Coronary Heart Disease (CHD) Leading cause of death in U.S. Narrowing coronary arteries –Atherosclerosis

Angina Pectoris - Pathophysiology Obstructed coronary artery Increased myocardial oxygen demand Lactic acid release Leads to pain Three types –Stable –Unstable –Prinzmetal’s: is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles. It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than directly by atherosclerosisangina vasospasmcoronary arteriesatherosclerosis

Angina Pectoris - Manifestations Chest pain Radiates Onset with exercise, etc. Relieved by rest, nitroglycerin (NTG) SOB, pallor, fear

Acute Coronary Syndrome Condition that includes: –Unstable angina –Acute myocardial ischemia with or without muscle damage Associated with coronary artery stenosis and atherosclerotic plaque

Acute Myocardial Infarction (AMI) Pathophysiology –Occluded coronary artery stops blood flow to part of cardiac muscle –Cellular death –Tissue necrosis –Description—heart area affected –Classification

AMI Manifestations Chest pain Radiates to shoulder, neck, jaw, arms Lasts longer than 15–20 minutes Not relieved with NTG Sense of impending doom SOB Diaphoresis Nausea and vomiting

AMI Manifestations (continued) Manifestations in women and elderly –May be atypical –Upper abdominal pain –No chest pain but other symptoms

AMI Complications Related to size and location of infarct Dysrhythmias Pump failure –Cardiogenic shock Pericarditis

Cardiac Dysrhythmias Pathophysiology –Due to altered formation of impulses or altered conduction of the impulse through the heart –Ectopic beats –Heart block –Reentry phenomenon –Classified to the site of impulse formation or the site and degree of conduction block

Types of Cardiac Dysrhythmias (continued) PVCs Ventricular tachycardia Ventricular fibrillation AV conduction blocks –First degree –Second degree –Third degree

Types of Cardiac Dysrhythmias Supraventricular Sinus tachycardia Sinus bradycardia PAC Atrial flutter Atrial fibrillation Junctional Ventricular dysrhythmias

ECG Changes in Angina Pectoris vs. Myocardial Infection

04/11/ Congestive Heart Failure Dr Ibraheem Bashayreh, RN,PhD

04/11/ Heart failure Normal heart function

04/11/ Congestive Heart Failure Definition Impaired cardiac pumping such that heart is unable to pump adequate amount of blood to meet metabolic needs Not a disease but a “syndrome” Associated with long-standing HTN and CAD Impaired cardiac pumping such that heart is unable to pump adequate amount of blood to meet metabolic needs Not a disease but a “syndrome” Associated with long-standing HTN and CAD

04/11/ Factors Affecting Cardiac Output Cardiac Output CO Preload AfterloadContractility Heart Rate Stroke Volume SV =X SV: the volume of blood pumped from one ventricle of the heart with each beat

04/11/ Factors Affecting Cardiac Output Heart Rate –In general, the higher the heart rate, the lower the cardiac E.g. HR x Systolic Volume (SV) = CO »60/min x 80 ml = 4800 ml/min (4.8 L/min) »70/min x 80 ml = 5600 ml/min (5.6 L/min) –But only up to a point. With excessively high heart rates, diastolic filling time begins to fall, thus causing stroke volume and thus CO to fall

04/11/ Heart RateStroke VolumeCardiac Output 60/min80 ml4.8 L/min 80/min80/ml6.4 L/min 100/min80/ml8.0 L/min 130/min50/ml6.5 L/min 150/min40/ml 6.0 L/min

04/11/ Factors Affecting Cardiac Output Preload –The volume of blood/amount of fiber stretch in the ventricles at the end of diastole (i.e., before the next contraction)

04/11/ Factors Affecting Cardiac Output Preload increases with: Fluid volume increases Vasoconstriction (“squeezes” blood from vascular system into heart) Preload decreases with Fluid volume losses Vasodilation (able to “hold” more blood, therefore less returning toheart)

