Term
| What is the difference between Cardiomyopathy and Heart Failure? |
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Definition
Heart failure is a constellation of clinical signs and symptoms reflecting either 1) inadequate CO or 2) excess fluid retention.
Cardiomyopathies are may or may not cause systolic myocardial dysfunction. |
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Term
| What signs/symptoms are associated with excess volume in HF? |
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Definition
1) Signs
- Distended JVP
- Elevated JVP pulsation
- S3
- Ascites
- Sacral/pedal edema
- Liver congestion
2) Symptoms
- Dyspnea or Orthopnea (when lying flat)
- Nocturnal dyspnea
- Abdominal bloating
- RUQ tenderness |
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Term
| What signs/symptoms are associated with decreased CO in HF? |
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Definition
1) Signs
- Decreased mentation and confusion
- Cool extremities
- Cyanosis/pallor
- Renal dysfunction
2) Symptoms
- Decreased appetite
- Weakness and fatigue
- Poor sleep
- Forgetfulness |
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Term
| How do the NYHA functional class system and the ACC/AHA Stages of HF systems differ in classification of HF? |
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Definition
1) NYHA based on inability to perform daily activities
- If patient responds to medical therapy, stage changes
- Stages I-IV
2) ACC/AHA based on progressiveness of illness
- not reversible based upon medical treatment
A- Risk factors
B- Structural changes with or w/o symptoms
C- Symptoms developed
D- end-stage HF |
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Term
| Why are heart failure rates rising despite falling CHD mortality rates? |
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Definition
Aging population with risk factors like HTN, Obesity, Valvular heart disease and CAD
**Also those that survive CHD tend to get HF, as it is the final stage of CVD** |
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Term
| Why might women have better survival compared to men with HF? |
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Definition
| They tend to have diastolic HF, rather than systolic HF. |
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Term
True or False:
African Americans have higher risk of HF due primarily to socioeconomic inequality. |
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Definition
False
This is an issue, but there are also differences in neurohormonal activation (NOS SNPs) in HF between races |
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Term
| What differentiates NYHA class II patients from class IV patients in terms of likely causes of mortality? |
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Definition
Class II tend to suffer SCD (arrythmias), while class IV tend to die of CHF.
SCD accounts for majority overall |
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Term
| What happens to HF incidence after age 45? |
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Definition
| Risk doubles every decade! |
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Term
What happens to the LV PV loops with
1) Systolic dysfunction?
2) Diastolic dysfunction? |
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Definition
1) Curve shifts to right and becomes thinner
- Lower contractility (ESPVR slope)
- Higher EDP for given EDV
- Decreased SV
2) Shifts loop upwards
- Normal contractility
- Decreased SV
- Maintained LVED volume results in higher LVED pressure (less filling volume for a given pressure) |
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Term
| What 2 factors contribute to plateau in the PV curve of a frank-starling relationship (i.e. changes in VR and/or LVEDP don't increase SV)? |
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Definition
1) Heart reached maximum contractile capacity
- Decreased calcium ability leads to decreased affinity of calcium for troponin C
- Sarcomeres may be too long and not overlap
2) Cardiac compliance reduced with heart disease |
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Term
| What are the main determinants of preload, afterload and inotropy and how might they relate to HF physiology? |
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Definition
1) Preload (Load on myocardial wall in diastole)
- VR
- Regurgitant blood from aortic or pulm stenosis
- DOES NOT EFFECT SV
2) Afterload (force resisting contraction)
- Stenosis or arterial stiffness would increase
3) Inotropy
- Increase in order to increase SV |
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Term
What effect would each of the following have on SV and LVEDV
1) decreased preload
2) decreasing afterload
3) increasing inotropy |
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Definition
1) No change in SV, but LVEDV is decreased
2) Increased SV, causing decrease LVEDV
3) Increased SV (and CO), but NOT LVEDV (changes ESV) |
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Term
| Why do inotropic agents not alter LV EDV, even though they increase SV? |
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Definition
Inotropes increase contractility and CO
SV= EDV-ESV, and increasing ESPVR slope increases contractility AND decreases ESV. So SV increases without a change in EDV
With inotropes, you are not changing peripheral resistance, so you still need a strong contraction (e.g. large pre-load from EDV). This is NOT the case with decreasing after-load, where you do not need the same force, so EDV can be decreased. |
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Term
| What are the 5 major determinants of CO? |
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Definition
1-4 influence SV
1) Preload
2) Afterload
3) Contractility
4) Relaxation
5) HR |
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Term
What changes in each of the following increase preload?
