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Pathophys > Cardiovascular pt 1 > Flashcards

Cardiovascular pt 1 Flashcards

1
Q

Atria

A

receiving chambers

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2
Q

ventricles

A

discharging chambers

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3
Q

right and left side act as____

A

separate pumps

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4
Q

____side receives oxygen-poor blood from tissues

A

Right
via pulmonary circuit
-pumps blood to lungs to get rid of co2 and pick up o2

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5
Q

____side receives oxygenated blood from lungs

A

left
via systemic circuit
-pumps blood to body tissues

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6
Q

cardiac muscle cells

A

-striated, branched, and interconnected
-joined by intercalated discs

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7
Q

cardiac muscle cells depend on

A

aerobic respiration to make ATP

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8
Q

Coronary arteries

A

spread over surface, penetrate myocardium
-left CA and right CA branch from aorta
-squeezing of myocardium compresses CAs, blocks blood flow

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9
Q

inner most layer of myocardium is_____

A

last to receive oxygenated blood

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10
Q

most prone to damage during ischemia

A

inner most layer of myocardium

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11
Q

collateral circulation

A

-the heart has connections btwn branches, protects from ischemia

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12
Q

needed for muscle contraction in heart

A

electrical activity

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13
Q

electrical activity in the heart takes place in

A

SA- Sinoatrial node (rate of heart beat)

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14
Q

SA sends electric signal to

A

Right and Left atriums and to Atrioventricular node -AV –>subendocardial branches–> right and left ventricles

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15
Q

innervation of heart originates from

A

medulla oblongata

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16
Q

Sympathetic NS

A

Norepinephrine
-leades to incr in Ca2+ release in myocardial cells (accelerated contractions)
-incr ca2+ reuptake (accelerated relaxation)

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17
Q

Parasympathetic NS

A

Acetylcholine
-opens k+ channels
-hyperpolarizes cell, making it less likely to fire

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18
Q

cardiac output

A

=stroke volume x heart rate (mL/min)

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19
Q

Stroke volume =

A

preload, afterload, and contractility
amount leaving with each beat. mL/beat

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20
Q

preload

A

amount of stretch in a muscle tissue before contraction
-effected by end-dystolic volume and venous return

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21
Q

Afterload

A

force against muscle, needed to contacts
-effected by aortic pressure and aortic valvular fxn

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22
Q

Contractility

A

how hard is heart pumping
effected by sympathetic simulation and myocardial oxygen supply

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23
Q

Heart rate

A

beat/min
-CENTRAL NERVOUS SYSTEM, autonomic NS, neural reflexes, atrial receptors. hormones

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24
Q

Aorta–> capillaries

A

blood velocity decreases
-further away from heart, are increases, resistance increases.

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25
Q

Capillaries–> vena cava

A

velocity increases.
-resistance decreases, area decreases

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26
Q

blood pressure

A

force that blood exerts against the vessel wall

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27
Q

systolic pressure

A

peak arterial BP, ventricular systole (contraction)

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28
Q

diastolic pressure

A

minimum arterial BP, diastole (relaxation)

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29
Q

factors effecting blood pressure

A

-cardiac output (CO= HR X SV)
-resistance to flow
-blood volume (mainly regulated by kidneys and RAAS)
-vessel diameter

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30
Q

HTN =

A

Incr CO, incr PR

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31
Q

____detect blood pressure

A

baroreceptors

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32
Q

factors affecting vessel diameter (peripheral resistance)-vasoconstrictors

A

myogenic- stretch
metabolic- endothelins
neural symph tone
hormonal- epi, norepi, angitensis lll, antidiuretic

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33
Q

Intrinsic factors

A

distribute blood flow to organs and tissues as needed.
myogenic and metabolic

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34
Q

extrinsic factors

A

maintains MAP mean artial pressure and redistributes blood during exercise and thermoregulation
neural and hormonal

