Review Course Part 1 Lesson 1

Front 1

Lesson 1 Objective

Back 1

Describe the pathophysiologic changes that occur in HF.

Front 2

Purpose of the Cardiovascular System

Back 2

Oxygen Delivery: distributes oxygen-rich blood to cells in different parts of the body

Waste Removal: transport of by-products of cellular metabolism including carbon dioxide and lactic acid

Synthesis and Regulation of Hormones: The heart produces several hormones, including atrial and B-type natriuretic peptide

Front 3

Heart Anatomical Position

Back 3

-The heart is slightly to the left center of the chest

-2/3 to the left of the midline and 1/3 to the right of the midline

-Size of a mans fist

-Lies behind the sternum between the points of attachment of the 2nd and 6th ribs

-The apex is the pointed end and is the area of the point maximal impulse

-The base is located superiorly and medially. It forms the upper borders of the heart and lies below the second rib

Front 4

Heart Anatomical Position

Back 4

Front 5

Heart Wall

Back 5

Front 6

The wall of the heart has three distinct layers of tissue.

Back 6

1. Epicardium: thin, fibrous external surface where the coronary arteries lie

2. Myocardium: thick, middle layer with involuntary cardiac muscle cells that contract to propel blood

3. Endocardium: innermost layer, forms the smooth lining of the heart's chambers and also helps form the heart's valves

Front 7

Cardiac Muscle

Back 7

Front 8

Cardiac Muscle

Back 8

Green: purkinje fibers
Orange: capillaries
Pink: muscle fibers
Cardiac muscle: striated, single nucleus branched

Front 9

Pericardium

Front 10

Pericardium

Back 10

Thin membranous, fibroserous sacSurrounds and protects heartConfines and stabilizes position of heart

Front 11

Pericardial Space

Back 11

Located between pericardium and epicardiumContains pericardial fluid that acts as lubricant

Front 12

Lymphatic System

Front 13

Lymphatic System

Front 14

Lymphatic System

Back 14

Most fluid is absorbed by tissue cellsExcess drains into lymphatic capillaries and is eventually returned to the cardiovascular circulation

Front 15

Cardiac Output (CO)

Front 16

Cardiac Output (CO)

Back 16

CO is the volume of blood pumped by the ventricle per minute* CO = stroke volume X heart rate
* Cardiac index (CI) represents CO that has been adjusted to a person’s size or body surface area (BSA). Dividing CO by BSA will provide the CI.
* Stroke volume (SV): is the volume of blood pumped from the ventricle with each beat.Calculated by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV)
* Stroke volume can be measured by echocardiogram

Front 17

Preload

Front 18

Preload

Back 18

The stretching of the cardiac myocytes prior to contraction.Preload is the basis of the Frank-Starling Law* Preload is increased in a failing heart due to volume overload
* Preload is decreased in the presence of hypovolemia

Front 19

Frank-Starling Law

Back 19

Increased end-diastolic fiber (sarcomere) length, volume, and pressure (increased preload) yields increased cardiac outputThis is a physiologic mechanism to allow for the CO to be responsive to increased activityHowever, excessive preload (as found in HF) exhausts the Frank-Starling mechanism, such that further increase in preload no longer increases cardiac output.

Front 20

Frank-Starling Law

Front 21

Afterload

Front 22

Afterload

Back 22

The amount of resistance the ventricle has to overcome in order to eject blood

* Reflective of aortic pressure for left ventricle and pulmonary artery pressure for the right ventriclePressure in the ventricles must be greater than systemic and pulmonary pressure to open aortic and pulmonic valvesAs arterial pressure increases; afterload increasesAs afterload increases; cardiac output decreases

Front 23

Vascular Resistance

Front 24

Vascular Resistance

Back 24

The resistance to blood flow that must be overcome to push blood from the heart through the circulatory systemSystemic vascular resistance (SVR) is the resistance the left ventricle must overcome to pump blood through the systemic, or peripheral, circulationPulmonary vascular resistance (PVR) is the resistance the right ventricle must overcome to pump blood through the vasculature of the lungs

