It pumps through the lungs (pulmonary circulation)

Heart

Where is the mediastinum?

above the diaphragm and between the lungs

-Pericardium: Parietal (outer) and visceral (inner; epicardium)

-Pericardial cavity and fluid; lubricates membrane that line the cavity.

-Myocardium

-Endocardium: CT and layer of squamous cells; continuous with endothelium of arteries.

The cambers of the Heart

Thickness

Valves of The Heart

Atrioventricular Valves

-Cusps attatched to the papillary muscles by chordae tendonae

             tricuspid valve (RIGHT) and the bicuspid valve (LEFT atrium and L Ventricle)

The Valves of the Heart

What and where are the semilunar Valves?

-Pulmonic semilunar valve (Right)

-Aortic Semilunar Valve (Left)

1. Atrial systol: heart is relaxed, blood flowing from the R & L atriums into the Ventricles

2. Isovolumetric ventricular contraction: Tricuspid and Bicusbid valves close

3. Ejection: semilunar valves open and blood flows out of L & R ventricle and into the lungs and systemic circulation.

4. Isovolumeric ventricular relaxation: Both tricuspid and bicuspid valves are closed and blood is let into the atrium

5.Passive Ventricular filling: tricuspid and bicuspid valves open and allow blood into the ventricles.

Conduction System

What does the SA Node do?

it is the pacemaker, it is innervated by the SNS and PSN; 75 APs/min

Conduction System

Atrioventricular Node (AV)

PNS ganglia receptors for vagus nerve; slows impulse conduction.

-Then proceed down to the Bundle of His (AV bundle)

-Right and left bundle branches

-Perkinke fibers

Electrocardiogram

The sum of all cardiac action potential

P-wave

Electrocardiogram

The sum of all cardiac action potential

PR interval

The time from the onset of the atrial activation to the onset of ventricular activation. The time necessary to tracel from the sinus node through the atrium, AV node, and His-Purkinke system to activate ventricular myocardial cells

Electrocardiogram

The sum of all cardiac action potential

QRS complex

sum of all ventricular depolarizations

Electrocardiogram

The sum of all cardiac action potential

ST interval

ventricular myocardium depolarized

Electrocardiogram

The sum of all cardiac action potential

QT interval

"electrical systole" of the ventricles. Varies inversly with heart rate

Cardiac Excitation

Automaticity

-Spontaneous depolarization to threshold potential; allows generation of AP without stimulus

-By "automatic cells"

-Membrane potential does not "rest" during phase 4; diastolic depolarization

Cardiac Exctability

Rhymicity

-Regular generation of AP

-SA node sets pace; fastest rate of depolarization; 60-100 spontanous depolarizations/minute; natural pacemaker

-AV node takes over if SA damaged; 40-60 per minute

-Purkinje fibers 30-40 beats/minute

Cardiac Innervation

ANS influences

-rate of impulse generation, depolarization and repolarization and strength of atrial and ventricular contracitons

-Important for rapid changes (vs. oxygen, glucose, hormones or other blood borne factors)

Cardiac Innervation

What do the SNS and PNS do?

They innervate all parts of the atria, ventricles SA and AV nodes.

-orriginate in the thoracic SC

-Branch into superior, middle and inferior cardiac nerves.

- Join the cardiac plexus at the root of the aorta.

Catecholamines (EPI>NE)

What do they do?

-They increase the HR (dromotomic)

-Decrease conduncion time

-Increase rhytmicity of AV node

-Binds with beta receptors to increase Ca influx and force contraction.

Originate in medulla and travel by way of vagus to join sympatheic fibers in cardiac plexus

-Decreases HR

- Slows condunction via AV

- More beta than alpha receptors; stimulates all 4 types of receptors strongly; NE stimulates them weakly or not at all

Adrenergic Receptors

Beta 1

mostly heart; SA, AV and myocardial cells of the atria and ventricles

B1 + epinephrine= increase of impulse generation and conduction and strength of contraction.

Adrenergic Receptors

Beta 2

mostly blood vessel smooth muscle

B2 + epinephrine= dilation of arterioles in coronary, liver, skeletal muscle; vasoconstriction in most vascular beds

(GI, Urinary)

Adrenergic Receptors

Alpha 1

Mostly blood vessel smooth muscle

-Alpha 1 and NE= vasoconstriction

Adrenergic Receptors

Alpha 2

Sympathetic ganglia and nerve terminals

-alpha2 and NE inhibits NE, allowing vasodilatiion

FRANK-STARLING LAW OF THE HEART

What determines the force of contractility?

