Transcript Cardiac Pathophysiology

Cardiac Pathophysiology
A Short Overview
1. The Pathophysiology of Congestive
Heart Failure (CHF)
Congestive heart failure is a syndrome that can
be caused by a variety of abnormalities,
including:
• Pressure and volume overload,
• loss of muscle,
• primary muscle disease or
• excessive peripheral demands such as high
output failure.
The Pathophysiology of CHF
The main causes of heart failure are:
 atherosclerosis (calcification of the arteries),
 hypertension or coronary artery disease (due to calcification of the
arteries).
Other diseases affecting the myocardium or heart valves can cause
heart failure :
• Myocardial inflammation, myocarditis
• Valve disease, endocarditis
• Heart rhythm disorders
• Pneumonia
• Pericardial effusion (pericarditis) or narrowing of the pericardium
• Hyperfunction of the thyroid, hyperthyroidism
• Heart disease, congenital or acquired
• Family history
In the usual form of heart failure, the heart muscle has reduced
contractility. This produces a reduction in cardiac output, which
then becomes inadequate to meet the peripheral demands of the
body.
Cardiac output = stroke volume X
heart rate (beats per minute)
NORMAL FOR MALE IS ABOUT 5.5 LITERS OF BLOOD
PUMPED BY THE HEART TO THE BODY EVERY
MINUTE
NORMAL FOR FEMALE IS ABOUT 5.0 LITERS PER
MINUTE
Left and Right-Sided CHF:
.
• Left heart failure occurs when the left ventricle
cannot pump blood to the body and fluid backs up
and leaks into the lungs causing shortness of breath.
• Right heart failure occurs when the right ventricle
cannot adequately pump blood to the lungs. Blood
and fluid may back up in the veins that deliver blood
to the heart. This can cause fluid to leak into tissues
and organs.
.•
Anything that may affect the heart rate, stroke
volume, and ejection fraction, may lead to the
heart pumping less efficiently. This can cause
blood to back up into the veins leading to the
heart, increasing pressure within the capillaries,
the smallest of blood vessels in the body and in
turn cause water (fluid) to leak into the interstitial
space (the space between cells that make up the
tissue and organs of the body).
• Consequently, ↓cardiac output results in →
↑pressure in capillary blood vessels→ water
leaking→ heart failure symptoms
Left Sided CHF:
.
The 4 primary determinants of left
ventricular (LV) performance are
generally altered as follows:
(1) There is an intrinsic decrease in
muscle contractility.
(2) Preload or left atrial filling pressure
is increased, resulting in pulmonary
congestion and dyspnea.
.
.
.
IMPORTANT TIP REGARDING LEFT
SIDED CHF:
Crackles on auscultation, hypoxia, shortness
of breath on exertion and often at rest,
cough, and paroxysmal nocturnal dyspnea.
Right-Sided CHF:
• May occur when the heart has to pump against
increased resistance in the blood vessels leading to the
lungs. As pressure rises in the pulmonary arteries and
veins, the right ventricle has to pump harder and may
not be able to overcome this higher pressure. Some
causes of right heart failure include the following:
• Pulmonary embolus (blood clot to the lung)
• Pulmonary hypertension (increased blood pressure
within the lung's blood vessels)
• Chronic obstructive pulmonary disease (COPD)
• Pulmonary valve stenosis or narrowing of the valve
that connects the right ventricle to the pulmonary
artery
.
.
2. The Pathophysiology of Deep
Vein Thrombosis (DVT)
•Deep vein thrombosis (DVT) occurs when a blood
clot (thrombus) forms in one or more of the deep
veins in the body, usually in the legs. DVT can cause
leg pain or swelling, but may occur without any
symptoms.
The Pathophysiology of DVT
• DVT can develop in the presence of certain
medical conditions that affect how the blood
clots. Deep vein thrombosis can also happen
with reduced movement, such as after
surgery, following an accident, or when the
patient is confined to a hospital or nursing
home bed.
• DVT is serious, because these blood clots can
break loose, travel through the bloodstream
and lodge in the lungs, blocking blood flow
(pulmonary embolism).
.
.
The warning signs of a pulmonary
embolism include:
• Unexplained sudden onset of shortness of
breath
• Chest pain or discomfort that worsens with a
deep breath or when patient coughs
• Patient complains of feeling lightheaded or
dizzy, or fainting
• Rapid pulse
• Coughing up blood
.
Pulmonary Emboli
3. The Pathophysiology of
Myocardial Infarction (MI)
Myocardial infarction (MI) (i.e., heart
attack) is the irreversible necrosis of heart
muscle secondary to prolonged ischemia.
The Pathophysiology of Myocardial
Infarction (MI):
This most commonly occurs when
a coronary artery becomes
occluded following the rupture
of an atherosclerotic plaque,
which then leads to the
formation of a blood clot
(coronary thrombosis). This
event can also trigger coronary
vasospasm. If a vessel becomes
completely occluded, the
myocardium normally supplied
by that vessel will
become ischemic and hypoxic.
Without sufficient oxygen, the
tissue dies.
The Pathophysiology of Myocardial
Infarction (MI):
• The damaged tissue is initially comprised of a
necrotic core surrounded by a marginal (or
border) zone that can either recover normal
function or become irreversibly damaged. The
hypoxic tissue within the border zone may
become a site for generating
arrhythmias. Collateral blood flow is an important
determinant of infarct size and whether or not
the border zone becomes irreversibly damaged.