04/11/ Factors Affecting Cardiac Output Starling’s Law –Describes the relationship between preload and cardiac output –The greater the heart muscle fibers are stretched (b/c of increases in volume), the greater their subsequent force of contraction – but only up to a point. Beyond that point, fibers get over-stretched and the force of contraction is reduced Excessive preload = excessive stretch → reduced contraction → reduced SV/CO

04/11/ Factors Affecting Cardiac Output Afterload –The resistance against which the ventricle must pump. Excessive afterload = difficult to pump blood → reduced CO/SV –Afterload increased with: Hypertension Vasoconstriction –Afterload decreased with: Vasodilation

04/11/ Factors Affecting Cardiac Output Contractility –Ability of the heart muscle to contract; relates to the strength of contraction.

04/11/ Factors Affecting Cardiac Output Contractility decreased with: –infarcted tissue – no contractile strength –ischemic tissue – reduced contractile strength. –Electrolyte/acid-base imbalance –Negative inotropes (medications that decrease contractility, such as beta blockers). Contractility increased with: –Sympathetic stimulation (effects of epinephrine) –Positive inotropes (medications that increase contractility, such as digoxin, sympathomimmetics)

04/11/ Pathophysiology of CHF Pump fails → decreased stroke volume /CO. Compensatory mechanisms kick in to increase CO – SNS stimulation → release of epinephrine/nor- epinephrine Increase HR Increase contractility Peripheral vasoconstriction (increases afterload) –Myocardial hypertrophy: walls of heart thicken to provide more muscle mass → stronger contractions

04/11/ Pathophysiology of CHF –Hormonal response: ↓’d renal perfusion interpreted by juxtaglomerular apparatus as hypovolemia. Thus: Kidneys release renin, which stimulates conversion of antiotensin I → angiotensin II, which causes: –Aldosterone release → Na retention and water retention (via ADH secretion) –Peripheral vasoconstriction

04/11/ Pathophysiology of CHF Compensatory mechanisms may restore CO to near-normal. But, if excessive the compensatory mechanisms can worsen heart failure because...

04/11/ Pathophysiology of CHF Vasoconstriction: ↑’s the resistance against which heart has to pump (i.e., ↑’s afterload), and may therefore ↓ CO Na and water retention: ↑’s fluid volume, which ↑’s preload. If too much “stretch” (d/t too much fluid) → ↓ strength of contraction and ↓’s CO Excessive tachycardia → ↓’d diastolic filling time → ↓’d ventricular filling → ↓’d SV and CO

04/11/ Congestive Heart Failure Risk Factors CAD Age HTN Obesity Cigarette smoking Diabetes mellitus High cholesterol African descent CAD Age HTN Obesity Cigarette smoking Diabetes mellitus High cholesterol African descent

04/11/ Heart failure Underlying causes/risk factors Ischemic heart disease (CAD) hypertension myocardial infarction (MI) valvular heart disease congenital heart disease 70% dilated cardiomyopathy

04/11/ Congestive Heart Failure Types of Congestive Heart Failure Left-sided failure –Most common form –Blood backs up through the left atrium into the pulmonary veins Pulmonary congestion and edema –Eventually leads to biventricular failure Left-sided failure –Most common form –Blood backs up through the left atrium into the pulmonary veins Pulmonary congestion and edema –Eventually leads to biventricular failure

04/11/ Congestive Heart Failure Types of Congestive Heart Failure Left-sided failure –Most common cause: HTN Cardiomyopathy Valvular disorders CAD (myocardial infarction) Left-sided failure –Most common cause: HTN Cardiomyopathy Valvular disorders CAD (myocardial infarction)

04/11/ Congestive Heart Failure Types of Congestive Heart Failure Right-sided failure –Results from diseased right ventricle –Blood backs up into right atrium and venous circulation –Causes LVF Cor pulmonale: failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart RV infarction Right-sided failure –Results from diseased right ventricle –Blood backs up into right atrium and venous circulation –Causes LVF Cor pulmonale: failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart RV infarction

