Heart Failure Flashcards
What is the CO for men? Women? Average?
Men- 5.6L/min Women- 4.9 Avg- 5.0
This is the law that states that the more volume in the heart, the greater # of stretch receptors that are activated, and therefore the heart will pump out more blood, leading to an increased CO
Frank-Starling law
The stretch receptor activation to increased volume will also trigger the SA node to do what?
Increase HR
If O2 consumption is high, will blood flow increase or decrease?
Increase
If there’s an increase in TPR, will CO oincrease or decrease?
Decrease CO = (arterial pressure)/TPR
What is the 1 mechanism to make the heart hypereffetive?
Hypertrophy
What can cause a hypoeffective heart?
MI, PANS, arrhythmia, and other common sense stuff
This cause of high CO is when theres an insufficiency of B1, which leads to vasodilation and decrease TPR.
Beriberi
This cause of high CO is when a commection between a major artery and major vein can decrease TPR.
AV fistula
This cause of high CO is when metabolism is increased in tissues from increased TH.
Hyperthyroidism
This cause of high CO is when decreased viscosity of the blood from low RBC count will decrease TPR.
Anemia
Contractility disease, decreased venous return, acute venous dilation, obstruction of large veins, and decreased tissue mass can cause either an increased or decreased CO?
Decreased
Increased venous return and SANS will do what, increase or decrease CO?
Increase
If there is a negative pressure in the RA, is there an increased or decreased venous return?
Increased
Likewise, a + pressure in the RA will cause what: an increased or decreased venous return?
decreased
This is the point when the pressure in the RA exceeds is so much that venous return is 0 (usually ~7mmHg)
Mean systemic filling pressure. (MSFP)
1 minute ater which arrhythmia does MSFP reached?
V fib
True or False: the higher the MSFP, the harder it is for the blood to flow back to the heart.
FALSE. The easier it is, because blood will keep flowing back to the heart at a wider range of pressures.
After an MI, CO is reduced and blood gets backed up in the veins, leading to an increase in pressure where?
RA
Due to the decreased CO, the sympathetics kick in, raising the MSFP from 7mmHg to what?
12-14mmHg
What % of blood loos do u need to affect the MAP and CO?
10%
This is the type of shock where there is hypovoluemia from blood loss, leading to decreased filling pressure and venous return.
Hemorrhagic shock
In hemorrhagic shock, the sympathetic NS helps increase MAP and CO, to prevent what stage of shock where u can die?
Irreversible shock
This is the type of shock where there is no loss of blood but vascular capacity increases a lot so that all the blood pools in the circulatory system.
Neurogenic shock
What things can cause neurogenic shocK?
general anesthesia, spinal anesthesia, brain dmg
This is the type of shock where an allergic condition causes decreased CO and MAP due to histamine release.
Anaphylactic shock
This is the type of shock where a bacterial infection spreads throughout the body and activates inflammatory responses on a massive scale.
Septic shock
This is the type of ventricular hypertrophy where higher pressures of the circulatory system cause thickening of the walls.
Pressure overload ventricular hypertrophy
True or False:In volume overload ventricular hypertrophy, big volumes dilate the heart, causing an increased mass but not necessarily thickening the walls.
True
Ischemic heart disease, HTN, Aortic and mitral valve disease, and myocardial diseases can cause which sided heart failure?
L sided
L-sided heart failure can cause congestion where?
Lungs
Edema in the lungs from L-sided heart failure present with what distinctive thing on X-ray?
Kerley B lines
Since the RAAS system can be activated in L-sided heart failure, what drugs can u use to treat it?
ACEi’s
L-sided heart failure or cor pulmonale can cause what sided heart failure?
OMG THE RIGHT. AJHFSDJIGNSDGSHDGHSGHSDHGHAHAHAHAFHHAHAHA
How does L-sided HF cause R-sided HF?
pulmonary congestion leads to RVH -> RHF
This is when the heart is unable to pump blood forward at a sufficient rate to meet the metabolic demands of the body
Heart failure
This is the ventricular wall tension at the end of diastole, right before the contraction, and determined by end-diastolic volume (EDV) or end-diastolic pressure (EDP).
Preload
Dehydration or hemorrhage can cause what to the EDV, increase or decrease it?
