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Patho Pharm > Cardio A/P > Flashcards

Cardio A/P Flashcards

1
Q

preload

A

amount of ventricular stretch

amount of volume in the ventricle at the end of
diastole

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2
Q

afterload

A

○ resistance against which the heart must pump to
circulate blood
○ increases cardiac workload

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3
Q

Heart wall layers

A

■ Pericardium- double walled heart sac
■ myocardium- muscle layer
■ endocardium- inner lining

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3
Q

myocardial contractility

A

heart rate: increased HR-> increased CO

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4
Q

Blood pressure regulation via

A

■ RAAS
■ Baroreceptors

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5
Q

difference between RAAS and Baroreceptors Blood pressure

A

The renin–angiotensin–aldosterone system (RAAS) is a critical regulator of blood volume and systemic vascular resistance on a long-term basis.

The baroreceptor reflex, on the other hand, responds in a short-term manner to decreased blood pressure. Arterial baroreceptors inform your autonomic nervous system of minor or rapid beat-to-beat changes in blood pressure.

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6
Q

What are the renin-angiotensin-aldosterone system (RAAS) steps?

A

When your blood pressure falls, your kidneys release the enzyme renin into your bloodstream.

Renin splits angiotensinogen, a protein your liver makes and releases, into pieces. One piece is the hormone angiotensin I.

Angiotensin I, which is inactive (doesn’t cause any effects), flows through your bloodstream and is split into pieces by angiotensin-converting enzyme (ACE) in your lungs and kidneys. One of those pieces is angiotensin II, an active hormone.

Angiotensin II causes the muscular walls of small arteries (arterioles) to constrict (narrow), which increases blood pressure. Angiotensin II also triggers your adrenal glands to release aldosterone and your pituitary gland to release antidiuretic hormone (ADH, or vasopressin).

Together, aldosterone and ADH cause your kidneys to retain sodium. Aldosterone also causes your kidneys to release (excrete) potassium through your urine.

The increase in sodium in your bloodstream causes water retention. This increases blood volume and blood pressure, thus completing the renin-angiotensin-aldosterone system.

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7
Q

How is the RAAS related to heart failure?

A

In particular, the RAAS releases more of the hormone angiotensin II to try to compensate for the lack of blood flow. This excess of angiotensin II subsequently makes heart failure worse. Scientists believe excess angiotensin II contributes to growth in the size of your heart.

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8
Q

How does the baroreceptor reflex work?

A

When there’s a change in your blood pressure, your artery walls respond accordingly. For example, with increased blood volume, your blood vessel walls stretch. In certain parts of your body, baroreceptors, which are special nerve endings, can “sense” artery wall stretch. This message goes to your brain, which interprets it as adequate blood pressure. In the absence of this stretch, your brain responds accordingly to raise your blood pressure.

If you stand up quickly, your baroreceptors sense a lack of stretching of the artery walls. This message goes to your brain, which interprets it as inadequate blood pressure. Your brain tells your blood vessels to tighten up in order to raise your blood pressure. This is just one way your body can control your blood pressure.

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9
Q

What triggers the baroreceptor reflex?

A

Any change in your body’s demand for blood can trigger your baroreceptor reflex. For example, your body may need to adjust your blood pressure when you:

Change your body position, such as when you stand.
See or experience something that frightens you.
Switch from walking to running

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10
Q

Common signs or symptoms of conditions associated with dysfunctional baroreceptor reflex

A

Unstable blood pressure.

Too much or too little blood reaching your organs.

Tachycardia.

Inability to raise heart rate appropriately.

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11
Q

Common treatments for the baroreceptor reflex

A

Midodrine.
Droxidopa.
Fludrocortisone.

