Transcript No Slide Title

Cardiovascular System
John P. McDonough,
CRNA, Ed.D., ARNP
Vessels

Arteries
– carry blood away from the heart
» oxygenated (except PA)

Veins
– carry blood to the heart
» desaturated (except PV)

Capillaries
– local circulation
– connects arteries to veins
“Great” Vessels

Vena cava
– superior & inferior
Pulmonary artery
 Pulmonary vein
 Aorta

Blood Flow Through the Heart
Rt Atrium
 Tricuspid valve
 Rt ventricle
 Pulmonic valve
 Lt atrium
 Mitral valve
 Lt ventricle
 Aortic valve

Structure of the Heart

Pericardium
– visceral
– parietal
– pericardial fluid

Myocardium
– contractile heart muscle

Endocardium
– cavity lining
Circulation to the Heart Itself

Lt main coronary artery
– Lt anterior descending
– Lt circumflex
Rt coronary artery
 Coronary perfusion

– occurs during diastole
– rate changes effect diastole only
Cardiac Conduction System
(electrical  mechanical function)

Sinoatrial (AS) node
– “pacemaker of the heart”
Intra-atrial conduction pathways
 Atrioventricular (AV) node
 Bundle of His
 Rt bundle branch
 Lt bundle branch

– Lt anterior & posterior facicles
Circulatory System
2 separate circuits, serially connected
 Output of one  the input of the other

– pulmonary, systemic

Heart is functions as 2 pumps
– Rt = pulmonary, Lt = systemic
Arteries
 Veins
 Capillaries

Adrenergic Control of Heart Rate

-adrenergic receptors (generally dilates
& excites)
– 1 found mostly in the heart (conduction
system)
– 2 found mostly in the lungs (bronchi), but also
in the coronary arterioles
Adrenergic Control of Heart Rate
-adrenergic stimulation will  heart rate &
dilate bronchi
 -adrenergic blockade will  heart rate &
constrict bronchi
 Norepinephrine binds with 1 receptors
 Epinephrine binds with 2 receptors

Adrenergic Control of Heart Rate

-adrenergic receptors
– some in the heart, but mostly in vessels

Stimulation causes constriction
Autonomic Control of Heart
Rate

Sympathetic
– thoracic chain ganglia
– neurotransmitter = norepinephrine (NE)

parasympathetic
– vagus nerve (CN-X)
– neurotransmitter = acetylcholine (Ach)
Other Controls of Heart Rate

Volume control
– Barinbridge reflex

Pressure control
– baroreceptors
Factors Effecting Cardiac Output
Preload
 Afterload
 Heart Rate
 Contractility

1, 300, 000 Myocardial
Infarctions yearly in the
United States
50%
are fatal
Risk Factors for CV Disease
Smoking
 Diabetes mellitus
 Hypertension
 Hyperlipidemia

Risk Factors for CV Disease
(con’t)
Genetic predisposition
 Obesity
 Sedentary life-style
 Type A personality

Hypertension
50 million Americans have it
 Diagnosed if >2 B/P measurements show:

– diastolic readings >90
– average of 2 systolic >140

Mortality rates:
–
–
–
–
white women
white men
black women
black men
4.7%
6.3%
29.3%
22.5%
Determinants of Hypertension

Essential hypertension
– stress
– diet
– genetic factors

Secondary hypertension
–
–
–
–
pheochromocytoma
renal vascular disease
Cushing’s syndrome
thyrotoxicosis
Effect of Vessel Diameter

With the same 100mg/Hg pressure driving:
– d=1  1 ml/min
– d=2  16 ml/min
– d=3  256 ml/min
Complications of Hypertension
Myocardial ischemia
 Ventricular failure
 Pulmonary edema
 Aortic dissection
 Intracerebral hemorrhage

Common Antihypertensives
Beta Blockers
Propanolol, esmolol,
metoprolol, atenolol
ACE Inhibitors
Captopril, enalapril,
Calcium
antagonists
Nifedipine, diltiazem
Blocks effect of
cate. at receptors.
Decreases HR &
CO
Dec conversion of
AT-1 To AT-2
Orthostatic
hypotension
Inhibits Ca++
uptake, dec
peripheral
resistance
Reflex tach,
hypotension
Bronchospasm,
bradycardia,
hypotension
Cardiomyopathies

Primary disorders of the muscle itself
– not related to CAD, HTN or valve disorders