Decrease
Conversely, a large IV infusion increases EDV, leading to a higher or lower CO?
Higher
So if you increase Preload, do u increase or decrease CO?
Increase!
This is hte ventricular wall tension during contraction, and the RESISTANCE that must be overcome to eject its contents.
Afterload
Pulmonary HTN, systemic HTN, and AR do what to the afterload: increase or decrease?
Increase
So if u increase afterload, does it increase or decrease CO?
Decrease
True or False: ionotropy is independent of preload and afterload, as it reflects the chemical or hormonal influences on the force of contraction.
True
True or False: B-blockers increase CO.
False. They decrease it by decreasing iontoropy
This is the volume of blood ejected from the ventrical during systole.
SV
How do u calculate SV using ESV and EDV?
SV = EDV - ESV basically: (volume ejected) = (volume of blood in LV before contraction) - (volume of blood in LV after contraction)
This is the fraction of EDV ejected from the ventricle during each contraction.
Ejection fraction
What is the normal EF?
55-75%
What is the eqn to calculate EF?
EF = SV/EDV basically, (% of total volume ejected) = (volume actually ejected)/(volume in LV that is capable of being ejected before contraction)
Do you understand this graph?
Point a- mitral valve opening in early diastole
Line ab- represents diastolic filling. Volume increases in association with a gradual rise in pressure. The onset of left ventricular systolic contraction causes the ventricular pressure rise. When the pressure in the left ventricle exceeds the left atrium you are at point b
Point b- closing of mitral valve
Line bc- isovolumetric contraction of the left ventricle (no blood leave b/c aortic valve is shut)
Point c-opening of the aortic valve. Happens when the pressure in the left ventricle rise to that in the aorta and ejection can begin
Line cd-Ejection of blood through the aortic valve. The volume within the ventricle decreases, but its pressure continues to rise until ventricular relaxation begins. The pressure for which the ventricle pumps against (afterload) is also represented by curve cd. Ejection ends during the relaxation phase, when the ventricular pressure falls below that of the aorta.
Point d-aortic valve closes.
Line ad- Isovolumetric relaxation which happens b/c as the ventricle continue to relax, its pressure declines while its volume stays the same (mitral valve has not opened yet). When the ventricular pressure falls below that of the left atrium, the mitral valve opens again (point a) and the cycle repeats.
Where on the graph is the EDV?
Point b
Where on the graph is ESV?
Point d
So the difference between point b and d can give you what?
SV
True or False: if you increase proload, afterload and contractility are kepts the same.
True
True or False: if you increase the proload, you increase the SV and increase the ESV.
False. ESV is the same
So how can you increase this preload without affecting afterload and ESV and contractility?
give a bunch of IV fluid
In HCM, compliance is reduced, and what happens to the slops of the filling curve? Is it steeper or longer?
Steeper
In HCM, is EDV increased or decreased?
Decreased, as the chamber can’t fill as much during diastole.
If Preload and Contractility are held constant but afterload is increased, is ESV increased?
Yes
Why is ESV increased in increased afterload, according to our eqn for SV?
If you increase somehting like systemic HTN, afterload is increased, and SV is decreased cuz the heart doesnt fill as much. On the graph, you’re creeping up that fixed ESPVR line, meeting it higher points, thus decreasing the SV
SV = EDV - (↑) ESV
this causes ↓ SV
If you increase the contractiliry of the heart, will the ESVPR line have a steeper or shallower slope?
Steeper (the ventrical empties more)
So increasing the contractility of the heart will do what to do the EDV? Increase or Decrease?
Decrease
(you push more out, so like normal EDV would be like 50mL, and now it’d be like 20mL)
So SV is increased with what changes in Preload, Afterload, and Contracility?
↑ Preload (higher point on EDVPR line)
↓ Afterload (lower point on ESVPR line)
↑ Contractility (shift ESVPR line upwards)
Impaired contractility or pressure overload can diminish the hearts ability to pump blood in what condition?
Systolic Heart failure
What happens to the ESVPR in heart failure? Why?
Decreases cuz contractility decreases.
What things can cause heart failure with a preserved ejection fraction?