STRETCH

-Length-tension relationship based on cross bridge theory

-More stretch= increased force of contraction

-End diastolic volume (EDV)

LENGTH-TENSION CURVES

-SNS curve A high CO or SV with same EDV

-Heart Failure Curve C; is over stretched

T=(P x R)/mu

Relationship between the transmural pressure (P) difference and the tension (T), radius (R), and thickness (mu) of the vessel wall.

         -The higher the pressure difference the more tension

         -The larger the radius the more tension

         -The thicker the wall the less tension

Application of Laplace's Law

Dilated CM

T=(P x R)/mu

Heart distended and the readius increased; to create the same pressure during ejection of blood, much larger wall tension  needs to be developed; dilated heart required more energy to pump the same amount of blood as compared to the heart of a normal size.

Application Of Laplace's Law

Aneurysm

T=(P x R)/mu

-As diameter increases, wall tension increases, which contributes to more increase in diameter and risk of rupture. Increased BP (systemic HTN) and increased aneurysm size increase arterial wall tension and therefore increase the risk for rupture.

-Pressure generated at the end of diastole (LVEDP)

-LVEDP=Left Ventricular End Diastolic Volume

-Determinded by LVEDV

-Think Starling's Law, when preload exceeds physiologic range further muscle stretch results in decreased CO

-Determined by 2 factors:

         1. Amount of venous return

         2. ESV; depndent on strength of contraction and  resistance to emptying

-Monitor EDP

-Treatment goals: maintain EDV and EDP that will maintain cardiac output

-Resistance to ejection during systole.

-Aortic systolic pressure is a good indicator; also affected by aortic valvular function.

-High afterload higher workload against which heart has to work; ejects less blood

         -EDV-ESV=stroke volume, blood moved with each beat

         -SV/EDV= EFx (ejection fraction)

-HTN chronically evevated TPR, chronic high afterload, high workload of the heart, hypertrophy of the myocardium (LVH)

Myocardial Contractility

STROKE VOLUME (=EDV-ESV)

What are the 3 factors that determine force of contraction?

-Depens on force of contraction and thus myocardial contractility. 3 factors determine force of contraction.

    1. Changes in stretching related to changes on preload

    2. Alterations in SNS

    3. Adequate oxygen supply

Myocardial Contractility

INOTROPIC AGENTS

What agents are a positve ionotrope?

What is a negative ionotrope?

-EPI or NE are the most important positive ionotropes (increases force of contraction)

-Acetylcholine negative ionotrope

Myocardial Contractility

OXYGEN AND CARBON DIOXIDE LEVELS

What happens to contractility with MILD hypoxemia?

What happens to contractility with SEVERE hypoxemia?

-Mild hypoxemia may increase contractility by increaseing myocardial response to catecholamines

-Severe hypoxemia contractility is depressed

HEART RATE

Cardiovascular control Center (CCC)

Where is it located?

What controls the HR at rest?

-Brain stem in the medulla with secondary ares in the hypothalamus, cerebral cortex and thalmus; internernerons

      -Nerve Fivers from CCC synapse with autonomic neurons

      -Carioexcitatory (parasympathetic excitation/sympathetic inhibition

      -Cardioinhibitory (parasympathetic excitation/sympathetic inhibition); HR at rest controlled by parasympathetic override effect of sympathetic on SA node

HR

NEURAL REFLEXES

Bainbridge Reflex

In what setting is this reflex seen?

change HR after infusions of blood/fluid; mediated by volume receptros in the atria; HR change depends on initial HR (if slow it will increase; if fast it will be slowed down)

HR

Neural Reflexes

BARORECEPTOR REFLEX

Where are the receptors located?

-facilitates HR and BP; mediated by pressure receptors in the aortic arch and carotid bodies; critical to maintaining contant tissue perfusion.

DECREASES HR

HR

ATRIAL RECEPTORS

What is stimulated to be released when there is increased level of volume in the Atria?

-In both atria

-Distention as a result of increased volume results in release of Atrial Natriuric Peptide (ANP); powerful diuretic and natriuretic to decrease BP and blood volume

HR

HORMONES AND BIOCHEMICALS

What is affected?

What does EPI do?

What does NE do?

What does TH do?

What is decreased and what does that result in?

