium and oxidize –> perceived as foreign = immune attack
  3. monocyte activation –> macrophages into blood and ingests and accumulates LDL = FOAM Cell
  4. cell proliferates, chemotaxis of other macrophages = increased Foam cells
  5. fatty streak forms - aggrigation of foam cells
  6. lads down fibrous plaque around/on top fatty streak = plaque formation in artery
  7. tissues induce clot formation = complicated lesion (plaque and clot) = primary cause of MI
58
Q

complicated lesion

A

made of plaque and blood clot - primary cause of MI

59
Q

coronary artery disease

A

any vascular disorder that narrows or occludes the coronary arteries
- atherosclerosis is most common form
RISK FACTORS: dyslipidemia, hypertension, smoking, diabetes, obesity/sedentary, atherogenic diet

60
Q

myocardial ischemia vs. miocardial infarction

A

ischemia: local deprivation of coronary blood supply
infarction: prolonged ischemia causing irreversable damage and cell death

61
Q

acute coronary syndromes

A
  • stable angina
  • unstable angina
  • prinsmetal angina
  • silent ischemia
  • transient ischemia
  • sustained ischemia
  • myocardial inflammation and necrosis
62
Q

angioplasty

A

inserted balloon into artery to open it up

63
Q

disorders of the pericardium

A

The pericardium is a membrane, or sac, that surrounds your heart. It holds the heart in place and helps it work properly. Problems with the pericardium include:
* Pericarditis - an inflammation of the sac. It can be from a virus or other infection, a heart attack, heart surgery, other medical conditions, injuries, and certain medicines.
* Pericardial effusion - the buildup of fluid in the sac
Cardiac tamponade - a serious problem in which buildup of fluid in the sac causes problems with the function of the heart

64
Q

disorders of the myocardium

A

cardiomyopathies - disease of the heart muscle itself

  • dilated cardiomyopathy - In DCM a portion of the myocardium is dilated, often without any obvious cause. Left or right ventricular systolic pump function of the heart is impaired, leading to progressive cardiac enlargement and hypertrophy, a process called remodeling
  • hypertriphic cardiomyopathy - heart muscle grows
  • restrictive cardiomyopathy - does not relax normally during the time between heartbeats when the blood returns from the body (diastole).
65
Q

disorders of endocardium

A
  • valvular dysfunction
  • valvular stenosis: occurs when there is narrowing, stiffening, thickening, fusion or blockage of one or more valves of your heart.
  • valvular regurgitation: mitral valve doesn’t close tight enough and lets some blood escape
  • acute rheumatic heart disease: a chronic heart condition caused by rheumatic fever that can be prevented and controlled. Rheumatic fever is caused by a preceding group A streptococcal (strep) infection. Treating strep throat with antibiotics can prevent rheumatic fever. Moreover, regular antibiotics (usually monthly injections) can prevent patients with rheumatic fever from contracting further strep infections and causing progression of valve damage.
66
Q

dysrhythmias

A

disturbance of heart rhythm

  • tachycardia
  • flutter
  • bradycardia
  • premature ventricular contractions
  • premature atrial contractions
  • asystole
67
Q

heart failure

A

inadequate perfusion of tissues with blood

- cannot pump blood forward

68
Q

left heart failure

A
  • systolic heart failure: inability to produce adequate cardiac output to perfuse tissues
  • from damage or scarring from an MI
  • Diastolic heart failure: pulmonary congestion despite normal store volume and cardiac output
  • ventricles can’t fill with blood because they won’t relax or are too thick
69
Q

right heart failure

A

commonly caused by diffuse hypoxic pulmonary disease

- results in increase in left vent. filling pressure that is reflected back into the pulmonary circulation

70
Q

high output failure

A

inability of heart to supply the body with blood-borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility

71
Q

SHOCK

A

cardiovascuar system fails to perfuse the tissues adequately

  • impaired oxygen use
  • impaired glucose use

Pathophysiology (13 decks)

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