Imopaired diastolic relaxation (MI), increased wall stiffness (LVH, fibrosis, restrictive CM), or both
What happens to the EDVPR in disastolic HF? Is it shifted up or down?
Up.
Pt’s with diastolic HF typically present with congestion where because of increased retrograde pressures?
Pulmonary and systemic veins.
1/2 of the patients with heart failure fall in to which category: systolic or diastolic HF?
Diastolic HF
(preserved ejection fraction)
Right-sided HF can result from sudden increases to what factor, typically in PE’s?
Afterload
True or False: the most common cause of right sided HF is the presence of left-sided HF
True!
Remember L-sided HF (like diastolic HF) increases retrograde pressures, causing R-sided HF
In the new york heart association classifications for chronic heart failure, what are the characteristics for class I HF?
No limitation on physical activity
In the new york heart association classifications for chronic heart failure, what are the characteristics for class II HF?
Slight limitation on activity, dyspnea with moderate exertion
In the new york heart association classifications for chronic heart failure, what are the characteristics for class III HF?
Marked limitation of activity, dyspnea with minimal exertion
In the new york heart association classifications for chronic heart failure, what are the characteristics for class IV HF?
Severe limitation of activity, Sx at rest.
This is the stage of chronic HF where the patient who is at risk has not develed dysfxn yet.
Stage A
In stage B, there is structural heart disease with HF, but what is lacking?
Sx
In stage C of HF, which 2 things are present?
Sx and strucutral dmg
In stage D of chronic HF, there is structural disease, and a marked increase of ______, despite Tx?
Sx
What is the 5 year mortality for HF pts?
45-60%
What is the 1 year mortality for pts with class III or IV HF?
40%
Which 2 drugs should u start the pt on if they have chronic HF with reduced EF (systolic HF)?
ACEi and B-blocker
The goal in the Tx of HF with preserved EF (diastolic HF) is to Tx the pulmonary and peripheral edema, using what type of drugs?
Diuretics
True or False: in diastolic HF, in addition to diuretics, you should give B-blockers, ACEi’s, or ARBs to reduce the mortality in these pts.
FALSE. These others have no demonstarted mortality benefit.
True or False: B-blockers should only be used in stable pts with systolic HF.
True
THis is the biventricular pacing where ht epacemaker stimulates both ventricles simultaneously, thus, resynchonizing the contractile effort.
Cardiac resynchronization therapy (CRT)
What are the 3 types of pts that are candidates for CRT?
- pts with advanced systolic dysfxn (LV EF < 35%)
- Prlonged QRS (>120msec)
- Continues Sx of HF despite Tx with drugs
What does digoxin/digitalis inhibit on the plasma membrane to increase intracellular Ca++?
Na+ pump
Wait wtf, how does inhibiting an Na pump increase Ca++ into the cell?
Na/Ca exchanger stops because Na gradient sucks –> increae in intracellular [Ca] –> increased contractility
True or False: digitalis is somewhat safe because it has a wide therapeutic window.
FALSE. it has a narrow one.
Pt’s taking what type of drugs cannot take digitalis because of toxicities?
non-K sparing diuretics
What is the most common arrhythmia produced by digitalis?
Ventricular extrasystoles (delayed afterdepolarization)
The vagal effect of digitalis on the SA node does what to the CV and refractory periods?
↓ CV
↑ RF
So what 2 types of arrhthmias is digitalis good for, espically since it ↓ CV and ↑ RF?
SVTs and AVNRTs
What is the mechanism of diuretics (furosemide) to treat pts with LV failur and CHF?
↓ preload
What is the mechanism for vasodilators (hydralazine) to treat HF pts?
↓ TPR –> ↓ afterload
What are the 2 main actions of ACEi’s (-pril’s) to treat HF pts?
- inhibits aldosterole release (↓ preload)
- inhibits ATII causing vasoconstriction (↓ afterload)
What do the aquaretics (conivaptan) block to ↓ preload?
vasopressin receptor V2
Aldosterone receptor antagonists (spironolactone) inhibit the reuptake of what in the kidney to ↓ preload?
Na+ and water
The whole point of the neurohormonal antagonists is to prevent the downregulation of which receptors, which can worsen CHF?
B-adrenergic receptors
