Heart Week 2A Flashcards
What is a vEnodilator?
NitroglycErin.
dereases prEload.
What is a vAsoldilator?
hydrAlAzine.
decreases AfterloAd.
What do ACE inhibitors and ARBs do to preload and afterload?
they both decrease preload and afterload.
ACE is given first, then ARBs if ACE is not well-tolerated.
What artery usually supplies the SA and AV nodes?
RCA
What are S1, S2, S3 and S4?
S1: mitral and tricuspid closing
S2: aortic and pulmonary valves closing
S3: early diastole, during rapid ventricular filling, associated with increased filling pressures (eg- regurgitation)
S4: “atrial kick”, late diastole, associated with ventricular hypertrophy, atrium must push against stiff LV wall.
What do the three elements do in the Renin-Angiotensin-Aldosterone axis?
Renin: decreased renal blood flow releases Renin, which begets…
Angiotensin: increases peripheral vascular resistance
Aldosterone: increases intravascular volume
What is the normal size of the mitral valve orifice?
4-6cm^2
What is the size of the mitral orifice for mild, moderate and severe disease?
(size of mitral orifice in cm^2)
mild: < 2
moderate: 1.0 - 1.5
severe: < 1
What is the normal size of the aortic orifice?
3-4 cm^2
What is the size of the orifice for moderate and severe aortic stenosis?
moderate: 1 - 1.5 cm^2
severe: <1 cm^2
What does stretching muscle fibers and holding them at fixed end points make the contractions stronger? What type of contraction is this?
a. muscle becomes more sensitive to Ca++
b. optimizes overlap of actin and myosin, increasing total number of cross bridges
This is an isometric contraction.
According to Frank-Starling, SV does what in relation to an increased preload?
SV increases.
In an isotonic contraction, what is the load that the muscles are contracting against?
The afterload.
In an isotonic contraction, what determines the final length of the muscle fiber?
The magnitude of the load it is contracting against. In cardiac muscle, this is the afterload.
Exposure to norepi does what to a cardiac contraction? And are the muscle fibers shorter or longer at the end?
It increases the force per contraction, and the muslce fibers have a shorter final length.
What are the three main components of CO?
a. contractility
b. preload
c. afterload
What is LaPlace’s Law?
wall stress = Pr/(2h)
pressure)(ventricle radius)/(2 x wall thickness
What can cause SV to rise?
a. up preload
b. down afterload
c. up contractility
What causes heart failure with a reduced ejection fraction?
a. impaired contractility: destruction of myocytes, MI, fibrosis
b. increased afterload
At what pressure will fluid leave pulmonary capillaries and enter the pulmonary interstitium?
> 20mmHg
What does heart failure with preserved ejection fraction lead to? And what does that lead to?
At first, it leads to increased ventricular volume and pressure during diastole. And that can lead to increased pulmonary pressure which can lead to pulmonary congestion (if pressure > 20mmHg).
When does heart failure with preserved ejection fraction occur? What are three things that can cause it?
It happens with impaired diastolic relaxation or increased ventricular stiffness. Can be cause by:
a. hypertrophy
b. cardiac tamponade
c. fibrosis
What is the equation to define BP?
BP = TPR x CO
What are three of the most important components of the neurohormonal reaction to heart failure?
a. adrenegic nervous system
b. renin-angiotensin-aldosterone
c. inreased production of antidiuretic hormones
Are chronic effects of the neurohormonal system beneficial?
no.
What are 3 immediate causes of stimulating the adrenergic system?
a. increase in heart rate
b. augmentation of ventricular contractility
c. vasoconstriction
When would the adrenergic system be stimulated?
Hypotension. Fall in CO is sensed by the baroreceptors, this increases sympathetc tone, and decreases parasympathetic tone.
What is the order of events of renin to angiotensin II?
a. decreased renal blood flow > release of renin
b. renin cleaves circulation angiotensin (A) to make AI.
c. angiotensin-converting enzyme cleave AI to make AII.
d. AII is a potent vasoconstrictor.
Where is aldosterone secreted from? How does it work?
It comes from the adrenal cortex.
It increases Na reabsorption from distal convoluted tubules, thus increasing intravascular volume.
What are the NY Heart Association classifications of heart failure?
- no limits on activity
- slight limit, eg- dyspnea running up stairs
- marked limitation of activity, eg- dyspnea while walking slow up stairs
- severe limitation of activity, eg- symptoms present even at rest.
Why use diuretics with heart failure? When should they be used?
promotes excretion of Na and water, thus reducing venous return and reducing preload. This should only be used with evidence of edema, such as hearing rales.
What are the vasodilating medicines?
a. ACEI
b. ARBs
c. Isosorbide Dinitrate (veins)
d. Hydralazine (arteries)
(*c and d can be used together when ACEIs and ARBs don’t work or are counter-indicated)
How do ACEIs work? Do they affect veins or arteries?
They inhibit the R-A-A system, specifically the aldosterone. They affect both veins and arteries.
(*also augments brady-kinin which helps with vasodilation)
What is the difference between concentric and eccentric hypertrophy?
Concentric: sarcomeres added in parallel, a result of chronic pressure overload, walls thicken.
Eccentric: sarcomeres add in series, a result of chronic volume overload, walls stay same size, but ventricles get bigger.
