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___________________ Case Study Part 2: CHF__________________________

Clinical Course Day 1:
The patient is admitted to the telemetry floor for diabetic ketoacidosis and becomes your patient. The patient has been started on IV fluids and an insulin drip. After 8 hours of being under your care the patient complains of increasing shortness of breath and believes her swelling of lower extremities is worsening. You obtain vital signs:
Vital Signs: T: 99.8; HR: 110; R: 32; B/P: 172/98; O2 sat: 90% on 2 Liters O2 per NC
Stat labs and chest x-ray are obtained, and an echocardiogram and EKG have been ordered.

Na 134 mEq/L K 5.1 mEq/L Cl 109 mEq/L HCO3 17 mEq/L BUN 44 mg/dL Cr 1.5 mg/dL
Glucose 180 WBC 12.7 x 103/mm3 Hb 13.6 g/dl / Hct43%
BNP: 1025pg/ml patient Troponin I, High Sens: 15

CXR: Cardiomegaly with pulmonary venous hypertension. Evidence of mild pleural effusion. No consolidation or atelectasis noted

ECHO = EF(ejection fraction) = 38% EKG = Sinus tachycardia with rare PVCs

_____________________________________________________________________________________

Answer the following questions based on the information above:

6)The patient is noted to be in congestive heart failure. What lab results and diagnostic tests support this diagnosis? (3 points)

7) What are the contributing factors for CHF noted in the patient history (2 points) and assessment findings noted in the physical exam (2 points) that contribute and/ or relate to this diagnosis? (hint: see H&P from week 1).

8) The patient is a known hypertensive on medication, but her blood pressure continues to rise. Name three early compensatory mechanisms occurring in heart failure and the expected effect in compensation (6 points)

Compensatory Mechanism

Expected Effect

9) What physical findings would you look for to differentiate left heart failure from right heart failure? (4 points)

APA 1 point Scholarly Work 1 point Total points 19

Blood Pressure Regulation
Atherosclerosis
Dyslipidemia
NUR 41500
Pathophysiology

Hypertension
A consistent elevation of systemic arterial blood pressure
The most common primary diagnosis in the United States
Occurs in 1 out of 3 Americans and in 2/3 of those older than 60.
Risk increases with age
More common in blacks and those with diabetes

Pathophysiology
Hypertension results from
A sustained increase in peripheral resistance
An increase in circulating blood volume
Or— both of the above

Definitions
Systolic pressure: arterial pressure during ventricular contraction(systole)
Diastolic pressure: the arterial pressure during ventricular filling(diastole)
Pulse pressure: the difference between systolic and diastolic pressure
Mean arterial pressure: the average pressure in the arterial system during ventricular contraction and relaxation

Arterial Blood Pressure
Represents the pressure of the blood as it moves through the arterial system
Cardiac output = HR x SV
Vascular resistance (VR)
Mean arterial pressure = CO x VR

Mechanisms of Regulation
Short-term regulation: corrects temporary imbalances in blood pressure
Neural mechanisms
Humoral mechanisms
Long-term regulation: controls the daily, weekly, and monthly regulation of blood pressure
Renal mechanism

Factors determining BP
Systolic pressure
The characteristics of the stroke volume being ejected from the heart
The ability of the aorta to stretch and accommodate the stroke volume
Diastolic pressure
The energy stored in the aorta as its elastic fibers are stretched during systole
The resistance to the runoff of blood from the peripheral blood vessels

Systolic and Diastolic Pressure

Factors affecting BP
Age
More common in younger men than younger women
More common in the elderly
Race
More common in blacks than whites
Socioeconomic group
More common in lower socioeconomic groups

Categories of Hypertension

Primary hypertension (essential hypertension)
Occurs without evidence of other disease
Secondary hypertension
Results from some other disorder, such as kidney disease
Complicated Hypertension
Chronic hypertension resulting in target organ damage

Classifications of Hypertension
Systolic/diastolic hypertension
Both the systolic and diastolic pressures are elevated.
Diastolic hypertension
The diastolic pressure is selectively elevated.
Systolic hypertension
The systolic pressure is selectively elevated.

