Cardiovascular Anatomy & Physiology

Objectives

Function Anatomy Cells Cardiac Output Oxygen Transport Pathologies

Cardiovascular Function Deliver oxygenated

blood to tissues- where diffusion and filtration occur

Transport blood back to lungs- where oxygen and carbon dioxide exchange occur

Cardiovascular System

Cardiovascular Structures

Surface anatomy of the human heart. The heart is demarcated by:

-1. A point 9 cm to the left of the midsternal line (lower left or apex of the heart)

-2. The seventh right sternocostal articulation (lower right side of heart)

-3. The upper border of the third right costal cartilage 1 cm from the right sternal line (upper right side of heart)

-4. The lower border of the second left costal cartilage 2.5 cm from the left lateral sternal line (upper left side of heart)

Human Heart

1.2.

3. 4.

Cells of the Cardiovascular System

Cardiac cells– pacemaker cells– cardiac myocytes

Vascular cells– endothelial cells– smooth muscle

cells

Cardiac Myocytes Conduct AP cell-to-cell via gap

junctions Are packed with contractile

elements Have well developed

sarcoplasmic reticulum which sequesters calcium

Are dependent on extracellular calcium for contraction

Action Potential

Increased intracellular free calcium

actin-myosin crossbridging

myocardial cell shortening

Calcium influx from ECF Calcium release from SR

How does membrane depolarization lead to mechanical contraction?

SR

Ca

Ca

Ca

ATP

ATP

CaNa

Ca++ channel

K

Na

digoxin

betareceptors cAMP

Na

Na channel

K

K channel

Achreceptor

Cardiac Muscle Cell

Heart SNS PSNS

inotropy + - chronotropy + - dromotropy + - lusitropy + -

Vessels

pulmonary/coronary constrictdilate

most others constrict no effect

ANS effects on heart and vessels

Cardiac Output

CO = HR x SV

THE most important variable in cardiac function!

pO2 lungs = 80-100 mm HgpO2 tissues = 30-40 mm Hg

SaO2 lungs = 95-100%SaO2 tissues = 60-80%

Oxygen Transport

98%96%94%92%89%83%75%

100908070605040

SaturationPaO2

Shift to left: affinity– alkalemia– hypothermia– hypocarbia– decreased

2,3DPG

Shifts in Hb-O2 Affinity

Shift to right: affinity– acidemia– hyperthermia– hypercarbia– increased

2,3DPG

Figure: 13-15The oxyhemoglobin dissociation curve

Carbon Dioxide TransportPhysical Solution: (5%)

PaCO2 X .06

Carbaminohemoglobin: (15%)HB N H

COO-

Bicarbonate ion (80%)CO2 + H2O H2CO3 H+ + HCO3

-

Red Cell Production iron folate vitamin B12 erythropoietin functional stem cells

Figure: 13-17The erythropoietin response to anemia, hypoxia, polycythemia

Cardiovascular Pathology

Anemia Heart Failure Valvular Defects Cardiomyopathies Congenital Defects Vascular Insufficiency

General Signs and Symptoms of Anemia

Increased respiration Increased heart rate Fatigue Decreased activity tolerance Pallor Murmur

Heart Failure Def: Inability to effectively PUMP the amount

of blood delivered to the heart Left ventricular ejection fraction (EF)

– Normal values: 60-80%– Important measure of heart failure

Etiologies: Many, but 2 main causes are hypertension and ischemia– MI– CIHD– Valve Disease– Congenital Defects– Cardiomyopathy

Figure: 19-5Interdependence of left and right heart function

Clinical presentation of CHFDiffers for left, right, or both ventricle failure

Left Ventricular Failure (LVF)Right Ventricular Failure (RVF)

Forward FailurePoor cardiac pumping = reduced CO

Backward FailureCongestion of blood behind the heart

Figure: 19-7Manifestations of left heart failure

Clinical presentation of LVFmost common presentation for CHFOften leads to RVF (biventricular failure)Common causes Left ventricular infarction Cardiomyopathy Aortic and mitral valvular disease Systemic hypertension

Forward effects – reduced CO leads to hypoxiaBrain hypoxia – restlessness, mental fatigue,

confusion, anxiety, impaired memory

Cardinal symptom – dyspnea (early sign)Hypoxemia results from impaired gas exchangeCyanosis results from deOxyHgb (late sign)

Arterial Blood Gas analysisCyanoticElevated Left arterial pressureAcute cardiogenic pulmonary edema – life threateningBolt-upright postureDyspnea and anxiety

