Rr-Symptoms-Orthopnea-Dyspnea

Front 1

CHF

Back 1

Heart is unable to pump blood at a rate sufficient ro meet the requirements of metabolizing tissues
Produces a complex of symptoms related to inadequate perfusion of tissues and retention of fluid (dyspnea, fatigues, pulmonary/periphery edema)

Front 2

Primary cause of CHF

Back 2

Impairment of the heart's ability to empty (systolic) and/or fill properly (diastolic dysfunction).

Front 3

Back 3

Front 4

Back 4

Front 5

Back 5

Front 6

Back 6

Front 7

Ventricular Remodeling

Back 7

Fundamental mechanism of myocardial dysfunction in heart failure
Hypertrophy and apoptosis of myocytes
Regression to a molecular phenotype that expresses fetal genes and proteins
Changes in the nature of the extracellular matrix

Front 8

Back 8

Front 9

What is a compensatory mechanism in response to a reduction in left ventricular systolic function?

Back 9

Activation of the sympathetic nervous system

Front 10

What's the first medication that should be administered in the ER for patients with CHF?

Back 10

Diuretics - for symptom relief

Front 11

JVP

Back 11

Important marker of the status of intravascular volume

Front 12

Back 12

Front 13

Regulation of Venous Return

Back 13

Affected by two main body pumps:
Respiratory pump:
Inspiration leading to decreased intrathoracic pressure resulting in increased venous return to the right atrium and an increase in preload.

Skeletal Muscle Pump:
Leg muscle contraction leads to increased venous return to right atrium and an increase in preload

Front 14

What can be targeted with meds for pts with HF?

Back 14

Afterload, preload, and contractility

Front 15

Diuretics

Back 15

Mainstay of heart failure management
Reduced fluid volume and preload
Reduction in heart size improves efficiency and reduces wall stress
Reduce edema

Front 16

Back 16

Front 17

Cardiac performance with systolic heart failure: preload

Back 17

Defined as LV filing
pressure/volume/fiber length

Relates to the Frank-Starling mechanism

Preload is usually increased because of increased blood volume and venous tone

Function of the curve is depressed

Reduction of high filling pressure is the goal of: salt restriction, diuretic therapy, and venodilators (nitrates)

Front 18

Back 18

Front 19

Preload

Back 19

Degree to which the myocytes are stretched prior to contracting
Related to the End Diastolic Volume
Atrial Pressure is a surrogate for preload
Affected by venous blood pressure and the rate of venous return

Front 20

How can you increase your Stroke Volume?

Back 20

By increasing preload up until point when curve plateaus

Front 21

Diuretic Side Effects

Back 21

Electrolyte abn
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypotension
Gout
Hearing loss (rare)
Increased incidence of digoxin toxicity
Renal insufficiency
Muscle cramps

Front 22

Back 22

Front 23

Pt with CHF has normal kidney function, which medication would you start?

Back 23

Enalapril (Ace-Inhibitor)

Front 24

Management after diuresis

Back 24

Afterload reduction
- ACE-I
- Hydralazine
- Nitroprusside (if severely hypertensive)

Front 25

Cardiac Performance with Systolic Heart Failure

Back 25

Resistance against which the heart must
pump (systemic vascular resistance)

• Failing heart is very sensitive to changes
in afterload

• Systemic vascular resistance is
increased due to increased sympathetic
activity and due to renin-angiotensin
system activation

• Reduced by: arterial vasodilators (ACE
inhibitors, ARBs, hydralazine)

Front 26

Afterload

Back 26

• Load against which the heart contracts to eject blood
• Tension within myocyte ≈ wall stress of the left ventricle during ejection
• Systolic aortic pressure is predominant determinant
• LV volume is another determinant
• Increased by HTN, aortic stenosis, coarctation of the
aorta , dilated LV cavity

Front 27

Neuro-hormonal response to CHF

Back 27

Front 28

Renin-Angiotensin-Aldosterone System

Back 28

Front 29

Back 29

Front 30

ACE-I primarily cause what change in the kidney?

Back 30

Dilation of the efferent arteriole

Front 31

Back 31

Front 32

Pt is tolerating enalapril with a systolic blood
pressure of 110/75. He continues to diurese on
diuretics. He can now lie flat and he is able walk the
hallways without any shortness of breath. You decide as his providing doctor to prescribe?

Back 32

BBlocker

Front 33

How do beta-blockers improve heart failure?

