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Patho/Pharm 2 > Cardio Patho > Flashcards

Cardio Patho Flashcards

1
Q

what is CO

A

volume of blood ejected from the ventricles in one minute

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2
Q

how is CO calculated

A

HR x SV

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3
Q

what impacts HR

A

SNS (epi & NE) & PSNS

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4
Q

what affects SV

A

preload, afterload (PVR), contractility

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5
Q

what is contractility

A

the ability of cardiac muscle to generate force of contraction during systole and push blood out of the ventricle against systemic vascular resistance (BP)

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6
Q

what affects preload

A

venous blood return & the amount of blood left in the ventricle after systole (end systolic volume)

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7
Q

what affects afterload

A

aortic pressure (aortic stenosis) and peripheral resistance (HTN)

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8
Q

what is the Frank-Starling law of the heart

A

normally, when the ventricle is stretched due to increased preload, the myocardium tension increases which leads to more contractility/force of contraction during next systole, leading to increased SV & CO

in HF, chronically increased preload leads to dysfunction, where actin/myosin fibres become disengaged due to overstretching, leading to no increased tension from increased preload and decreased CO

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9
Q

what is the RAAS

A

in response to decreased CO (hypoperfusion) or SNS activation (from CNS baroreceptors), renin is released from kidney, which converts angiotensinogen from liver into angiotensin I

ACE from the lungs then converts A1 into A2

A2 causes vasocontriction, which leads to elevated BP & decreased GFR, as well as stimulating release of ADH & aldosterone

aldosterone & ADH lead to Na & water retention, which also increases BP (afterload) and preload

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10
Q

what happens as a result of RAAS in HF

A

chronic SNS activation leads to cycle of decreasing contractility, increased preload & afterload due to Na & water retention, and worsening left HF

this causes pulmonary edema, hypertrophy, and cardiac apoptosis/necrosis

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11
Q

what is NPS

A

natriuretic pepetides:

Atrial NPS - released from atrial stretch
BNP - released from ventricles when stretched

act as antagonist to RAAS and decrease preload & afterload through vasodilation (not enough to compensate for effects of HF)

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12
Q

what is HFpEF

A

heart failure with preserved ejection fraction (LVEF>50%)

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13
Q

what is HFmEF

A

heart failure with mid-range ejection fraction (LVEF41-49%)

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14
Q

what is HFrEF

A

heart failure with reduced ejection fraction (LVEF<40%)

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15
Q

what are the four main etiologies of HFrEF

A
  1. ischemic (CAD)
  2. Rheumatic valvular diesase (from strep)
  3. HT heart disease
  4. COPD
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16
Q

what are some main risk factors for HF

A

male, age, CAD w/ hx MI, HTN, valvular heart disease, smoking/substance misuse, obesity, DM, genetics, chemo/radiation

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17
Q

what are some symptoms of HF (pt presenting complaints)

A

dyspnea, orthopnea, paroxysal nocturnal dyspnea, fatigue/weaknes, decreased activity tolerance, nocturia, confusion, decreased appetite, palpitation

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18
Q

what are signs found on assessment of HF?

A

tachycardia, hypotension, decreased o2 sat, weight gain, increased JVP/positive HJR, pulmonary rales, displaced LV apex, extra heart sounds, ascites, hepatomegaly, peripheral edema, cool extremities

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19
Q

what is the gold standard biomarker for HF

A

BNP

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20
Q

what are tests used to diagnose HF

A

ECG, CXR, BNP, labwork (cbc, coags, troponin, lytes/creatinine, glucose/a1c, lipid profile, tsh)

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21
Q

what are the most effective diuretics available

A

loop diuretics

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22
Q

how are loop diuretics used in the treatment of HF

A

promote fluid & electrolyte loss, decrease HTN & diastolic pressures, reduce preload and thus systemic congestion/edema and resolve symptoms like dyspnea & SOB (due to pulmonary edema)

23
Q

what causes HTN

A

increase in CO (hr, SV) or PVR (vasoconstriction, increased blood viscosity)

24
Q

what are risk factors for HTN

A

physical inactivity, low intake of fruits/veggies, overweight/obese, DM, CKD

25
Q

what are long term effects of HTN

A

CV disease, Cerebrovascular disease, renal disease, peripheral arterial disease, hypertensive retinopathy

