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Cardiology Exam 2 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Hemodynamics of Systolic HF

A
  • Dec contractility (pumping problem)
  • Breakdown of Frank Starling Law where inc venous return no longer inc SV b/c dec contractility; inc preload actually worsens problem
  • Inc LVEDV, inc LVEDP, dec contractility, dec SV
  • Compensation:
  • inotropes to inc contractility to overcome high afterload
  • Dec afterload w/ vasodilators so do not have to achieve same pressure to eject
  • Dec preload w/ diuretics b/c achieve same SV at lower pressure
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2
Q

Hemodynamics of Diastolic HF

A
  • Stiff ventricle, dec compliance (filing problem)
  • Dec compliance means the EDPVR shifts up so the same change in volume will cause a much greater change in pressure (this limits EDV b/c you can only have so much EPV)
  • Inc LVEDP but same or lower LVEDV, same contractility, dec SV
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3
Q

What are the two broad categories of signs/symptoms? (examples for ea)

A
  • Inc volume = SOB, orthopnea (sob when laying), swelling/bloating, RUQ tender, inc JVP, wet crackles or rales, S3, liver congestion (palpate below costal margin), ascites, edema
  • Low CO = Weakness, fatigue, nausea, dec appetite, poor sleep, forgetfulness, confusion, cool extremities, cyanosis or pallor, renal dysfunction, end-organ dysfunction
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4
Q

How does the neurohormonal system make CHF worse?

A
  • Symp NS = vasoconstriction via alpha receptors (inc afterload and inc myocardial stress) –> even more symp stimulation
    • Long term neg effects - Myocardial necrosis and apoptosis
  • RAAS
    • Inc reabsorption and stimulate aldosterone to further inc reabsorption –> inc preload (BAD)
    • Arterial vasoconstriction –> inc afterload (BAD)
    • Stimulate myocardial fibrosis and cellular hypertrophy (long-term)
  • Vasopressin
    • Vasoconstriction –> inc afterload (BAD)
    • Inc water reabsorption –> inc preload (BAD)
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5
Q

LV Remodeling in HF

A
  • Progressive change in size and shape of heart in response to myocardial injury, excessive neurohormonal activation and altered loading conditions
  • LV dilation - to accommodate inc vol w/o inc LVEDP

1st - myocyte hypertrophy to compensate to overload

2nd - inc myocyte spacing due to fibrosis and collagen deposition (sympathetic stimulation and RAAS contribute to inflammation and fibrosis)

3rd- myocyte necrosis and apoptosis (due to genetic mutations, cytokines, catecholamines, angiotensin AND dec blood flow due to spacing) –> dec myofilament density –> dilated

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6
Q

Drugs to Dec Mortality and Progression from HF (7)

A
  • ACEi
  • Angiotensin Receptor Blockers
  • Aldosterone Blockade
  • Beta blockers
  • Hydralazine + Nitrates
  • Neprilysin Inhibitor
  • Ivabradine
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7
Q

Drugs/Tx to Dec Complications in HF (2)

A
  • Prevent stroke (esp if CHF is secondary to anterior wall MI)- anti-coagulation (Warfarin)
  • Prevent arrhythmias - ICD if LVF < 35%
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8
Q

Drugs to Dec Symptoms in HF (3)

A
  • Diuretics
  • Digoxin
  • Inotropes (last resort)
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9
Q

Mechanical Support for De-comp HF

A
  • IABP
    • Inflated in systole - neg press acts as suction to pull blood from LV –> aorta
    • Delated in diastole - divert flow to coronary arteries and improves LV function (less LVEDP/LVEDV)
    • Downsides - infection, requires bedrest which is bad if volume overloaded, timed w/ ECG so does not work if have arrhythmia
  • LV Assist Device
    • Implanted pump; receives blood from LV then returns it to aorta
    • Battery operated
  • Temporary fix b/f cardiac transplant is possible
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10
Q

Pathology of R Heart Failure

A

NUTMEG LIVER (blood backs up into hepatic sinusoids –> red dots amongst normal brown background of liver; begins in centrilobulbar region - hepatic veins)

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11
Q

Pathology of L Heart Failure

A

HEART FAILURE CELLS IN ALVEOLI (macrophages in alveoli eating up excess fluid)

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12
Q

ACE inhibitors

A
  • prevent angio-II which –> dec BP (afterload) but more importantly dec fibrosis by angio-II (dec remodeling)
  • Interchangeable, can use at any stage of heart failure, usually pick 2
  • Side effects - dry cough from bradykinin , hyperkalemia, worse renal funct, angioedema
  • Ramipril, Captopril, trandolapril, enalapril
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13
Q

ARBs

A
  • equivalent to ACEi so use if cannot use ACEi

- Valsartan/candesartan

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14
Q

Aldosterone Blockade

A
  • used in addition to angio-II blockers (further reduces remodeling) b/c aldosterone levels go back to normal after 12 wks of ACEi or ARBs
  • Careful of hyperkalemia
  • Only use if LV dysfunction not just in at risk group
  • Eplerenone, spironolactone
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15
Q

Beta Blockers for HF

A
  • initial dec in CO (can make symptoms worse - tired/vol overload) but long term prevent and even reverse remodeling
  • Must dec volume (diuresis) 1st and careful if asthma
  • Best in mild to moderate CHF
  • Carvedilol good b/c non-selective
  • Contra-indicated if asthma
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16
Q

Hydralazine + Nitrates

A
  • inhibits oxidase path and produces NO

- Use if ACEi/ARB intolerant (ex - renal dysfunction) OR in black population

17
Q

Neprilysin Inhibitors

A
  • Neprilysin breaks down good things like endogenous natriuretic peptides so blocking it keeps these active
  • Reserve for more severe patients
  • Sacubitril (comes in combo pill w/ valsartan ARB = Entresto)
18
Q

Ivabradine

A
  • purely chronotropic; dec HR to inc diastolic filling time; works by binding and inhibiting funny channel (dec slope of pacemaker potential in SA node)
  • Really only dec admissions not mortality so no US guidelines yet
19
Q

Diuretics in HF

A

Careful b/c CHF pts have more narrow acceptable volume range; too little volume can lead to hypotension/dehydrated and need certain preload to achieve SV OR too much volume can lead to volume overload

20
Q

Inotropes in HF

A
  • Inhibit Na-K pump –> now have inc Na+ so blunt the Na-Ca exchanger –> inc Ca++ in cell –> inc contractility/BP –> reflexive inc in parasympathetic tone (slow AV node)
  • Inc CO and makes heart more efficient/less oxygen demand b/c dec HR
  • Side effects - TRIAD (CNS yellow vision, cardiac arrhythmias/block and GI nausea)
  • Can be toxic if too slow - heart block
21
Q

Digoxin in HF

A
  • direct beta agonists (dobutamine and epi) OR PDE inhibitors which inc Ca++ in cell (milrinone or enoximone)
  • Inc contractility
  • Use when such LV dysfunction that inc vol and inc filling pressures will not make diff; have to “whip heart” to contract
  • For very sick patients w/ marked dec CO (severe fatigue, mental status change, extreme hypotension)
  • Side effects - hypotension, arrhythmias, worsened ischemia b/c inc oxygen demand of heart, inc mortality

Cardiology Exam 2 (13 decks)

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