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CARDIOVASCULAR DISEASES. REVIEW . How many chambers are in the heart? How does the blood flow through the heart? What vessels take blood AWAY from the heart? What vessels take blood TO the heart? What is Pulse Pressure? What is Cardiac Output? What is Stroke Volume?.

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review
REVIEW
  • How many chambers are in the heart?
  • How does the blood flow through the heart?
  • What vessels take blood AWAY from the heart?
  • What vessels take blood TO the heart?
  • What is Pulse Pressure?
  • What is Cardiac Output?
  • What is Stroke Volume?
terms associated with stroke volume
Terms associated with Stroke Volume
  • Preload – degree of stretch of the cardiac muscle fibers at the end of diastole
    • Direct effect on stroke volume: more blood then causes more effective contraction
  • Afterload – pressure the ventricle myocardium must overcome to eject blood during systole
  • Systemic vascular resistance - resistance of the systemic pressure to the left ventricle ejection
slide4

Pulmonary vascular resistance - resistance of the pulmonary pressure to the right ventricle ejection

  • Ejection fraction – percentage of the end – diastole volume that is ejected with each stroke (42 – 50%) (used to assess contractility)
  • Contractility – the force generated by the contracting myocardium under any given condition
    • Increased contractility leads to increased stroke volume
effects of aging
Effects of Aging
  • Aging heart muscle can provide adequate CO until emotional /physiological stress
  • Less activity can lead to left ventricular atrophy
  • Decreased elasticity and widening of the aorta
  • Thickening & rigidity of the cardiac valves
  • Increased connective tissue in the SA & AV nodes
  • LEADS to decreased contractility, increased left ventricular ejection, & delayed conduction
differences in males females
Differences in Males & Females
  • WOMAN HEART
    • Smaller in size
    • Smaller coronary arteries
      • Occlude easier with atherosclorosis
      • Makes angioplasty more difficult
    • Higher stroke volume, ejection fraction, resting HR
    • Shorter SA to AV node conduction
differences continued
Differences continued
  • Female hormones such as estrogen protect women from developing coronary artery disease (CAD)
  • Estrogen affects
    • cholesterol level
    • Reduce LDL
    • Increases HDL
    • Improve blood flow
  • Menopause – decreased estrogen causes women to be at equal risk for CAD with men
signs symptoms to evaluate
Signs & Symptoms to evaluate
  • Chest discomfort
    • Angina Pectoris
    • MI
  • SOB
    • Left ventricular failure; CHF
  • Edema/weight gain
    • Rt ventricular failure; CHF
  • Palpitations
    • Dysrhythmias; valvular disease; ventricular aneurysm; electrolyte imbalance
  • Fatigue
    • Associated with numerous heart conditions
  • Dizziness
    • Postural hypotension; dysrhythmias; vasovagal effect; cerebrovascular disorders
activity exercise on heart disease
Activity & Exercise on Heart disease
  • Decreases in activity tolerance are usually gradual
  • Easily Fatigued after activity is an early indication of progressing disease
  • After activity, patients may experience chest pain, SOB, palpitations
sleep rest
Sleep & Rest
  • Progressing disease has symptoms when the patient is at rest
  • Increasing the number of pillows to sleep
  • Awakening due to SOB (paroxysmal noturnaldyspnea)
  • Awakening chest discomfort
pulse pressure
Pulse Pressure
  • Systole – Diastole= Pulse Pressure
  • Normal: 30 – 50 mmHg
  • Increases in conditions that increase stroke volume
    • Anxiety
    • Exercise
    • bradycardia
  • Decreases in abnormal conditions
    • Shock
    • Heart failure
    • hypovolemia
postural orthostatic pressure
Postural (orthostatic) pressure
  • When BP drops significantly after the patient assumes the upright position
  • Symptoms
    • Dizziness
    • Lightheadedness
    • syncope
  • Causes
    • Hypovolemia
    • Inadequate vasoconstrictor mechanisms
    • Insufficient autonomic effect on vascular constriction
assessing orthostatic hypotension
Assessing Orthostatic hypotension
  • Have the patient lie supine & flat as symptoms permit for 10 minutes before taking BP & HR
  • Check supine before doing upright measurement
  • Check & compare supine, sitting, & standing pressures & HR
  • Wait 1 – 3 minutes after each postural change before measuring BP
normal findings
NORMAL findings
  • LYING to sitting/standing
    • HR increases 5 – 20 beats above resting
    • Systole is the same or slightly decreases (w/in 10 mm Hg)
    • Slight increase in diastole (5 mm Hg)
auscultation of the heart
Auscultation of the heart
  • Aortic area – 2ndintercostal space Rt of sternum
  • Pulmonic area – 2ndintercostal space LT of sternum
  • Erb’s point – 3rdintercostal space to LT
  • Right ventricular/tricuspid area – 4th & 5th IC to left @ midclavicular line
  • Left ventricular/apical area – 5th IC to left sternum @ midclavicular line
  • Epigastric area – below the xiphoid process
heart sounds
Heart Sounds
  • S1 – closing mitral /tricuspid valve
    • Heard loudest at the apex
  • Systole
  • S2 – closing aortic & pulmonic valves
    • Sometimes the pulmonic is slightly late causing a split S2
    • Heard loudest at the base of the heart
  • Diastole
slide17

