Cardiovascular System- Pathophysio

Internal structures of the heart?

-Interatrial septum
-pectinate muscles
-interventricular septum
-trabeculae carneae

Interatrial septum

wall that separates atria

Pectinate muscles

internal ridges of myocardium in right atrium and both auricles

Interventricular septum

wall that separates ventricles

Trabeculae carneae

internal ridges in both ventricles

Chordae Tendinae

Fibers (heart strings) attatched to the heart valves -- pull valves shut, preventing back flow of blood

Valves of the heart?

-Right AV (tricuspid) valve
-Left AV (bicuspid/mitral) valve
-Pulmonary valve
-Aortic valve

Atrioventricular valves

Separate atria from ventricles

Blood flow through AV valves?

one way ONLY, from the atria through the ventricles

Semilunar valves

Separate ventricle from arterial system

Blood flow through the semilunar valves?

one way ONLY, from the ventricles to the arterial blood system

Tricuspid valve (right AV valve)

between right atrium and right ventricle

Pulmonary valve

between right ventricle and pulmonary artery

Bicuspid (mitral) valve (left AV valve)

between left atrium and left ventricle

Aortic valve

between left ventricle and systemic arteries

When ventricle begins to contract (ventricular pressure > atrial pressure), AV valves will...

shut to prevent backflow intro atria

When ventricular pressure > arterial pressure, semilunar valves will...

open and ejection begins

When ventricular pressure < arterial pressure, semilunar valves will...

shut to prevent backflow into ventricle

When ventricular pressure < atrial pressure, AV valves will...

open to fill atria and ventricles with blood

Atrial contraction

pushing the last bit of blood into the ventricles before it contracts

What kind of blood comes in through the superior vena cava, through the tricuspid valves?

De-oxygenated blood

Mitral valve prolapse (MVP)

flaps of mitral valve protrude into left atrium because of pressure in left ventricle - blood leaks back into atrium

Causes of mitral valve prolapse?

-Congential defect
-Damage to chordae tendinae
-Typically with females

Symptom triad for MVP

Profound fatigue, palpitations, dyspnea

How would you diagnose a mitral valve prolapse?

TEE (transesophegeal echocardiogram)

Mitral valve stenosis

-Narrowing of the mitral valve from scarring
-tied to rheumatic heart disease
-thickened valve causes "snap" heard in early diastole
-portions of valves are fixed, therefore open when should be closed and creates pressure differences between L atria and L ventricle

Symptom triad for mitral valve stenosis

-Dyspnea
-Fatigue
-Orthopnea

Aortic stenosis

-Disease of aging
-Narrowing of aorta
-Usually caused by valve calcification or post rheumatic fever

Risk factors for aortic stenosis

-Obesity
-Smoking
-Lifestyle
-High cholesterol

Symptoms of aortic stenosis

-Angina
-Exertional syncope

Left coronary artery (LCA) branches

anterior interventricular branch and circumflex branch

Anterior interventricular branch

supplies blood to interventricular septum and anterior walls of ventricles

Circumflex branch

passes around left side of heart in coronary sulcus, supplies left atrium and posterior wall of left ventricle

Right coronary artery (RCA) branches

right marginal branch and posterior interventricular branch

Right marginal branch

supplies lateral right atrium and ventricle

Posterior interventricular branch

supplies posterior walls of ventricles

What happens if the walls of the ventricles (pushing blood out to the rest of the body) are faulty?

Deoxygenation/lack of O2 -- if not repaired, cell death in areas lacking blood flow

Angina pectoris

-partial obstruction of coronary blood flow that causes chest pain

-pain caused by ischemia, often activity dependent

Myocardial infarction (MI)

-complete obstruction causes death of cardia cells in affected area
-pain or pressure in chest that often radiates down left arm

Common heart attack (MI) warning signs

-Pain or discomfort in chest
-Lightheadedness, nausea, or vomiting
-Jaw, neck or back pain
-Discomfort or pain in arm or shoulder
-Shortness of breath

Arteries

carry blood away from heart

Veins

carry blood to the heart

Heart cycle

repeating pattern of contraction and relaxation

Systole

contraction of heart

Diastole

relaxation of the heart

What area of the heart fills with blood when relaxed?

atria

Atria contract and relax together, as do ventricles (T/F).

True

Ventricular contraction

-systole
-follows atrial contraction after 0.2 second delay

Ventricular filling

-diastole

-up to 80% before atria contract --> this is why a person can live with atrial fib but dies with ventricular fib

Cardiac rate

heart rate (the events of cardiac cycle)

End diastolic volume

total amount of blood in ventricles at end of diastole

Stroke volume

amount of blood ejected when ventricles contract

End systolic volume

blood left in ventricles at end of resting person's ventricular contraction

Cardiac output (CO)

-amount of blood ejected by ventricle in 1 minute
-about 4-6 L/min at rest
-cardiac output = HR x stroke volume

Cardiac reserve

-difference between resting and maximal CO
- increases with fitness, decreases with disease

What is stroke volume governed by?