Non-modifiable Risk Factors for Hypertension
Family history
Age-due to arterial stiffness
Race
Gender

Modifiable Risk Factors (lifestyle)
High salt intake
Obesity
Excess alcohol consumption
Dietary intake of potassium, calcium, and magnesium
Oral contraceptive drugs
Stress

Stress does not cause hypertension but it can exacerbate it
14

Target Organ Damage in Complicated Hypertension
Heart
Hypertrophy, angina, heart failure, MI, sudden death
Brain
TIA, stroke, aneurysm, thrombosis, hemorrhage, dementia
Peripheral vascular
Atherosclerosis
Kidney
Nephrosclerosis, renal insufficiency or renal failure
Retinal vascular disease, exudates, hemorrhage

Pharmacological Tx
Diuretics
β-adrenergic–blocking drugs
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers
Calcium-channel–blocking drugs
Central α2-adrenergic agonists
α1-adrenergic receptor blockers
Vasodilators

Question
Renal failure results in Na+ and water retention. This results in hypertension. How would you classify this type of hypertension?

Primary hypertension
Secondary hypertension
Malignant hypertension
Systolic hypertension

Answer: secondary hypertension

Most common causes of secondary HTN:
Kidney disease –this is the number 1 cause of secondary hypertension
Adrenal cortical disorders
Pheochromocytoma
Coarctation of the aorta
Sleep apnea

Types of Hypertension in Pregnancy

Gestational hypertension
Chronic hypertension
Preeclampsia/eclampsia
Preeclampsia superimposed on chronic hypertension

Diagnosis & Tx of Hypertensionin Pregnancy
Early prenatal care
Refraining from alcohol and tobacco use
Salt restriction
Bed rest
Carefully chosen antihypertensive medications

Hypertension in Children
Blood pressure norms are based on age, height, and gender-specific percentiles.
Secondary hypertension is the most common form in this group
Kidney abnormalities
Coarctation of the aorta
Pheochromocytoma and adrenal cortical disorders
In infants, hypertension is associated most commonly with high umbilical catheterization and renal artery obstruction caused by thrombosis.

Orthostatic Hypotension
Definition
An abnormal decrease in blood pressure on assumption of the upright position
Causes
Decrease in venous return to the heart due to pooling of blood in lower part of body
Inadequate circulatory response to decreased cardiac output and a decrease in blood pressure

Causes of Orthostatic Hypotension
Conditions that decrease vascular volume
Dehydration (prolonged vomiting, GI suction)
Diuretics
Diaphoresis
Conditions that impair muscle pump function
Bed rest (↓ Fluid Volume)
Spinal cord injury
Conditions that interfere with cardiovascular reflexes
Medications
Disorders of autonomic nervous system
Effects of aging on baroreflex function

Clinical Manifestations Orthostatic Hypotension
Dizziness
Visual changes
Head and neck discomfort
Poor concentration while standing
Palpitations
Tremor, anxiety
Presyncope, and in some cases syncope

Question
Increased vascular compliance may contribute to which condition?

Systolic hypertension
Orthostatic hypotension
Diastolic hypertension

26

Answer
Systolic hypertension
Orthostatic hypotension: Orthostatic hypertension is the result of lower pressures, and increased compliance would decrease the vascular resistance and result in lower pressures.
Diastolic hypertension

Atherosclerosis
Arteriosclerosis
Thickening and hardening of the vessel wall.

Formation of a lesions called a plaques.

Results in ischemic syndromes that can vary widely in their severity and clinical manifestations.

The leading cause of coronary artery and cerebrovascular disease.

Evolution of Atherosclerosis

Pathophysiology of Atherosclerosis
Atherosclerosis begins with injury to the endothelial cells that line artery walls.

Possible causes of endothelial injury:
Smoking
Hypertension
Diabetes,
Increased levels of low-density lipoprotein (LDL)
Decreased levels of high-density lipoprotein (HDL)
Autoimmunity

Pathophysiology (Cont.)
Injured endothelial cells become inflamed. Inflammation plays a fundamental role in mediating the steps in the initiation and progression of atherogenesis.
The next step in atherogenesis occurs when inflamed endothelial cells express adhesion molecules that bind macrophages and other inflammatory and immune cells.
Macrophages are activated by binding to damage-associated molecular patterns (DAMPs) released from injured cells.
Hyperlipidemia, diabetes, smoking, and hypertension contribute to LDL oxidation and its accumulation in the vessel wall.
Lipid-laden macrophages are now called foam cells, and when they accumulate in significant amounts, they form a lesion called a fatty streak.