-Affects arteries, arterioles, venules, capillaries and contractility of myocardium

-EPI dilates blood vessels of liver and skeletal muscle and increases myocardial contractility

-NE increases HR, contractility and constricts BV

-Thyroid hormone enhance sympathetic activity to increase CO

-decrease in GH, TH, adrenal hormones results in Bradycardia, reduced CO and low BP

VEINS

What they have to help?

VEINS

ENDOTHELIUM

-It is a life support tissue

-Enables growth, promotes contraction or relaxation (vasomotion) and involved in repair, antithrombogenesis and fibronolysis

-performs functions via synthesis and release of vasoactive chemicals

endothelium-dependent vasocontriction

What are factors that cause vascontriction in the endothelium?

-Thromboxane A2 (which is what ASA inhibits)

-Endothelin: located in the endothelium tissue

 --ACE Converts angiotensin I into angiotensin angiotensin II that metabolizes bradykinin which is a vasodilator.

Endothelium Dependent Vasodilation

What factors cause dilation in the Endothelium?

-A variety of exogenous pharmacologic substances, platelet-derived factors, and shear stress can promote the release of nitric oxide synthase (NOS).

-Prostacyclin (PGi2) causes relaxation of vascular smooth muscle cells by cyclic adenosine monophosphate (cAMP)- dependent mechanism, and both nitric oxide and PGI2 inhibit platelet aggregation.5-HT, serotonin; ADP, adenosine diphosphate; ATP, adenosine triphosphate

What are factors that affect blood flow?

F=P/R

(flow proportional to pressure but inversily proportional to resistance.)

-Pressure difference; high to low

-Resistance: diameter and length

Factors Affecting Blood Flow

Poiseuille's law

R= 8 (viscosity) (length)/pi (v^4)

-Very smal changes in vessel radius result in big changes in resistance.

Factors Affecting Blood Flow

What items have Neural control of total peripheral resistance?

-Change in diameter of the vessles

-Baroreceptors

-Arterial chemoreceptors

Factors Affecting Blood Flow

How do hormones affect blood movement?

EPI, NE, antidiuretic hormone, renin-angiotensin-aldosterone system, natriuretic peptides, adrenomedullin insulin, and others

Factors Affecting Blood Flow

VELOCITY

distance traveled/unit of time (cm/min); directly related to blood flow (ml/min) and indirectly related to cross sectional area (decreased area increased velocity vs. increased area dereases; as vessels cross sectional are increases flow decreases)

Factors Affecting Blood Flow

LAMINAR VS. TURBULENT FLOW

concentric layers of flow at different velocities; less velocity near the wall related to cohesive attraction between fluid and wall

Factors Affecting Blood Flow

VASCULAR COMPLIANCE

C=VP

-Related to ratio of elastic muscle fibers (veins>arteries; elastic>muscular); compliance determines a vessels response to pressure changes; eg. In the venous system for a small increase in pressure a large volume of blood can accommodate

(*veins are very compliant and will easily expand)

BP=CO x PR

CO=HR x SV

-Located on aortic arch and corotid sinue.

-Action potentials are conducted to the cardioregulatory and vsomotor center.

-The HR can be decreased by the parasympathetic system

-The HR and SV can be increased by sympathetic system

-Sympathetic system can also constrict or dilate blood vessels

-They are located in the medulla oblongata and the carotid and aortic bodies detect changes in blood oxygen, carbon dioxide and pH.

-Action potentials are conducted to the medulla oblongata. in response the vasomotor center can cause vasoconstriction or dilation of blood vessels by the sympathetic system and the cardioregulatory center can cause changes in pumping activity of the heart through the parasympathetic and sympathetic systems.

-Antidiuretic Hormone (ADH) and renin-angiotensin and aldosterone tend to increase water retention and thus increase plasma volume.

-The natriuretic peptides antagonize these mechanisms by promoting water loss and sodium loss, thus promoting a decrease in total plasma volume. NPs, ACE angiotensin converting enzyme

What are the effects of hormones?

ANGIOTENSIN II

-Vasoconstriction

-It stimulates the relaese of aldosterone

-Growth promoter; myocyte and vascular hypertrophy and progression of HTN and HF

-Stimulates thirst

- Release of ADH

-Increase SNS output

Effects of Hormones

Angiotensin II Receptors

AT1

Where are they located?

-heart, vascular smooth muscle, andothelial cells, nerve endings adrenal cortex, liver, kidney brain.