Lungs are congested but systemic venous system is not

http://upload.wikimedia.org/wikipedia/commons/c/c9/Coronary_arteries.png

Summary

Anemia Heart Failure Valvular Defects Cardiomyopathy Congenital Defects Vascular Insufficiency

Valvular Disorders Abnormalities of Valve function:

– Stenosis & Regurgitation Etiology

– congenital– rheumatic– degenerative calcification– infective

Diagnostic Evaluation: Echo-doppler

Common Valve Disorders Mitral Stenosis Mitral Regurgitation Aortic Stenosis Aortic RegurgitationMitral valve lies between the left atrium and left ventricle.

Stenosis – obstruction to blood flow thru cardiac valves that are not opening completely

Regurgitation – retrograde blood flow through a cardiac valvewhen the valve is closed

Differential Diagnosis of Murmur Mitral Stenosis

– Increased Left Arterial Pressure– Loud S1 opening snap at apex– Murmur rare, if present, short

diastolic– atrial fibrillation is common

Mitral Stenosis

0

30

60

90

120

LA/LVgradient

Differential Diagnosis of Murmur Mitral Regurgitation

– Systolic Murmur– Radiates to left axilla– Pansystolic, blowing– Prominent S3

0

30

60

90

120

large regurgitant V-wave

Mitral Regurgitation

Differential Diagnosis of Murmur Aortic Stenosis

– Mid systolic– Crescendo-decrescendo– Radiates to neck– S4 prominent– Angina, syncope common

Aortic Stenosis

0

40

90

180

LV/Aorticpressure gradient120

Differential Diagnosis of Murmur Aortic Regurgitation

– Diastolic murmur– Bounding Pulse “waterhammer”– Wide pulse pressure

Aortic Regurgitation

0

40

90

180

120

normalaorticpressure

aortic pressure with AorticRegurgitation

Cardiomyopathy Dilated

– enlarged heart chambers– poor contractility

Hypertrophic– outflow obstruction– ischemia

Restrictive– impaired diastolic filling

Congenital Heart DefectsAcyanotic L to R shunt

– Atrial Septal Defect

– Ventricular Septal Defect

– Patent Ductus Arteriosus

Cyanotic R to L shunt

– Transposition– Tetralogy of

Fallot

Shock

Defining Characteristic: Oxygen Delivery to one or more tissues is below basal requirements leading to hypoxic and immunologic injury.

Types of Shock:– Hypovolemic– Cardiogenic– Distributive (e.g. anaphylactic, septic,

neurogenic) Manifestations: Signs and symptoms of tissue

ischemia and death.

Diagnosis of Shock Tachycardia Hypotension (orthostatic) Peripheral hypoperfusion

(slow capillary refill, cool, mottled)

Oliguria or anuria Metabolic acidosis In septic shock: fever, chills

General Treatment Measures

Supine position Oxygen Analgesics Labs: CBC, ABG, Renal panel, Type & X, UA Cardiac Monitoring CVP Monitoring (at least) Volume replacement

(colloid vs crystalloid vs blood) Vasoactive Drugs

Septic Shock Usually caused by gram negative

bacteria. Monoclonal antibody to endotoxin may be used.

Don’t be fooled by high cardiac output, still have insufficient blood volume to fill the tank.

Oxygen consumption is often low due to abnormal distribution and shunt. Look for increased consumption with treatment.

Mortality is high: 40-80%

Vascular System

Arterial InsufficiencyVenous Insufficiency

Risks for Vascular Insufficiency Arterial

– smoking– atherosclerosis– inflammatory:Bu

ergers– trauma– DIC– emboli from LV– vasospasm– diabetes

mellitus

Venous– stasis of

bloodflow immobility R heart failure prolonged

standing obesity pregnancy

– trauma– hypercoagulabl

e high platelets high

hematocrit

Pathophysiology of Insufficiency

Heart Pump

arterialvenous

capillaryischemiaedema

Arterial Insufficiency Flow Downstream

ischemiaacute chronic

PainPallorPulselessnessParesisParalysisPoikilothermy

Intermittent claudicationAtrophy (skin, hair)Thickening of nails

Venous InsufficiencyObstruction of Venous Drainage

capillary hydrostatic pressure

edema, stasis

pain risk of pulmonaryembolus

stasis ulcers and skin changes

Thrombophlebitis Deep Vein

(DVT)– Extremity

Edema– General leg

pain– Fever

High Risk of PE Treatment

– immobilize– anticoagulate– treat risk

factors

Superficial– local

Inflammation warm tender red swollen

– Collateral veins minimize edema

Low Risk of PE

Assessment of Cardiac Function

Electrical FunctionContractile Function

Is Electrical Conduction Normal?