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12
Q

Calculate Mean Arterial Pressure

A

MAP= SBP +2(DBP) all divided by 3

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13
Q

Define MAP

A

the average pressure in the circulation, based on length of cardiac
cycle

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14
Q

Define Primary (Essential) Hypertension

A

constant elevation of systemic arterial BP

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15
Q

Causes/pathophysiology of hypertension (primary)

A

● SNS hyperactivity
● Overactive RAAS
● Defect in natriuresis
● Insulin resistance
● Inflammation and endothelial dysfunction

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16
Q

Values for Normal BP

A

<120 and <80

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17
Q

Values for Pre

A

120-139

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18
Q

Values for stage 1 hypertension

A

140-
159

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19
Q

BP value that indicates Hypertensive Crisis

A

Diastolic BP >140 mmHg

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20
Q

Complicated HTN – multiorgan effects

A

stroke, acute encephalopathy, retinopathy, MI, general atherosclerosis, albuminuria, proteinuria, renal failure

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21
Q

Orthostatic Hypotension – criteria/how to assess

A

Decrease in systolic BP of at least 20 mmHg or diastolic BP of at
least 10 mmHg within 3 minutes of moving to standing position

■ 1. Have pt lie down for 5 mins
■ 2. Measure BP
■ 3. Have pt stand
■ 4. Repeat BP measurements after standing for 1 and 3 minutes

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22
Q

Varicose veins complications

A

○ Leads to venous hypertension, blood stasis, and
tissue hypoxia
○ Can lead to venous stasis ulcers which do not heal
because they do not get enough oxygenation

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23
Q

Thrombus:

A

blood clot attached to vessel wall

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24
Q

Embolus:

A

detached/moving thrombus

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25
Q

Embolism:

A

obstruction of a vessel by an embolus

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26
Q

Virchow’s triad:

A

factors that promote thrombus formation

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27
Q

Risk factors for – Virchow’s triad:

A

● Stasis of blood flow
○ Bed rest, immobilization
● Endothelial damage
○ Trauma, caustic intravenous medications
● Blood hypercoagulability
○ Inherited hypercoagulability, medications, pregnancy

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28
Q

Homan’s sign

A

Homan’s Sign (or Homans Sign) is a classic test for DVT (Deep Vein Thrombosis). The test is positive if the patient experiences (severe) calf pain when the ankle is passively dorsiflexed.

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29
Q

difference between true vs. false aneurisms

A

■ False: extravascular hematoma that communicated with the
intravascular space
■ True: involves all three layers of the arterial wall

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30
Q

Describe Fusiform/saccular aneurisms

A

Saccular looks like a skin tag on a vessel. ranges from 5-20cm in diameter. Often contains a thrombus.

Fusiform looks like a obese part of the vessel. “circumferential dilation of vessel”. Up to 20cm in diameter. Usually found in BIG arteries like to aorta, abdominal aorta, and iliac (inguinal) arteries

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31
Q

describe pulsatile hematoma

A

false aneurism that creates hematoma on the outside of the vessel wall. causes ventricular aneurisms and aortic dissections

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32
Q

Which aneurism has high rate of morbidity and less mortality

A

false

33
Q

atherosclerosis Pathophysiologic process, steps in depth

A

■ INJURY damage to endothelium
● LDL enters intima and is oxidized
● Oxidized LDL generates proinflammatory lipids that induce
adhesion molecules
● Monocytes convert to macrophages and are recruited ->
phagocytize oxidized LDL and transform to foam cells
(macrophages that eat up too many LDLs look like sea foam)
● Foam cells present oxidized LDL to T cells
● Cytokines are secreted that are proinflammatory and
procoagulant

■ Fatty streak: accumulation of foam cells
● More T cell recruitment
● More macrophages, inflammation, smooth muscle cell
proliferation, and damage

■ Fibrous plaque: development of fatty streak
● Smooth muscle cells proliferate and produce collagen and
migrate over fatty streak to create fibrous plaque
● Fibrous plaques calcify
● Lumen of vessel narrows
■ Complicated lesion: unstable plaques can rupture prior to occlusion
of vessel
● Rupture is caused by an immune response to endothelial
injury
● Rupture exposes underlying tissue, causes plaque adhesion,
initiating clotting cascade, and rapid thrombus formation
● Thrombus formation can occlude resulting in ischemia and
infarction

