Cardio Patho Flashcards
what is CO
volume of blood ejected from the ventricles in one minute
how is CO calculated
HR x SV
what impacts HR
SNS (epi & NE) & PSNS
what affects SV
preload, afterload (PVR), contractility
what is contractility
the ability of cardiac muscle to generate force of contraction during systole and push blood out of the ventricle against systemic vascular resistance (BP)
what affects preload
venous blood return & the amount of blood left in the ventricle after systole (end systolic volume)
what affects afterload
aortic pressure (aortic stenosis) and peripheral resistance (HTN)
what is the Frank-Starling law of the heart
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
what is the RAAS
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
what happens as a result of RAAS in HF
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
what is NPS
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)
what is HFpEF
heart failure with preserved ejection fraction (LVEF>50%)
what is HFmEF
heart failure with mid-range ejection fraction (LVEF41-49%)
what is HFrEF
heart failure with reduced ejection fraction (LVEF<40%)
what are the four main etiologies of HFrEF
- ischemic (CAD)
- Rheumatic valvular diesase (from strep)
- HT heart disease
- COPD
what are some main risk factors for HF
male, age, CAD w/ hx MI, HTN, valvular heart disease, smoking/substance misuse, obesity, DM, genetics, chemo/radiation
what are some symptoms of HF (pt presenting complaints)
dyspnea, orthopnea, paroxysal nocturnal dyspnea, fatigue/weaknes, decreased activity tolerance, nocturia, confusion, decreased appetite, palpitation
what are signs found on assessment of HF?
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
what is the gold standard biomarker for HF
BNP
what are tests used to diagnose HF
ECG, CXR, BNP, labwork (cbc, coags, troponin, lytes/creatinine, glucose/a1c, lipid profile, tsh)
what are the most effective diuretics available
loop diuretics
how are loop diuretics used in the treatment of HF
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)
what causes HTN
increase in CO (hr, SV) or PVR (vasoconstriction, increased blood viscosity)
what are risk factors for HTN
physical inactivity, low intake of fruits/veggies, overweight/obese, DM, CKD
what are long term effects of HTN
CV disease, Cerebrovascular disease, renal disease, peripheral arterial disease, hypertensive retinopathy
what are key vasodilating hormones
natriuretic peptides
what are vasoconstrictive hormones
angiotensin II, ADH, epinephrine, NE
who is considered high risk for HTN
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%
what is the treatment target for a high risk HTN individual
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
who is considered moderate-to-high risk for HTN
target organ damage, multiple CV risk factors & FRS 10-14%
what is treatment criteria/target for moderate risk HTN individuals
initiate medical therapy if >=140/90, aim for below that
who are low risk for HTN
no target organ damage, no CV risk factors, FRS <10%
what is treatment criteria/target for low risk HTN individuals
> =160/100, aim for below 140/90
what is AOBP
automated office blood pressure - patient’s BP taken alone by automated machine
with is OBPM
office BP measurement - provider in room, take 3x, discard 1st and average second and third; assess both seated and standing for orthostatic hypotension
what is the preferred out of office BP monitoring method
ambulatory BP readings –> worn for 24hrs, takes BP q20min
what is the most sustained cardiac arrhythmia
afib
in afib, instead of the normal path of electrical impulses and conduction patterns there is a combination of what two phenomenon
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
what are two things people are at increased risk for with afib?
blood clots & VTE
what are the four pathological mechanisms that can lead to AF
- cardiac structuralling remodeling (particularly in the atria)
- genetic causes (chromosome 10)
- electrical remodeling (can be due to lyte imbalances)
- idiopathic
what is the difference between primary and secondary afib
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
what is paroxysmal afib
continuous AF episode >30s but stops within 7days
what is persistent afib
continuous AF that lasts longer than 7 days but less than 1 year
what is longstanding AF
continuous AF lasting longer than 1 year but rhythm control strategies are being sought out
what is permanent AF
continuous AF for which a therapeutic decision has been made NOT to pursue NSR (ie no treatment)
what are ECG features of AF (4)
- irregularly irregular rhythm
- no P waves
- absence of isoelectric baseline
- variable ventricular rate
what lab work would you order for afib
CBC, coags, lytes (including Ca & Mg), renal/liver/thyroid panel, fasting lipids, fasting glucose & AIC
what is the CHADS-65 Score
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
what risk factors are noted in the Framinham risk score
age, sex, HDL, total cholesterol, systolic BP (treated vs not treated), smoker, diabetes
when do you initiate treatment for the intermediate FRS patients
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
what are statin indicated conditions
atherosclerosis
aortic aneurysm
DM >40years OR >30 with 15 year duration of disease
CKD (>50, eGFR <60, or ACR >3)
when do you need to add a therapy on top of a statin used for primary prevention?
non HDL-C >2.6 or LDL-C >2 or ApoB >0.8 on max statin dose
when do you need to add a therapy on top of a statin used for secondary prevention?
non HDL >2.4 or lDL >1.8 or ApoB >0.7