Front 25

Heart Failure (HF) Definition

Back 25

* HF is a complex clinical syndrome which can result from any structural or functional cardiac disorder that impairs ability of the ventricle to fill with or eject blood
* Cardinal symptoms are fatigue and dyspnea, and clinical signs are fluid retention and exercise intolerance
* HF is a progressive clinical syndrome that involves the interaction of multiple systems in the body

Back

Front 26

Causes of HF

Back 26

1. Coronary artery disease/myocardial infarction
2. Hypertension
3. Valvular disease
4. Genetic (e.g. Duchenne muscular dystrophy, certain hypertrophic cardiomyopathies)
5. Congenital abnormalities (e.g tricuspid atresia, septal defects)
6. Peripartum cardiomyopathy
7. Infiltrative cardiomyopathy (e.g amyloidosis, sarcoidosis, hemochromatosis)
8. Infections and inflammatory processes(e.g viral myocarditis, Chagas disease)
9. Metabolic disorders (e.g. hyperthyroidism, diabetes mellitus)
10. Toxins (alcohol, chemotherapy, radiation therapy, illicit drugs)
11. Incessant arrhythmias

Front 27

The Autonomic Nervous System

Front 28

The Autonomic Nervous System

Back 28

Short term control of blood pressure and heart rate

The Autonomic Nervous System

* Stress Response
* Sympathetic

Flight or Fight
* Parasympathetic​Rest and Digest

​​Antagonistic-most organs receive impulses from both divisions

Front 29

Renin-Angiotensin Aldosterone

Front 30

Renin-Angiotensin Aldosterone

Back 30

Long term control of blood pressure and volume

Front 31

Sympathetic Stimulation

Front 32

HF Pathophysiology

Front 33

Neurohormones in HF

Back 33

Atrial natriuretic peptide (ANP). Synthesized in atrial myocytesB-Type natriuretic peptide (BNP). Synthesized in ventricular myocytes* intrinsic diuretic; promotes natriuresis in fluid volume overload
* BNP secreted by ventricles secondary to wall stress/stretch, indicating high pressures. BNP is therefore a biomarker of cardiac pressure overload:Response to natriuretic peptides is attenuated in HF
* Elevated BNP is a significant predictor of mortality; corresponds proportionately with worsened HF/fluid retention
* May be higher secondary to renal failure, in women and older individuals; and lower in the presence of obesity

Front 34

Opposition of Neurohormonal Forces in HF

Front 35

Physiology of Endogenous hBNP

Front 36

Neurohormonal Activation

Front 37

Vasopressin (Anti-diuretic Hormone)

Back 37

Released in response to arterial underfilling/reduced volume via high pressure baroreceptorsRegulates retention of water by stimulating renal tubular reabsorptionCauses congestion and hyponatremia

Front 38

Endothelin (ET)

Back 38

Vasoconstrictor peptide expressed in the myocardium stimulated by hypoxia, ischemia, neurohormonesIncreased levels contribute to progression of left ventricular dysfunction and secondary pulmonary hypertension

Front 39

Dysregulation of the Immune System

Back 39

HF causes immune activation of pro-inflammatory cytokines:* Tumor Necrosis Factor (TNF-α), Interleukin (IL-1, IL-6)
* These are over-expressed in the systemic circulation and myocardium. Sustained over-expression contributes to central and peripheral manifestations
* Effects of pro-inflammatory cytokines on left ventricular function:Exert negative inotropic effect
* Induce abnormalities in cardiac metabolism
* Promote myocardial remodeling
* Cardiomyocyte hypertrophy
* Necrosis and Apoptosis (programmed cell death)
* Endothelial dysfunction

Front 40

Types of HF

Front 41

Diastolic Dysfunction or HF with Preserved Ejection Fraction (HFpEF)

Back 41

HF symptoms with EF > 50%Caused by hypertrophic CM, HTN, Ischemia, AgeImpairment of left ventricular myocardial relaxation and diastolic ventricular filling; increased left ventricular wall stiffness; reduced left ventricular compliance

Front 42

Systolic Dysfunction or HF with Reduced Ejection Fraction (HFrEF)

