Unit 5 Part 1 Flashcards
network of highways connecting muscles and organs through an extensive system of vessels that transport blood, nutrients, and waste.
Cardiovascular System
Different Types of Molecules Move Through The Cardiovascular System
Nutrients
Oxygen
Metabolic wastes
Hormones
heat
from digested food to cells
Nutrients
from lungs to cells
Oxygen
from cells to excretory organs.
Metabolic wastes
regulate body activities
Hormones
maintain body temperature (constrict or dilate)
heat
Three interrelated components of the Cardiovascular System
- Blood (transport vehicle)
- Heart (pump)
- Blood vessels (network of tubes)
Other Components of the Hemovascular System
Bone marrow
* Liver
* Spleen
* Lymph system
Other Components of the Hemovascular System
-Bone marrow -red and yellow
-Liver
-Spleen
-Lymph system
– Acts as a filter
– Produces all the PROCOAGULANTS essential to
hemostasis and blood coagulation
(PROTHROMBIN and CLOTTING FACTORS)
– formation of Vitamin K
– Stores excess iron
– Produces HEPDICIN , a key regulator of iron balance
Liver
procoagulants
(PROTHROMBIN and CLOTTING FACTORS)\
Hematopoietic
Filtration
Immunologic
Storage
Spleen
Able to produce RBCs during fetal development
Hematopoietic
Remove old and damaged RBCs from circulation
Removes hemoglobin from RBCs and returns iron
component to the bone marrow for reuse
Filters out bacteria, especially encapsulated
organisms
Filtration
Contains a rich supply of lymphocytes,
monocytes, and stored immunoglobulins
Immunologic:
Stores RBCs and approximately 30% of total
mass of platelets
Storage:
transports substances between body cells and the
external environment
blood
liquid connective tissue
blood
mixture of formed elements and plasma
blood
living blood cells & platelets
formed elements
the fluid matrix
plasma
Physical characteristics of blood
* ___ than water
* Temperature about ___ higher than oral or rectal body temperature
* Alkaline pH ??
* ___ of total body weight
* L in adult male
* L in adult female
More viscous
1 degree celsius
7.35 to 7.45
~8%
5-6
4-5
Functions of Blood
➢Transport and Distribution
➢Regulation of Internal Homeostasis
➢Protection
➢Transport and Distribution
delivery: ?
removal: ?
O2, nutrients, and hormones
CO2 and metabolic wastes
➢Regulation of Internal Homeostasis
– body temperature
– pH
– fluid volume
– composition of the interstitial fluid/lymph
➢Protection
– necessary for inflammation and repair
– prevents blood loss by hemostasis (coagulation)
– prevents infection
2 parts of blood sample
Plasma
Formed elements
– ~55% of the volume
– straw colored liquid on top
Plasma
~45% of the volume
– red blood cells (99%)
– buffy coat - white blood cells and platelets (1%)
Formed elements
white blood cells and platelets (1%)
buffy coat
➢ 92% WATER
➢ 7% PROTEINS
➢Important for osmotic balance
➢ 1.5% OTHER SOLUTES
PLASMA
(60%)
–transports lipids
–steroid hormones
Albumin
(4%) - blood clotting
Fibrinogen
(35%) – many different proteins with a wide variety of functions
–globulin classes α, β, and γ
* 1% other regulatory proteins
Globulins
carried to various organs for removal
Waste products
glucose and other sugars, amino acids, lipids, vitamins and minerals
Nutrients
- enzymes
- hormones
Regulatory substances
O2
, CO2
, N2
Gases
Electrolytes
(ions)
➢ >99% RED BLOODCELLS
➢ <1% WHITE BLOOD CELLS and THROMBOCYTES (platelets)
FORMED ELEMENTS
➢LIVING CELLS
➢Erythrocytes, or Red Blood Cells (RBC’s), for O2 and
CO2 transport
➢RBCs’ hemoglobin also helps buffer the blood
rbc
– neutrophils
– eosinophils
– basophils
- Granular leukocytes (granulocytes)
– lymphocytes - T cells, B cells
–monocytes → tissue macrophages
Agranular leukocytes (agranulocytes)
pump of blood in an hour
300 quarts
heartbeat
a day
per year
lifetime
100,000 times
35 million
2,700,000,000
largest artery in the body
diameter of a garden hose
aorta
small that it takes ten of them to
equal the thickness of a human hair
Capillaries
body has about __liters (__ quarts) of blood.
