Heart Failure Flashcards
What drugs are relied upon in heart failure?
Hypertensives; however, BP reduction is not often the goal
Define Heart Failure
- a progressive clinical syndrome that can result from any changes in cardiac output or function that may impair the ability of the ventricle to fill with or eject blood
What is the fundamental problem in heart failure?
- Decreased cardiac output
What occurs in the kidneys if cardiac output is decreased?
Glomerular pressure will decrease and renin will be released from juxtaglomerular cells
RAAS Activation; however, RAAS will not improve GFR significantly
RAAS will continue to function 24 hours a day
Fluid retention, edema, increase in vascular volume (volume overload)
Describe the relationship between the amount of blood coming into the right atrium and the amount of blood leaving the left ventricle? What happens if venous return is higher than cardiac output?
- The amount of blood that returns to the heart is the same amount that is pumped out. In healthy heart, an increased venous return will result in higher cardiac output.
- Venous system preceeding the right atriums capacity –> Backup of blood and veins become more congested
- An increase of blood in the venous system leads to an increased amount of pressure and fluid in the venous system.
What is pre-load?
- The degree to which the ventricle is stretched before it contracts
What ventricle is important for preload?
- Left Ventricle –> Cardiac output is highly limited,
Increased amount of blood returning than normal
High pressure on top of ventricle so during diastole the ventricle is bombarded with blood.
In patients with heart failure, what is the pre-load?
Preload (e.g. filling pressures) are high because of the high volume of blood being returned but not cleared.
Not able to to pump all the blood returning from venous system, blood back up and increases preload.
How does RAAS effect preload during heart failure?
- High preload is exacerbated by RAAS activation (increased blood volume because kidneys are retaining fluid)
- As a result, RAAS reduces urine output and increases intravascular volume.
Starling’s Law of the Heart (Frank-Starling Law)
- the energy (force) of contraction is proportional to the initial length of the cardiac muscle fiber
- Increase preload stretch = increase work of the heart
- Enables a healthy heart to immediately increased preload
How does the body respond to decreased cardiac output?
Baroreceptors (SNS) –> Not stretched, turn on SNS –> high levels of norepinephrine –> RAAS activated
Constant atrial stretch will result in ANP –> Vasodilation
Delievery of oxygenated blood impaired –> Brain (fatigue and muscles (exercise intolerance)
Ventricular hypertrophy and remodelling
Primary Symptoms of Heart Failure
- Dyspnea (shortness of breath)
- Fatigue (both during exercise and at rest)
Two types of heart failure:
1) Heart failure with perserved ejection fraction (HFpEF)
2) Heart failure with reduced ejection fraction (HFrEF)
Define ejection fraction
Ejection fraction is the % of blood left in the left ventricle that is not pumped out during contraction
Heart Failure with reduced ejection fraction (HFrEF)
- Left ventricular systolic dysfunction “contraction dysfunction”
- Normal Ejection Fraction –> 50-75%
- Ejection Fraction with HFrEF = 25%
Heart Failure with preserved ejection fraction (HFpEF)
- Diastolic Dysfunction “relaxation dysfunction”
Left ventricular hypertrophy –> thickening of muscular wall - Ejection fraction is in normal range but Cardiac Output is low
Do the symptoms vary between HFrEF and HFpEF?
- Symptoms would not be different; however, treatment is different
HFrEF –> 100 mL in ventricle in diastole –> 75 mL left
- 15 mL of blood pushed out (systole)
HFpEF –> 35 mL in ventricle (diastole) –> 10 mL left
- 15 mL of blood pushed out (systole)
Two most common causes of heart failure
- Heart Attack (75% of HFrEF cases)
- Hypertension
Is cardiac muscle replaced when it dies?
No
Heart attacks cause cardiac injury, heart does not replace cardiac muscle –> once its gone, its gone –> poor contraction as a result
Drugs used for HFrEF
- Volume overload –> Loop diuretics, TZD and SGLT-2 inhibitor (excrete sugar in urine)
- RAAS ACtivation - Valsartan/sacubitril or ACEI/ARBs alone –> MRA (aldosterone antagonist –> spirlactone)
- SNS activation –> Beta-blockers
Are diuretics used in HFrEF?
- Reduce symptoms associated with fluid retention
- Volume overload
- High preload
- Edema
- Pulmonary Congetsion
Orthopena
What drugs can be used for RAAS involvement in HFrEF?
- One of the three options:
ACEI
ARB’s
Valsartan/sacubitril - Angiotensin II and aldosterone –> vasoconstriction, cardiac remodelling (fibrosis, hypertrophy, and apoptosis), SNS activation, Na+ and fluid retention
Can mineralcorticoid antagonists be used in HFrEF?
- YES
- aldosterone concnetrations can still be high despite ARBS/ACEI’s
- Benefits of further aldosterone blockade:
reduce cardiac fibrosis and remodelling
reduce inflammatory trigger
reduce progression of arterial narrowing (artherosclerosis)
Can beta-blockers be used in HFrEF?
- Yes
- Benefits:
Reduce exposure of cardiac cells to norepinephrine (over time becomes poisonous) - May reverse some remodelling of cardiac tissue (hypertrophy)
- Lower Heart Rate –> improves ventricular filling time