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35
Q

factors affecting vessel diameter (peripheral resistance)-vasodilators

A

metabolic-O, CO, H, K, prostaglandins, adenosine, nitric oxide
neural- symph tone
hormonal- atrial natriuretic peptide

36
Q

Evaluating CV fxn imaging to show structure

A

-chest radiograph- x-ray
CT
MRI

37
Q

Gives information about the conduction of the heart muscle and activity of pacemaker cells

A

Electrical activity

38
Q

Exercise stress test

A

Demonstrates how CV system responds to physical stress

39
Q

Indicators to evaluate CV fxn

A

Heart rate, cardiac output, cardiac index, stroke volume, oxygen consumption and mean arterial pressure

40
Q

Hypertension

A

Consistent elevated blood pressure over time

41
Q

Systolic

A

> = 140 mmhg

42
Q

Diastolic

A

> = 90mmHg

43
Q

Hypertension increases risk for

A

MI, Kidney dx, stroke, other vascular complications

44
Q

95% of cases are _____and 5% are ______

A

Primary (essential, idiopathic) secondary

45
Q

Secondary hypertension can be from

A

Obesity, drug-induced, hyperthyroidism, drug-induced, aldosteronism, crushing’s syndrome, renal hyper tension

46
Q

Hypertension risk factors

A

1.Family hx/ inherited defects: insulin sensitivity, RAAS, renal sodium excretion, insulin, symph NS activity
2. Lifestyle: high Na+, low Ca=, K+ or Mg+, smoking, heavy alcohol consumption
3. Metabolic syndrome; hypertension, dyslipdemia, glucose tolerance
4.Other conditions: obesity, dm, glucose intolerance

47
Q

“Silent killer”

A

Hypertension

48
Q

Effects of hypertension on the body

A

-damages multiple organs w/o outward symptoms
-results from incr vascular resistance

49
Q

RAAS

A

Renin-angiotensin-aldorestrone system

50
Q

Patho for HTN

A

-chronic incr in MAP (mean arterial pressure)
-Increased vascular tone (VSM constriction) = increased peripheral resistance
-inc blood volume

51
Q

activation of SNS temporarily increases______

A

BP and HR
-fight of flight
-maintains BP and tissue perfusion

52
Q

Prolonged activation promotes _______

A

Vascular remodeling
-insulin resistance, endothelial dysfunction
-procoagulant effects

53
Q

Prolonged activation may be due to:

A

-incr production of Epi and NE
-incr receptor reactivity to Epi and NE

54
Q

Role of RAAS

A

-Maintains BP, tissue perfusion
-Contributes to atherosclerosis, renal dx, cardiac hypertrophy

55
Q

Over activation of RAAS

A

-Salt and water retention
-incr in vascular resistance
- lots of angiotensin II (Ang II)

56
Q

Ang II

A

A potent vasoconstrictor

57
Q

High levels of Ang II lead to :

A

-Endothelial dysfunction
-athsclerotic plaque formation
-platelet aggregation
-risk of thrombus

58
Q

Vascular remodeling —>

A

Further promotes hypertension

59
Q

Natriuretic hormones

A

-Atrial natriuretic peptide (ANP)
-Brain natriuretic peptide (BNP)

60
Q

natriuretic peptides……

A

-modulate real Na2+ excertion by enhancing renal blood flow and GFR
-induced systemic vasodilation
-suppress aldosterone (of RAAS0
-Inhibit SNS
-require adequate Ca2+, Mg2+, K+ to fxn properly

61
Q

In HTN Increase serum levels of ANP and BNP

A

-heart failure
-atherosclerosis
-ventricular hypertrophy

62
Q

Contributors to hypertension

A

-inflammation -kidneys suffer damage —> initiates inflammatory response
-endothelial dysfunction- release of inflamm cytokines, decrease prod of vasodilators and incr vasoconstrictors
-obesity-linked to inflamm, vascular remodeling, endothelial dysfunction, insulin resistance. Changes in leptin
-DM/insulin resistance- insulin resistance even in pts w/o DM, decr vasodilator realest by ECs. Incr salt, water retention, activity of RAAS and SNS