Dilated cardiomyopathy
– toxins, ETOH, infection, nutrition,

Hypertrophic cardiomyopathy
– usually congenital

Restrictive cardiomyopathy
– usually infiltrative disease process
Congestive Heart Failure
(a symptom complex)
Each side of the heart can fail separately
 Left HF is a frequent cause of right HF

– frequent, but the not the only

S/S Left heart failure
– dyspnea
– pulmonary congestion

S/S Right heart failure
– peripheral edema
– vein distention
Treatment of CHF
Rate control
 Digitalis glycosides (lanoxin)
 Diuretics
 Phosphodiesterase (PDE) inhibitors

Cardiac muscle extracts the largest amount of
oxygen because of the extensive work the heart
does (manifested as contractility) even during rest.
At rest: 8-10 ml O2/min/100g of myocardium.
During exercise this can increase by a factor of 10.
But what drives the contraction
process in myocytes?
Answer: ATP
As demand goes up, inotropic response of the
heart increases and the coronary vasculature
adapts by vasodilating to provide an adequate
oxygen supply.
If, due to atherosclerotic disease, the coronary
arteries are unable to sustain the myocardium,
ischemia ensues and the flow is predicted by:
Q =  P r4/ 8 n L
where r is radius of vessel, n is viscosity and L is vessel length.
Factors in Supply & Demand

Decreased supply
–
–
–
–
reduced content
reduced coronary flow
increased LV pressure
fixed vascular
obstruction

Increased demand
–
–
–
–
–
positive chronotropism
positive inotropism
increased LV volume
increased wall tension
increased afterload
Visualization of intracellular oxygenation:
Microspectrophotometry
Reference: Takahashi, E. and K. Doi. Visualization of oxygen level inside a single cardiac
myocyte. Am. J. Physiol. 268: H2561-H2568, 1995.
Aerobic environment
Happy myocytes
Anoxic environment
Myocytes not happy
History
 Pain
 Dyspnea
 Palpitation
 Edema
 Syncope
 Fatigue
&
Weakness
 Cyanosis
Hemodynamic to Formulae
BP = CO x SVR
 CO = SV x HR
 SV = LVEDV - LVESV
 SVR = MAP - CVP x 80 / CO

– normal = 800-1200 dyne/sec/cm-5
Congestive Heart Failure
(diagnostic problems)
Volume overload
 Bronchospasm
 Pneumonia
 Pulmonary embolism
 Ischemically mediated pulmonary edema

Characteristics of Chest Pain

ANGINA
– retrosternal, diffuse
– Lt arm, jaw, back
– aching, dull, pressing,
squeezing,
– minutes
– effort, emotion, eating
cold
– rest, NTG

PROBABLY NOT
– Lt inframam, localized
– Rt arm
– sharp, cutting,
shooting,
– seconds, hours, days
– respiration, posture,
motion
– nonspecific
Cardiac Causes of Chest Pain



CAD
aortic valve disease
pulmonary
hypertension



mitral valve prolapse
pericarditis
IHSS
Pulmonary Causes of Chest Pain
pulmonary embolism
 pneumonia
 pleuritis
 pneumothorax

Musculoskeletal Causes of Chest
Pain
costochondritis
 arthritis
 muscular spasm
 bone tumor

GI Causes of Chest Pain
ulcer disease
 bowel disease
 hiatal hernia
 pancreatitis
 cholecystitis

Other Causes of Chest Pain

Vascular
– aortic dissection

Emotional
– anxiety
– despression
Common Causes of Palpitations




extrasystoles
tachyarrthymias
bradyarrthymias
drugs



smoking
caffeine
thyrotoxicosis
Common Causes of Dyspnea

Cardiac
– Lt failure
– mitral stenosis

Pulmonary
–
–
–
–
obstructive disease
asthma
restrictive disease
pulmonary HTN



Emotional
High altitude exposure
Anemia
Physical Exam of the Heart




inspection
blood pressure
assess arterial pulse
assess JV pulse




percussion
palpation
auscultation
evaluation of edema
Murmur Description





timing in cycle
location
radiation
duration
intensity




pitch
quality
relationship to position
relationship to
respiration
Grading of Murmurs (I-V/VI)
I lowest intensity
 II low intensity
 III medium intensity (without thrill)
 IV medium intensity (with thrill)
 V loudest murmur with scope on chest
 VI loudest, heard with scope off chest

Location of Murmurs within Cardiac Cycle
“Shape” of Murmurs
Three Most Important
Survival Factors
 MYOCARDIAL
PRESERVATION
 MYOCARDIAL PRESERVATION
 MYOCARDIAL PRESERVATION
“Dead meat don’t beat!”