Download Pathophysiologic Basis for Health Deviations 437

Patho 437 - Cardiac - Page 1
The Cardiovascular System
Quick review of the heart circulation:
Blood from body --> superior/inferior vena cavas --> RA --> tricuspid valve -->
RV --> pulmonic valve --> to lungs --> pulmonary vein (only vein to carry
oxygenated blood) --> LA --> mitral valve --> LV -- aortic valve --> to body thru
aorta
With Right sided failure --> things collect in periphery
With Left sided failure --> things collect in the lungs
Atria
Ventricles
Valves
Atrioventricular: Rt = tricuspid, Lt. = mitral
Semilunar valves: aortic and pulmonic
“Noises” (heart sounds) due to closure of valves (healthy valves make no noise when
opening)
S1 is syncrhonous with the carotid.
Splitting of S1
Split S2
physiological
paradoxical splitting
Wide-splitting S2
Causes: RBBB, pulmonic stenosis, after Valsalva maneuver
Fixed splitting S2
Causes: Atrial-Septal Defect (ASD)
S3 (ventricular gallop) =
normal in children, in adults, means CHF!!!
S4 (atrial gallop)
May hear S4 in: post MI, hyperthyroidism, * aortic stenosis (very
common in elderly...valve worn out, faints since blood not getting to
brain), * chronic HTN (most common cause)
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“Silences” are also important:
Systole = between S1 and S2
Diastole = between S2 and next S1
Systolic murmurs = some are pathologic
• aortic stenosis
• idiopathic hypertrophic subaortic stenosis (IHSS)
• pulmonic stenosis
• tricuspid regurgitation
• VSD (ventricular septal defect)
• mitral regurgitation
• mitral valve prolapse
Diastolic murmurs = all are pathologic
• aortic regurgitation
• pulmonary regurgitation
• mitral stenosis
Combination: rheumatic heart disease:
- systolic murmur of mitral regurgitation
- diastolic murmur of mitral stenosis
Cardiac Contraction
Systole = ventricular contraction (maximal peripheral pressure generated);
Diastole = resting portion of the cardiac cycle (blood filling the ventricles); elastic recoil
of large vessels maintains flow
1.
Passive diastole: pressure in the left atrium (LA) is higher than in left
ventricle (LV); mitral valve opens and blood passively flows into ventricle
(approximately 60 cc. enters passively)
2.
Active diastole: atrial contraction in response to SA node stimulation =
“atrial kick” (= 20 cc)
Stroke volume = the amount of blood ejected from the LV with normal heartbeat.
Normal SV is 80 cc, which goes into the aorta.
There is a cardiac reserve of approximately 40 cc left in the LV at any one time.
Left Ventricular End Diastolic Volume (LVEDV) = Cardiac reserve + passive diastole
+ active diastole = 120 cc.
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Cardiac output (CO): the amount of blood pumped out of the heart in one minute
Cardiac output = SV X HR
What regulatory mechanisms help maintain cardiac output?
Permanent pacemakers
ICHD (Inter-Society commission for Heart Disease Resources) code for
pacemakers contains 5 main components:
- Chamber-paced
- Chamber-sensed
- Mode of response to sensed electrical impulses (inhibited or triggered)
- Rate modulation
- Multi site pacing
Contractility = intrinsic myocardial property independent of influences such as preload
and afterload.
Affected by:
• ANS stimulation
• humoral agents (e.g., prostaglandins, calcium, angiotensin, potassium)
• metabolic conditions (e.g., hypoxemia)
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Monitoring parameters: cardiac index, ejection fraction, preload, afterload
- Cardiac index =
CO
BSA (Body surface area)
2
Normal Cardiac index = approx. 2.8 - 4.0 L/min/m
As CI decreases, CO decreases, meaning increasing severity of failure
2.8 - 4.0
2.2 - 2.7
1.8 - 2.1
< 1.8
Normal
Mild
Severe
Cardiogenic shock
- Ejection Fraction = the percentage of the blood emptied from the ventricle during
systole; it averages 60-70%.
- Preload: the volume or pressure in the left ventricle at end-diastole; the myocardium is
normally compliant (distensible), so end-diastolic volume results in maximum stretching
of the myocardial fibers
Normal preload: Normal LVEDV = 120 cc; results in LVEDP of 10 torr
Preload increases with:
• stiff ventricle (fibrosis, hypertrophy, scar tissue)
• vasoconstriction
• overhydration
2 consequences of increased preload (--> decreased CO with decreased SV):
1.
increased pulmonary pressure
2.
decreased undamaged contractility because less contraction because of
chronic volume
Preload decreases with:
• vasodilation
• diuresis
• atrial natriuretic factor (ANF)
A peptide secreted by the atrial tissue of the heart in response to an increase in BP.