Pathophysiology (Cont.)
Macrophages also release growth factors that stimulate smooth muscle cell proliferation. Smooth muscle cells in the region of 610endothelial injury proliferate, produce collagen, and migrate over the fatty streak, forming a fibrous plaque.

Many plaques, however, are “unstable,” meaning they are prone to rupture even before they affect blood flow significantly and are clinically silent until they rupture

Plaques that have ruptured are called complicated plaques. Once rupture occurs, exposure of underlying tissue results in platelet adhesion, initiation of the clotting cascade, and rapid thrombus formation.

The thrombus may suddenly occlude the affected vessel, resulting in ischemia and infarction. Aspirin or other antithrombotic agents are used to prevent this complication of atherosclerotic disease.

Signs and Symptoms
Partial vessel obstruction may lead to transient ischemic events, often associated with exercise or stress.

As the lesion becomes complicated, increasing obstruction with superimposed thrombosis may result in tissue infarction. Obstruction of peripheral arteries can cause significant pain and disability.

Coronary artery disease (CAD) caused by atherosclerosis is the major cause of myocardial ischemia and is one of the most important health issues in the United States.

Atherosclerotic obstruction of the vessels supplying the brain is the major cause of stroke.

Treatment of Atherosclerosis

Obtaining a complete health history (including risk factors and symptoms of ischemia) is essential.

Physical examination may reveal arterial bruits and evidence of decreased blood flow to tissues.

Laboratory data that include measurement of levels of lipids, blood glucose, and hs-CRP are also indicated.

Current management with drugs aimed at stabilizing and reversing plaques before they rupture.

Prevention includes implementation of an exercise program, smoking cessation, and control of hypertension and diabetes where appropriate while reducing LDL cholesterol level by diet or medications, or both.

Dyslipidemia

The term lipoprotein refers to lipids, phospholipids, cholesterol, and triglycerides bound to carrier proteins. Lipids (cholesterol in particular) are required by most cells for the manufacture and repair of plasma membranes. Cholesterol is also a necessary component for the manufacture of such essential substances as bile acids and steroid hormones. Although cholesterol can easily be obtained from dietary fat intake, most body cells also can manufacture cholesterol.

The cycle of lipid metabolism is complex. A series of chemical reactions in the liver results in the production of several lipoproteins that vary in density and function. These include very-low-density lipoproteins (VLDLs), primarily triglyceride and protein; low-density lipoproteins (LDLs), mostly cholesterol and protein; and high-density lipoproteins (HDLs), mainly phospholipids and protein.

Dyslipidemia (or dyslipoproteinemia) refers to abnormal concentrations of serum lipoproteins. It is estimated that nearly half of the U.S. population has some form of dyslipidemia, especially among white and Asian populations.
Combination of genetic and dietary factors.
Secondary causes:
Diabetes, hypothyroidism, pancreatitis, and renal nephrosis, as well as the use of certain medications.