Back 33

•Upregulation of beta receptors
•Improved coupling of beta receptors to
secondary intracellular signals
•Alterations in myocardial metabolism
•Improved calcium transport
•Inhibition of renin-angiotensin system
•Inhibition of endothelial and cytokine
release

Front 34

Back 34

Front 35

Digoxin

Back 35

Glycoside derived plant species from genus digitalis (foxglove)
Only cardiac glycoside available in US
Chemically consists of a steroid nucleus linked to a lactone ring and a series of sugars

Front 36

Direct Effects of Digoxin:

Back 36

a. Positive inotropic effect
– Due to a direct effect to
increase the contractile state
of the myocardium
– Increases stroke volume

b. Increases vagal tone
– Slows heart rate

Front 37

Secondary effects of digoxin

Back 37

a. Decreased heart rate
b. Arterial and venous dilation
c. Decreased venous pressure
d. Normalized arterial baroreceptors

Front 38

Digoxin: Molecular site of action

Back 38

• Positive inotropic effect due to
inhibition of the Na+,K+-ATPase
– results in increased intracellular [Na+]
thereby decreasing driving force for Ca2+extrusion by Na+/Ca2+ exchanger
– indirectly results in increased
intracellular concentration of Ca2+

• K+ competes for binding of digoxin
to the Na+,K+ -ATPase

Front 39

Electrophysiological actions of digoxin

Back 39

• At therapeutic concentrations, mainly related to
increased vagal nerve activity
– Reduced firing rate of SA node
– Decreased conduction velocity in AV node
– Heart block can develop

• Main observation on the ECG – increased PR
interval

Front 40

Pharmacokinetics of Digoxin

Back 40

• t ½ = 36 h (permits daily dosing)

• Orally absorbed (60 – 75% absorbed)

• Excreted unchanged by the kidneys (renal elimination)

• Max. increase in contractility observed at serum concentration of 1.4 ng/ml

• Neurohormonal benefits occur at lower concentrations (0.5 – 0.8 ng/ml)

Front 41

Adverse effects and toxicity of Digoxin

Back 41

Front 42

Clinical use of digoxin

Back 42

Not a first-line treatment

• Use limited to heart failure patients with LV systolic
dysfunction in atrial fibrillation or in some cases to
patients in sinus rhythm who remain symptomatic despite maximal therapy with other therapies

• If used, administer a low dose that maintains serum
levels between 0.5-0.8 ng/ml

Front 43

HF prognosis correlates most strongly with?

Back 43

Impaired renal function

Front 44

What increases contractility?

Back 44

↑ intracellular Ca2+
– ↓ extracellular Na+ (↓ activity Na+/K+ pump
– Catecholamines (↑ Ca2+ pump in SR)
– Digoxin (↓ Na+/K+ pump → ↑ intracellular Ca2+)

Front 45

What decreases contractility ?

Back 45

– B1 blockade (↓ cAMP)
– Non-dihydropyridine Ca2+ channel blockers (verapamil
and diltiazem)
– Acidosis
– Hypoxia and hypercapnea

Front 46

Back 46

Front 47

Back 47

Front 48

Back 48

Front 49

Diastole

Back 49

- Initiated by T-wave on ECG
- Isovolumic relaxation
- Mitral and tricuspid valves open
- Early rapid filling
- Slow filling
- Atrial contraction

Front 50

Systole

Back 50

- Initiated by QRS complex on ECG
- Isovolumic contraction
- Rapid ejection
- Reduced ejection

Front 51

Back 51

Front 52

What is true regarding ejection fraction (LVEF) in patients with heart failure?

Back 52

A dilated, thin-walled ventricle usually has a reduced LVEF

Front 53

Back 53

Front 54

Back 54

Front 55

Back 55

Front 56

Back 56

Front 57

Back 57

Shifts the curve

Front 58

A 56-year-old man presents with a 1-week history
of palpitations and shortness of breath. He has a
longstanding history of poorly controlled
hypertension. Physical examination reveals an
elevated blood pressure of 190/98 mm Hg, elevated
jugular venous pressure (JVP), mild hepatomegaly,
bilateral pedal edema, and rales at the lung bases.
Diagnostic studies reveal concentric left ventricular
hypertrophy without significant valvular
abnormalities on echocardiogram.

What drug is beneficial in the treatment of
the patient's condition by virtue of both
afterload and preload reduction?

Back 58

ACE-I

ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II (AII)
through ACE and thus results in favorable modification of the neurohormonal
activation in heart failure. They cause favorable hemodynamic effects by
causing peripheral vasodilatation, afterload, and blood pressure reduction.
They also bring about reduction in the preload through the reduction of
aldosterone, which in turn decreases sodium and fluid retention.

Front 59

Loop Diuretics

Back 59

reduce preload by reducing fluid volume

Front 60

Procainamide

Back 60

class Ia antiarrhythmic agent used in ventricular and
supraventricular arrhythmias.