Gallop – blood filling the ventricles is impeded during diastole

    • Sounds like a galloping horse
    • During rapid ventricular filling
    • CHF: myocardial disease; ventricles fail to eject all blood during systole
  • Snaps & Clicks
    • Stenosis of the mitral valve
    • Early in diastole that is high pitched best heard at left sternal border
slide18

Murmurs – turbulent flow of blood\critically narrowed valve

  • Malfunctioning valve allowing regurgitant blood flow
    • Defect of the ventricular wall
    • Defect between the aorta & pulmonary artery
  • Friction Rub
    • Pericarditis
    • Grating sound heard in systole & diastole
    • Abrasion of the pericardial surface during cardiac cycle
inspecting extremities
Inspecting Extremities
  • Capillary Refill – slow peripheral flow rate
  • Vascular changes
  • Hematoma
  • Peripheral edema
  • Clubbing
  • Lower extremity ulcers – may be present in arterial and/or venous insufficiency
respiratory findings related to cv disease
Respiratory findings related to CV disease
  • Tachypnea – heart failure
  • Cheyne – Stokes respirations – Severe Left ventricular failure
  • Dry, hacky cough – pulmonary congestion r/t heart failure
  • Crackles – heart failure
  • Wheezes – pulmonary edema or SE of beta blockers (heart medication)
cardiac enzymes
Cardiac Enzymes
  • Are elevated during/after MI
  • Released from injured cells when the cell membranes rupture due to prolonged hypoxia
  • Isoenzymes come only from cardiac cells
  • CreatineKinase (CK) & CK – MB are the most specific for MI; they are the first to elevate
  • lactic dehydrogenase & its isoenzyme elevate 2 – 3 days later
  • Troponin I is a contractile protein only in cardiac muscle. Elevates within 3 – 4 hours after insult
cholesterol levels hdl ldl
Cholesterol Levels & HDL, LDL
  • Cholesterol should be less than 200 mg/dL
    • Used for what?
    • Where is it found?
    • Sources?
    • Contributing factors: age, gender, diet, exercise, & stress
  • LDL – normal is less than 130 mg/dL
    • Primary transporter of cholesterol into cell
  • HDL – normal MALE: 35 – 65 FEMALE: 35 – 85
    • Transport cholesterol away from the cell to the liver for excretion
electrolytes
Electrolytes
  • Sodium
    • Fluid balance
    • Hyponatremia – fluid excess
    • Hypernatremia – fluid deficit
  • Magnesium – absorption of CA & maintains K+ stores;
    • Hypomagnesemia – lengthens QT interval
  • Calcium
    • Blood coagulability & neuromuscular activity
    • Hypocalcemia/hypercalcemia – causes dysrhythmia
  • Potassium
    • Affected b/ renal function
    • Decreased by diuretic (used to treat CHF)
    • Hypokalemia – cardiac irritability
    • Hyperkalemia /hypokalemia – lead to ventricular fibrillation or cardiac standstill
coagulation studies
Coagulation studies
  • Formation of a thrombus is initiated by injury to a vessel wall or tissue
  • Partial thromboplastin time (PTT)
    • Measure the activity of the intrinsic pathway
    • Normal: 25 – 38 seconds
  • Prothrombin time (PT)
    • Measures the extrinsic pathway activity & monitored during anticoagulation therapy
    • Normal: less than 13 seconds
  • International Normalized Ratio (INR)
    • Provides a standard method for reporting PT
    • Patient receiving anticoag therapy: 2.0 – 3.0
  • Heparin & Coumadin – drugs that provide anticoagulation therapy
slide25
ECG
  • Universal diagnostic tool
  • 12 Lead shows the activity from 12 different views
  • Used to diagnose dysrhythmias, conduction abnormalities, enlarged heart chambers, myocardial ischemia/infarction
  • Hypo/hyper calcemia; hypo/hyper kalemia
reading ekg s
Reading EKG’s
  • Waveform represents the functions of the heart’s conduction activity
  • Printed on graph paper
  • Time & rate measured on horizontal axis
  • Amplitude or voltage is measured on vertical axis
  • Represented by P Q R S T
slide27