04/11/ Congestive Heart Failure Types of Congestive Heart Failure Right-sided failure –Venous congestion Peripheral edema Hepatomegaly Splenomegaly Jugular venous distension Right-sided failure –Venous congestion Peripheral edema Hepatomegaly Splenomegaly Jugular venous distension

04/11/ Congestive Heart Failure Types of Congestive Heart Failure Right-sided failure –Primary cause is left-sided failure –Cor pulmonale RV dilation and hypertrophy caused by pulmonary pathology Right-sided failure –Primary cause is left-sided failure –Cor pulmonale RV dilation and hypertrophy caused by pulmonary pathology

04/11/ Acute Congestive Heart Failure Clinical Manifestations Pulmonary edema (what will you hear?) –Agitation –Pale or cyanotic –Cold, clammy skin –Severe dyspnea –Tachypnea –Pink, frothy sputum Pulmonary edema (what will you hear?) –Agitation –Pale or cyanotic –Cold, clammy skin –Severe dyspnea –Tachypnea –Pink, frothy sputum

04/11/ Chronic Congestive Heart Failure Clinical Manifestations Fatigue Dyspnea –Paroxysmal nocturnal dyspnea (PND) Tachycardia Edema – (lung, liver, abdomen, legs) Nocturia Fatigue Dyspnea –Paroxysmal nocturnal dyspnea (PND) Tachycardia Edema – (lung, liver, abdomen, legs) Nocturia

04/11/ Chronic Congestive Heart Failure Clinical Manifestations Behavioral changes –Restlessness, confusion,  attention span Chest pain (d/t  CO and ↑ myocardial work) Weight changes (r/t fluid retention) Skin changes –Dusky appearance Behavioral changes –Restlessness, confusion,  attention span Chest pain (d/t  CO and ↑ myocardial work) Weight changes (r/t fluid retention) Skin changes –Dusky appearance

04/11/ Congestive Heart Failure Classification Based on the person’s tolerance to physical activity –Class 1: No limitation of physical activity –Class 2: Slight limitation –Class 3: Marked limitation –Class 4: Inability to carry on any physical activity without discomfort Based on the person’s tolerance to physical activity –Class 1: No limitation of physical activity –Class 2: Slight limitation –Class 3: Marked limitation –Class 4: Inability to carry on any physical activity without discomfort

04/11/ Congestive Heart Failure Diagnostic Studies Primary goal is to determine underlying cause –Physical exam –Chest x-ray –ECG –Hemodynamic assessment Primary goal is to determine underlying cause –Physical exam –Chest x-ray –ECG –Hemodynamic assessment

04/11/ Congestive Heart Failure Diagnostic Studies Primary goal is to determine underlying cause –Echocardiogram (Uses ultrasound to visualize myocardial structures and movement, calculate EF) –Cardiac catheterization Primary goal is to determine underlying cause –Echocardiogram (Uses ultrasound to visualize myocardial structures and movement, calculate EF) –Cardiac catheterization

04/11/ Acute Congestive Heart Failure Nursing and Collaborative Management Primary goal is to improve LV function by: –Decreasing intravascular volume –Decreasing venous return –Decreasing afterload –Improving gas exchange and oxygenation –Improving cardiac function –Reducing anxiety Primary goal is to improve LV function by: –Decreasing intravascular volume –Decreasing venous return –Decreasing afterload –Improving gas exchange and oxygenation –Improving cardiac function –Reducing anxiety

04/11/ Acute Congestive Heart Failure Nursing and Collaborative Management Decreasing intravascular volume –Improves LV function by reducing venous return –Loop diuretic: drug of choice –Reduces preload –High Fowler’s position Decreasing intravascular volume –Improves LV function by reducing venous return –Loop diuretic: drug of choice –Reduces preload –High Fowler’s position

04/11/ Acute Congestive Heart Failure Nursing and Collaborative Management Decreasing afterload –Drug therapy: vasodilation, Angiotensin-converting enzyme ( ACE) inhibitors –Decreases pulmonary congestion Decreasing afterload –Drug therapy: vasodilation, Angiotensin-converting enzyme ( ACE) inhibitors –Decreases pulmonary congestion