Front 61

hydralazine

Back 61

used to reduce the afterload by decreasing peripheral vascular resistance and increasing heart rate, stroke
volume, and cardiac output.

Front 62

While performing an in vitro experiment on canine
myocardial cells, you administer an experimental
pharmacological agent that acts as a positive inotropic
cardiac agent. Administration of this same agent to
smooth muscle cells results in smooth muscle relaxation. What medication is the experimental agent most similar to?

Back 62

Milrinone

Used short-term in the treatment of decompensated heart failure. Milrinone is a positive inotropic cardiac agent that increases cellular cAMP by inhibiting phosphodiesterase III. On the other hand, this medication results in smooth muscle relaxation, leading to peripheral vasodilatation. Milrinone's vasodilating, inotropic action increases cardiac output and reduces left ventricular pressures without producing significant changes in heart rate and blood pressure.

Front 63

Amiodarone

Back 63

class III cardiac agent that prolongs the action potential duration and the QT interval on ECG by blocking potassium currents in cardiac muscle cells. The medication is used to treat ventricular arrhythmias and is also highly effective in treating supraventricular arrhythmias, such as atrial fibrillation.

Front 64

A 78-year-old female who is a known case of
congestive cardiac failure presents to the clinic with
complaints of a 2-day history of ulcers on her right
foot. Examination reveals bilateral pitting pedal
edema with 2 small 2X2 cm venous ulcers at the
medial malleolus of her right foot along with
increased jugular venous pressure (JVP),
hepatomegaly, and S3 gallop on cardiac
auscultation. The patient is advised to consider
compression stocking for the venous ulcer.

Application of compression stocking helps
reduction of edema through which of the
following hemodynamic mechanism?

Back 64

Increasing tissue hydrostatic pressure

Front 65

If left untreated, what is a long-term
complication of this patient's condition?

Back 65

Myocarditis

This patient's history and clinical picture is suggestive of Lyme disease. Lyme disease is an inflammatory disease characterized by a skin rash, joint
inflammation, and flu-like symptoms; it is caused by the bacterium Borrelia burgdorferi and is transmitted by the bite of a deer tick. The figure shows the classic appearance of the rash, erythema chronica migrans.

Front 66

A 60-year-old man you have been treating for
congestive heart failure symptoms has been
diagnosed with diabetes mellitus. The
endocrinologist who made the diagnosis
decided to treat the patient with glipizide 5mg
daily since his blood glucose readings are
280mg/dl. You manage the patient's congestive
heart failure with enalapril 10 mg daily, and he
takes a furosemide 20 mg daily if he needs it.

What kind of effect on the patient's hyperglycemia may be expected in these settings?

Back 66

Co-administration of ACE inhibitors (captopril,
enalapril) and oral sulfonylurea hypoglycemics
results in an increase of the hypoglycemic
effect, for which more careful monitoring of
blood glucose is advised to avoid pronounced
hypoglycemia. Co-administration of thiazide,
but not loop diuretics, results in a decrease of
hypoglycemic effect. There are no
documented interactions of furosemide and
sulfonylureas.

Front 67

A 72-year-old man presents with double vision,
weakness, fatigue, nausea, and abdominal
discomfort. He describes seeing everything
greenish. He suffers from congestive heart
failure and is treated for that with digoxin,
furosemide, and potassium. He has been taking
acetylsalicylic acid since a TIA 2 years ago. He
also takes amoxicillin for a urinary tract
infection.

What medication can cause his symptoms?

Back 67

Digoxin

Front 68

A 55-year-old man presents with dyspnea,
paroxysmal nocturnal dyspnea, nocturia, and
anorexia for the past 3 weeks. On examination,
he has mild pedal pitting edema. What is the
most common cause of his condition?

Back 68

Coronary Artery DIsease

Front 69

A 50-year-old man presents for physical
examination, which shows that when lying at an
angle, the vertical distance between his sternum
and the top pulsation of his jugular vein is 2 cm.
On inspiration, it increases to 3.5 cm. On
auscultation, his heart has a regular rate and no
murmur is heard. His lungs are clear to
auscultation. X-ray shows that his heart is a
normal size and there is no evidence of
pulmonary congestion. Cardiomyopathy is
suspected.

What is most likely the underlying cause in this patient?

Back 69

Amyloidosis is a possible cause of restrictive
cardiomyopathy. This patient presents with signs
and symptoms of restrictive cardiomyopathy. An
increase in central venous pressure with
inspiration is called Kussmaul's sign. Normally,
there is a decrease in jugular venous pressure
with inspiration. Kussmaul's sign can be seen with
restrictive cardiomyopathy. The heart is normal
sized with restrictive cardiomyopathy