test 1 Flashcards
1
Q
What is Heart Failure (HF)
A
- 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
2
Q
Two Major Types of Heart Failure
A
- Systolic and Diastolic
3
Q
Systolic Failure
A
- Reduced pumping action (contractility)
- Reduced ejection fraction
- ~50% of HF patients
* “younger”
4
Q
Diastolic Failure
A
- Stiffening and loss of adequate relaxation
- Reduced filling and cardiac output
- ~50% of HF patients
* “older”
5
Q
Heart failure causes edema how (2)
A
- 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
6
Q
HF Treatment Goals (3)
A
- Reducing symptoms
- Slow disease progression
- Improve survival
7
Q
Causes of Heart Failure (6)
A
- Ischemia
- Cardiomyopathy
- Myocarditis
- HTN
- Valve disease
- Congenital defects
8
Q
Ischemia leading to HF
A
- Coronary artery disease
- Multiply MIs
- Most common
9
Q
Cardiomyopathy leading to HF
A
- Damage to the heart muscle
- Infection
- Alcohol abuse
- Drug abuse
- Genetics
10
Q
Myocarditis leading to HF
A
- 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
11
Q
HTN leading to HF
A
- Heart has to work harder to pump blood to body
* Causes heart to become thicker and stiffer
12
Q
Valvular Disease leading to HF
A
- Stenosis
* Insufficiency
13
Q
Congenital Defects leading to HF
A
- Bicuspid aortic valve
- Renal artery stenosis
- Coarctation of aorta
- Cushing’s syndrome
14
Q
HF Symptoms
A
- Shortness of breath (dyspnea)
- Orthopnea
* Dyspnea lying down - Fatigue
- Peripheral edema
- Decreased exercise tolerance
15
Q
Three Major Compensatory Mechanisms
A
- Increased sympathetic activity
- Activation of the renin-angiotensin aldosterone
system - Myocardial hypertrophy
16
Q
Increased Sympathetic Activity as a compensatory mechanism
A
- 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
17
Q
Activation of the Renin-angiotensinaldosterone
System (RAAS) as a compensatory mechanism
A
- 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
18
Q
Myocardial Hypertrophy as a compensatory mechanism
A
- Thickening of the heart muscle
* Decrease in size of the chambers - Chambers dilate
19
Q
Cardiac Remodeling
A
- 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
20
Q
Seven Classes of Drug for Treatment of Heart Failure
A
- ACE inhibitors
- ARBs
- Aldosterone blockers
- β-blockers
- Diuretics
- Direct vaso - and venodilators
- Inotropic agents
21
Q
what do ACE Inhibitors do
A
- 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
22
Q
ACE Inhibitors: Adverse Effects
A
- DRY MOUTH
- Rash
- Fever
- Angioedma
- Hypotension
- Hyperkalemia
- Fetal malformations
23
Q
what do Angiotensin Receptor Blockers (ARBs) do
A
• 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
24
Q
ARBs: Adverse Effects
A
- Similar to ACE inhibitors
* Less risk of cough - Should not be combined with ACE inhibitors
* Similar mechanism and adverse effects - Teratogenic
25
what do Aldosterone Antagonists do
* Block aldosterone
* Prevents salt and water retention
* Prevents myocardial hypertrophy
26
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
27
β-blockers: Adverse Effects
* Bradycardia
* Hypotension
* Fatigue
* Insomnia
* Sexual dysfunction
* Alter lipid panel
* Decrease HDL
* Increase triglycerides
28
what do Diuretics do
* Relieve pulmonary congestion and peripheral edema
* Decrease plasma volume
* decrease preload/afterload
* Loop diuretics commonly used
29
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
30
what does Hydralazine do
* Relaxes vascular smooth muscle mainly in arteries and arterioles
* Decreases SVR and CO by releasing nitric oxide from the endothelium
31
what does Hydralazine and isosorbide dinitrate do
* Fixed dose combo (Bidil)
| * Been shown to improve survival in the African/American community
32
Vaso – and Venodilators: Adverse Effects
* Headache
* Hypotension
* Reflex tachycardia
33
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
34
Inotropes: Cardiac Glycosides/Digitalis
* Come from the digitalis (foxglove) plant
* Low therapeutic index
* Digoxin
35
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
36
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)
37
Digoxin: Adverse Effects
* Digoxin toxicity
* Arrhythmias
* Anorexia
* Nausea
* Vomiting
* Blurred vision
* Severe Toxicity
* V-Tach
* Administration of digoxin antibody
* Digibind
38
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
39
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
40
how do inotropes work
1. binding of a β-agonist, such as dopamine or dobutamine, activates adenylyl cyclase, which produces cAMP
2. cAMP activates protein kinase, which in turn phosphorylates Ca2+ channels
3. Phosphorylation of Ca2+ channels increases Ca2+ flow into the cell, causing increased force of contraction of the heart
4. Phosphodiesterases inhibitors prevents hydrolysis of cAMP and, thus, prolonging the action of protein kinase
41
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
42
Stage B of Heart Failure
* Structural heart disease, no symptoms
* Diagnosed with HF
* ACE inhibitor or ARBs prescribed
43
Stage C of Heart Failure
* Cardiac dysfunction present
* Symptomatic
* β-blockers added
44
Stage D of Heart Failure
```
•Remain symptomatic despite optimal drug
therapy and treatment
•Surgical options necessary
•Heart transplant
•LVAD or BiVAD
•Pacemaker placement
```
45
what is stage A
- at high risk for HF but without structural heart disease or symptoms of HF
46
what is stage B
- structural heart disease but without signs or symptoms of HF
47
what is stage C
- structural heart disease with prior or current symptoms
48
what is stage D
advanced HF