63
Q

Complicated HTN

A

HTN that is sustained and causes organ damage

64
Q

Vascular remodeling

A

-VSM cells undergo hypertrophy, hyperplasia
-fibrosis in the vessel wall
-decr blood flow, causing damage to organs

65
Q

Heart

A

-LV hypertrophy—>bigger heart means more O2 demand, impaired contractility
-congestive heart failure
-coronary artery dx
-Myocardial infarction
-Aorta and other large vessels prone to aneurysms
-damage to vessel walls from high pressure can initiate clotting cascade (thrombus)

66
Q

Vascular beds cannot stand pressure. Capillaries ____and cause____

A

Rupture, ischemia

67
Q

HTN Treatments-lifestyle

A

-less sodium
-less saturated fat
-adjust caloric intake to reach optimal weight
-exercise that promotes endurance
-smoking cessation, reduced alcohol

68
Q

Pharmacological treatments

A

-Diuretics
-Beat-blockers
-ACE inhibitors

69
Q

Diuretics

A

-decrease blood volume by increasing urine production
-classes defined by site of action in nephron

70
Q

Beta-blockers

A

Slow HR, reduce workload of heart
Beta-adrenergic antagonists-block action of Epi and nE on the heart

71
Q

ACE inhibitors

A

ACE=angiotensin-converting enzyme) inhibitors
-prevent conversion of Ang I and Ang II

72
Q

Aneurysm

A

Dilation or outward ballooning of vessel wall or cardiac chamber

73
Q

Aneurysm characteristics

A

-thoracic or abdominal aorta- conduit arteries that endure high stress/pressure
-weak point in vessel or ventricular wall (necrotic muscle) becomes stretched by high pressure
-wall continues to weaken, becomes more fibrotic

74
Q

Aneurysm risk factors/causes

A

-arteriosclerosis and hypertension found in half of patients bc of vascular remodeling
-infection (syphilis)
-injury/truama to the chest
-genetic susceptibility

75
Q

Aneurysm treatment

A

-goal is to reduce blood volume and blood pressure to prevent rupture
-diuretics, beat-blockers
-surgery : stent placement for rapid, growing over 5 cm

76
Q

Aneurysms diagnosed with ____

A

Imaging, CT, MRI, etc

77
Q

Thrombus

A

Blood clot in a vessel; healthy response to injury intended to stop bleeding

78
Q

Embolus

A

Any thing that is circulating in the bloodstream

79
Q

Two threats if arterial thrombus

A

-Grows large enough to occlude vessel, cause ischemia and infract
-may dislodge and become thrombembolus

80
Q

thrombembolus

A

Clot that travels until it occludes a vessel

81
Q

Arterial thrombus/ embolism risk factors/causes

A

-inappropriate activation of the clotting cascade
-the heart

82
Q

Inappropriate activation of the clotting cascade bc of :

A

-endothelial damage
-inflammation
-infection
-traumatic injury
-obstructions that cause blood pooling
-may be bc of HTN, Atherosclerosis

83
Q

Most common cause of thromboembolus is___

A

The heart.
-valve dx of heart arrhythmias disturb blood flow
-cause formation of thrombus
-dislodged clot usually ends up in lower extremities
-may also go to coronary arteries or cerebral circulation

84
Q

Endothelium

A

NO and PGI2 maintain blood flow and inhibition platelet activity

85
Q

Platelets

A

-activation causes them to clump together, stopping bleeding

86
Q

Pharmacological treatments for arterial thrombus

A

-indirect clotting inhibitors (warfarin, heparin)
-direct thrombin inhibitors (hirudin)
-thromolytics-administered with clotting inhibitors

87
Q

Surgical treatments for arterial thrombus

A

-ballon-tipped catheter to remove or compress thrombus
-catheter may also directly deliver thrombolytic drug

Pathophys (11 decks)

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