5.6
6
circulation of blood
minute
day
3 times every minute
total of 19,000 km (12,000 miles)
___ have bigger anatomical hearts
males
location of heart
mediastinum
broad superior portion of heart
Base
inferior end, tilts to the left, tapers to point
Apex
– Carry blood from the right ventricle to the lungs
– Blood is deoxygenated
Pulmonary Arteries
– Carry blood from the lungs to the left atrium
– Blood is oxygenated
Pulmonary Veins
– Carries blood from the body to the right atrium
– Blood is deoxygenated
Superior & Inferior Vena Cava
– Carries blood from the left ventricle to the body
– Blood is oxygenated
Aorta
like a cone on its side between the lungs
heart
- surrounds heart, keeps your heart in it’s place (like a father-in-law with the gun collection)
- Allows heart to beat without friction, room to expand and resists excessive expansion
Pericardium
Superficial, tough, elastic
Fibrous Pericardium
Thinner, delicate, double layer
Serous Pericardium
– fused to the fibrous pericardium
Parietal Layer
Parietal Layer
Parietal Layer
outside slippery layer
Epicardium-/visceral pericardium
muscle of heart
myocardium
inside the heart
Endocardium
- Atrial walls are thinnest
- Right ventricle thinner than left ventricle
– pumps blood shorter distance - Left ventricle walls thickest
- Right and left ventricles pump same volume of
blood with each beat
Myocardium
- Interatrial septum
- Pectinate muscles
- Interventricular septum
- Trabeculae carneae
- Chordae tendineae
- Heart Valves
Endocardium
– wall that separates atria
Interatrial septum
– internal ridges of myocardium in right atrium and
both auricles
- Pectinate muscles
– wall that separates ventricles
Interventricular septum
– internal ridges in both ventricles walls
Trabeculae carneae
cords connecting to the tricuspid and mitral valves
Chordae tendineae
inflammation of the pericardium
Pericarditis
-chest pain
-pericardial friction rub (creaking sound)
Acute Pericarditis
-pericardial fluid accumulates—compress heart
-Cardiac tamponade -fluid in the pericardial cavity
compressing the heart, can stop the heart beat
-cancer and tuberculosis
chronic pericarditis
inflammation of the myocardium
myocarditis
– viral infection, rheumatic fever,
exposure to radiation or certain chemicals,
medications
-fever, fatigue, chest pain, irregular or rapid
heart beat, joint pain, breathlessness
Myocarditis
inflammation of the endocardium
Endocarditis
entry halls
atria
little bellies
ventricles
– 2 superior, posterior chambers
– receive blood returning to heart
Right and left atria
– 2 inferior chambers
– pump blood into arteries
Right and left ventricles
resting pulse rate
kid
adult
90-120
slows to an ave. of 72
- Vessels that carry blood to and from the lungs
- Pulmonary circuit is a short, low-pressure circulation
Right side is the pump for the pulmonary circuit
- Vessels that carry the blood to and from all body tissues
- Systemic circuit blood encounters much resistance in
the long pathways - Anatomy of the ventricles reflects these differences
– Left side is the pump for the systemic circuit
blood flow in the heart
Right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries →
lungs → pulmonary veins → left atrium → bicuspid valve → left ventricle → aortic semilunar valve → aorta→ systemic circulation
- Ensure one-way blood flow
- Semilunar valves
- Atrioventricular (AV) valves
Heart Valves
- control flow into great arteries
Semilunar valves
from right ventricle into pulmonary trunk
Semilunar valves pulmonary:
from left ventricle into aorta
Semilunar valves aortic
right AV valve has
3 cusps (tricuspid valve)
left AV valve has
2 cusps (mitral, bicuspid valve)
- cords connect AV valves to papillary muscles (on floor of ventricles)
chordae tendineae
The valves of the heart open and close in
response to
pressure changes as the heart contracts and relaxes
AV Valve Mechanics when Ventricles relax
pressure drops, semilunar valves close, AV valves open, blood flows from atria to ventricles
AV Valve Mechanics when Ventricles contract
AV valves close (papillary m. contract and pull on chordae tendineae to prevent prolapse), pressure rises, semilunar valves open, blood flows into great vessels
systole
contraction
diastole
relaxation
narrowing of heart valve opening
that restricts blood flow; stiff= heart workload
increased
Stenosis
failure of valve to close completely backflow and
repump
Insufficient/Incompetent valve
– scar formation; congenital anomaly
Mitral stenosis
left ventricle→left atrium; mitral valve prolapse
Mitral insufficiency
(aorta→left ventricle)
Aortic stenosis, aortic insufficiency
streptococcal infection of throat;
bacteria trigger an immune response in which
antibodies produced attack and inflame connective
tissues in joints, heart valves (aortic, mitral)
Rheumatic fever
act of listening to heart sounds
Auscultation
Due to vibrations in the blood caused by valves
closing and opening
Heart Sounds
Four sounds but only two loud enough to hear by
stethoscope which are
(S1 and S2)
long, booming sound AV valves closing
(mitral and tricuspid)
S1 = lub
short, sharp sound SL valves closing
(aortic and pulmonary)
S2 = dub
blood turbulence during ventricular filling
(relaxed)
S3
blood turbulence during atrial
systole/ventricular filling (active)
S4
systole, atrioventricular valves, tricuspid, and mitral close
s1 lub
diastole, pulmonic, aortic valve
s2 dub
Represents the closure of the mitral and tricuspid valves
First heart sound(S1)
Represents the closure of the aortic and pulmonary valves
Second heart sound (S2)
It is created by the blood coming from the atria into the
ventricles during the early diastolic filling phase. Occurs
just after S2.