Back 42

Decreased contractility EF < 40%CAD, Valve disease, Ischemic and Idiopathic CMPDecreased stroke volumeImpaired contraction with forward or backward failure

Front 43

Differentiating Between the Definitions of HF

Back 43

Decompensated

Advanced

Reduced Ejection Fraction

Preserved Ejection Fraction

Front 44

Decompensated

Back 44

Decompensated HF exists when the LV is unable to maintain cardiac output to meet the demands of the body and worsening symptoms emerge

Front 45

Advanced

Back 45

Advanced HF exists when symptoms and NYHA class are refractory to medical management

Front 46

Reduced Ejection Fraction

Back 46

HF with reduced ejection fraction exists when there is a reduced LVEF with HF symptoms.The LV is commonly dilated

Front 47

Preserved Ejection Fraction

Back 47

HF with preserved ejection fraction exists when patient present with symptoms of heart failure but the LVEF is normal.

Front 48

Normal Cardiac Pressures

Front 49

Central venous pressure (CVP) 0-5 mm Hg

Back 49

Pressure of blood in the vena cava, near the right atriumReflects the amount of blood returning to the heartGood approximation of right atrial pressure

Front 50

Right ventricular pressurevc

Back 50

Systolic – 15-30 mm HgDiastolic – 0-5 mm Hg

Front 51

Pulmonary artery pressure

Back 51

Systolic – 15-30 mm HgDiastolic – 5-10 mm Hg

Front 52

Pulmonary capillary wedge pressure (PCWP) 6-12 mm Hg

Back 52

Indirect pressure of left atrial pressurePulmonary edema reflective of PCWP >25 mm Hg

Front 53

Left ventricular systemic pressure (systolic)

Back 53

100-140 mm Hg

Front 54

Pulmonary vascular resistence (PVR)

Back 54

(PAP-PCWP)* 80 } / (CO) =150-250 dynessec/cm^5PAP- PCWP/ CO= PVR in wood unitsAn increase in PVR can result in RV failureAbnormally high PVR can be a contraindication to cardiac transplantation as it could cause RV dysfunction in the transplanted heart

Front 55

Systemic vascular resistance (SVR)

Back 55

SVR = (MAP - CVP) x 80 / CONormal SVR range is 800 - 1200 dyn·s·cm−5

Front 56

Intra-cardiac Pressures Guide Diagnosis and Treatment of HF

Back 56

Compensatory mechanisms increase blood flow in addition to cardiac filling pressures to maintain pumping function and supply adequate blood flowDamaged myocardium stretches out of shape causing increased filling pressures

Front 57

Fluid Imbalance in HF

Front 58

Fluid Imbalance in HF

Back 58

Blood plasma and the interstitial fluid exchange readily through the thin walls of the capillariesThe primary forces that govern this exchange are:* Outward hydrostatic pressure
* Inward oncotic pressure (osmosis)

Front 59

Fluid Imbalance in HF

Back 59

When the heart’s function is compromised, venous hydrostatic pressure rises. The increased venous pressure is transmitted back to the capillaries.* Sodium and water retention result in increased capillary hydrostatic pressure and decreased capillary oncotic pressure
* In the setting of HF, net flow of fluid goes into the interstitial space, resulting in excess fluid accumulation, or edema
* Volume overload results from inappropriate renal sodium and water retention (decreased sodium and water excretion) in the setting of already normal or increased extra cellular fluid volume.

Front 60

More on Fluid Imbalance…

Back 60

Baroreceptor sensing of arterial under filling can occur as result of a decrease in cardiac output, even though blood volume is not decreasedNeurohormonal mechanisms are activated and cause renal sodium and water retentionEstimated 15% of total blood volume resides in arterial circulation; total blood volume increased primarily by expansion of blood volume in venous circulation, which then produces peripheral edema and ascites

Front 61

Perils of Elevated Pulmonary Vascular Resistance (PVR)

Back 61

In patients with end stage HF, elevated PVR is a possible contraindication to cardiac transplantationElevated PVR causes RV dysfunction or failure and death in heart transplant recipients especially in the first month after transplant

