Heart Failure Flashcards
Characterized by a high risk for HF without structural heart disease or symptoms (i.e. hypertension, atherosclerosis, diabetes, obesity, etc.)
Stage A
Structural heart disease without the development of HF
-Prior MI, depressed LV ejection fraction, LVH
Stage B
Characterized by structural heart disease with current or prior symptoms
Stage C
Classified as end-stage HF
Stage D
The fraction of blood ejected by the ventricle relative to its end diastolic volume
Ejection Fraction
How do we find ejection fraction?
EF = (SV / LVEDV) * 100
Normally, ejection fraction is greater than
50-60%
Preload is the myocardial stretch, which can be found as
Preload = EDV / /EDP
Force of myocardial contraction and is independent of preload or afterload
Contractility
Characterized by decreased capacity to eject blood due to decreased contractility
-LVEF is usually less than 40-50%
HF with Reduced EF
Characterized by abnormal diastolic function due to increased stiffness
-LVEF is greater than 50%
HF with preserved EF
Ventricles fill at higher than normal pressures with
HF w/ preserved EF
When the RV becomes thin-walled and more compliant leading it to accept a wide range of volume w/out change in filling pressures
RV Failure
The most common cause of RV failure is
LV failure
If RV failure is due to lung process, we call it
Cor Pulmonale
Has a limited benefit in severely decreased contractility
Frank-Starling Mechanism
Serves to maintain perfusion to vital organs by increasing SVR and increasing intravascular volume
Neuro-Hormonal Activation
The acute effects are beneficial but the chronic effects are deleterious
Neuro-Hormonal Activation
Characterized by increasing sympathetic and decreasing parasympathetic output to the heart and periphery
Neuro-hormonal activation
Cleaves angiotensinogen to AN-I
Renin
Cleaves AN-I to AN-II
ACE
A potent vasoconstrictor that stimulates thirst and increases aldosterone and Na retention, which thus increases volume
AN-II
Secreted by the posterior pituitary and functions to increase water retention in distal nephron
ADH/Vasopressin
Beneficial hormones that respond to stretch and increase Na+ and water retention
Natriuretic peptides (ANP and BNP)
ANP and BNP promote
Vasodilation
ANP and BNP inhibit
Renin secretion
Used in diagnosis of HF
BNP levels
Ventricular remodeling and hypertrophy reduces wall stress and maintains
Contractility
Characterized by cardiac cachexia, tachypnea, and tachycardia with rales and decreased BS
Left sided HF
We will see a diffuse apical impulse and a weak pulse with
Left sided HF
Characterized by increased JVD and hepatic enlargement with ascites and leg edema
Right sided HF
What labs suggest chronic HF?
Decreased Na and Hgb w/ increased creatinine
Function in water and Na+ elimination which decreases intravascular and diastolic volumes
Diuretics
The most potent diuretics are
Loop diuretics
Less potent, but additive diuretics
Thiazides
Venous vasodilators used to increase venous capacitance and decrease LV preload
Nitrates
Arteriolar vasodilators used to decrease SVR which increases CO and thus increases BP
Hydralazine and Prazosin
Balanced venous and arterial vasodilators
ACE inhibitors and ARBs
Decrease AN-II and aldosterone while increasing bradykinins
ACE inhibitors
Limit maladaptive remodeling and improves survival
ACE inhibitors
Complete AN-II inhibition w/ no effect on bradykinins
ARBs
Similar efficacy and survival benefit as ACE inhibitors, but can be an alternative if patient gets ACE-induced cough
ARBs
Improve survival, especially in AA
-Alternative if ACE inhibitor/ARB intolerant
Hydralazine/Nitrates
Phosphodiesterase inhibitor used to increase ventricular contractility
Milrinone
Blunts sympathetic drive and slows AVN conduction
Digoxin
Inhibits Na+/K+ ATPase which increases intracellular Ca2+
Digoxin
Improves symptoms and reduces hospitalizations, but has no effect on survival
Digoxin
How do we treat patients with HF w/ reduced EF
Aldosterone Antagonists
What are two examples of aldosterone antagonists?
Spironoloactone and eplerenone
Blunt cardiac fibrosis and remodeling
Spironolactone and eplerenone
In patients taking the aldosterone antagonists, we need to monitor
K+ levels
When we have LVEF that is less than 35%, what can we use for SCD prevention?
AICD
We want to avoid overdiuresis with
Right-sided HF
The majority of patients with acute decompensated HF have what is classified as
Wet and Warm HF (Normal perfusion at rest w/ presence of congestion)
The number one goal to treat wet and warm is
Diurese
We want to keep wet and warm patients on
Beta-blockers
May be added to diuretic therapy w/ wet and warm in absence of symptomatic hypotension and still w/ severe HF
Vasodilators
Causes rapid improvement in congestion and is useful in pulmonary edema and severe hypertension
Vasodilators
Peripheral edema means that the
Right side of heart is affected
A low EF and low output syndrome w/ marginal BP and unresponsiveness to vasodilators
Wet and Cold HF
Shows a poor response to diuretics and worsening renal function
Wet and Cold HF
How do we treat patients w/ wet and cold HF?
IV inotropes
Usually do not get admitted unless they are in end-stage
Patients with Dry and cold HF
For dry and cold HF, what do we give if:
- ) BP is ok?
- ) BP is low?
- ) Vasodilators
2. ) Inotropes
Characterized as stable and chronic HF
Dry and Warm HF
In patients w/ advanced HF w/ reduced EF, are used in conjunction with ACE inhibitors
Beta-Blockers