-Majoirty of II activity (growth promotion, vasoconstriction, aldosterone secretion inhibition of renin, sypathetic outflow, stimulate inflammation)

-ACE-1 and ARB for preventative and reparative strategies

Effects of Hormones

Angiottensin II

AT2

BLOCKS the effect of angiotensin II and its ability for AT1 to have effect on vascular, cardiac and renal

fetal tissue, adrenal medulla, renal tubules, vasculature, uterus, ovaries

       -Opposes At1 receptors

       -Induces vasodilation

       -Mediated by NO

Regulation of Coronary Circulation

CORONARY PERFUSION PRESSURE

(F=P/R)

-Differnce between pressure in the aorta and pressure in coronary vessels; aortic pressure is the driver

-During systole: aortic valves cusps obstruct coronary artery blood flow; coronary arteries compressed by ventricular contraction; most oxygen provided by myoglobin

-Most coronary blood flow occurs during diastole

Regularton of Coronary Circulation

AUTOREGULATION

individual vessels regulate blood flow.

-With decrease in perfusion pressure or increase in metabolic needs, myocardial cells release CO2, H, K, adenosine that promotes vasodilation

Regulation of Coronary Circulation

Autonomic Regulation

-Sympathetic nerves cause increased coronary flow despite vascocontriction because of increased myocradial metabolism (because of SNS stimulation of HR and contracitlity); metabolic autoregulation overrides neurogenic influences.

-Capillary outflow exceeds venous reabsorption (3L/day)

-Special vascular system that picks up excess tissue fluid and returns it to the blood.

-Consists of lymphatic vessels and nodes; one way valves with closed ends; fluids back to venous system and heart via lymphatic duct and thoracic duct and thoracic duct into right and left subclavian veins.

Cardiography and Holter Monitoring

-typically 12 lead electrocardiogram

-info about HR and rhythm, the effects of electrolytes and drugs on the heart, and electrical orientation of the cardiac muscle

-detect disturbances in impulse generation condunction

elicit clinical manifestations of cardiovascular disease that might not be present at rest

the use of a radiotracer imaging technique such as SPECT

-detects structural and functional cardiac abnormalities over time

-Is used to measure the oxygen content and pressure of blood in the heart's chambers and to inject contrast media for x-ray examination of the size and shape of the chambers and valves.

-Injection of contrast medium into cardiac arteries (coronary angiogram), on the other hand permits visualization of the coronary circulation and every tissue perfused by the coronary arteries.

Varicose Veins

Mechanism of Action

-A vein in which blood is pooled

-Trauma

-Gradual venous distention

Varicose Vein

clinincal manifestation

- distended, torturous, and palpable veins

Chronic Venous insufficiency

Mechanism of Action

Chronic Venous insufficiency

Clinical Manifestations

DVT

Mechanism of Action

Obstruction of venous flow leading to increased venous pressure

DVT

Patho

            hypercoagulable states

DVT

Clinical Manifestation

Increased risk for clots

Thrombus Formation in Veins

Mechanism of Action

Thromboembolus: detached thrombus

Thrombus Formation in Veins

Patho

inflammation

Thrombus Formation in the Veins

Clinical Manifestations

Aneurysm

Mechanism of Action

Aneurysm

Patho

Aneursym

Clinical Manifestations

Aortic: often asymptomatic, dyspnea, pain, dysphagia, decreased blood flow to an extremity

Embolism

Mechanism of Action

Embolism

Patho

Embolism

Clinical Manifestations

Embolism of central origin causes dysfunction and pain

Peripheral Artery Disease

Mechanism of Action

Increased O2 demand that could not be supplied

Peripheral Artery Disease

Patho

Also called intermittent claudcaion

Peripheral Artery Disease

Clinical Manifestations

Pain with ambulation that stops when stops ambulating

Claudication

Thromboangiitis Obliterans (Buerger Disease)

Mechanism of Action

Can often lead to gangrenous lesions

Thromboangiitis Obliterans (Buerger disease)

Patho

Thromboangiitis Oblinterans (Buerger disease)

Clinical Manifestations

Young men who smoke

Raynaud's Disease

Mechanism of Action

Disease is primary vasospastic disorder of unknown origin

Raynauds Phenomenon and Disease

Patho

Changes in skin color and sensation

Raynauds

Clinical Manifestations

changes in skin color

painful

pallor

numbness

cold sensation in digits

rubor often accompanies throbbing and paresthesias

Hypertension (Primary)

Mechanism of Action

Hypertension (Primary)

Patho

Hypertension (Primary)

