test 1 Flashcards
What is Heart Failure (HF)
- Progressive disorder in which the heart is unable to pump sufficient blood to meet the needs of the body
- Impaired ability of the heart to adequately fill with and/or eject blood
Two Major Types of Heart Failure
- Systolic and Diastolic
Systolic Failure
- Reduced pumping action (contractility)
- Reduced ejection fraction
- ~50% of HF patients
* “younger”
Diastolic Failure
- Stiffening and loss of adequate relaxation
- Reduced filling and cardiac output
- ~50% of HF patients
* “older”
Heart failure causes edema how (2)
- Increase in venous pressure -> increased capillary filtration = edema
- decrease CO -> decreased blood pressure -> increased sympathetic activity and decreased renal blood flow -> increased renin, angiotensin II -> increase aldosterone -> increased sodium and water retention = edema
HF Treatment Goals (3)
- Reducing symptoms
- Slow disease progression
- Improve survival
Causes of Heart Failure (6)
- Ischemia
- Cardiomyopathy
- Myocarditis
- HTN
- Valve disease
- Congenital defects
Ischemia leading to HF
- Coronary artery disease
- Multiply MIs
- Most common
Cardiomyopathy leading to HF
- Damage to the heart muscle
- Infection
- Alcohol abuse
- Drug abuse
- Genetics
Myocarditis leading to HF
- Inflammation of the heart
- Viral
* Common cause - Many viruses implicated
* Coxsackie V viruses
* Epstein-Barr virus (EBV)
* Cytomegalovirus (CMV)
* Hepatitis C
* Herpes
* HIV - May or may not fully or completely resolve
* Might require valvular surgery
HTN leading to HF
- Heart has to work harder to pump blood to body
* Causes heart to become thicker and stiffer
Valvular Disease leading to HF
- Stenosis
* Insufficiency
Congenital Defects leading to HF
- Bicuspid aortic valve
- Renal artery stenosis
- Coarctation of aorta
- Cushing’s syndrome
HF Symptoms
- Shortness of breath (dyspnea)
- Orthopnea
* Dyspnea lying down - Fatigue
- Peripheral edema
- Decreased exercise tolerance
Three Major Compensatory Mechanisms
- Increased sympathetic activity
- Activation of the renin-angiotensin aldosterone
system - Myocardial hypertrophy
Increased Sympathetic Activity as a compensatory mechanism
- Baroreceptors sense a decrease in BP
* Activates the SNS - Results in increased HR, contractility, and vasoconstriction
- Enhanced venous return
* Increases preload - Increased stroke volume and CO
Activation of the Renin-angiotensinaldosterone
System (RAAS) as a compensatory mechanism
- Decrease flow to the kidney, due to low CO, causes release of renin
- Leads to an increase angiotensin II levels
- Leads to an increase in aldosterone
- Leads to increase in blood volume
* More blood is returned to the heart
Myocardial Hypertrophy as a compensatory mechanism
- Thickening of the heart muscle
* Decrease in size of the chambers - Chambers dilate
Cardiac Remodeling
- Alteration in the structure (dimension, mass, shape) of the heart in response to hemodynamic load and/or cardiac injury
- Cellular changes
* Myocyte hypertrophy, necrosis, fibrosis
Seven Classes of Drug for Treatment of Heart Failure
- ACE inhibitors
- ARBs
- Aldosterone blockers
- β-blockers
- Diuretics
- Direct vaso - and venodilators
- Inotropic agents
what do ACE Inhibitors do
- Block the enzyme that cleaves angiotensin I to form angiotensin II
- Reduces inactivation of bradykinin
- Reduces secretion of aldosterone
- Reduces afterload and preload
* Increase CO - Been shown to significantly improve patient survival
- Indicated in patients will all stages of LV failure
ACE Inhibitors: Adverse Effects
- DRY MOUTH
- Rash
- Fever
- Angioedma
- Hypotension
- Hyperkalemia
- Fetal malformations
what do Angiotensin Receptor Blockers (ARBs) do
• Block the angiotensin II receptors
• Block angiotensin II action
• Actions are similar to ACE inhibitors
• Reduce afterload and preload which increases CO
•Used in patient who cannot tolerate ACE inhibitors
• Severe cough
• angioedema (rapid edema of the area beneath the skin)
- decreases cell proliferation (decrease in tumors or number of cells)
- decreases hypertrophy
ARBs: Adverse Effects
- Similar to ACE inhibitors
* Less risk of cough - Should not be combined with ACE inhibitors
* Similar mechanism and adverse effects - Teratogenic