Third heart sound (S3)
It is created by atrial contraction at the late diastolic phase. It
occurs just before S1
Fourth heart sound (S4)
Normal heart sound
First heart
sound(S1
)
splitting is heard (the lungs
and veins expand so the
venous return increases to
the right side of the heart.)
Second heart sound (S2
)
causes an increase in
blood flow thru the
pulmonary valve.
the lungs
and veins expand so the
venous return increases to
the right side of the heart.
NB: S3
is almost
always pathologic. It is
caused by diseased of
the left ventricle
(dilated left ventricle,
poor-contracted left
ventricle, dilated
cardiomyopathy, MI)
Third heart
sound(S3
)
Normally,
heard in
healthy young
people.
Fourth heart
sound (S4
)
swishing sound heard
when there is turbulent or abnormal blood
flow across the heart valve.
Heart Murmur
murmurs present
without any medical or heart conditions
(childhood murmurs, pregnancy)
Innocent murmurs
Causes heart murmur
– Valvular heart diseases
most common valvular disease
cardiomyopathy; septal defect
Functional causes heart murmurs
anemia, hyperthyroidism
Derived from increased turbulence
Systolic Murmurs
- Increased flow across normal SL valve or into a
dilated great vessel - Flow across an abnormal SL valve or narrowed
ventricular outflow tract - e.g. aortic stenosis - Flow across an incompetent AV valve - e.g. mitral
regurgitation - Flow across the interventricular septum
Systolic Murmurs
Almost always indicate heart disease
1. Early decrescendo diastolic murmurs
2. Rumbling diastolic murmurs in mid- or late
diastole
Diastolic Murmurs
– signify regurgitant flow through an incompetent
semilunar valve
* e.g. aortic regurgitation
Early decrescendo diastolic murmurs
– suggest stenosis of an AV valve
- Rumbling diastolic murmurs in mid- or late
diastole
Atria and ventricles contract in coordinated
manner
Ensures correct blood flow
electrical events
* Control and coordinate activity of contractile cells
Conducting system
mechanical events
* Produce powerful contractions that propel blood
Contractile cells
striated, short, fat,
branched, and interconnected
Cardiac muscle cells
connects to the fibrous skeleton
Connective tissue matrix (endomysium)
wide but less numerous
T tubules
Numerous large mitochondria
(25–35% of cell
volume)
junctions between cells
anchor cardiac cells
Intercalated discs:
prevent cells from separating during
contraction
Desmosomes
allow ions to pass; electrically
couple adjacent cells
Gap junctions
behaves as a functional
syncytium
Heart muscle
contractile fibers have stable
resting membrane potential
Depolarization
period of maintained depolarization
Plateau
recovery of resting membrane potential
Repolarization
time interval during which second
contraction cannot be triggered
Refractory period
-Cardiac muscle tissue contracts on its own
-Does not need hormonal or neural stimulation (These will change the force)
automaticity or autorhythmicity
Repeatedly generate action potentials that trigger
heart contractions
Cardiac muscle tissue contracts on its own
Conducting Myocardium
unstable resting potentials
pacemaker
potentials
for rising
phase of the action potential
calcium influx
Made up of two types of cells that do not
contract:
»Nodal cells
»Conducting cells
The Conducting System
(responsible for
establishing rate of contraction)
»Nodal cells
(distribute the
contractile stimulus to general
myocardium)
»Conducting cells
generates impulses about
90-100 action potentials per minute
Sinoatrial (SA) node
delays the impulse
approximately 0.1 second; 40-50 action
potentials per minute
Atrioventricular (AV) node
Impulse passes from atria to ventricles via
the
atrioventricular bundle
carry the impulse toward the
apex of the heart
Bundle branches
carry the impulse to the heart
apex and ventricular walls
Purkinje fibers
Normal sinus rhythm
60-100 beats/min
abnormality of the heart
rhythm
Cardiac arrhythmia
heart rate slow (<60 beats/min)
Bradycardia
heart rate fast (>100 beats/min)
Tachycardia