Criteria for Dyslipidemia

Optimal Near-Optimal Desirable Low Borderline High Very High

Total cholesterol <200 200-239 ≥240 LDL <100 100-129 130-159 160-189 ≥190 Triglycerides <150 150-199 200-499 ≥500 HDL <40 ≥60 The role of LDL in Dyslipidemia LDL is responsible for the delivery of cholesterol to the tissues, and an increased serum concentration of LDL is a strong indicator of coronary risk. High dietary intake of cholesterol and saturated fats, in combination with a genetic predisposition to accumulations of LDL in the serum (e.g., dysfunction of the hepatic LDL receptor), result in high levels of LDL in the bloodstream. LDL also plays a role in endothelial injury, inflammation, and immune responses that have been identified as being important in atherogenesis. The term LDL describes several types of LDL molecules. Measurement of LDL subfractions allows for a better prediction of coronary risk. HDL and VLDL Low levels of HDL cholesterol also are a strong indicator of coronary risk. HDL is responsible for “reverse cholesterol transport,” which returns excess cholesterol from the tissues to the liver for processing or elimination in the bile. HDL also participates in endothelial repair and decreases thrombosis. It can be fractionated into several particle densities (HDL-2 and HDL-3) that have different effects on vascular function. Exercise, smoking cessation,weight loss, fish oil consumption, and moderate alcohol use result in modest increases in HDL level. Despite the wealth of evidence that HDL plays an important role in preventing atherosclerotic coronary disease, studies have suggested that raising overall levels of HDL is not adequate to prevent cardiovascular disease. Niacin and fibrates are drugs that can cause modest increases in HDL levels that are not correlated with an improvement in cardiovascular risk in individuals without documented coronary disease (primary prevention). Drugs that are aimed specifically at increasing HDL levels include recombinant apolipoprotein A-I (ApoA-I) mimetics, thiazolidinediones (used to treat diabetes), and cholesteryl ester transfer protein inhibitors, but they have not been shown to be effective in preventing heart disease. Other lipoproteins associated with increased cardiovascular risk include elevated levels of serum VLDLs (triglycerides) and increased lipoprotein(a) levels. Triglycerides are associated with an increased risk for CAD, especially in combination with other risk factors such as diabetes. HDL and VLDL, continued Risk Factors Risk Factors Hypertension is responsible for a twofold to threefold increased risk of atherosclerotic cardiovascular disease. Cigarette smoking. Both direct and passive (environmental) smoking increase the risk of CAD. Diabetes mellitus. Good diabetic control is linked to reduced risk for CAD. Obesity/sedentary lifestyle. It is estimated that 65% of the adult population in the United States is overweight or obese, and an estimated 47 million U.S. residents have a combination of obesity, dyslipidemia, hypertension, and insulin resistance, called the metabolic syndrome, which is associated with an even higher risk for CAD events. Atherogenic diet. Diet plays a complex role in atherogenic risk. Diets high in salt, fats, trans-fats, and carbohydrates have all been implicated. HEART FAILURE NUR 41500 Heart Failure Costs estimated >$35 billion in the US
Leading cause of hospitalization of patients over 65 years in age.

Condition usually progresses with time

Function of the heart

Moves deoxygenated blood from the venous system through the right heart into the pulmonary circulation
Moves the oxygenated blood from the pulmonary circulation through the left heart into the arterial system
Right and left heart must maintain an equal output to function properly.

Heart Failure
Heart Failure Physiology
Heart unable to maintain adequate CO to meet body demands

Action of compensatory mechanisms

CO = HR x SV
(amount blood pumped every minute)

Heart Failure
Caused by any condition that reduces the pumping ability of the heart.

The consequence
 stroke volume and ejection fraction from
 increase in the residual volume left in the ventricle at the end of systole.

Over time, this extra remaining volume begins to dilate the ventricle.

COMPENSATORY Mechanisms–Early
Sympathetic Nervous System Stimulation
A. Reflex stimulation of SNS occurs in HF
Autoregulation

B. Helps perfuse heart & brain –
Blood gets diverted from skin, kidneys & GI tract to coronary & cerebral circulation

C. When HF persists too long & SNS overused:
May cause dysrhythmias
May wear out SNS nerve endings & exhaust supply of norepinephrine

COMPENSATORY Mechanisms–Early
Salt & Water Retention:

A: ↑ circulatory volume  ↑ venous return
in an attempt to ↑ CO

B: In HF, this mechanism makes heart work harder by ↑ blood volume & giving heart more blood to pump

C: The diversion of blood from kidneys & reduced CO both cause reduced renal perfusion

COMPENSATORY Mechanisms-Early
Renin-Angiotensin Aldosterone Mechanism.
This reduced renal perfusion leads to stimulation of Renin Angiotension cycle

Angiotensin II acts as vasoconstrictor, stimulating release of ADH (antidiuretic hormone)  retains water in circulation

RA cycle leads to release of aldosterone which ↑ tubular reabsorption of Na+ & water follows Na+ – end result is retention of sodium & water

COMPENSATORY Mechanisms–Early
Frank-Starling mechanism

Increases ventricular preload causing greater stroke volume (Increases CO)

This mechanism is only adaptive to a point.
Eventually mechanism fails as ventricle becomes overfilled & muscle becomes overstretched .