what do Aldosterone Antagonists do
- Block aldosterone
- Prevents salt and water retention
- Prevents myocardial hypertrophy
what do β-blockers do
- Prevent changes that occur because of chronic activation of the SNS
- Decrease HR
- Inhibit renin release
- Decrease remodeling, hypertrophy, and cell death
- Recommended for all patients with chronic, stable HF
- Metoprolol, Bisoprolol, and carvedilol reduce morbidity and mortality
β-blockers: Adverse Effects
- Bradycardia
- Hypotension
- Fatigue
- Insomnia
- Sexual dysfunction
- Alter lipid panel
* Decrease HDL
* Increase triglycerides
what do Diuretics do
- Relieve pulmonary congestion and peripheral edema
- Decrease plasma volume
* decrease preload/afterload - Loop diuretics commonly used
what does Isosorbide dinitrate do
- Causes vascular smooth muscle relaxation
- Converts nitrite ions to nitric oxide which causes an increase in cGMP leading to dephosphorylation of myosin light chain
- Causes dilation of large veins
* Reduces preload
what does Hydralazine do
- Relaxes vascular smooth muscle mainly in arteries and arterioles
- Decreases SVR and CO by releasing nitric oxide from the endothelium
what does Hydralazine and isosorbide dinitrate do
- Fixed dose combo (Bidil)
* Been shown to improve survival in the African/American community
Vaso – and Venodilators: Adverse Effects
- Headache
- Hypotension
- Reflex tachycardia
what do Inotropes do
- Increase intracellular Ca2+ concentration
* Enhance cardiac contractility
* Increase CO - Associated with reduced survival
* Except digoxin
* Only used for short period
* Hospital setting
Inotropes: Cardiac Glycosides/Digitalis
- Come from the digitalis (foxglove) plant
- Low therapeutic index
- Digoxin
how does Digoxin work
- Inhibits the Na+ /K+ - adenosine triphosphatase (ATPase)
- Reduces ability of myocyte to actively pump Na+ out of cell
* Increases intracellular Na+ - Increases intracellular Ca2+
- Increases cardiac contractility
when is digoxin used
- Indicated in patients with severe HF
* After initiation with ACE inhibitors, β-blockers, and diuretic therapy - Reduced HF admissions and improved survival
* Low doses - Long half-life
* 30-40 hours - Tolerated at low doses
* (0.5-0.8 ng/ml)
Digoxin: Adverse Effects
- Digoxin toxicity
* Arrhythmias
* Anorexia
* Nausea
* Vomiting
* Blurred vision - Severe Toxicity
* V-Tach - Administration of digoxin antibody
* Digibind
what does Dobutamine do
- β-agonist: positive inotropic effect
- Increases cAMP which activates protein kinase
* Protein kinase phosphorylates slow Ca2+ channels
* Increases Ca2+ entry into myocardial cell enhancing contraction - Given by IV infusion
- Used in short-term treatment of HF
* Hospital setting
what does Milrinone do
- Phosphodiesterase inhibitor
- Increases cAMP which activates protein kinase
* Protein kinase phosphorylates slow Ca2+ channels
* Increases Ca2+ entry into myocardial cell enhancing contraction - Short-term IV therapy
how do inotropes work
- binding of a β-agonist, such as dopamine or dobutamine, activates adenylyl cyclase, which produces cAMP
- cAMP activates protein kinase, which in turn phosphorylates Ca2+ channels
- Phosphorylation of Ca2+ channels increases Ca2+ flow into the cell, causing increased force of contraction of the heart
- Phosphodiesterases inhibitors prevents hydrolysis of cAMP and, thus, prolonging the action of protein kinase
Stage A of Heart Failure
- High risk, no symptoms
- HTN
- DM
- Family history
- High sodium and alcohol intake
- Poor diet and exercise
- Loop diuretics prescribed
Stage B of Heart Failure
- Structural heart disease, no symptoms
- Diagnosed with HF
- ACE inhibitor or ARBs prescribed
Stage C of Heart Failure
- Cardiac dysfunction present
- Symptomatic
- β-blockers added
Stage D of Heart Failure
•Remain symptomatic despite optimal drug
therapy and treatment
•Surgical options necessary
•Heart transplant
•LVAD or BiVAD
•Pacemaker placementwhat is stage A
- at high risk for HF but without structural heart disease or symptoms of HF
what is stage B
- structural heart disease but without signs or symptoms of HF
what is stage C
- structural heart disease with prior or current symptoms
what is stage D
advanced HF