26
Q

what are key vasodilating hormones

A

natriuretic peptides

27
Q

what are vasoconstrictive hormones

A

angiotensin II, ADH, epinephrine, NE

28
Q

who is considered high risk for HTN

A

anyone with DM, anyone >75, anyone >50 with a systolic BP 130-180 and one of the following risk factors

-CVD
-CKD
-Framinham risk score >15%

29
Q

what is the treatment target for a high risk HTN individual

A

Non-diabetic: initiate medical therapy if SBP >=130 and aim to get below 120

Diabetic: initiate medical therapy if SBP >=130 130 OR DBP>80 and aim to get under 130/80

30
Q

who is considered moderate-to-high risk for HTN

A

target organ damage, multiple CV risk factors & FRS 10-14%

31
Q

what is treatment criteria/target for moderate risk HTN individuals

A

initiate medical therapy if >=140/90, aim for below that

32
Q

who are low risk for HTN

A

no target organ damage, no CV risk factors, FRS <10%

33
Q

what is treatment criteria/target for low risk HTN individuals

A

> =160/100, aim for below 140/90

34
Q

what is AOBP

A

automated office blood pressure - patient’s BP taken alone by automated machine

35
Q

with is OBPM

A

office BP measurement - provider in room, take 3x, discard 1st and average second and third; assess both seated and standing for orthostatic hypotension

36
Q

what is the preferred out of office BP monitoring method

A

ambulatory BP readings –> worn for 24hrs, takes BP q20min

37
Q

what is the most sustained cardiac arrhythmia

A

afib

38
Q

in afib, instead of the normal path of electrical impulses and conduction patterns there is a combination of what two phenomenon

A

focal ectopic activity & the reentry of elecrtrical impulses

-electrical impulses originate from the ectopic atrial foci instead of the SA note; unsynchronized firing of electrical impulses and irregular activation of the atria

39
Q

what are two things people are at increased risk for with afib?

A

blood clots & VTE

40
Q

what are the four pathological mechanisms that can lead to AF

A
  1. cardiac structuralling remodeling (particularly in the atria)
  2. genetic causes (chromosome 10)
  3. electrical remodeling (can be due to lyte imbalances)
  4. idiopathic
41
Q

what is the difference between primary and secondary afib

A

primary is the result of a pathological process within the body, secondary is self-limiting and reversible, usually due to surgery, sepsis, MI, thyrotoxicosis, or pulmonary disease

42
Q

what is paroxysmal afib

A

continuous AF episode >30s but stops within 7days

43
Q

what is persistent afib

A

continuous AF that lasts longer than 7 days but less than 1 year

44
Q

what is longstanding AF

A

continuous AF lasting longer than 1 year but rhythm control strategies are being sought out

45
Q

what is permanent AF

A

continuous AF for which a therapeutic decision has been made NOT to pursue NSR (ie no treatment)

46
Q

what are ECG features of AF (4)

A
  1. irregularly irregular rhythm
  2. no P waves
  3. absence of isoelectric baseline
  4. variable ventricular rate
47
Q

what lab work would you order for afib

A

CBC, coags, lytes (including Ca & Mg), renal/liver/thyroid panel, fasting lipids, fasting glucose & AIC

48
Q

what is the CHADS-65 Score

A

stroke risk assessment: patient should be on anticoagulants if in afib and has 1 or more of the following:
C - congestive HF
H - HTN
A - age 65+
D - diabetes
S - stroke/TIA

49
Q

what risk factors are noted in the Framinham risk score

A

age, sex, HDL, total cholesterol, systolic BP (treated vs not treated), smoker, diabetes

50
Q

when do you initiate treatment for the intermediate FRS patients

A

LDL >=3.5mmol/L
*if <3.5 still consider initiating treatment if:
1. Apo B >=1.2g/L OR
2. non HDL >=4.3

also men >50 and women >60 with 1 risk factor:
-low HDL, impaired FG, >waist circumference, smoker, HTN

51
Q

what are statin indicated conditions

A

atherosclerosis
aortic aneurysm
DM >40years OR >30 with 15 year duration of disease
CKD (>50, eGFR <60, or ACR >3)

52
Q

when do you need to add a therapy on top of a statin used for primary prevention?

A

non HDL-C >2.6 or LDL-C >2 or ApoB >0.8 on max statin dose

53
Q

when do you need to add a therapy on top of a statin used for secondary prevention?

A

non HDL >2.4 or lDL >1.8 or ApoB >0.7

Patho/Pharm 2 (7 decks)

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