P wave – is the electrical impulse from the SA node through the atria (atrial depolarization)

    • Normal: 2.5 mm or less in height and .11 second duration
  • QRS Complex – ventricular muscle depolarization; less than .12 seconds in duration
    • Depression after P wave is the Q wave that is .04 seconds
    • Positive deflection after P wave is R wave
    • Negative deflection after R is the S wave
slide28

T wave – represents ventricular muscle repolarization (resting state); after QRS wave & usually in the same direction of the QRS complex

  • U wave – represents the repolarization of Purkinje fibers; may be seen in hypokalemia or HTN
  • PR interval – beginning of P wave to beginning of QRS complex.
    • Time for SA node stimulation, atrial depolarization, & conduction through the AV node
    • Normal .12 - .20 seconds
slide29

ST segment – early ventricular repolarization; lasts for end of QRS to beginning of T wave

    • Beginning of ST segment is identified by a change in the thickness of the terminal portion of the complex
  • QT interval – total time for ventricular depolarization & repolarization ; beginning of QRS to end of T wave
    • .32 - .40 seconds
interpreting ekg
Interpreting EKG
  • 1 minute strip has 300 large squares & 1500 small squares
  • 15 large boxes in 3 seconds; 5 lg boxes/1 sec
  • Calculate the HR: count the R peaks in 6 seconds & multiply by 10
  • If the R peaks are equal distance apart, then the rate is regular
dysrhythmia disorders
Dysrhythmia disorders
  • Formation of new electrical activity or alteration in the electrical activity
  • Review of normal conduction
    • What are the structures & the steps to electrical activity?
slide32

Sinus Bradycardia

    • SA node fires at a slower than normal rate
    • Slower metabolic needs, vagal stimulation, medications, increased ICP, MI (inferior wall)
  • Sinus Tachycardia
    • Faster than normal rate
    • Blood loss, anemia, shock, hypervolemia, hypovolemia, CHF, pain, fever, exercise
slide33

Sinus Arrhythmia

    • SA nodes creates an irregular rhythm; increases during inspiration & decreases during expiration
    • Causes: heart disease, valvular disease
atrial dysrhythmia
Atrialdysrhythmia
  • Atrial Flutter
    • Atrium beats 250 – 400 times/minute
    • Too fast for the AV node to send all to ventricles
  • Atrial Fibrillation
inflammatory disorders
Inflammatory Disorders
  • Endocarditis – inflammation of endocardium
    • Bacterial – leaflets of the mitral valve erode due to bacteria
    • Libman – Sacks – found in patients with lupus
  • Myocarditis – inflammation of the muscle
    • Acute (usually caused by a virus)
    • Chronic
  • Pericarditis – inflammation of the sac/outer layer
    • Acute
    • Chronic
valvular disease
Valvular Disease
  • Mitral Valve Prolapse
    • Usually benign
    • Causes
      • Calium degeneration
      • Inflammatory endocarditis
      • MI
    • Complications
      • Arrhythmia
      • Cardiomyopathy
      • Heart failure
slide37

Mitral Valve Stenosis

    • Hardening of the mitral valve caused by calcification/fibrosis
    • Narrowing of the valve opening
    • Dialation of the left atrium
    • S & S
      • Dyspnea on exertion
      • Paroxysmal nocturnal dyspnea/orthopnea
      • Fatigue/weakness
      • Right sided heart failure
      • crackles
slide38