04/11/ Acute Congestive Heart Failure Nursing and Collaborative Management Improving cardiac function –Positive inotropes Improving gas exchange and oxygenation –Administer oxygen, sometimes intubate and ventilate Reducing anxiety –Morphine Improving cardiac function –Positive inotropes Improving gas exchange and oxygenation –Administer oxygen, sometimes intubate and ventilate Reducing anxiety –Morphine

04/11/ Chronic Congestive Heart Failure Collaborative Care Treat underlying cause Maximize CO Alleviate symptoms Treat underlying cause Maximize CO Alleviate symptoms

04/11/ Chronic Congestive Heart Failure Collaborative Care Oxygen treatment Rest Biventricular pacing Cardiac transplantation Oxygen treatment Rest Biventricular pacing Cardiac transplantation

04/11/ Chronic Congestive Heart Failure Drug Therapy ACE inhibitors Diuretics Inotropic drugs : drugs that influence the force of contraction of cardiac muscle Vasodilators  -Adrenergic blockers ACE inhibitors Diuretics Inotropic drugs : drugs that influence the force of contraction of cardiac muscle Vasodilators  -Adrenergic blockers

04/11/ Chronic Congestive Heart Failure Nutritional Therapy Fluid restrictions not commonly prescribed Sodium restriction –2 g sodium diet Daily weights –Same time each day –Wearing same type of clothing Fluid restrictions not commonly prescribed Sodium restriction –2 g sodium diet Daily weights –Same time each day –Wearing same type of clothing

04/11/ Chronic Congestive Heart Failure Nursing Management Nursing Assessment Past health history Medications Functional health problems Cold, diaphoretic skin Past health history Medications Functional health problems Cold, diaphoretic skin

04/11/ Chronic Congestive Heart Failure Nursing Management Nursing Assessment Tachypnea Tachycardia Crackles Abdominal distension Restlessness Tachypnea Tachycardia Crackles Abdominal distension Restlessness

04/11/ Chronic Congestive Heart Failure Nursing Management Nursing Diagnoses Activity intolerance Excess fluid volume Disturbed sleep pattern Impaired gas exchange Anxiety Activity intolerance Excess fluid volume Disturbed sleep pattern Impaired gas exchange Anxiety

04/11/ Chronic Congestive Heart Failure Nursing Management Planning Overall goals: –  Peripheral edema –  Shortness of breath –  Exercise tolerance –Drug compliance –No complications Overall goals: –  Peripheral edema –  Shortness of breath –  Exercise tolerance –Drug compliance –No complications

04/11/ Chronic Congestive Heart Failure Nursing Management Nursing Implementation Acute intervention –Establishment of quality of life goals –Symptom management –Conservation of physical/emotional energy –Support systems are essential Acute intervention –Establishment of quality of life goals –Symptom management –Conservation of physical/emotional energy –Support systems are essential

04/11/ What is Blood Pressure? The force of blood against the wall of the arteries. Systolic- as the heart beats Diastolic - as the heart relaxes Written as systolic over diastolic. Normal Blood pressure is less than 130 mm Hg systolic and less than 85 mm Hg diastolic.

04/11/ High Blood Pressure A consistent blood pressure of 140/90 mm Hg or higher is considered high blood pressure. It increases chance for heart disease, kidney disease, and for having a stroke. 1 out of 4 Americans have High Bp. Has no warning signs or symptoms.

04/11/ Why is High Blood Pressure Important? Makes the Heart work too hard. Makes the walls of arteries hard. Increases risk for heart disease and stroke. Can cause heart failure, kidney disease, and blindness.

04/11/ How Does It Effect the Body? The Brain High blood pressure is the most important risk factor for stroke. Can cause a break in a weakened blood vessel which then bleeds in the brain.

04/11/ The Heart High Blood Pressure is a major risk factor for heart attack. Is the number one risk factor for Congestive Heart Failure.

04/11/ The Kidneys Kidneys act as filters to rid the body of wastes. High blood pressure can narrow and thicken the blood vessels. Waste builds up in the blood, can result in kidney damage.

