Heart Failure

Front 1

What are the causes of right sided heart failure?

Back 1

PE, COPD, interstial lung disease (sarcoidosis), chronic lung infection, pulmonary hypertension, left sided heart failure, stenosis of pulmonary valve, right ventricular infarct, ARDS

Front 2

What are the clinical syndromes of coronary heart disease?

Back 2

ACS (MI and unstable angina), angina pectoris, sudden death, chronic ischemic heart disease

Front 3

95%, 75%, 60% each relate to what kind of specific stenotic changes within the heart?

Back 3

95%= angina a rest; 75% angina w/ work; 60% = colateralization of vessels

Front 4

Which comes first in the pathogenosis of atherosclerosis? A. Macrophages infiltrate wall and oxidize lipids B. Plaque formation on intimal wall

Back 4

A.Macrophages infiltrate wall and oxidize lipids

Front 5

What are th 4 factors that determine myocardial oxygen consumption?

Back 5

Heart Rate
Afterload
Contractility
Wall Tension

Front 6

What is the significance of creatine kinase as it relates to the heart?

Back 6

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.

Front 7

What is the problem in stable angina? How is it fixed?

Back 7

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.

Front 8

If a patient has stable angina, what do we need to tell them so that they do not develop unstable angina?

Back 8

Change diet (reduce sat. fat intake), get lipids down, increase exercise.

Front 9

What are 2 other names for Prinzmetal Angina?
How do we treat this condition;

Back 9

Unstable angina and variant angina.
Treatment:
(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.

Front 10

What is the purpose of each of the treatments of a patient with angina? (10 drugs; NOT 3+ procedures yet)

Back 10

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

Front 11

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?

Back 11

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.

Front 12

How can interpretation of elevated ST segments be similar and different to T wave inversion?

Back 12

ST segment elevation can mean ischemic changes BUT not necessarily injury. Inverted T waves mean injury.

Front 13

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?

Back 13

Troponin (<.4ng/ml & elevated w/in 3 hrs) and CK-mb (<6% of total CK & elevated w/in 3 hours). Longest= LDH (160 hrs)

Front 14

Why is it that there is an accumulation of lactate in an ischemic event?

Back 14

Because lactate is a product of anaerobic metabolism which is the metabolism of ischemic areas.

Front 15

What are the 4 main factors that affect CO?

Back 15

HR, (SV), preload, afterload, contractility

Front 16

What are the causes of right sided heart failure?

Back 16

PE, COPD, interstial lung disease (sarcoidosis), chronic lung infection, pulmonary hypertension, left sided heart failure, stenosis of pulmonary valve, right ventricular infarct, ARDS

Front 17

What are the 2 cranial nerves that the baroreceptors affect?

Back 17

IX, X

Front 18

What needs to be be done adn what meds need to be administered to reduce preload?

Back 18

vasodilation-nitro, morphine

Front 19

What are three elements that can increase afterload?

Back 19

aortic stenosis, vascular resistance, increased diastolic pressure

Front 20

What is the response to reduced SV immediately, after hours, after weeks?

Back 20

Immediately- Baroreceptor activation
Hours- RAS
Weeks- LVH

Front 21

What are the majority of HF classified as: systolic or diastolic?

Back 21

Systolic

Front 22

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?

Back 22

Systolic: <40%
Diastolic: >50%
Elderly HF= diastolic HF

Front 23

Which 3 of the valvular defects are involved with systolic HF?

Back 23

aortic stenosis, aortic regur, mitral regur

Front 24

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?

Back 24

mitral stenosis; tamponade

Diastolic

Front 25

Of the cardiomyopathies, which 2 are associated with diastolic HF?

Back 25

Restrictive, hypertrophic

Front 26

What grouping of effects are consistant between HF- backward effects or forward effects? What are those effects that they have in common?

Back 26

Forward effects of restlessness, confusion, anziety, oliguria, fatigue, faint pulses, & increased HR.

Front 27

What are common backwards effects of right sided HF?

Back 27

Spleenomegally, hepatomegally, JVD, ascities, anorexia, subcutaneous edema

Front 28

What are common backwards effects of left sides HF?

