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Heart Failure 2


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What are the causes of right sided heart failure?
PE, COPD, interstial lung disease (sarcoidosis), chronic lung infection, pulmonary hypertension, left sided heart failure, stenosis of pulmonary valve, right ventricular infarct, ARDS
What are the clinical syndromes of coronary heart disease?
ACS (MI and unstable angina), angina pectoris, sudden death, chronic ischemic heart disease
95%, 75%, 60% each relate to what kind of specific stenotic changes within the heart?
95%= angina a rest; 75% angina w/ work; 60% = colateralization of vessels
Which comes first in the pathogenosis of atherosclerosis? A. Macrophages infiltrate wall and oxidize lipids B. Plaque formation on intimal wall
A.Macrophages infiltrate wall and oxidize lipids
What are th 4 factors that determine myocardial oxygen consumption?
Heart Rate
Wall Tension
What is the significance of creatine kinase as it relates to the heart?
It is the enzyme that converts ATP plus creatine to APD plus creatine phosphate and vice versa. This is all during glycolysis and the necessary production of ATP to make the cardiac cell have the energy it needs to contract. If that cell dies, the enzyme lyses out of the cell and is deteched on cardiac enzyme tests.
What is the problem in stable angina? How is it fixed?
Problem: vessel is partially blocked for a moment and that causes patient chest pain due to decreased availability of O2. Fixed: by rest and nitro.
If a patient has stable angina, what do we need to tell them so that they do not develop unstable angina?
Change diet (reduce sat. fat intake), get lipids down, increase exercise.
What are 2 other names for Prinzmetal Angina?
How do we treat this condition;
Unstable angina and variant angina.
(Hit the ER door)- 325 mg chewed asprin, subligual nitro, O2, run EKG. Get history/physical and cardiac enzymes going. Get them started on IV nitro, IV morphine, (IV metoperol only in MI-use CCB in angina) clopidegril, ACE if not already on one, & LMWH/anti-coag (Lovenox). Use GPIIaIIIb inhibitor (Abciximab) if patient going to receive PCI OR if high risk patient.
What is the purpose of each of the treatments of a patient with angina? (10 drugs; NOT 3+ procedures yet)
1.aspirin: anti-platlet, 2.O2: need O2 to ischemic areas, 3/4.IV&subling. nitro: need to drop BP by venodilation, 5.morphine: reduce pain and thus sympath. stimulation, 6.metoperol: reduce sympath. stimulation and pain (only in MI not variant angina), 7.clopidegril: antiplatelet, 8.LMWH: Xa/hitting clotting cascade, 9.Abciximab: anti-platelet drug that inhibits final platelet aggregation stage (used prior to PCI, 10.ACE: vasodilator/RAA inhibitor
What is the PCI and what are the 2 possible procedure following the PCI to treat angina/MI? What are the restenosis rates in these procedures? What is the surgical option and restenosis rate?
PCI is percutaneous coronary intervention. It involves angiography and ink mapping out the occluded arteries. Balloon angioplasty, stent placement are the possibilities from there. Balloons have a 30-40% restenosis rate and stents have 20-30%.
Surgical option is harvesting saphenous vein or internal mammary artery to do a CABG. Restenosis is highest with this route at 95% w/ mammary artery and 50% w/ saphenous vein each after 5 years.
How can interpretation of elevated ST segments be similar and different to T wave inversion?
ST segment elevation can mean ischemic changes BUT not necessarily injury. Inverted T waves mean injury.
What are the 2 most cardiac specifc enzyme to order in a suspected MI? What is the reference range for each? What cardiac enzyme stays elevated for the longest time?
Troponin (<.4ng/ml & elevated w/in 3 hrs) and CK-mb (<6% of total CK & elevated w/in 3 hours). Longest= LDH (160 hrs)
Why is it that there is an accumulation of lactate in an ischemic event?
Because lactate is a product of anaerobic metabolism which is the metabolism of ischemic areas.
What are the 4 main factors that affect CO?
HR, (SV), preload, afterload, contractility
What are the 2 cranial nerves that the baroreceptors affect?
What needs to be be done adn what meds need to be administered to reduce preload?
vasodilation-nitro, morphine
What are three elements that can increase afterload?
aortic stenosis, vascular resistance, increased diastolic pressure
What is the response to reduced SV immediately, after hours, after weeks?
Immediately- Baroreceptor activation
Hours- RAS
Weeks- LVH
What are the majority of HF classified as: systolic or diastolic?
What kind of EF is systolic HF associated with? What kind of EF is diastolic HF associated with?
Which type of HF is more associated with the elderly?
Systolic: <40%
Diastolic: >50%
Elderly HF= diastolic HF
Which 3 of the valvular defects are involved with systolic HF?
aortic stenosis, aortic regur, mitral regur
Name 2 cardiac problems that can lead to obstruction of left ventricle filling.
Which type of HF (systolic or diastolic) do these conditions lead to?
mitral stenosis; tamponade

