211 exam 2 ch18 part 1

Epicardium myocardium endocardium

The heart muscles are self excitable

Too much fluid compresses the heart which limits pumping ability

Inserting a syringe into the pericardial cavity to drain excess fluid

Inflammation of the pericardium, ther togethere is not enough serous fluid. Over time serous layers can stick

Pericarditis

Excess inflammatory fluid seeps into pericardial cavity and causes cardiac tamponade

Simple squamous epithelium

Limits the spread of action potentials to specific paths

A shallow depression in the interracial septum

Foramen ovale

The ventricles

Increase atrial volume

Collateral routes to ensure blood delivery to the heart even if major vessels are blocked

Tissue death and heart attack

Arteries are compressed during heart contraction

Blood supply to the heart itself

Merging cardiac veins

Temporary ischemia

Reduced blood flow

Stress induced spasms of the coronary arteries

Prolonged ischemia

Acromegaly

Lack of oxygen

Contraction

Initiating depolarization of the heart

The autonomic nervous system

Sets the pace of the heart

Carry impulses to the heart apex and ventricular walls

Irregular heart rhythms

Pumping action

Depolarization of SA node an atria

Ventricular depolarization

Ventricular repolarization

When AV valves close

When SL valves close

One full heartbeat

Contraction of heart muscle

Relaxation of heart muscle

Volume of blood in each ventricle at end of ventricular diastole

120ml

Volume of blood remaining in each ventricle after systole

The same

When the right ventricle ejects more blood than the left

When fluid accumulates in the pulmonary tissue

When the left ventricle ejects more blood than the right

Fluid accumulation in the systemic tissue.

Failure of either ventricle to eject blood effectively

Persistent high blood pressure

Removing fluid

When the ventricles stretch and become flabby

Genetics

Cells enlarge and ventricles cannot pump enough blood for the body

Volume of blood pumped out by each ventricle in one minute

HR X SV heart rate x stroke volume

Volume of blood pumped out by a ventricle with each beat

Difference between resting and maximal cardiac output

Greater with fitness

Preload, contractility, afterload

Stroke volume is proportional to end diastolic volume

Venous return

Preload (degree of stretch) of cardiac muscle cells before they contract equals stroke volume

Degree of stretch of cardiac muscle cells

Inotropic agents

They increase contractility

Hypercalcemia

They decrease contractility

Acidosis (created by hypercapnia)

The arterial blood pressure the ventricles must overcome to eject blood

Lung disease

Decrease Sv

Hypertrophy of the myocardium → eventually causes failure

Increase heart rate

Decrease heart rate

Increasing heart rate

Autonomic nervous system

In the medulla oblongata

The cardioaccelatory center

Sympathetic nervous system

epinephrine

Acetylcholine

Stress

Pressure sensors

Aortic arch

It increases HR to increase BP

It decreases HR to decrease BP

Epinephrine

Epinephrine is released from the adrenal medulla and increases HR and contractility

Thyroxine is released from the thyroid gland and increases HR

The effects of epinephrine and norepinephrine

For normal heart function

K t

Its a high level of potassium (k+) in the blood

It is a low level of potassium in the blood

It depresses the heart

Increases HR and contractility

Age

Persistent resting heart rate above 100bpm

Elevated body temperature