Unit 5 Part 1 Flashcards by Aubs Ganda

network of highways connecting muscles and organs through an extensive system of vessels that transport blood, nutrients, and waste.

Cardiovascular System

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Different Types of Molecules Move Through The Cardiovascular System

Nutrients
Oxygen
Metabolic wastes
Hormones
heat

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from digested food to cells

Nutrients

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from lungs to cells

Oxygen

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from cells to excretory organs.

Metabolic wastes

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regulate body activities

Hormones

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maintain body temperature (constrict or dilate)

heat

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Three interrelated components of the Cardiovascular System

Blood (transport vehicle)
Heart (pump)
Blood vessels (network of tubes)

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Other Components of the Hemovascular System

Bone marrow
* Liver
* Spleen
* Lymph system

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Other Components of the Hemovascular System

-Bone marrow -red and yellow
-Liver
-Spleen
-Lymph system

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– 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

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procoagulants

(PROTHROMBIN and CLOTTING FACTORS)\

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 Hematopoietic
 Filtration
 Immunologic
 Storage

Spleen

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Able to produce RBCs during fetal development

Hematopoietic

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 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

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Contains a rich supply of lymphocytes,
monocytes, and stored immunoglobulins

Immunologic:

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Stores RBCs and approximately 30% of total
mass of platelets

Storage:

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transports substances between body cells and the
external environment

blood

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liquid connective tissue

blood

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mixture of formed elements and plasma

blood

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living blood cells & platelets

formed elements

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the fluid matrix

plasma

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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

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Functions of Blood

➢Transport and Distribution
➢Regulation of Internal Homeostasis
➢Protection

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➢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

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)

blood turbulence during atrial systole/ventricular filling (active)

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

1. Increased flow across normal SL valve or into a dilated great vessel 2. Flow across an abnormal SL valve or narrowed ventricular outflow tract - e.g. aortic stenosis 3. Flow across an incompetent AV valve - e.g. mitral regurgitation 4. 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

2. 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

amount of blood pumped out by a ventricle with each beat; ml per beat

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

1. Preload 2. Contractility 3. 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

1. Duration of ventricular diastole 2. 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:

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

Unit 5 Part 1 Flashcards

(241 cards)