1) Total body volume
2) Body position
3) Venous tone
4) Atrial contraction
5) Skeletal muscle contraction
6) Intra-pericardial pressure
7) Intra-thoracic pressure
8) valvular heart disease |
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Definition
1) Increase (hydration/perfusion)
2) Standing to supine
3) Venocontraction
4) Sinus rhythm (vs. atrial fibrillation)
5) Increased contraction
6) Pericardiocentesis (reduce the pressure)
7) Inspiration
8) Aortic regurgtiation (LV) or Pulmonic regurg (RV) |
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Term
| How can you clinically approximate changes in preload? |
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Definition
Swan Ganz catheter in pulmonary artery to estimate LA pressure
** things that cause LA pressure to decrease (blood loss, loss of vascular tone, tension pneumothorax/increased intrathoracic pressure) will decrease preload** |
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Term
| Why do you give arterial vasodilators in systolic heart failure? What kinds of drugs do you give? |
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Definition
Decrease afterload (heart is particularly sensitive to afterload in systole, when contraction is impeded).
Give ACE inhibitors or ang-2 blocker to increase SV and improve CO. |
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Term
| Why does LVED pressure increase, but LVED volume remain constant in diastolic dysfunction? |
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Definition
| Decreasing compliance means that less of a change in volume will cause a greater increase in pressure (change in afterload). |
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Term
| What does wall stress have to do with the major risk factors for HF? |
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Definition
Laplace: T= Pr/thickness
1) HTN or stenosis (after-load)
- increased pressures, so wall stress increases
- hypertrophy will follow to compensate
2) Regurgitation/Volume overload (Pre-load)
- LV dilates to accomodate increasing pressures (increasing compliance), and increased radius increases wall stress |
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Term
True or False:
Afterload does not affect contractility. |
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Definition
False!
Preload does not effect contractility
Afterload requires an increase in contractility to maintain sV (otherwise SV and CO will go down). |
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Term
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Definition
Hallmark of HF caused by 1) myocardial injury, 2) altered loading conditions or 3) Excessive neurohormonal activation.
1) LV dilation accommodates increased volume without increasing LVED pressure
- long term increases wall stress cause histological changes: poor actin/myosin overlap correlates with clinical deompensation (transitioning from B to C or D) |
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Term
What adaptive changes occur as LV pump function declines due to underling injury?
How can these changes be a problem over time? |
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Definition
Changes
1) Salt/water retention (maintain SV)
2) SNS activation (preserve CO)
3) Vasodilatory molecules (NO, naturetic peptides, prostaglandins) to increase pre-load and decrease afterload
Problems
1) Neurohormonal increase in vascular resistance to maintain BP ultimately can lead to myocardial deterioration |
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Term
| How does Adrenergic activation differ from activation of the RAAS pathway? |
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Definition
1) Adrenergic activation responds to decreased MAP
2) RAAS activation is initiated by perceived decrease in intravascular VOLUME. |
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Term
| What cellular pathological changes occur in HF? |
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Definition
1) Myocyte necrosis and apoptosis (challenging to measure) causes replacement of myocytes with collagen and fibrosis, leading to dysfunction of viable myocardium
2) Disrupted myocardium has decreased capillary permeability and increased wall stress (so you get poor blood supply and hypertrophy) |
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Term
| Why are clinical sympathetic responses reduced in HF, despite increasing levels of catecholamines? |
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Definition
B-adrenergic desensitization.
Remember, these chemicals are trying to increase heart rate and contractility (B1) to maintain perfusion pressures |
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Term
| What is the role of the RAAS system in HF? How can it be bad? |
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Definition
Activated in response to volume loss (dehydration or bleed).
1) Renin in kidneys cleaves angiotensiogen to ang-1
2) ACE converts ang-1 to ang-2
3) ang-2 increases sodium reabsorption in proximal renal tubules AND stimulates aldosterone
**ang-2 also causes fibrosis and hypertrophy in myocardium via endothelin and TNF, as well as increasing afterload by causing arterial vasoconstriction** |
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Term
| How does ADH (Vasopressin) signaling relate to HF? |
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Definition
Produced in posterior hypothalamus and stored in pituitary
1) Increased plasma osmolality or decreased circulating volume leads to ADH release
2) V1 receptors cause vasoconstriction and V2 receptors in kidneys result in water reabsorption
3) In HF, high ADH levels lead to increased afterload and hyponatremic volume overload. |
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Term
| What are the effects of ANP and BNP in HF? |
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Definition
Get rid of excess fluid (overwhelmed in HF by RAAS and ADH)
Both increase peripheral vascular capacitance and decrease tone, thereby decreasing BOTH preload and after-load. They are useful biomarkers, but not treatments.