34
Q

atherosclerosis (4 steps)

A

injury, fatty streak, fibrous plaques, complicated lesion

35
Q

Stable vs. unstable plaque in atherosclerosis

A

■ Stable: thick fibrous cap
■ Unstable: thin cap, thick lipid pool, prone to rupture

36
Q

Head/neck assessment findings for atherosclerosis

A

■ Bruits heard in carotid artery
■ Xanthelasmas: small fat deposits around the eyelids
■ Arcus senilis: lipid ring around cornea

37
Q

define Cholesterol:

A

Lipoproteins that are regulated by the liver

38
Q

3 types of cholesterol

A

LDL, HDL, triglycerides

39
Q

Differentiate LDL

A

LDL (PROTEIN): deliver cholesterol to tissue (increase plaque formation)
○ key in atherosclerosis and endothelial damage
○ high levels associated with CAD

40
Q

Differentiate HDL

A

HDL: reverse cholesterol transport (from tissue to liver)
○ endothelial repair
○ low levels associated with CAD, carries mostly good
proteins

41
Q

Differentiate triglycerides

A

fat other than cholesterol

42
Q

Identify optimal levels LDL

A

LDL <100

43
Q

Identify optimal levels HDL

A

HDL >60

44
Q

Identify optimal levels TRIGLYCERIDES

A

Triglyceride <150 is desirable, 150-199 is borderline, 200-499
is high

45
Q

Identify optimal levels TOTAL CHOLESTEROL

A

Total cholesterol <200 desirable, 200-239 is borderline, >240
is high

46
Q

atherosclerosis is the primary risk factor for

A

coronary artery disease,
myocardial ischemia, and acute coronary syndromes

47
Q

Intermittent claudication:

A

pain with ambulation D/T PAD and/or hypertension

48
Q

Define Coronary Artery Disease:

A

a continuum of diseases from atherosclerosis to
myocardial ischemia to myocardial infarction

49
Q

Pathophysiology of Angina

A

build-up of lactic acid, stretch causes irritation to
myocardial nerve fibers

50
Q

Define Angina pectoris

A

Angina pectoris is chest pain or discomfort secondary to myocardial
ischemia - heaviness, pressure or pain may radiate to back,

51
Q

Angina pectoris physical assessment findings:

A

● may have normal physical
● heart assessment: tachycardia, gallops/murmurs, carotid
artery bruits, ECG changes (T wave inversion, ST segment
depression)
● head/neck: xanthelasmas, arcus senilis

52
Q

Describe RAAS

A

body thinks it doesn’t have enough fluid. Juxtaglomerular cells in kidneys release renin into circulation. Renin goes to liver which activates angiotensinogen which turns into angiotensin 1. Then angiotensin converting enzyme (ACE) turns angiotensin 1 into angiotensin 2. Angiotensin affects the vasculature, adrenal cortex, and posterior pituitary gland to increase BP.

53
Q

What does angiotensin 2 do to the body

A

narrows blood vessels, constricting blood flow to kidneys which limits organ’s ability to secrete water

it makes the adrenal cortex release aldosterone which tells kidneys to keep water and sodium in the blood (decreases urination)

causes posterior pituitary gland to release ADH (antidiretic hormone) which causes kidneys to hold onto water and enacts thirst

54
Q

3 types of NATRIURETIC
HORMONES?

A

Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide (BNP), C-Type Natriuretic Peptide (CNP)

55
Q

functions of NATRIURETIC
HORMONES?

