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Pathophysiology > Cardiology Review (Exam 2) > Flashcards

Cardiology Review (Exam 2) Flashcards

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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
what are the consequences of artherosclerosis
compromising blood flow nutrient exchange impaired plaque development --> rupture of plaque
26
what is the largest driver in the development if dyslipidemia subsequent atherosclerosis
inflammation
27
how are LDL particles cleared from the blood?
HDL picks up and brings excess to the liver LDL returned to the liver through LDL receptors
28
describe the steps in the development of atherosclerosis
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
29
what is hypertriglyceridemia and what causes it?
type of severe dyslipidemia excessive triglycerides leads to CV damage can be from diabetes
30
what are the consequences go hypertriglyceridemia
extreme elevations lead to acute pancreatitis nausea, vomiting, persistent epigastric abdominal pain, fever, low bp, high levels of pancreatic enzymes, etc.
31
what is peripheral artery disease? intermittent claudication?
plaques in the peripheral arteries (limbs) pain in the extremities due to reduced oxygen supply; pain due to exercise at rest is fine
32
what is ischemic heart disease? what are the symptoms?
plaques in the coronary arteries; can lead to MI angina
33
what is acute coronary syndrome? what are the three types?
sudden obstruction or rupture of plaques lead to thrombus formation in coronary arteries types: unstable angina, NSTEMI, STEMI
34
what are the symptoms of ACS
angina, sweating, dizziness, loss of consciousness, abnormal breathing
35
what happens after ACS? What is cardiac remodeling
congestive heart failure/arrhythmia scar tissue forms and heart can't contract or relax like normal tissue
36
what is heart failure?
reduction in cardiac output
37
what causes heart failure?
some acute ischemic event to the heart long standing HTN
38
what are symptoms of heart failure?
tachycardia, peripheral edema, pulmonary edema, trouble breathing, cough, fatigue, etc.
39
what is the difference between reduced ejection fraction and preserved ejection fraction heart failure
reduced - dilated ventricles, cardiac output decreased, thinner walls preserved - stiffened myocardium, thicker walls, muscles can't relax
40
41
what are the compensatory mechanisms involved in HF
activation of RAAS activation of SNS increase cardiac output
42
what objective measure can be clinically followed to determine the status of a patients heart failure
weight
43
what two factors have a direct effect on cardiac output
stroke volume and heart rate
44
how does preload and after load affect stroke volume?
preload - increase preload, increase stroke volume afterload - increase after load, decrease stoke volume
45
how does fluid volume and vessel diameter affect preload?
fluid volume - inc volume, inc preload diameter - larger, dec preload
46
what is after load? how does vessel diameter effect it?
afterload - resistance the left ventricle overcomes to pump blood to the aorta larger diameter, lowers pressure, dec afterload
47
how does contractility affect stoke volume?
increase contractility, increase stroke volume
48
what affect does activation of beta1 receptors have on contractility? M2 receptors?
beta1 - inc contractility M2 - dec contractility
49
how does preload affect contractility?
volume goes up, pressure should go up increase preload, increase contractility
50
how does cardiac remodeling affect heart failure?
scarring makes heart worse --> inc failure
51
what is acute decompensated heart failure?
sudden worsening of heart failure
52
how are ADHF patients categorized based on perfusion and volume?
perfusion - warm (stable) and cold (hypo perfusion) volume - dry (stable, no fluid) and wet (fluid overload)
53
what is an arrhythymia
irregular heart rhythm or rate
54
what causes arrhythmias
energy drinks, drugs, damage to cardiac tissue, imbalance in electrolytes, etc.
55
what are the symptoms of arrhythmia?
palpitations, chest discomfort, light headedness depends on the type of arrhytmia
56
what are the three most common ways to classify arrhythmias?
location, how they effect the heart and the type of conduction abnormality
57
what are pacemaker cells? what is automaticity?
pacemaker cells - generate action potential automaticity - don't need input from the nervous system to create an action potential
58
what are the two sets of pacemaker cells in the heart?
SA node AV node
59
How does the sympathetic and parasympathetic nervous system affect heart rate? what receptors are involved?
sympathetic - increases heart rate parasympathetic - decreases heart rate beta1 receptors
60
depolarization at phase 0 occurs due to influx of
sodium
61
phase 1 notch is due to efflux of
potassium
62
phase 2 plateau is due to influx of ____ and eflux of ____
calcium potassium
63
phase 3 depolarization is due to
potassium efflux
64
what does the P wave in the EKG represent? QRS wave? T wave?
P wave - atrial depolarization QRS wave - ventricular depolarization T wave - ventricular repolarization
65
describe what heart block arrhythmia is
block does not allow full action potential failure of normal propagation of action potentials from atrium to ventricle
66
which arrhythmia are more common?
tachyarrythmia
67
describe the normal pathway of action potential starting from SA node
SA node --> AV node --> down bundle branches
68
what is an ectopic pacemaker?
cardiac cells gain automaticity and begins to spontaneously depolarize
69
what is atrial fibrillation? what causes A fib?
atrium cannot effectively contract, can form thrombus causes - ischemia, HTN, damage to myocardium
70
what are the consequences of A fib?
stroke and heart failure
71
what is ventricular fibrillation? what causes V fib
ectopic centers in ventricular area, can't pump properly, most dangerous causes - ectopic pacemakers
72
what are the consequences of vfib
death
73
what is shock
lack of blood flow leading to organ failure, impairment of cellular metabolism
74
name and describe 3 types of shock
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 (18 decks)

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