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how can you differentiate between acute and chronic regurgitation
acute regurgitation= ventricle doesnt have time to dilate, increased volume leads to sudden increase in pressure, therefore LVEDV and LVEDP increase

symptomatic: dyspnea, pulmonary edema, low CO
chronic regurg= happens gradually, ventricles dilate to compensate for excess volume. therefore increased volume (LVEDV) does not necessarily lead to an increase in pressure (LVEDP)
what is ejection fraction
(EDV-ESV)/LVEDV

SV/LVEDV
what happens to the pressure volume curve as preload increases
preload increases, LVEDV increases and stroke volume time increases.

time spent in isovolumetric contraction decreases

in a healthy heard LVESV does not increase
what happens to the pressure volume curve with different afterloads
have a longer isovolumetric contraction to reach a pressure significant enough to overcome the afterload.

more energy is spent in isovolumetric contraction, less time for systolic ejection
what happens to the pressure volume curve with increased contractility
with the same EDV :

lower contractility: increased ESV and decreased SV

higher contractility: decreased ESV and increased SV
what is the slope of the end systolic pressure volume relationship line a function of
contractility. steeper slope is more contractile

when contractility increases slope increases
what are the compensatory mechanisms to low cardiac output
increased HR (reflex tachy)

RAAS and SNS activation

remodelling: increased volume and increased preload -->dilatation to reduce wall stress-->eccentric hypertrophy
what defines hypovolemic shock
inadequate circulating volume

causes
hemorrhage, burns, vomitting
what defines cardiogenic shock
inadequate perfusion to heart

causes
MI, valve dysfunction
what defines distributive shock
excessive blood vessel dilation

causes
anaphylaxis, sepsis, neurogenic (vasodilation due to loss of SNS function)
what defines obstructive shock
physical obstruction of great heart vessels
tamponade
tension pneumothorax
pulmonary embolus
air embolus
what is the definition of heart failure
inability to pump sufficient blood to the body, or to only be able to do so under high pressures or high volumes

LOW CO= HEART FAILURE
what are 3 ways you can get heart failure
1. low preload (mitral stenosis, hypertrophy, mass in ventricle)

2. high afterload (reduced SV, more time spent in isovolumetric contraction) (AV stenosis, HTN)

3. reduced contractility, damage to heart muscle(ischemia/necrosis)
if left ventricular end diastolic pressure is high, what can it indicate
diastolic dysfunction
what are 3 causes of left heart failure (2 diastolic, 1 systolic)
Diastolic:

impaired relaxation (hypertrophy, increased LVEDP)

impaired filling (obstruction)

Systolic:
high afterload
how is HTN related to CHF
it's not: CHF is a failure to pump blood out of the heart, therefore results in hypotension
how is Angina related to CHF
it's not related at all
treatment of acute heart failure
Lasix (furosamide, loop diuretic)
Morphine
Nitro, Natiuretic peptides
Oxygen
Pressors (increase SNS stimulation of heart to increase forward flow of blood)
treatment of chronic heart failure
ACEi
B blocker
ARB
Digoxin
Nitrates
Spironolactone

difference between acute and chronic heart failure treatment?
acute you do NOT give any ACEi, no beta blocker. these slow the heart.

Want to increase the forward flow of blood (prevent low perfusion to tissues), therefore give pressor to stimulate heart
Examples of pressors (inotropes)

When are they given
dobutamine, dopamine, epi, norepi

given in ACUTE situations
IDEDNMP

describe their MOA
beta agonists
alpha agonists



increase systemic vasoconstriction, increase inotropy of heart
how do you calculate VO2 max
CO* (CaO2-CvO2)

aka the amount of blood that leaves the heart, and the amount of O2 that is extracted from this blood
what is the effect of morphine on CHF
sympatholytic centrally
reduces systemic catecholamines --> decrease HR, BP

reduces SOB, agitation and myocardial oxygen demand
What 2 drugs are contraindicated in acute heart failure
beta blockers and ace inhibitors
what are the effects of digoxin
increased inotropy (via inhibiting NaK exchanger

More Na in the cell, no longer favorable to pump Na in and Ca out therefore more Ca in the cell for contraction

Vagoylytic to the heart, decrease HR
what 2 conditions use dig
Atrial fibrillation (reduce AV conduction and slow ventricular rate)

Chronic HF (increase heart inotropy)
ACC/AHA stages of heart failure
A: at risk but no structural disease or symptoms

B: structural disease, no heart failure (asymptomatic)

C: structural disease with prior or current failure (symptomatic)

D: refractory heart failure
NYHA functional class of heart failure
I: asymptomatic heart failure

II: mild heart failure, symptomatic with moderate exertion

III: moderate heart failure: symptomatic with minimal exertion

IV: Severe HF, symptomatic at rest