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Pathophysiology > Cardiology Review (Exam 2) > Flashcards

Cardiology Review (Exam 2) Flashcards

1
Q

Describe the path of blood from the vena cava to the aorta

A

vena cava –> right atrium –> right ventricle –> lungs –> left atrium –> left ventricle –> aorta –> body

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2
Q

name the four chambers of the heart

A

left ventricle
left atrium
right ventricle
right atrium

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3
Q

where does the right side of the heart pump to? the left?

A

right - pulmonary circulation
left - systemic circulation

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4
Q

what are the physical differences between arteries and veins

A

arteries - thicker tunica media, smooth musculature due to high pressure, low volume
veins - more narrow, low pressure, high volume

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5
Q

describe the hierarchy of vasculature from the largest vessels down to the smallest

A

arteries/veins
arterioles/venules
capillaries

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6
Q

the definition of hypertension

A

any blood pressure >130/>80

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7
Q

what causes hypertension

A

genetics, sodium retention, diet, exercise amount, etc.
increase in peripheral resistance

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8
Q

what is the difference between systolic and diastolic blood pressure

A

systolic - heart contraction
diastolic - heart relaxation

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9
Q

what are the symptoms of hypertension

A

asymptomatic!!!

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10
Q

what are the consequences of untreated hypertension

A

organ failure - occurs after 20 years

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11
Q

which receptors are responsible for vasoconstriction

A

alpha1
beta 1 in heart and kidneys

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12
Q

which receptors are responsible for vasodilation

A

beta 2 - skeletal and smooth muscle

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13
Q

what two factors have a direct effect on blood pressure?

A

peripheral resistance and cardiac output

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14
Q

describe the RAAS system. how does it work to regulate blood pressure?

A

activates renin when pressure is low
activation of RAAS increases blood volume, which increases blood pressure

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15
Q

what other endogenous compounds can affect blood pressure?

A

prostacyclins (inflammatory mediators)
nitric oxide
naturetic peptides

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16
Q

What is ADH/Vasopressin and how does it affect blood pressure

A

anti diuretic hormone (part of RAAS)
inc water reabsorption –> increase in blood volume –> inc blood pressure

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17
Q

what are some factors that may contribute toward the Patho of hypertension?

A

sodium retention
over activation of RAAS
overactivation of SNS
vascular endothelial dysfunction

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18
Q

describe the actions of beta1, beta2, alpha1, and alpha2 receptors and where they are located

A

beta1 - vasoconstrictor, heart (inc contractility)
beta 2 - vasodilator, lungs
alpha 1 - vasoconstrictor, attires/veins
alpha2 - presynaptic neuron, stops flow of ACh

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19
Q

describe how lipids are processed and transported in the body

A

packaged into cholymicrons –> intestines to liver –> breakdown with lipoprotein lipase, makes VLDL –> VLDL leaves liver into blood stream –> drops nutrients in the body –> converts to IDL then LDL, LDL back to liver via LDL receptors

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20
Q

why are lipoproteins needed?

A

water is waterbased

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21
Q

Which lipoproteins contain Apo-B? Apo-A?

A

Apo-B: chylomicrons, VLDL, IDL, LDL
Apo-A: HDL

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22
Q

purpose of HDL

A

picks up excess cholesterol in the blood and brings it back to the liver

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23
Q

what is dyslipidemia

A

abnormal blood lipid levels caused by inflammation

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24
Q

what are the symptoms of dyslipidemia

A

asymptomatic

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25
Q

what are the consequences of artherosclerosis

A

compromising blood flow
nutrient exchange impaired
plaque development –> rupture of plaque

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26
Q

what is the largest driver in the development if dyslipidemia subsequent atherosclerosis

A

inflammation

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27
Q

how are LDL particles cleared from the blood?

A

HDL picks up and brings excess to the liver
LDL returned to the liver through LDL receptors

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28
Q

describe the steps in the development of atherosclerosis

A

inflammation event –> LDL attracted to site –> immune system triggers VLDL out of liver –> LDL and WBCs converge –> WBC killed and becomes foam cell –> generates plaque

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29
Q

what is hypertriglyceridemia and what causes it?

A

type of severe dyslipidemia
excessive triglycerides leads to CV damage
can be from diabetes

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30
Q

what are the consequences go hypertriglyceridemia

A

extreme elevations lead to acute pancreatitis
nausea, vomiting, persistent epigastric abdominal pain, fever, low bp, high levels of pancreatic enzymes, etc.

31
Q

what is peripheral artery disease? intermittent claudication?

A

plaques in the peripheral arteries (limbs)
pain in the extremities due to reduced oxygen supply; pain due to exercise at rest is fine

32
Q

what is ischemic heart disease? what are the symptoms?

A

plaques in the coronary arteries; can lead to MI
angina

33
Q

what is acute coronary syndrome? what are the three types?