• Infarcted tissue does not contribute to tension
generation during systole, and therefore can
alter ventricular systolic and diastolic
function and disrupt electrical activity within the
heart.
.
.
.
Myocardial Infarction
Myocardial infarctions produce clinical symptoms that
include:
• intense chest pain that may radiate into the neck, jaw
or arms (i.e., referred pain),
• a sense of substernal heaviness, squeezing or pressure,
• shortness of breath (dyspnea),
• fatigue,
• fainting (syncope),
• nausea,
• sweating (diaphoresis),
• anxiety,
• sleeplessness,
• hypertension or hypotension (depending in part on the
extent of cardiac damage),
• tachycardia and arrhythmias.
.
The Pathophysiology of Myocardial Infarction
(MI):
Recent clinical research indicates that the
symptoms may be very different between
men and women. Chest pain is less common
in women. Instead, their most common
symptoms are weakness, fatigue and
dyspnea.
The pathophysiology of acute myocardial infarction is
complex.
• Loss of viable myocardium impairs global cardiac function,
which can lead to reduced cardiac output, and if damage is
severe, to cardiogenic shock.
• Systolic and diastolic dysfunction are associated with
ischemic myocardium. If left ventricular function is
significantly impaired, pulmonary congestion and edema can
occur.
• Ischemia can also precipitate abnormal cardiac rhythms and
conduction blocks that can further impair function and
become life-threatening in some cases.
• Reduced cardiac output and arterial pressure can
elicit baroreceptor reflexes that lead to activation of
neurohumoral compensatory mechanisms (e.g., activation of
sympathetic nerves and the renin-angiotensin-aldosterone
system) similar to what occurs during heart failure.
,
.
• The pain and anxiety associated with
myocardial infarction further activates the
sympathetic nervous system, which causes
systemic vasoconstriction and cardiac
stimulation (this explains why some patients
become hypertensive and have tachycardia).
• While sympathetic activation helps to
maintain arterial pressure, it also leads to a
large increase in myocardial oxygen
demand that can lead to greater myocardial
hypoxia, enlarge the infarcted region,
precipitate arrhythmias, and further impair
cardiac function.
Cardiac Anatomy & Physiology
Quiz
1. In the systemic circuit, the _____________
half of the heart pumps __________ blood to all
body tissues and then _________ blood flows
back to the heart.
a. right; deoxygenated; oxygenated
b. right; oxygenated; deoxygenated
c. left; deoxygenated; oxygenated
d. left; oxygenated; deoxygenated
2. In the pulmonary circuit, the __________ half
of the heart pumps __________ blood to the
alveoli of the lungs, and then _____________
blood flows back to the heart.
a. right; deoxygenated; oxygenated
b. right; oxygenated; deoxygenated
c. left; deoxygenated; oxygenated
d. left; oxygenated; deoxygenated
3. The predominant driving force that
moves blood back to the heart in the
veins is:
a. active transport
b. passive transport
c. the closing of one-way valves
d. the beating of the heart
e. the skeletal muscle contractions
4. Which of the following procedures involves a
segment of a leg vein being used to provide an
alternate pathway for blood flow past a point of
obstruction between the aorta and a coronary
artery?
a. angioplasty
b. coronary angiography
c. heart transplant
d. coronary bypass
5. Which of the following valves directs blood
flow from the left atrium to the left ventricle?
a.
b.
c.
d.
Mitral
Tricuspid
Aortic
Pulmonic
6. The layer of squamous cells that lines the
cardiac chambers and valves is called the:
a. myocardium
b. endocardium
c. epicardium
d. pericardium
7. Which of the following statements is true?
a. The AV node stimulates the atria.
b. The vagus nerve supplies both the SA and
AV nodes.
c. Sympathetic nerve stimulation reduces the
heart rate.
d. Parasympathetic nerve stimulation
reduces the heart rate.
8. The echocardiogram (ECG/EKG) is
especially useful in the measurement of
the:
a. coronary blood flow and location of
obstructions.
b. Structures and motion of the heart within
the chest.
c. Structures and function of the lungs.
d. All of the above.
9. What effect does stimulation of the
sympathetic nervous system have on the
arterioles?
a. Dilation, which results in increased vascular
resistance, and increased blood pressure.
b. Constriction, which results in increased
vascular resistance, and decreased blood
pressure.
c. Constriction, which results in increased
vascular resistance, and increased blood
pressure
d. Dilation, which results in decreased vascular
resistance, and decreased blood pressure.
10. Which of the following conditions impedes
blood flow from the left atrium to the left
ventricle, and can be heard as a lub dub
whoosh:
a. Aortic Stenosis
b. Pulmonary Valvular Stenosis
c. Mitral Stenosis
d. Tricuspid Stenosis
11. What is the pathophysiologic phenomenon
underlying disseminated intravascular
coagulation (DIC)?
a.
b.
c.
d.
Clotting that leads to bleeding
Elevated platelet and fibrinogen levels
Inadequate cardiac output
Mast cell degranulation
12. A patient with heart failure complains of
awakening intermittently during the night with
shortness of breath. Which of the following
terms is appropriate for this clinical
manifestation?
a.
b.
c.
d.
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Cyanosis