COMPENSATORY Mechanisms

CHF: classifications
Left/Right
High-output/Low-output
Systolic/Diastolic

Right-sided vs.
Left-sided failure
Classified as to which side of heart is failing
However, whether left or right, eventually, the failure becomes general & involves both sides

Right-sided Failure
Represents failure of the right heart to pump blood forward into the pulmonary circulation
Blood backs up in the systemic circulation
Causes peripheral edema (dependent extremities) and venous congestion of the abdominal organs
Also Manifests as weight gain
1000mL = 1 Kg (2.2#)
If congestion & edema severe enough 
engorged liver with death of liver cells,
external jugular veins remain engorged even when the person stands (JVD)
Ascites, hepatomegaly

Left-sided Failure
Represents failure of the left heart to move blood from pulmonary circulation into systemic circulation
Blood backs up in the pulmonary circulation
Fluid moves out of capillaries into surrounding alveoli
Excess fluid in lung tissue interferes with gas exchange
More respiratory signs (DOE, SOB) & Pulmonary Edema (complication)

The Role of
Increased Afterload (PVR) on the Pathogenesis of Heart Failure
Afterload: the amount of resistance the blood must overcome to be pumped out of the heart

HF Video

S/S of CHF
1.Edema – (right sided)

Mostly due to capillary pressure with fluid leaking into surrounding tissues

Salt & water retention adds to pressure –

Nocturia (Urination during nighttime)

when person is lying down dependent fluid in extremities is redistributed to central circulation & can then be excreted

S/S of CHF
2.Respiratory Symptoms – (left sided)

Dyspnea: Nocturnal dyspnea may occur when dependent edema 1st returns to general circulation & overloads pulmonary circulation

Bronchospasm may occur

May need several pillows to sleep(orthopnea)

S/S of CHF
3. Fatigue & weakness – (> w/ Left)
May occur with left-sided failure
CO is less

CO may be so low that circulation to brain may be impaired which leads to CNS disturbances  memory, confusion, ….. (Left or right sided)

5. Cardiac Arrhythmias

S/S of CHF

6. Renal impairment– In most cases this is a pre-renal cause of AKI

7.Cachexia (> w/ right sided)
Cardiac wasting due to poor intake of food & congestion of GI organs 
Impairing digestion & absorption

8. Cyanosis – (either / both)
Late sign of failure
due to poor oxygenation of blood &/or low output failure

The American Heart Association & the American College of Cardiology Stages of HF (2001)
Stage A: Patients at high risk (risk factors present) for developing HF in future but no functional or structural heart disorder

Stage B: Diagnosed by an ejection fraction (amount of blood pumped out of left ventricle w/ each heartbeat) below 40% (norm 55 % or >) but no past or current symptoms.

Stage C: Heart failure diagnosed, with past or current symptoms, including SOB, fatigue, & reduced exercise tolerance.

Stage D: Advanced symptoms of heart failure after receiving optimal medical care, requiring hospital-based support, heart transplant or palliative care.

New York Heart Association
Classification of HF
Rank from Class I to IV according to functional limitations & severity of symptoms.

Class Patient Symptoms

Class I (Mild) No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).

Class II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.

Class III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.

Class IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

CHF DIAGNOSIS
Diagnosed primarily by clinical picture:

Assess Risk factors (common causes)
Ischemic Heart Disease / CAD (over 50%)
Hypertension
Cardiac Arrhythmias
Cigarette Smoking
Obesity
Diabetes
Congenital Heart Disease
Valvular Heart Disease
(much higher in older populations)

*

CHF Diagnostics
Blood Test
B-type Natriuretic Peptide (BNP)

BNP is a substance secreted from the ventricles in response to changes in pressure (stretching) – protective mechanism

Occurs when heart failure develops & worsens.

The level of BNP in the blood increases when heart failure symptoms worsen, & decreases when the heart failure condition is stable.
Half-life of 20 minutes (measures current ventricular status)

When released this polypeptide decreases systemic vascular resistance and central venous pressure by

Increasing diuresis
Vasodilatation

BNP
BNP level in a person with heart failure – even someone whose condition is stable – is higher than in a person with normal heart function.

Patients with CHF, BNP values will generally be above 100 pg/ml

Results
BNP levels below 100 pg/mL – no heart failure
BNP levels of 100-300 pg/mL – suggest heart failure is present
BNP levels above 300 pg/mL – indicate mild heart failure
BNP levels above 600 pg/mL – indicate moderate heart failure.
BNP levels above 900 pg/mL – indicate severe heart failure.

CHF DIAGNOSIS
EKG to see if underlying rhythm or conduction problems (r/o MI)

Chest X-Ray

Echocardiogram (assesses pumping strength and EF)

Hemodynamic monitoring to assess fluid overload

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