1) ANP stored in granules rapidly released from atrial myocardium, ventricular myocardium and kidneys (short half-life with large fluctuation)
2) BNP is mainly in ventricular myocardium (longer half-life and less fluctuation) |
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Term
| What are the basic strategies for lowering mortality in HF? |
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Definition
1) Reduce progress (neurohormonal intervention)
- ACE-I/ARB/Aldosterone blockers/Beta blockers/Nitrates/Hydralazines
2) Prevent complications (stroke and arrhythmias)
- Anticoagulation (Warfarin) for AWMI
- Arrhythmia (ICD if EF < 35% and maybe Beta-blocker) |
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Term
| What are the basic strategies for making a patient with HF feel better? |
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Definition
| Hemodynamic intervention to reduce volume overload (Diuretics) and increase CO (Positive inotropes) |
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Term
| What do endothelin and TNF have to do with LV remodeling and progression of HF? |
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Definition
These factors are activated by angiotensin 2 when it binds to AT1 receptor (low CO activates RAAS system).
These factors eventually lead to
1) Myocardial hypertrophy and fibrosis
2) Vasoconstriction and Na/Water retention (through aldosterone) in periphery |
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Term
| What is the utility of using an Ace-inhibitor to treat CHF progression? |
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Definition
Captopril (short-acting) and Enalapril (long-acting)
You want to prevent fibrosis, hypertrophy, vasoconstriction and water retention (high BP). They improve symptoms and prevent mortality
**Don't work with LV dysfunction** |
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Term
| What are the important side effects and contraindications of Ace inhibitor use for HF? |
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Definition
SE
1) Cough (bradykinin mediated)**
remember, most common cause is CHF, itself, so be sure!
2) Renal toxicity
3) Angioedema
4) Hyperkalemia
Contraindications
1) Renal failure |
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Term
| How does the action of an angiotensin receptor blocker differ from an ACE-inhibitor. Why use an ARB? |
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Definition
ARB's like Candesartan or Valsartan ($$$) inhibit the VT1 receptor, rather than the production of ang-2.
Use em' in Ace-intolerance (Cough ONLY), or as additive (not well supported. |
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Term
| A patient with distended JVP, S3 heart sound and difficulty breathing is on an Enalapril and develops a bad cough. What do you do? |
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Definition
This is ACE-inhibitor intolerance (Enalapril is long-acting ACE-i).
Put them on an ARB like Candesartan or Valsartan instead. |
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Term
| Why might you use an aldosterone receptor antagonist like Spironolactone in addition to an an ACE-inhibitor like Enalapril or Captopril? |
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Definition
ACE-inhibitors block aldosterone initially, but it ESCAPES after 12 weeks.
Addition of receptor blocker improves HF in class III-IV (anything above risk) |
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Term
| Why might you prescribe a beta-blocker for treatment of HF? |
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Definition
Use in class II-III (maybe IV), except Carvedilol is only agent useful for severe case (non-selective with alpha activity).
Rationale: Sympathetic overdrive that occurs in response to decreased CO in HF eventually leads to
1) cardiac injury/hypertrophy/arrhythmia
2) vasoconstriction
3) sodium retention in kidneys
Beta blocker will be initially negatively-inotopic, but will then be balanced by enhanced myocardial recovery (arresting remodeling and potentially reversing it)
**also prevent arrhythmia** |
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Term
| Why might you give your HF patients water pills when you are starting them on a new drug? |
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Definition
If it is a beta-blocker like Carvedilol, they may experience transient worsening of LV dysfunction/CO as well as fluid retention.
You want to prepare them for this, so that they will gain the benefits of stunted LV remodeling and arrhythmia protection down the line. |
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Term
| What are the major contraindications for beta-blocker use in HF? |
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Definition
1) Active volume overload
2) Hypotension
3) Bronchospasm (COPD OK, but not asthma)
4) Bradycardia (symptomatic or high-degree AV block especially) |
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Term
| What is the utility of nitrates and hydralazines in HF treatment? When is their use appropriate? |
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Definition
1) NO is good for contractility, vasodilation and stopping apoptosis (Nitrates kick it up)
Free radicals are bad for DNA (Hydralazines stop them)
2) Use in patients with renal dysfunction, where ACE-I/ARB are innefective.