Of the cardiomyopathies, which 2 are associated with diastolic HF?
Restrictive, hypertrophic
What grouping of effects are consistant between HF- backward effects or forward effects? What are those effects that they have in common?
Forward effects of restlessness, confusion, anziety, oliguria, fatigue, faint pulses, & increased HR.
What are common backwards effects of right sided HF?
Spleenomegally, hepatomegally, JVD, ascities, anorexia, subcutaneous edema
What are common backwards effects of left sides HF?
Dyspnea, paroxsysmal nocturnal dyspnea on exertion, orthopnea, cough, cyanosis, basilar crackles
What is it about ventricular remodeling that makes it detrimental to the heart?
Crazy, mutant myocytes are formed!
What chemical is activated during remodeling and what can we do about it? Why would we rather have fibrosis than remodeling?
AngII- use an ACE
We would rather have fibrosis than remodeling because fibrosis at least does not have mutant cells causing problems (as they would if left up to their own devices)
Describe the process that baroreceptors have on the heart?
The baroreceptors are activated and communicate with the brain to stimulate the SNS. This will in turn increase HR and contractility.
Briefly describe the different stages of heart failure- how many, how physical limitation changes throughout the stages.
There are 4 stages of HF.

Class I: No limitation of physical activity
Class II: Slight limitation of activity. Dyspnea and fatigue with moderate physical activity (e.g. walking up stairs quickly)
Class III: Marked limitation of activity. Dyspnea with minimal activity (e.g. slowly walking up stairs)
Class IV: Severe limitation of activity. Symptoms are present even at rest
A. What percentage of patients are alive after 5 years after a diagnosis of HF?
B. What percentage of patients are alive after 1 year if they are classified as a Class III or IV?
A. Only 50% of patients remain alive 5 years after the diagnosis of heart failure is made.

B. NYHA Class III or IV have a 1 year survival rate of 40%
When looking at a CXR how big should the heart be in relation to the diaphram?
1/2 the size.
When is BNP released from the heart?
What is BNP diagnostic for?at what level?
What other disease stage does an above normal BNP rule out?
BNP is released when ventricles are distended due to increased volume and pressure- tells the kidneys to unload volume.
BNP > 100 is diagnosic for CHF.
This level of >100 rules out COPD.
In terms of treatment of HF, what are 2 surgical procedures and 2 lifestyle changes that would help to treat the underlying condition?
Surgery: CABG and valve replacement.
Lifestyle: lower sodium intake adn alcohol intake. Alcohol causes fatty deposits on the the heart thus making the it less compliant and able to stretch.
What treatment of HF would we use to treat the acute symptoms?
Diuretic, vasodilator, positive ionotrop, reduce dietary sodium.
When using diuretics in HF, what are three possible problems that can occur if you get over zealous with the medication?
decreased CO, electrolyte imbalance, or RENAL FAILURE
When using a diuretic in HF, what are the 2 reasons to use them?
pulmonary edema or pulmonary congestion
Can you use a thiazide with a decreased GFR?
NO. Need normal renal function to use a thiazide.
In a physical exam, how would you detect pulmonary edema?
Rales- use lasix
What is another name for digitalis glycoside? Is this drug a positive or negative inotrop; positive or negative chronotrope?
What is a another commonly used positive inotrope in HF?
Positive inotrope and negative chronotrope.

Dopamine (beta agonist)
Administering 2-5 MCG's of digitalis produces what effect on the kidney?
What is the affect of 5-10 MCG's of digitalis?
-Increases renal blood flow

-Increased positive inotrophy and negative chronotrophy
What type of HF do we NOT WANT to use positive inotropes?
diastolic dysfunction
When it comes to vasodilators, what are the 3 common choices?
ACE (dilates arterial and venous vessels), NTG (venodilator), hydralizine (arterial dilator).
What are the acute symptoms of a patient with pulmonary edema?
Acute left-sided heart failure
Tachypnea, cold-clammy skin, coughing “frothy” sputum representing transudation of fluid into the alveoli
How do we treat that patient that has pulmonary edema?
Seat patient upright;, give O2, MgSO4 IVP, LASIX IVP, and NTG IV- Possible inotropic agents (negative inotropes in diastolic HF and positive inotropes in systolic HF)
Chamber dilation can occur in HF as a compensatory mechanism.
A. What are the two types of chamber dilation?
A. Eccentric and concentric
When chamber dilation begins in cardiac compensation of HF, what are 2 causes of new sacromeres aligning in series with old sarcomeres in that dilation process?
Causes:Mitral regurg and aortic regurg
-preload occurs
-(eccentric dilation)
Within cardiac compensatory dilation process, what are 2 causes of the sarcomeres aligning parallel to eachother?
Causes:Aortic stenosis and HTN
- afterload occurs
-(concentric dilation)
Which type of compensatory dilation is more forgiving in terms of impairing the hearts ability to restore CO?
If a patient comes into your office w/ syncope, what are the 3 broad classifications you are going to consider in evaluating the cause?
What is the most common cause of syncope?
Vasovagal, followed by cardiogenic
What does the treatment of syncope entail?
Treatment: After establishing the cause, treatment may include a pacer, vasovagal treatment, beta blockers, anticholingergics, vasoconstrictors, and maneuvers to decrease venous pooling.
When diagnosing syncope, what tests are going to be helpful?
Diagnosis: EKG, Holter, Electrophysiologic testing with patients that have high risk cardiogenic factors. Tilt table testing for vasovagal.

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