P

Q S

R

T

ECG Assessment Rate? Conduction Abnormality?

– Dysrhythmias– Conduction blocks

Ischemia/Infarction? LVH?

Cardiovascular Pathophysiology

Afterload – The resistance that must be overcome to eject blood from a cardiac chamber. Left ventricular afterload is correlative withthe resistance in the systemic vasculature.

Preload – The volume of blood that remains in the cardiac chamber prior to systole.

Classification of Hypertension

CategoryNormal <130 <85 Recheck in 2 years

High Normal 130-139 85-89 Recheck in 1 year

HypertensionStage 1 (mild) 140-159 90-99 Confirm within 2 moStage 2 (mod) 160-179 100-109 Eval or refer 1 moStage 3 (severe) 180-209 110-119 Eval or refer 1 weekStage 4 (very sev) >210 >120 Eval or refer

immediately

SBP DBPRecommended

Followup

Differential Diagnosis of Hypertension Primary Hypertension (95%) Secondary Hypertension

– Contraceptive use– Renal disease– Renal artery stenosis– Cushing’s syndrome– Pheochromocytoma– Pregnancy induced hypertension

Treatment? Diuretics, beta blockers, ACE

inhibitors, calcium channel blockers, alpha blockers

Consider age, ethnicity, coexisting disorders, cost, lipid profile

Figure: 18-2Lipoprotein transport

Chylomicron 85% triglyceride 5% cholesterol

VLDL 55% triglyceride 20% cholesterol

LDL 5% triglyceride 55% cholesterol 20% protein

HDL 5% triglyceride 20% cholesterol 50% protein

Figure: 18-3Type I - IV atherosclerotic plaques

Types I-IIIAsymptomaticArterial wall narrowing

Types IV-VIPredispose to ischemicepisodes

Ischemic Heart Disease Etiology:

– Coronary Atherosclerosis Risks: Clinical Syndromes:

– angina pectoris– myocardial infarction– chronic ischemic heart disease– sudden cardiac death

Pathogenesis of Atherosclerosis

Lipid accumulates in vascular wall

Macrophages infiltrate the wall and oxidize the lipids

Cell injury and release of local growth factors(Angiotensin II)

Plaque formation on intimal wall

Demand > Supply: Angina

Perfusion pressurefixed stenosisoxygen content

SUPPLY

DEMAND

afterloadcontractilitypreload heart rate

How to increase supply? How to decrease demand?

Pathogenesis of Ischemia

Plaque Disruption or Breakdown

Tissue Thromboplastin Exposed

Platelet Aggregation and Clotting Cascade Activated

Thrombus Formation

Acute Ischemia

StableAngina

Patho: Fixed stenosis Thrombus Thrombus>75% + lysis with occlusion

Pain: predictable unpredictable unpredictablerelieved by not relieved not relievedrest (3-5 min) rest rest (>15-30)

Serum Enz: not elevated not elevated elevated

UnstableAngina MI

Ischemic Syndromes

Indicative Leads show: Ischemia: ST elevation or depression

T-wave peaking, flattening, inversion

Bigger than normal Q-waves

ECG Changes with Ischemia

Q

ST elevation

Decreased Myocardial Perfusion

Partially ischemic cells

Anaerobic metabolismand lack of ATP

No ATP

Ion leak across cell membrane

ST changes Dysrhythmias

Cell rupture and death

Q-waves ElevatedEnzymes

Totally ischemic cells

Sequela of Myocardial Infarction

Figure: 18-9Summary of events following MI

Figure: 18-8Time course of serum marker elevations after MI

Serum markers released from damaged cardiac cells

Cardiac isozymes – MI indicators creatine kinase (CK-MB) only present up to 72 hrs troponin I (present longer) troponin T (present longer)

Decreased Stroke Volume

IMMEDIATE HOURS WEEKS

baroreceptoractivation

SNS

SV, CO SV, COSV, CO

RAS activity

fluid retained

preload

Increased LVwall tension

ventricularhypertrophy

Compensatory Response to Decreased Stroke Volume

Differential Diagnosis of Chest Pain

Cardiac ischemia Chest wall trauma,

costochondritis Pleural pain - pneumonias Pneumothorax Gastrointestinal (GERD)