It influences BP, blood volume, and CO. It increases the excretion of sodium and
water in urine, thereby lowering blood volume and BP and influencing CO. Its
secretion rate depends on glomerular filtration rate and inhibits sodium
reabsorption in distal tubules. These actions reduce the workload of the heart.
• loss of atrial kick
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- Afterload: resistance against which the ventricle must pump (resistance faced by any
heart chamber in systole)
3 phases of systole:
1.
isovolumetric contraction - contraction of fibers to increased pressure
(90% of oxygen used here)
2.
systolic ejection - valve opens and blood ejects into aorta (approximately
80 cc, if normal) (10% of oxygen used here)
3.
peripheral run-off - semilunar valves still open, but blood ---> periphery
Affected by:
• anatomical characteristics of the arterial system (e.g., aortic stenosis)
• vasoconstriction (increases) or vasodilation (decreases)
• increased blood viscosity (e.g., polycythemia, high altitude, dehydration, chronic
hypoxia)
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Pathophysiologic Basis for Health Deviations 437
The Cardiovascular System - Critical Thinking Exercise
Determine whether each of the following problems is a primary preload problem or a
primary afterload problem.
1.
cardiogenic shock
2.
tricuspid regurgitation
3.
inferior vena cava obstruction
4.
mitral stenosis
5.
coarctation of the aorta
6.
pulmonary vascular hypertension
7.
pulmonic stenosis
8.
aortic insufficiency
9.
subclavian stenosis
10.
hypervolemia
11.
hyperthermia
12.
hypothermia
13.
hypovolemia
14.
ventricular-septal defect
15.
histamine
16.
hypoxia
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Quick review of conduction system of heart:
Impulse arises in SA node --> AV node --> bundle of His --> bundle branches -->
Purkinje fibers
Cardiac Action Potentials:
depolarization - electrical activation of the muscle cells; caused by the movement of
electrically charged solutes (ions) across cardiac cell membranes
repolarization - = reactivation; occurs the same way as depolarization
Normal myocardial cell depolarization and repolarization occur in four phases:
1.
Phase 0 (fast sodium current)= depolarization; represents rapid sodium entry into
the cell
Type I anti-arrhythmic drugs (quinidine, procainamide/Pronestyl, Lidocaine)
2.
Phase 1 = early repolarization; calcium slowly enters --> decrease in action
potential
3.
Phase 2 (also called the plateau) is a continuation of repolarization, with slow
entry of calcium and sodium into the cell.
Type IV anti-arrhythmic drugs (calcium channel blockers)
4.
Phase 3 - potassium is moved out of the cell (efflux)
Type III anti-arrhythmic (amiodarone, bretylium)
5.
Phase 4 (slow sodium) - return to resting membrane potential
Type II anti-arrhythmic drugs (beta-blockers).
refractory period
Configuration of typical action potential on EKG:
P wave = atrial depolarization
P-R segment or interval = 0.12 - 0.20 sec (movement of impulse from atrial to AV
node)
QRS complex = ventricular depolarization (0.06 - 0.10 sec)
ST interval = normally isoelectric (flat baseline); from end of S to beginning of T wave
T wave = ventricular repolarization
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Pathophysiology of the Cardiovascular System: Adults and Children
There are numerous pathophysiological problems which occur involving the CV system.
These include diseases of the arteries and veins, disorders of the heart wall, and
manifestations of heart disease, such as dysrhythmias and heart failure.
There are also the various types of shock, including cardiogenic, hypovolemic,
neurogenic, anaphylactic, and septic shock.
We will be limiting our discussion to the types of problems most commonly seen in the
practice of family nurse practitioners, including:
Diseases of the Arteries and Veins
 Atherosclerosis
 Hypertension
 Peripheral arterial disease
 Varicose veins and chronic venous insufficiency
 Thrombus formation in veins
 Superior vena cava syndrome
 Ischemic heart disease
Diseases of the Heart Wall
 Valvular dysfunction: murmurs
 Acute rheumatic fever and rheumatic heart disease
 Infective endocarditis
Manifestations of heart disease
 Dysrhythmias: atrial fib
 Heart failure
Diseases of the Arteries and Veins
Arteriosclerosis: a chronic disease of the arterial system characterized by abnormal
thickening and hardening of the vessel walls.