Front 62

Myocardial Remodeling

Back 62

Alteration in the structure (dimensions, mass, shape) of the heart muscle in response to the hemodynamic changes and/or cardiac injury in association with neurohormonal activation

A remodeled heart is less elliptical and more spherical

Left ventricular dilatation

Left ventricular hypertrophy

LV remodeling may occur with a process that can create volume overload such as:

* Aortic stenosis
* Hypertension
* Valvular incompetence such as mitral regurgitation​

Front 63

Cardiorenal Syndrome

Back 63

Cardiorenal syndrome occurs when reduction in cardiac output results in disproportionate reduction in renal perfusion

Leads to diminished glomerular filtration rate (GFR) and increased serum creatinine levels

Worsening renal function:* Change in serum creatinine >0.3 mg/dL or >25% over baseline (normal range: adult male: 0.8 to 1.4 mg/dL; adult female: 0.6 – 1.4 mg/dL)
* >70% of patients will experience increase in creatinine during hospitalization
* 20% to 30% of patients experience increase of >0.3 mg/dL
* Any increase of >0.3 mg/dL is associated with longer length of stay and increased mortality

Front 64

Cardiorenal Syndrome

Back 64

Cardiorenal Syndrome is a complex interaction between the heart and kidneys resulting in bidirectional injury and dysfunction

•There are 5 subcategories

◦ADHF leading to acute renal failure (ARF)

◦Chronic HF leading to chronic kidney disease (CKD)

◦ARF leading to cardiac event

◦CKD leading to worsening CV disease

◦Acute illness (i.e. sepsis) leading to simultaneous heart and kidney failure

Front 65

Pathophysiology of Cardiorenal Syndrome

Front 66

Hyponatremia

Back 66

Hyponatremia defined as serum sodium concentration <136 mmol/L

•Mild hyponatremia is seen in approximately 25% of patients with acute HF

•Hyponatremia poses significantly greater risk of death after discharge

•Reduction in cardiac output triggers hyponatremia

Front 67

Hyponatremia as a Prognostic Tool

Back 67

Hyponatremia is one of the strongest predictors for poor outcomes in HF patients

•Hyponatremia may be caused by multiple factors:

◦RAAS: Aldosterone causes sodium and water retention.

◦Antidiuretic Hormone, Vasopressin

◦Impaired renal function leads to a decreased ability of the kidneys to excrete sodium and water.

•Efforts should be made to limit nephrotoxic medications and therapies such as:

◦Dye loads

◦Non-steroidal anti-inflammatory drugs (NSAIDs)

◦Antibiotics

Front 68

Diuretic Resistance

Back 68

Diuretic Resistance is the persistence of congestion despite diuretic therapy

◦May result from renal under-perfusion

◦Distal tubules develop hypertrophy

◦There is enhanced sodium reuptake downstream from loop diuretic site of action

◦Oral absorption of loop diuretics is impaired in the setting of gut hypoperfusion and edema

•Treatments ◦Restricting sodium intake◦Change timing of diurectic dose

◦Use of combination diuretic therapies.

◦Ultrafiltration and hemodialysis

Front 69

1. This is the resistance against which the ventricle must generate pressure in order to eject blood out of the heart during systole:

Choose one:

Preload

End-diastolic volume

Afterload

Pulmonary vascular resistance

Back 69

Afterload

Front 70

2. Which of the following BNP concentrations is consistent with a diagnosis of severe or acute decompensated heart failure (ADHF)?

Choose one:

5 pg/mL

76 pg/mL

269 pg/mL

4,000 pg/mL

Back 70

4,000 pg/mL

Front 71

3. Which statement is false regarding HFpEF?

Choose one:

Impairment of left ventricular relaxation

Increased left ventricular wall stiffness; reduced compliance

Impaired diastolic ventricular filling

Not as common as HFrEF

Back 71

Not as common as HFrEF

Front 72

4. Pathologic remodeling occurs with:

Choose one:

Pressure overload (eg, aortic stenosis, hypertension)

Volume overload (eg, valvular regurgitation)

Following cardiac injury (eg, MI, myocarditis, or idiopathic dilated cardiomyopathy)

All of the above

Back 72

All of the above