Classification (increased/decreased)
Heart rate
Classification (regular/irregular)
Heart rhythm
Classification (supraventricular / ventricular)
Site of origin
Classification (narrow/broad)
Complexes on ECG
- Composite record of action potentials produced by all the heart muscle fibers
- Electrodes placed on body surface
- Graphed as series of up and down waves produced during each heartbeat
- Instrument called electrocardiograph
Electrocardiogram (ECG or EKG)
- Electrodes placed on body surface
– arms and legs and six positions on chest
produces 12 different tracings
electrocardiograph
ECG Waves
- P wave
- QRS complex
- T wave
- atrial repolarization usually not visible
– atrial depolarization
P wave
– ventricular depolarization
– onset of ventricular contraction
QRS complex
– ventricular repolarization
– just before ventricles start to relax
T wave
– masked by larger QRS complex
atrial repolarization usually not visible
Cardiac action potential arises in___
* ___ wave appears
SA node
P
Action potential enters___ and out over ventricles
* __ complex
* Masks __
AV bundle
QRS
atrial repolarization
- Begins shortly after QRS complex appears and continues during S-T segment
Contraction of ventricles/ ventricular systole
Repolarization of ventricular fibers
- T wave
period between the start of one
heartbeat and the beginning to the next
Cardiac cycle
During atrial systole, ventricles
relax
During ventricle systole, atria
relax
- All events associated with one heartbeat
- In each cycle, atria and ventricles alternately contract
and relax - Forces blood from higher pressure to lower pressure
- During relaxation period, both atria and ventricles
are relaxed
Cardiac Cycle
volume of blood
ejected from left (or right) ventricle into aorta
(or pulmonary trunk) each minute
Cardiac Output (CO)
Cardiac Output (CO) formula
stroke volume (SV) x heart rate (HR)
number of heart beats per
minute
HR
amount of blood pumped out by
a ventricle with each beat; ml per beat
SV
Cardiac Output and Cardiac Reserve
- In typical resting male
5.25L/min = 70mL/beat x 75 beats/min
Entire blood volume flows through
pulmonary and systemic circuits each minute
difference between
maximum CO and CO at rest
Cardiac reserve
Factors Influencing Cardiac Output
Heart rate
Positive chronotropic factors
Negative chronotropic factors
rate of depolarization in
autorhythmic cell
Heart rate
factors increase heart
rate
Positive chronotropic factors
factors decrease heart
rate
Negative chronotropic factors
Stroke volume usually remains relatively
constant.
Changing heart rate is the
most common way to change cardiac
output
- Increased heart rate
- Sympathetic nervous system
- Crisis
- Low blood pressure
- Increased heart rate
- Hormones
- Epinephrine
- Thyroxine
- Sympathetic nervous system
- Hormones
- Exercise
- Decreased blood volume
- Increased heart rate
- Parasympathetic nervous system
- High blood pressure or blood volume
- Dereased venous return
- Decreased heart rate
force of contraction in
ventricular myocardium
stroke volume
stroke volume
- Preload
- Contractility
- Afterload
– Degree of stretch on the heart before it contracts
– Greater preload increases the force of contraction
Preload
– the more the
heart fills with blood during diastole, the greater
the force of contraction during systole
* Preload proportional to end-diastolic volume (EDV)
Frank-Starling law of the heart
2 factors determine EDV
- Duration of ventricular diastole
- Venous return
volume of blood returning to right
ventricle
Venous return
– Strength of contraction at any given preload
– Positive inotropic agents
– Negative inotropic agents
Contractility
increase contractility
* Often promote Ca2+ inflow during cardiac action
potential
* Increases stroke volume
* Epinephrine, norepinephrine, digitalis
Positive inotropic agents
decrease contractility
* Anoxia, acidosis, some anesthetics, and increased K+
in interstitial fluid
Negative inotropic agents
– Pressure that must be overcome before a
semilunar valve can open
Afterload