Atherosclerosis: a form of arteriosclerosis in which the thickening and hardening of the
vessel walls are caused by soft deposits of intraarterial fat and fibrin that harden over
time.
• The lesions of atherosclerosis occur primarily within the tunica intima (innermost
layer) and include the fatty streak, fibrous plaque, and the advanced or complicated
lesion.
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Hypertension: consistent elevation of systemic arterial blood pressure.
primary hypertension: combined systolic and diastolic hypertension with no known
cause (also called essential or idiopathic hypertension.
secondary hypertension: caused by altered hemodynamics associated with a primary
disease, such as arteriosclerosis.
isolated systolic hypertension: elevated systolic blood pressure accompanied by normal
diastolic BP
Peripheral arterial disease
• Tissue damage generally occurs below the arterial obstruction. The amount of
damage depends on the extent of the arterial blockage, on the nature of the decreased
arterial blood flow (chronic or acute), and on the location of the destruction.
• Causes of PAD: 1) vasoconstriction (Raynaud’s), 2) lack of blood flow
 At risk: familial tendency, smokers, hyperlipidemia, HTN, DM obesity (same ones as
for atherosclerosis)
 Chronic PAD: The disease is asymptomatic in its early stages. Most patients initially
seek treatment for a characteristic leg pain known as intermittent claudication.
• Acute PAD: due to thrombus or embolus; severe, acute pain below the level of
obstruction.
Chronic venous insufficiency
 Venous problems are the most prevalent
 Venous system inclusdes deep system (high pressure), superficial system (low
pressure) and the perforating veins which carry blood between the two systems
 Can have vein problems, valve problems, or a combination of both
 Sx: dull ache or heavy feelings in legs which worsens with prolonged standing.
• Physical signs: varicosities, edema, arterial tenderness, hyperpigmentation, stasis
• Also: thick, yellow nails; pain relieved with elevation of leg
 Varicose veins: in superficial veins, esp. around ankles; 90% related to vavular
incompetence (due to congenital defects, DCT); 10% due to obstruction; 2-4X more
prevalent in women; increased frquency with pregnancy, age, obesity, prolonged
standing
 Venous ulcers: superior and posterior to the medial malleoli and garter area; irregular
edges, erythematous borders, moist bed, wound slough, granulation base, stasis
dermatitis, tenderness
• Venous ulcers need compression device (for mild disease 20-30 mm Hg, for
significant disease: 40-50 mm Hg) Note: TED hose only provide 10-12 mm Hg.!
Need “medi” hose, elastic wraps, Unna’s boot, SCDs.
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Thrombus formation in veins
• Venous thrombi are more common than arterial thrombi, because flow and pressure
are lower in the veins than in the arteries.
Superior vena cava (SVC) syndrome: a progressive occlusion of the SVC that leads to
venous distention in the upper extremities and head.
Causes?
Signs/symptoms?
Ischemic heart disease
• CAD, myocardial ischemia, and MI form a pathophysiologic continuum that impairs
the pumping ability of the heart by depriving the heart muscle of blood-borne oxygen
and nutrients.
• ischemia, a local state in which the cells are temporarily deprived of blood supply.
They remain alive but are unable to function normally.
• Persistent ischemia or the complete occlusion of a coronary artery causes infarction,
or death, of the deprived myocardial tissue.
• Myocardial ischemia develops if coronary blood flow or the oxygen content of
coronary blood is not sufficient to meet the metabolic demands of myocardial cells.
Ischemia occurs if demand exceeds supply.
• Angina pectoris is chest pain caused by myocardial ischemia.
Supply is reduced by:
• hemodynamic factors (increased resistance in coronary vessels, hypotension, or
decreased blood volume
• cardiac factors (decreases of diastolic filling time, increases in HR, valvular
incompetence)
• hematologic factors (oxygen content of the blood)
• systemic disorders that reduce blood flow or the availability of oxygen (shock)
Demand is increased by:
• high systolic BP
• increased ventricular volume
• increased thickness of the myocardium (LVH caused by increased systemic resistance,
such as occurs with aortic valve stenosis and HTN)
• increased HR resulting from exercise, stress, hyperthyroidism, anemia, or
hyperviscosity of the blood (polycythemia)
• conditions that heighten the myocardium’s contractile response
Risk factors include:
• hyperlipidemia
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hypertension
cigarette smoking
diabetes mellitus
genetic predisposition
obesity (esp. upper body obesity)
sedentary lifestyle
hormone therapy
alcohol
women and CAD
Type A personality
Disorders of the Heart Wall
Valvular dysfunction: murmurs
• Disorders of the endocardium, the innermost lining of the heart wall, all damage the
heart valves, which are made up of endocardial tissue.