-preload, contractility, afterload

How would an increased preload or contractility affect stroke volume (SV)?

increased SV

How would a decreased afterload affect stroke volume (SV)?

decreased SV

Preload

amount of tension in ventricular myocardium before it contracts

Increased preload means what for contraction?

increased force of contraction

Preload: Frank-Starling Law

-stroke volume is directly proportional to end diastolic volume
-ventricles eject as much blood as they receive
-the more stretched (increased preload), the harder they contract

Afterload

pressure in arteries above semilunar valves opposes opening of valves (i.e. blood pressure)

How does an increased afterload affect stroke volume?

decreased SV

Any impedance (i.e. COPD) in arterial circulation will lead to an _______ afterload

increased afterload

Continuous increase in afterload (lung disease, atherosclerosis, etc.) causes...

hypertrophy of myocardium; may lead it to weaken and fail

"Lub"

first heart sound, closing of the AV valves

"Dub"

second heart sound, closing of the semilunar valves

Heart murmurs

abnormal heart sounds as a result of abnormal flow

Cardiac muscle structure

-short, branched cells, one central nucleus
-less sarcoplasmic reticulum, large T-tubules
-intercalated discs
-gap junctions

What joins myocytes end to end?

intercalated discs

What increases surface area of the intercalated discs?

interdigitating folds

Mechanical junctions of intercalated discs

tightly join myocytes

Gap junctions of cardiac muscle structure

electrical junctions that allow ions to flow from ell to cell

Metabolism of cardiac muscle

-aerobic respiration
-rich in myoglobin and glycogen
-large mitochondria
-organic fuels (fatty acids, glucose, ketones)
-fatigue resistant

Cardiac conduction system properties

myogenic and autorhythmic

Myogenic

heartbeat originates within heart

Autorhythmic

regular, spontaneous depolarization

Components of the cardiac conduction system?

SA node, AV node, Bundle of His, Right/Left bundle branches, Purkinje fibers

Sinoatrial node (SA)

primary pacemaker, initiates heartbeat, and sets HR

Atrioventricular node (AV)

the electrical gateway to the ventricles and a secondary pacemaker

Bundle of His

pathway that transmits AV node signals

Right/Left bundle branches

divisions of the bundle of His that enter the interventricular septum

Purkinje Fibers

spread upward from the heart apex throughout the ventricular myocardium

Sympathetic cardiac nerve supply

-nerves arise from upper thoracic spinal cord, through sympathetic chain to cardiac nerves
-innervate the ventricular myocardium
-can raise HR to 230 bpm

Parasympathetic cardiac nerve supply

-right vagal nerve to SA node

-left vagal nerve to AV node

-vagal tone: normally slows HR to 70-80 bpm

Cardiac rhythm includes

sinus rhythm, premature ventricular contraction (PVC), ectopic foci- region of spontaneous firing

Sinus rhythm

-set by SA node at 60-100 bpm
-adult at rest is 70-80 bpm (vagal inhibition)

Premature ventricular contraction (PVC)

caused by hypoxia, electrolyte imbalance, stimulants, stress, etc.

Ectopic foci- region of spontaneous firing (not SA node)

-nodal rhythm: set by AV node, 40-50 bpm
-intrinsic ventricular rhythm: 20-40 bpm

Depolarization of SA node

-each depolarization creates one heartbeat
-SA node at rest fires at 0.8 sec, about 75 bpm

Pacemaker potential

gradual depolarization from -60 mV, slow influx of Na+

SA node resting membrane potential

NO stable resting membrane potential

Action potential

-occurs at threshold of -40 mV
-depolarizing phase to 0 mV
-repolarizing phase

What ions enter during the depolarizing phase of the SA node?

Ca2+ in

What ions enter during the repolarizing phase of the SA node?

-K+ out
-at -60 mV K+ channels close, pacemaker potential starts over

Action potential of myocyte

1) Na+ gates open
2) Rapid depolarization
3) Na+ gates close
4) Slow Ca2+ channels open
5) Ca2+ channels close, K+ channels open

Summary of heart contraction

-depolarization causes/occurs during cardiac contraction
-repolarization causes/occurs during cardiac relaxation

During depolarization of the heart...

atria and ventricles produce AP and are depolarized in systole (contraction)

During repolarization of the heart...

Atria and ventricles repolarize at beginning of diastole (relaxing)

EKG

reflects conduction of action potential in heart