Back 28

Dyspnea, paroxsysmal nocturnal dyspnea on exertion, orthopnea, cough, cyanosis, basilar crackles

Front 29

What is it about ventricular remodeling that makes it detrimental to the heart?

Back 29

Crazy, mutant myocytes are formed!

Front 30

What chemical is activated during remodeling and what can we do about it? Why would we rather have fibrosis than remodeling?

Back 30

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)

Front 31

Describe the process that baroreceptors have on the heart?

Back 31

The baroreceptors are activated and communicate with the brain to stimulate the SNS. This will in turn increase HR and contractility.

Front 32

Briefly describe the different stages of heart failure- how many, how physical limitation changes throughout the stages.

Back 32

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

Front 33

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?

Back 33

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%

Front 34

When looking at a CXR how big should the heart be in relation to the diaphram?

Back 34

1/2 the size.

Front 35

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?

Back 35

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.

Front 36

In terms of treatment of HF, what are 2 surgical procedures and 2 lifestyle changes that would help to treat the underlying condition?

Back 36

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.

Front 37

What treatment of HF would we use to treat the acute symptoms?

Back 37

Diuretic, vasodilator, positive ionotrop, reduce dietary sodium.

Front 38

When using diuretics in HF, what are three possible problems that can occur if you get over zealous with the medication?

Back 38

decreased CO, electrolyte imbalance, or RENAL FAILURE

Front 39

When using a diuretic in HF, what are the 2 reasons to use them?

Back 39

pulmonary edema or pulmonary congestion

Front 40

Can you use a thiazide with a decreased GFR?

Back 40

NO. Need normal renal function to use a thiazide.

Front 41

In a physical exam, how would you detect pulmonary edema?

Back 41

Rales- use lasix

Front 42

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?

Back 42

Positive inotrope and negative chronotrope.

Dopamine (beta agonist)

Front 43

Administering 2-5 MCG's of digitalis produces what effect on the kidney?
What is the affect of 5-10 MCG's of digitalis?

Back 43

-Increases renal blood flow

-Increased positive inotrophy and negative chronotrophy

Front 44

What type of HF do we NOT WANT to use positive inotropes?

Back 44

diastolic dysfunction

Front 45

When it comes to vasodilators, what are the 3 common choices?

Back 45

ACE (dilates arterial and venous vessels), NTG (venodilator), hydralizine (arterial dilator).

Front 46

What are the acute symptoms of a patient with pulmonary edema?

Back 46

Acute left-sided heart failure
Tachypnea, cold-clammy skin, coughing “frothy” sputum representing transudation of fluid into the alveoli

Front 47

How do we treat that patient that has pulmonary edema?

Back 47

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)

Front 48

Chamber dilation can occur in HF as a compensatory mechanism.
A. What are the two types of chamber dilation?

Back 48

A. Eccentric and concentric

Front 49

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?

Back 49

Causes:Mitral regurg and aortic regurg
-preload occurs
-(eccentric dilation)

Front 50

Within cardiac compensatory dilation process, what are 2 causes of the sarcomeres aligning parallel to eachother?

Back 50

Causes:Aortic stenosis and HTN
- afterload occurs
-(concentric dilation)

Front 51

Which type of compensatory dilation is more forgiving in terms of impairing the hearts ability to restore CO?

Back 51

Eccentric

Front 52

If a patient comes into your office w/ syncope, what are the 3 broad classifications you are going to consider in evaluating the cause?

Back 52

Cardiovascular
Noncardiovascular
Unexplained

Front 53

What is the most common cause of syncope?

Back 53

Vasovagal, followed by cardiogenic

Front 54

What does the treatment of syncope entail?

Back 54

Treatment: After establishing the cause, treatment may include a pacer, vasovagal treatment, beta blockers, anticholingergics, vasoconstrictors, and maneuvers to decrease venous pooling.

Front 55

When diagnosing syncope, what tests are going to be helpful?

Back 55

Diagnosis: EKG, Holter, Electrophysiologic testing with patients that have high risk cardiogenic factors. Tilt table testing for vasovagal.