Increase in afterload causes stroke volume to
decrease
what increases afterload
Hypertension and atherosclerosis
Regulation of Heart Beat
– Autonomic Regulation
–Nervous System Control
– Chemical Regulation
– Originates in cardiovascular center of medulla oblongata
– Increases or decreases frequency of nerve impulses in
both sympathetic and parasympathetic branches of ANS
Autonomic regulation
Noreprinephrine effects In SA and AV node
speeds rate of spontaneous
depolarization
Noreprinephrine effects In contractile fibers
fibers enhances Ca2+ entry increasing
contractility
releases acetylcholine
Parasympathetic nerves
decreases heart rate by slowing rate of spontaneous
depolarization
acetylcholine
activates
sympathetic
neurons
Cardio-acceleratory
center
controls
parasympathetic
neurons
Cardio-inhibitory
center
Chemical regulation of heart rate
Hormones
- Epinephrine and norepinephrine increase heart rate
and contractility - Thyroid hormones also increase heart rate and
contractility
Chemical regulation of heart rate
cations
- Ionic imbalance can compromise pumping effectiveness
- Relative concentration of K+, Ca2+ and Na+ important
Abnormality of cardiac function that leads to the
inability of the heart to pump blood
Congestive Heart Failure
- Causes a decreased tissue perfusion as a result of
decreased CARDIAC OUTPUT
Congestive Heart Failure
inability of the heart to pump blood to meet the
body’s basic metabolic demands
Congestive Heart Failure
Congestive heart failure (CHF) is caused by:
– Coronary atherosclerosis
– Persistent high blood pressure
– Multiple myocardial infarcts
– Dilated cardiomyopathy (DCM) – main pumping
chambers of the heart are dilated and contract
poorly
– Valve disorders
– Congenital defects
Congestive heart failure (CHF) is caused by:
– Coronary atherosclerosis
– Persistent high blood pressure
– Multiple myocardial infarcts
– Dilated cardiomyopathy (DCM) – main pumping
chambers of the heart are dilated and contract
poorly
– Valve disorders
– Congenital defects
Left Heart Failure
- Dyspnea
- Dec. exercise tolerance
- Cough
- Orthopnea
- Pink, frothy sputum
Right Heart Failure
- Dec. exercise tolerance
- Edema
- HJR / JVD
- Hepatomegaly
- Ascites
- Results from LEFT ventricular wall damage or
dilatation - Left ventricular and atrial end-diastolic
pressures increase and cardiac output decreases - Impaired left ventricular filling results in
congestion and increased pulmonary vascular
pressures - REMEMBER: “L”eft and “L”ung, the fluid “backs
up” to lungs
Left-sided failure
- Caused by pulmonary hypertension and left heart
failure - Pulmonary hypertension causes increased pressure
that right ventricle must pump against, so right
ventricle cannot empty; hypertrophy and dilatation
result - Right ventricle distention leads to blood
accumulation in systemic veins - REMEMBER: “R”ight and “R”est of the body, the
fluid “backs up” to rest of body
Right-sided failure
Systolic– “can’t pump”
– Aortic Stenosis
– HTN
– Aortic Insufficiency
– Mitral Regurgitation
– Muscle Loss
* Ischemia
* Fibrosis
* Infiltration
Diastolic- “can’t fill”
– Mitral Stenosis
– Tamponade
– Hypertrophy
– Infiltration
– Fibrosis
Evaluation of Heart Failure
- HEART SOUNDS
- Systolic Murmurs
- Diastolic Murmurs
- S3: Rapid filling of a diseased ventricle
- CXR
- EKG
Evaluation of Heart Failure
* Systolic Murmurs
– Mitral Regurg
– Aortic Stenosis
Evaluation of Heart Failure
* Diastolic Murmurs
– Mitral Stenosis
– Aortic Insufficiency
Evaluation of Heart Failure
* CXR
– Kerley’s lines : A and B
– Pulmonary Edema
– Cephalization
– Pleural Effusions (bilateral)
Evaluation of Heart Failure
* EKG
– Left atrial enlargement
– Arrhythmias
– Hypertrophy (left or right)
Treatment of CHF
- Treat Precipitating Factor(s)
- Adjust Heart Rate
- Decrease Preload
- Decrease Afterload
- Increase Contractility
- Increase Oxygenation
Treatment of CHF – UNLOAD ME
- U – upright position
- N – Nitrates
- L - Lasix
- O - Oxygen
- A - ACEi
- D - Digoxin
- M - Morphine
- E - ECG