Treatment of Cardiac Ischemia Stable angina

– SL nitroglycerin– Platelet inhibitor (e.g. ASA 325mg

qod)– beta blocker– add long acting nitrate (remove at

night)– add calcium channel blocker (not

verapamil)

Treatment of Cardiac Ischemia If ECG shows signs of current

ischemia– Continuous ECG monitoring, Labs– Oxygen– Give ASA– Relieve pain with SL nitro, morphine– Evaluate for thrombolytic therapy– Decrease MVO2: bedrest, pain relief,

etc– Manage dysrhythmias,

hemodynamics

Heart FailurePathophysiological stateAbnormality of cardiac function to supply blood to meet demandPumps only from abnormally elevated diastolic filling pressure

EtiologyMyocardial failureHigh demand on heart with near normal cardiac functionInadequate adaptation of cardiac myocytes to increased wall stress

Causes circulatory failure but converse is not always true

AdaptationsFrank-Starling mechanism – increased preload sustains cardiac performanceMyocardial hypertrophy – mass of contractile tissue increasesNeurohumoral Activation –

Adrenergic cardiac nerves causes release of NE Positive inotropyActivation of RAA system – salt and water retention (increased preload, increased energy expense)Release vasoconstrictive agents which increase afterloadIncreased cAMP causes increased calcium entry

Positive inotropy, negative lusitropyIncreased energy expenditure and reduced CO which further stimulates RAA system

Calcium overload may cause arrythmia and sudden deathCardiac AngII may cause negative lusitropy, positive inotropy, positive afterload, increased myocardial energyexpense

Congestive Heart Failure

Systolic dysfunctionReduced myocardial contractilityCongestion is result of fluid backup in heartCommon cause is myocardial cell death – MI (neg inotropy)EF less than 50%Chronic overexcitation of b receptor SNS may be exacerbate conditionB receptor blockers – treatment

Heart failure –Signs, symptoms CHFReduced stroke volumeReduced cardiac output

Reduced EF (typically < 40%; severe if EF<20%)

Can result from most cardiac disorders.Most common causes of CHF is myocardial ischemia from coronary artery disease, hypertension and dilated cardiomyopathy

Congestive Heart Failure

Diastolic dysfunctionReduced myocardial relaxationVentricle is not compliant and does not fill effectivelyVentricle filling dependent on Ca2+ uptake (active phase of diastolic relaxation)Passive phase (myocardial stretch) impairedCommon cause is myocardial cell death – MI (neg inotropy)

Heart failure –Signs, symptoms CHF (congestion; edema)Reduced stroke volumeReduced cardiac outputNear normal EF > 50%

Factors Affecting Cardiac Output Heart Rate (chronotropy) Contractility (inotropy) Preload Afterload

How is Heart Rate Regulated? Intrinsic pacemaker rate = 100 bpm Autonomic Influences

– SNS------> B1 receptor-------> Increased HR

– PSNS-> Muscarinic (Ach)--> Decreased HR

Stretch Reflex (Bainbridge): Increased filling------> Increased HR

Drugs: ANS drugs, digitalis

Anything that increases Ca++ availability in the heart muscle cell will increase Contractility.

Anything that decreases Ca++ availability in the heart muscle cell will decrease Contractility.

What would be the effect of:– SNS– PSNS– Digoxin– Ca++ channel blocker– B1 blocker

What Factors Affect Contractility?

Preload: Volume Work of the Heart

preload

S.V.

The Frank-Starling Law of the Heart: Increased preload increases force of contraction

Afterload: Pressure work of the Heart Increased Afterload occurs with

increased resistance to ejection of blood from the ventricle– Increased Systemic Vascular

Resistance– Increased Diastolic Blood Pressure– Aortic Stenosis

Increased Afterload: Decreased stroke volume

Constitution of normal bloodParameter Value

Hematocrit45 ± 7 (38–52%) for

males42 ± 5 (37–47%) for

femalespH 7.35–7.45

base excess −3 to +3PO2

10–13 kPa (80–100 mm Hg)

PCO24.8–5.8 kPa (35–45 mm

Hg)HCO3

− 21–27 mM

Oxygen saturation Oxygenated: 98–99%Deoxygenated: 75%

ANEMIAS

ANEMIAS

How can the different types of anemia be differentiated?