• Endocardial damage can be either congenital or acquired.
• The usual cause of acquired valvular dysfunction is inflammation of the endocardium
secondary to acute rheumatic fever or infectious endicarditis.
• In valvular stenosis, the valve orifice is constricted and narrowed, impeding the
forward flow of blood and increasing the workload of the cardiac chamber “in front”
of the diseased valve.
• In valvular regurgitation (also called insufficiency or incompetence), the valve
leaflets, or cusps, fail to shut completely, permitting blood flow to continue even
when the valve is supposed to be closed
Murmurs: occur due to:
• increased blood flow over normal valves (pediatrics, pregnancy after 28th week, after
heavy exercise)
• blood flow over constricted valves (aortic stenosis, mitral stenosis)
• regurgitation (aortic, mitral, or tricuspid regurgitation)
• blood going wrong way (ASD, AVD)
Acute rheumatic fever and rheumatic heart disease
Rheumatic fever is a diffuse, inflammatory disease caused by a delayed immune
response to infection by the group A beta-hemolytic streptococcus. In its acute form,
rheumatic fever is a febrile illness characterized by inflammation of the joints, skin,
nervous system, and heart.
If untreated, rheumatic fever can cause scarring and deformity of cardiac structures
resulting in rheumatic heart disease.
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Acute rheumatic fever (ARF)
• Epidemiology:
crowded population, poor public hygiene
• Occurs most frequently in children between ages 5 and 15.
• Only 3% of those in whom pharyngeal streptococcal infection develops acquire acute
rheumatic fever (ARF).
• Because the beta-hemolytic streptococcus infection must persist for some time to
cause ARF, appropriate antibiotic therapy given within the first 9 days of infection
usually prevents progression to rheumatic fever (infective endocarditis).
• Inflammation may subside before Rx is initiated. However, still may have caused
damage to heart valves.
• With damage to valves, increased risk of recurrent ARF after any subsequent
pharyngeal infection.
• 10% of people who develop ARF will progress to rheumatic heart disease.
Rheumatic heart disease
• Endocardial
• Valves lose elasticity and leaflets may adhere to one another
• Aschoff bodies
• Pericardial inflammation
• Cardiomegaly and CHF
• Conduction defects (prolonged PR, widened QRS) and atrial fibrillation
• Many of the common clinical manifestations of ARF - fever, lymphadenopathy,
arthralgia, N, V, epistaxis, abd. pain, and tachycardia - are associated with other
disorders as well and are by no means diagnostic of the disease.
• The major specific manifestations of ARF are carditis, acute migratory
polyarthritis, chorea (sudden aimless, irregular, involuntary movements = St.
Vitus dance), and erythema marginatum (truncal rash which looks like ringworm
as macules fade), which may occur singly or in combination after a latent period of 15 weeks after streptococcal infection of the pharynx.
• Dx: positive throat culture
• A high or rising antistreptolysin O antibody titer (ASO)
• Tx: 10-day regimen of oral PCN or erythromycin
Infective Endocarditis: general term used to describe inflammation of the endocardium,
especially the cardiac valves.
• Risk factors for infective carditis include acquired valvular heart disease (esp.
MVPP and implantation of prosthetic heart valves.
• Other risk factors: congenital lesions associated with highly turbulent flow, such as
ventricular septal defect; a previous attack of infective endocarditis, male gender, IV
drug abuse, long-term indwelling vascular catheterization, and recent cardiac surgery.
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3 critical elements needed:
1) The endocardium (heart valve) must be “prepared,” usually by endothelial
damage, for microorganism colonization.
2) Blood-borne microorganisms must adhere to the damaged endocardial surface.
3) The adherent microorganisms must proliferate and promote the propagation of
infective endocardial vegetation.
Manifestations of Heart Disease
Dysrhythmias: (arrhythmia): a disturbance of heart rhythm.
Range in severity from occasional “missed” or rapid beats to serious disturbances
that impair the pumping ability of the heart, contributing to heart failure and
death.
Heart failure: the inability of the heart to supply the body and heart muscle itself with
adequate circulatory volume and pressure.