A

vasodilation, naturiesis, decreased renin

56
Q

Brain Natriuretic Peptide (BNP)

A

ventricle is stretched

57
Q

Dx tests for angina

A

● Stress test
● coronary arteriography
● noninvasive: CT, MRI, ultrasound
● single photon emission computerized tomography

58
Q

types of angina

A

stable, unstable, silent, prinzmetal or variant:

59
Q

describe stable angina

A

caused by gradual luminal narrowing and hardening
○ recurrent, predictable chest pain
○ cannot vasodilate with increased myocardial demand
○ transient 3-5 mins
○ usually relieved by nitroglycerin or rest

60
Q

describe prinzmetal or variant angina

A

caused by coronary vasospasm,
decreased vagal cavity, decreased NO, hyperactive SNS
○ unpredictable
○ almost always occur during rest, at night during REM

61
Q

describe silent angina

A

mental stress induced ischemia
○ asymptomatic, may be a problem with LV afferent
sympathetic nerve innervation
○ DM is the most common cause

62
Q

describe unstable angina

A

a form of acute coronary syndrome
○ occurs randomly or unpredictably and is unrelated to
any obvious trigger
○ considered a medical emergency - escalates rapidly,
signals that plaques are complicated and MI is
pending
○ reversible myocardial ischemia that results from a
sudden obstruction of a coronary

63
Q

the damage from a Myocardial Infarction becomes irreversible after how many minutes

A

20

64
Q

two most common causes of an MI

A

● Decreased blood supply - increased demand
● Unstable angina

65
Q

Pathophysiology of ischemia

A

● begins 8-10 seconds after decreased blood flow
● aerobic to anaerobic metabolism
● glycogen decreases
● hydrogen ions, lactic acid increase (ACIDOSIS)

● loss of intracellular ions (K, Mg, Ca)
● release of catecholamines
● inflammatory cascade at injury
● angiotensin II release
○ vasoconstriction/fluid retention
○ growth factor for cardiac smooth
muscle/fibroblast/myocyte = remodeling

66
Q

what intracellular ions do cardiac cells need to function

A

(K, Mg, Ca)

67
Q

What would Increase in biomarkers: Troponin I, CK-MB indicate

A

MI

68
Q

What would ST segment elevation indicate

A

MI

69
Q

symptoms of MI

A

chest pain, HTN, diaphoresis, N/V, pale, cyanotic

70
Q

Arteriosclerosis vs. Atherosclerosis

A
  • Arteriosclerosis:
    – thickening and hardening of the vessel wall.
  • Atherosclerosis:
    – Form of arteriosclerosis that is caused by the
    accumulation of lipid-laden macrophages within
    the arterial wall, which leads to lesions called
    plaques.
    – Leading cause of:
  • coronary artery disease
  • cerebrovascular disease
71
Q

4 steps to Atherosclerosis disease progression

A

1.INJURY – DAMAGED ENDOTHELIUM
2.FATTY STREAK
3.FIBROUS PLAQUE
4.COMPLICATED LESION

72
Q

Describe a STEMI

A

○ ST segment elevation MI
○ Greater damage, change in ECG seen at this point (ST
Elevation)
○ Complete obstruction has probably occurred
○ Biomarkers also elevated
○ Transmural – infarction through the wall
○ HIGHEST RISK FOR HEART FAILURE AND
COMPLICATION

73
Q

men vs women symptoms of MI

A

women often have unique presentations of MI with additional symptoms such as palpitations, jaw or neck pain, shortness of breath, fatigue, or epigastric symptoms including indigestion.

men, such as chest pain described as pain, pressure, tightness, or discomfort

74
Q

ECG changes with: Ischemia

A

T wave inversion, ST wave segment depression

75
Q

ECG changes with: Injury

A

ST segment elevation, increased biomarkers Troponin I and
CK-MB

76
Q

ECG changes with: Infarction

A

deep Q waves after 24 hours

77
Q

how to calculate bp

A

cardiac output x systemic vascular resistance = blood pressure

78
Q

how to calculate cardiac output

A

heart rate plus stroke volume

79
Q

how to calculate hypertension

A

volume x vasoconstriction

Patho Pharm (15 decks)

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