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)
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)
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 (
2. Active
diastole: atrial contraction in
response to SA node stimulation = atrial kick (= 20 cc)
Stroke volume = the amount of
blood ejected from the
There
is a cardiac reserve of approximately 40 cc left in the
Left Ventricular
End Diastolic Volume (LVEDV) = Cardiac reserve + passive diastole +
active diastole = 120 cc.
Cardiac output
(CO): the amount of blood pumped out of the heart
in one minute
Cardiac
output = SV X HR
Permanent pacemakers
ICHD (Inter-Society commission for
Heart Disease Resources) code for pacemakers contains five 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)
Monitoring
parameters: cardiac index, ejection fraction, preload,
afterload
- Cardiac
index
= CO
BSA (Body
surface area)
Normal Cardiac index = approx. 2.8 -
4.0 L/min/m2
As CI decreases, CO decreases,
meaning increasing severity of failure
2.8 - 4.0
2.2 - 2.7 Mild
1.8 - 2.1 Severe
< 1.8 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
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
- 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)
**************************************************************************************************
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
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
Pathophysiology
of the Cardiovascular System: Adults and
Children
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.
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 (Raynauds), 2) lack of
blood flow
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
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
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,
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.
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 myocardiums
contractile response
Risk
factors include:
hyperlipidemia
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 endocarditis.
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.
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
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 1-5
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.
MVP 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.
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.
Right
heart failure (cor pulmonale):
Lung
disease
Increased pulmonary vascular
resistance Decreased
oxygen supply
Increased force of RV
contraction
Increased
RV oxygen demand RV
hypoxia
Decreased
force of RV
contraction
Increased
RV end-diastolic
pressure
Increased
RV preload
Increased
RA preload
Peripheral
edema
Left
heart failure (congestive heart failure)
Increased
systemic vascular resistance
Increased force
of
Increased
Increased
Decreased systemic BP ¬Decreased force
of
Decreased coronary artery Increased LV end-diastolic pressure
blood flow
Increased
Increased LA preload
Pulmonary edema
Increased pulmonary vascular resistance
RV failure
On
venous side:
decreased CO --> decreased venous
return --> increased blood caught in venous tree
--> increased venous pressure --> increased preload --> fluid unable
to move out of tissue back into circulation and increased pushed out of capillaries
--> EDEMA
On
arterial side:
Decreased CO + decreased venous
return --> baroreceptors activated (** Here is bodys
mistake/misdiagnosis: Msg. is
wrong: body thinks that because there is
decreased blood returning to the
heart, that there must be a hemorrhage!) -->
msg. to brain --> activates adrenergic (sympathetic) nervous system
--> increased BP --> also, kidneys activated to shut down -->
decreased renal perfusion --> more angiotensin II released --> increased
BP; increased aldosterone released --> increased sodium and water retention
--> increased BP. (Ultimate
result: increased peripheral resistance)
Signs/Symptoms:
Venous:
increased venous pressure (jugular
pulsates)
loss of appetite (blood in mesentary pushes
on stomach; feels full)
rales
dyspnea
cyanosis (nail beds, gingiva)
pitting edema (wherever pressure is
greatest: legs in ambulatory patient,
sacral area in bedfast patient) (* Non-pitting
edema is due to such things as collagen diseases)
Arterial:
tachycardia secondary to beta-stimulation
cardiac arrhythmia
HTN
oliguria (low urinary output); specific
gravity increases
cardiac hypertrophy (works harder -->
thickened wall --> poor ejection fraction)
Low-output
failure: biventricular failure due to cardiomyopathies
and myocardial infection (myocarditis).
Begins with a loss of contractility and a decrease in CO
High-output
failure: the inability of the heart to adequately
supply the body with blood-borne nutrients, despite adequate blood volume and
normal or elevated myocardial contractility.
The heart increases its output, but the bodys metabolic needs are still
not met. Common causes are anemia,
septicemia, hyperthyroidism, and beriberi.