Aortic Stenosis

    • Congenital aortic valve defect
    • Due to rheumatic fever
    • Treatment
      • Digoxin Nitroglycerine
      • Diuretics
    • S & S
      • Exertionaldyspnea
      • Syncope
      • Angina, palpitations
      • Left sided failure
hypertension
Hypertension
  • Essential – progressive
  • 90% cases
    • Could be from mechanisms that:
      • Control cardiac output
      • Systemic vascular resistance
      • Blood volume
  • Secondary
    • Caused by another disorder
    • Less than 10% cases
silent killer
Silent Killer
  • Affects other organs in the body
    • Brain
      • Narrowed blood vessels will have clotted blood & cause strokes
      • Weakened blood vessel walls can lead to hemorrhage
    • Eyes
      • Increased BP cause hemorrhage in retina
      • Swelling of optic disc leads to blindness
    • Kidneys
      • Arterioles harden & restrict O2 to glomeruli
different drugs for htn
Different Drugs for HTN
  • Diuretics
  • Beta Blockers
  • ACE Inhibitors
thiazide diuretics
Thiazide Diuretics
  • Generic: Hydrochlorothiazide
  • Effective & most cost-efficient
  • Usually tried first
  • Increases excretion of water, sodium, chloride, & potassium
  • Treats: edema, uncomplicated HTN, prophylaxis of kidney stones, electrolyte imbalance
  • SE: Hypokalemia, hypochloremia, muscle weakness, postural hypotention, vertigo, HA, fatigue, lethargy, hyperglycemia, elevated uric acid
  • CI: diabetes, gout, severe renal disease, impaired liver function
  • Interactions: NSAIDS, corticosteroids, digitalis
beta adrenergic blocker
Beta-Adrenergic Blocker
  • Inderal (propranolol) & Tenormin (atenolol)
  • Used in patients with angina, postmyocardial infarction
  • SE: hypotension, vertigo, syncope, bradycardia, irritability, confusion, insomnia, N & V, Brochospams (in asthma), hypoglycemia,
  • CI: Major surgery, diabetes, renal or liver impairment, bradycardia, asthma, COPD
  • Interactions: Antidepressants
  • Potentiate the hypotensive effects in:
    • Diuretics
    • Tranquilizers
    • Tagamet
    • Other cardiac drugs
    • alcohol
calcium channel blockers
Calcium – Channel blockers
  • Cardizem (diltiazem) & Procardia (nifedipine)
  • Used in patients with diabetes or high coronary risk
  • Suppress the Calcium in muscle contraction; reducing excitability & dilates coronary arteries
  • SE: hypotension, HA, vertigo, bradycardia, edema, N, constipation, & abdominal discomfort
  • CI: heart block, heart failure, pregnancy, children
  • Interaction: lithium, diuretics, barbiturates
ace inhibitors
ACE Inhibitors
  • Angiotensin – converting enzyme inhibitors
  • Catopril & enalapril
  • Decreases vasoconstriction (no change in CO or HR)
  • Usually used with diuretic therapy
  • Used in patients with heart disease, diabetes, renal disease
  • SE: rash, loss of taste perception, severe hypotension, chronic dry cough, nasal congestion, hyperkalemia
  • CI: Lupus, heart failure, angioedema, pregnancy
  • I: diuretics, vasodilators, K+ sparing diuretics, NSAIDS
heart failure
Heart Failure
  • Myocardium can’t pump effectively enough to meet the body’s needs
  • Possible Causes
    • Increased pressure/volume resulting myocardial function
    • Left ventricular remodeling
    • Altered hemodynamics to maintain CO
    • Hormonal changes that accelerate HR & increase EF
slide47

Classifications

    • Right or Left sided
      • Right – result of ineffective Rt ventricular contraction due to infarction, PE, back flow due to Lt side failure
      • Left – ineffective Lt ventricular contraction leading to pulmonary congestion & decreased CO
    • Systolic or diastolic
      • Systolic – LT ventricle can’t pump to body
      • Diastolic – left ventricle can’t relax & fill appropriately leading to decreased SV
    • Acute or chronic
      • Acute – the compensatory mechanisms kick in; fluid status is normal
      • Chronic – S & S present for some time, compensatory mechanisms kicked in & fluid overload is present
signs symptoms
Signs & Symptoms

Left

RIGHT

Edema

Jugular vein distention

Hepatomegaly

Generalized weight gain

  • Dyspnea
  • Cough
  • Tachycardia
  • Fatigue
  • Muscle weakness
  • Edema
  • Weight gain
  • Crackles
cardiomyopathy
Cardiomyopathy
  • Refers to the disease of the heart muscle fibers
  • 3 classes
    • Dilated - affects systolic function
    • Hypertrophic – primarily affects diastolic function
    • Restrictive – stiffness of the ventricle caused by left ventricular hypertrophy or endocardial fibrosis
cad coronary artery disease
CAD (Coronary Artery Disease)
  • Progressive buildup of atherosclerotic plaque in the coronary arteries
  • Risk factors
    • High LDL’s
    • Uncontrolled HTN
    • Sex (Men are more prone)
    • Smoking
    • Heredity
angina
Angina
  • Usually upon exertion
  • Abnormal stress test or Echocardiogram findings
  • Chest pain
  • May show up as a reversible ST
  • Progressively will become worse & severity over time
angina vs mi
Angina vs MI
  • Angina
    • Pain is burning, squeezing, substernal
    • Lasts 5 – 15 minutes
    • Usually related to exertion, stress, cold, exercise
    • Relief: nitroglycerin, rest, oxygen
    • Hypotension/HTN, tachy or bradycardia
    • Cardiac enzymes WNL
  • MI
    • Severe substernal pain, chest, shoulders, hand
    • Lasts greater than 15 minutes
    • Occurs all of sudden
    • May be preceded by unstable angina
    • Relief: MS, reperfusion of cardiac tissue
    • Hypo/hyper tension, palpable precordial pulse, muffled heart sounds, arrhythmia
    • Cardiac markers: Elevated
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