A

sudden obstruction or rupture of plaques lead to thrombus formation in coronary arteries
types: unstable angina, NSTEMI, STEMI

34
Q

what are the symptoms of ACS

A

angina, sweating, dizziness, loss of consciousness, abnormal breathing

35
Q

what happens after ACS? What is cardiac remodeling

A

congestive heart failure/arrhythmia
scar tissue forms and heart can’t contract or relax like normal tissue

36
Q

what is heart failure?

A

reduction in cardiac output

37
Q

what causes heart failure?

A

some acute ischemic event to the heart
long standing HTN

38
Q

what are symptoms of heart failure?

A

tachycardia, peripheral edema, pulmonary edema, trouble breathing, cough, fatigue, etc.

39
Q

what is the difference between reduced ejection fraction and preserved ejection fraction heart failure

A

reduced - dilated ventricles, cardiac output decreased, thinner walls
preserved - stiffened myocardium, thicker walls, muscles can’t relax

40
Q
A
41
Q

what are the compensatory mechanisms involved in HF

A

activation of RAAS
activation of SNS
increase cardiac output

42
Q

what objective measure can be clinically followed to determine the status of a patients heart failure

A

weight

43
Q

what two factors have a direct effect on cardiac output

A

stroke volume and heart rate

44
Q

how does preload and after load affect stroke volume?

A

preload - increase preload, increase stroke volume
afterload - increase after load, decrease stoke volume

45
Q

how does fluid volume and vessel diameter affect preload?

A

fluid volume - inc volume, inc preload
diameter - larger, dec preload

46
Q

what is after load? how does vessel diameter effect it?

A

afterload - resistance the left ventricle overcomes to pump blood to the aorta
larger diameter, lowers pressure, dec afterload

47
Q

how does contractility affect stoke volume?

A

increase contractility, increase stroke volume

48
Q

what affect does activation of beta1 receptors have on contractility? M2 receptors?

A

beta1 - inc contractility
M2 - dec contractility

49
Q

how does preload affect contractility?

A

volume goes up, pressure should go up
increase preload, increase contractility

50
Q

how does cardiac remodeling affect heart failure?

A

scarring makes heart worse –> inc failure

51
Q

what is acute decompensated heart failure?

A

sudden worsening of heart failure

52
Q

how are ADHF patients categorized based on perfusion and volume?

A

perfusion - warm (stable) and cold (hypo perfusion)
volume - dry (stable, no fluid) and wet (fluid overload)

53
Q

what is an arrhythymia

A

irregular heart rhythm or rate

54
Q

what causes arrhythmias

A

energy drinks, drugs, damage to cardiac tissue, imbalance in electrolytes, etc.

55
Q

what are the symptoms of arrhythmia?

A

palpitations, chest discomfort, light headedness
depends on the type of arrhytmia

56
Q

what are the three most common ways to classify arrhythmias?

A

location, how they effect the heart and the type of conduction abnormality

57
Q

what are pacemaker cells? what is automaticity?

A

pacemaker cells - generate action potential
automaticity - don’t need input from the nervous system to create an action potential

58
Q

what are the two sets of pacemaker cells in the heart?

A

SA node
AV node

59
Q

How does the sympathetic and parasympathetic nervous system affect heart rate? what receptors are involved?

A

sympathetic - increases heart rate
parasympathetic - decreases heart rate
beta1 receptors

60
Q

depolarization at phase 0 occurs due to influx of

A

sodium

61
Q

phase 1 notch is due to efflux of

A

potassium

62
Q

phase 2 plateau is due to influx of ____ and eflux of ____

A

calcium
potassium

63
Q

phase 3 depolarization is due to

A

potassium efflux

64
Q

what does the P wave in the EKG represent? QRS wave? T wave?

A

P wave - atrial depolarization
QRS wave - ventricular depolarization
T wave - ventricular repolarization

65
Q

describe what heart block arrhythmia is

A

block does not allow full action potential
failure of normal propagation of action potentials from atrium to ventricle

66
Q

which arrhythmia are more common?

A

tachyarrythmia

67
Q

describe the normal pathway of action potential starting from SA node

A

SA node –> AV node –> down bundle branches

68
Q

what is an ectopic pacemaker?

A

cardiac cells gain automaticity and begins to spontaneously depolarize

69
Q

what is atrial fibrillation? what causes A fib?

A

atrium cannot effectively contract, can form thrombus
causes - ischemia, HTN, damage to myocardium

70
Q

what are the consequences of A fib?

A

stroke and heart failure

71
Q

what is ventricular fibrillation? what causes V fib

A

ectopic centers in ventricular area, can’t pump properly, most dangerous
causes - ectopic pacemakers

72
Q

what are the consequences of vfib

A

death

73
Q

what is shock

A

lack of blood flow leading to organ failure, impairment of cellular metabolism

74
Q

name and describe 3 types of shock

A

hypovolemic shock - low fluid volume from bleeding
cardiogenic shock - damage/dysfunction of the heart from MI
distributive shock - leaky blood vessels and excessive vasodilation (ex: septic shock)

Pathophysiology (15 decks)

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