**Hydralazine is a worry for anti-histone antibodies (induced-lupus)**
**Both reduce BP** |
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Term
| How can you control arrhythmia in HF? |
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Definition
1) ICD if EF< 35% (PROTECTS FROM DEATH)
2) Beta blocker may work
3) Anti-arrhythmics are BAD, except amiodarone is neutral |
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Term
| How can you help a patient with CHF breathe better? |
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Definition
Treat volume status (mostly), and CO if needed
1) Diuretics
2) Digoxin
3) Positive inotropes (Dobutamine)
4) Mechanical intervention (CRT, LVADs) |
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Term
Describe the 4 classes of CHF in terms of hemodynamic problems.
How are these split into forrester hemodynamic subsets? |
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Definition
Remember, CHF is a problem where the heart can either not sustain adequate perfusion, or can only due so at very high LVEDP!
1) Class I gets normal Cardiac index (CO/SA) at low LVEDP
2) Class II gets normal Cardiac index, but only at high LVEDP
3) Class III cant get Cardiac index up, but is not overloaded
4) Class IV cannot get Cardic index no matter what LVEDP
Wet is volume overload and cold is reduced CO
I is warm dry
II is warm wet
III is cold dry
IV is cold wet |
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Term
A patient has a JVP> 5cm with lung crackles, high filling pressures and normal CO.
What class do they belong to? |
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Definition
They are Warm and Wet (class II)
They have good CO, but are volume overloaded (JVP, lung crackles and high filling pressures) |
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Term
A patient has a JVP< 5cm with minimal crackles, no edema, increased creatinine and low CO.
What class do they belong to? |
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Definition
| This patient is not volume overloaded (JVD<5cm, minimal crackles and no edema), but has reduced CO (Cold Dry) |
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Term
How should you proceed medically for a patient with HF in each of the following classes?
1) Warm Dry
2) Warm Wet
3) Cold Dry
4) Cold Wet |
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Definition
1) Nada
2) Volume is issue, so Diuretics (II)
3) CO is issue, so inotropes (III)
4) Kitchen sink (IV) |
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Term
| Why should you be careful prescribing loop diuretics? Does it matter that a patient has CHF? |
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Definition
They are POTENT, and not self limited. You don't want to get them dehydrated!
Monitor renal function, but you have some room to work with in CHF |
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Term
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Definition
1) Contractility
2) Parasympathetic effects (decrease AV conduction velocity and increase effective refractory period)
** can make heart block in toxic concentrations**
3) Depolarizes resting membrane potential, decreased APD and enhanced automaticity (steeper phase 4)
**Arrhythmia risk** |
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Term
| What are the major contraindications for Digoxin use in CHF? |
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Definition
1) Cardiac
- A tach
- AV block
- Bradycardia
- Ventricular extrasystole
- Arrhythmia
2) CNS***** (yellow vision)
3) GI- Nausea |
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Term
| What EKG changes do you see in a patient on Digoxin? |
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Definition
Remember, Digoxin ONLY TREATS SYMPTOMS
1) Decreased R-T interval
2) T-wave inversion
3) Uncoupled P waves (toxic concentrations)
4) Bigeminy (toxic concentrations) |
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Term
True or False:
Digoxin can reduce mortality in CHF |
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Definition
False!
Only symptoms, and look out for nausea + arrhythmia + visual "halo" |
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Term
| When should you use Inotropes in CHF? |
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Definition
1) Beta agonists like Dobutamine/Epi and 2) PDE-inhibitors like Milrinone/Enoximone
**Stop those beta-blockers**
Cold and Wet (IV) to increase contractility
Use if
1) Signs of severely decreased CO
- Hypotension, renal insufficiency, mental status changes
2) Signs of refractory volume overload
- Lung congestion, peripheral edema, JVP |
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Term
| What are some major complications of using Beta-agonists like Dobutamine and Epinephrine or PDE-inhibitors like Milrinone and Enoximone? |
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Definition
Inotropes
1) Hypotension
2) Sinus tach
3) A fib
4) Ventricular ectopy/tachycardia
5) Ischemia (O2 demand)
6) Death!! |
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Term
| True or False: Digoxin and DIuretics improve symptoms but not survival in CHF. |
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Definition
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Term
True or False:
Dobutamine and Milrinone improve function but worsen survival. |
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Definition
| True! This is true of positive inotropes in CHF |
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