04/11/ The Eyes Can eventually cause blood vessels to break and bleed in the eye. Can result in blurred vision or even blindness.

04/11/ The Arteries Causes arteries to harden. This in turn causes the kidneys and heart to work harder. Contributes to a number of problems.

04/11/ What causes High Blood Pressure? Causes vary Narrowing of the arteries Greater than normal volume of blood Heart beating faster or more forcefully than it should Another medical problem The exact cause is not known.

04/11/ Who can develop High Blood Pressure? Anyone, but it is more common in: African Americans- get it earlier and more often then Caucasians. As we get older. 60% of Americans over 60 have hypertension. Overweight, family history High normal bp: /85-89 mm Hg.

04/11/ Detection Dr.’s will diagnose a person with 2 or more readings of 140/90mm Hg or higher taken on more than one occasion. White-Coat Hypertension Measured using a spygmomameter.

04/11/ Tips for Having your blood pressure taken. Don’t drink coffee or smoke cigarettes for 30 minutes before. Before test sit for five minutes with back supported and feet flat on the ground. Test your arm on a table even with your heart. Wear short sleeves so your arm is exposed.

04/11/ Tips for having blood pressure taken. Go to the bathroom before test. A full bladder can affect bp reading. Get 2 readings and average the two of them. Ask the Dr. or nurse to tell you the result in numbers.

04/11/ Categories of High Blood Pressure Ages 18 Years and Older) Blood Pressure Level (mm Hg) Category Systolic Diastolic Optimal** < 120 < 80 Normal < 130 < 85 High Normal 130–139 85–89

04/11/ Categories of High Blood Pressure High Blood Pressure Stage 1 140–159 /90–99 Stage 2 160–179 /100–109 Stage /110

04/11/ Preventing Hypertension Adopt a healthy lifestyle by: Following a healthy eating pattern. Maintaining a healthy weight. Being Physically Active. Limiting Alcohol. Quitting Smoking.

04/11/ DASH diet Dietary Approaches to Stop Hypertension. Was an 11 week trial. Differences from the food pyramid: an increase of 1 daily serving of veggies. and increase of 1-2 servings of fruit. inclusion of 4-5 servings of nuts,seeds, and beans.

04/11/ Tips for Reducing Sodium Buy fresh, plain frozen or canned “no added salt” veggies. Use fresh poultry, lean meat, and fish. Use herbs, spices, and salt-free seasonings at the table and while cooking. Choose convenience foods low in salt. Rinse canned foods to reduce sodium.

04/11/ Maintain Healthy Weight Blood pressure rises as weight rises. Obesity is also a risk factor for heart disease. Even a 10# weight loss can reduce blood pressure.

04/11/ Be Physically Active Helps lower blood pressure and lose/ maintain weight. 30 minutes of moderate level activity on most days of week. Can even break it up into 10 minute sessions. Use stairs instead of elevator, get off bus 2 stops early, Park your car at the far end of the lot and walk!

04/11/ Limit Alcohol Intake Alcohol raises blood pressure and can harm liver, brain, and heart

04/11/ Quit Smoking Injures blood vessel walls Speeds up process of hardening of the arteries.

04/11/ Other Treatment If Lifestyle Modification is not working, blood pressure medication may be needed, there are several types: Diuretics-work on the kidney to remove access water and fluid from body to lower bp. Beta blockers-reduce impulses to the heart and blood vessels.

04/11/ Other Treatment ACE inhibitors- cause blood vessels to relax and blood to flow freely. Angiotensin antagonists- work the same as ACE inhibitors. Calcium Channel Blockers- causes the blood vessel to relax and widen. Alpha Blocker- blocks an impulse to the heart causing blood to flow more freely.

04/11/ Other Treatment Alpha-beta blockers- work the same as beta blockers, also slow the heart down. Nervous system inhibitors- slow nerve impulses to the heart. Vasodilators- cause blood vessel to widen, allowing blood to flow more freely.

04/11/ Conclusion Hypertension is a very controllable disease, with drastic consequences if left uncontrolled.