Laboratory Diagnosis of Anemia– Low Hematocrit– Low Hemoglobin– Low RBC count

Red Cell Indices – MCV (size) microcytic, normocytic

macrocytic– MCHC (color) hypochromic,

normochromic

MCV MCV

low normal high

Normocytic acute bleeding aplastic hemolytic low

erythropoietin malignancy

Macrocytic low Vit B12 low folate

Microcytic iron deficiency hemoglobinopat

hy chronic disease lead poisoning

Polycythemia

red cell mass

normal

Relativepolycythemia

increased

check erythropoietin

high

Secondary- hydrate

- assess lung and kidney function

low

Vera

- assesswbc, platelets

Polycythemia

Cardiovascular System Physiology

Figure: 19-2Compensatory mechanisms in heart failure

These mechanisms attempt to improve cardiac outputSNS activation – early response to reduced CO Increased heart rate Increased contractility Increased arterial vasoconstriction Increased renin release

Chronic SNS activation Increased afterload Increased workload = Reduced CO

Decreased CO reduces kidney perfusionActivates RAA system ultimately leading to increased fluid retentionDecreased EF = Increased Preload = Reduced CO = Reduced GFR = Increased Fluid Retention = Increased RAS activation = Increased Blood volume= Increased Chamber volume =Increased Contraction (myocardial stretching)

Higher Preload = Increased Contractility = Increased CO

Left Heart Failure

LVFBackward

effectsForwardeffects

EF

Left Ventricularpreload

CO

RASactivation

TissueperfusionFluid

retention

Left atrialpressure

PulmonaryPressure

Right ventricular afterload

Right ventricular hypertrophy

PulmonaryCongestion & edema

(dysfunction)

Forward FailurePoor cardiac pumping = reduced CO

Backward FailureCongestion of blood behind the heart

Right Heart Failure

RVFBackward

effectsForwardeffects

EF

Right Ventricularpreload

Output to LV

RASactivation

Tissueperfusion

Fluidretention

Right atrialpressure

Systemic VenousCongestion

Forward FailurePoor cardiac pumping = reduced CO

Backward FailureCongestion of blood behind the heart

Left ventricularCO

Figure: 19-9Manifestations of right heart failure

Clinical presentation of RVFOften results from LVFCommon causes LVF Right MI Pulmonary disorders that increase pulmonary resistance increased right ventricular afterload reduce lung vascularization hypoxemia, emphysema, embolus RV compensates by increasing preload and hypertrophy Cardiomyopathy Aortic and mitral valvular disease Systemic hypertension

Forward effects – reduces CO via action on LVBackward effects – congestion of systemic venous system Impaired function of liver, portal system, spleen, kidneys, peripheral subcuatenous tissues, brainEdema apparent in lower extremities

Systemic system is congested but pulmonary system is not

In biventricular heart failure – both systemic venous and pulmonary systems are congested

Principles of Heart Failure Treatment GOAL: Optimize Cardiac Output

and Minimize Cardiac Workload– Management of Preload– Management of Afterload– Management of Contractility

Drugs used in the management of Heart Failure (table 19-3)

4

0

1 2

3K+ out Na+ in

K+ out

Ca++ in

Phases of the Ventricular Action Potential

Depolarized (-)

Hyperpolarized (+)

-70 mV

Also see Fig 13-16

CO2 transport in Blood1. Dissolved CO22. Carbaminoglobin3. Bicarbonate ion

Chlorideshift

Cardiovascular System

Cardiovascular Structures

Structure diagram of the human heart from an anterior view. Blue components indicate de-oxygenated blood pathways and red components indicate oxygenated pathways.

Pacemaker Cells SA node, AV node, Purkinje fibers Spontaneously generate action

potentials Vary rate in response to ANS Action potentials are associated

with opening of slow calcium ion channels

Almost no contractile elements

Spontaneous Phase 4 depolarization

RMP

threshold -40 mV

-60 mVNa

Ca K out

pacemaker cells are leaky to sodium at rest

What is the basis of automaticity?

ANS Influences on Ion Flux

Sympathetic: NE, E stimulates Beta receptors leading

to opening of Na/Ca channels.

The cell depolarizes faster.

Parasympathetic: acetylcholine stimulates muscarinic receptors leading to opening of K channels. Potassium leak out offsets sodium influx. The cell depolarizes

slower.

SNS (T1-L2)

PSNS (Cn IX, X)

alpha-MN

Ach

Ach

AchN2 (nicotinic)

muscle

Ach muscarinic receptor

M1 to M5

N1 NE

nicotinic

nicotinic

a1, a2

b1, b2, b3receptor

N1

Autonomic NERVES