Clinical Manifestations

>160 or >100

Hypertension (secondary)

Mechanism of Action

HTN (secondary)

Patho

See page 1153

-Renal parenchymal disease, renovascular disease, renin-producing tumors, Renal failure, Primary sodim retention

-Endocrine: acromegaly, hypothyroidism, hyercalemia, hyperthyroidism, adrenal disorders, coritcal disorders, cushings syndrome, primary aldosteronism

-Vascular Disorders: Coarction of the aorta

HTN (secondary)

Clinical manifestation

Obstruction sleep apnea

Complicated HTN

Mechanism of Action

Kidney, brain, heart, extremities, and eyes

Complicated HTN

Patho

endothelia dysfunction, AngII catecholamines, IR and inflammation contribute

Complicated HTN

Clinical Manifestations

Malignant Hypertension

Mechanism of Action

EMERGENCY

Diastolic BP over 160

Malignant HTN

Clinical Manifestations

Orthostatic HTN

Mechanism of Action

   -Chronic: secondary to disease or idiopathic

Orthostatic HTN

Patho

Orthostatic HTN

Clinical Manifestations

Atherosclerosis

Mechanism of Action

Occurs throughout body

atherocsclerosis

Patho

Thickening and hardening caused by accumulation of lipid-laden marcrophages in the arterial wall

Complixated plaque

atheroscelorosis

Clinical Manifestation

TIA's often associated with exercise stress

Leading cause of stroke

Coronary Artery Disease

Mechanism of Action

Atheroscloerosis is most common cause

Coronary Artery Disease

Patho

Myocardial cells become ischemic within 19 sec; lactic acid build up; remain viable for 20 min

Coronary Artery Disease

Clinical Manifestations

Angina pectoris

Acute Coronary Syndrome

Mechanism of Action

Myocardial Infarction: prolonged ischemia causing irreversible damage to heart muscles

Acute Coronay Syndromes

Patho

Myocardial Infarction

Mechanism of Action

Myocardial infarction

Patho

4. repair

Myocardial Infarction

Clinical Manifestation

Acute Pericarditis

Mechanism of Action

Acute Pericarditis

Patho

Can result from MI, trauma, neoplasm, surgery, bacterial infection, radiation therapy

Acute Pericarditis

Clinical Manifestation

Dilated Cardiomyophathy

Mechanism of Action

IHD, valvular heart disease, renal failure, ETOH, drugs, DM, nutritional

Dilated Cariomyopathy

Patho

Dilated Cardiomyopathy

Clinical Manifestation

Hypertrophic Cardiomyopathy

Mech of action

Serious risk for arrhythmias and sudden death

Hypertrophic Cardiomyopathy

Patho

Hypertrophic Cardiomyopathy

Clinical manifestations

Restrictive Cardiomyopathy

Mechanism of Action

Myocardium rigid and non-compliant

Restrictive Cardiomyopathy

Patho

Restrictive Cardiomyopathy

Clinical Manifestations

Cardiomegaly and dysrhythmias are common

Aortic Stenosis

Mechanism of Action

Aortic Stenosis

Patho

Causes diminished blood flow from left ventricle to aorta, increases pressure in left ventricle, left ventricular hypertrophy, increased workload, increased oxygen demand, angina

Aortic Stenosis

Clinical Manifestations

Mitral Stenosis

Mechanism of Action

Impairs flow of blood from left atrium to left ventricle

Mitral Stenosis

Patho

-Incomplete emptying of left atria, elevated atrial pressure, dilation and hypertrophy

Mitral Stenosis

Clinical Manifestations

Pulmonday congestion and right heart failure

Aortic Regurg

mechanism of action

Aortic Regurg

Patho

Aortic Regurg

Clinical Manifestation

Dysrhythmias and endocarditis common

Mitral Regurg

Mechanism of Action

Backflow from left ventricle to left atrium during systole; increased volume of left atrium

Mitral Regurg

Patho

Left ventricle dilated and hypertrophied to maintain CO; may end in left failure

Mitral regurg

Clinical Manifestations

-Well trolerated for years until ventricle failure occurs

Tricuspid Regurg

Mechanism of Action

Tricuspid regurg

Patho

Mitral Valve Prolapse

Mechanism of Action

Mechanism Valve Prolapse

Patho

Autosomal dominant x-linked inheritance

Mitral Valve Prolapse

Clinical Manifestations

Some increase risk for endocarditis, cardioembolic stroke, sudden death