Cardiovascular Anatomy & Physiology
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Transcript of Cardiovascular Anatomy & Physiology
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
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