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90 Cards in this Set

  • Front
  • Back
C.O. in a young healthy male =
C.O in a young healthy female =
5.6 L/min
4.9 L/min
Control of C.O. by venous return
Frank - Starling the amount of blood presented to a ‘normal’ heart will be the amount pumped out the left side
Stretch of the S.A. node causes the atria to discharge faster and the heart to pump faster
Bainbridge reflex stretched right atrium causes a nerve impulse to the vasomotor center and increases rate autonomically
CO is proportional to _____

CO is proportional to _____
tissue O2. use.

1/Total Peripheral Resistance when AP is constant.
High C.O. From low peripheral resistance
Beriberi – vit. B deficiency (esp. B1)
AV shunts
Hyperthyroidism – metabolism h
Anemia – reduced viscosity and reduced O2 delivery
Normal C.O. can increase up to _________ before the heart becomes the limiting factor
13 L/min (2.5 times normal)
High C.O.
Cardiac failure – about a thousand reasons
Low blood volume – shock
Acute venous dilation – sympathetic system outage
Obstruction of large veins
Decreased tissue mass – esp. in geriatric patients w/ low mm. mass – demand is low, venous return is low
Intrapleural pressure (IPP) shifts cardiac output because it affects atrial filling
Normal intrathoracic pressure = -4mmHg
Intrapleural pressure shifts during inspiration -2mmHg and expiration + 2mmHg
During exercise – up or down 50 mmHG
Positive pressure breathing – pushes on atria
Open chest removes IPP
Cardiac tamponade – Fluid in the pericardium
Transmural pressure across heart wall is
for example, RAP-IPP, for right atrium.
Measurement of cardiac output
Electromagnetic flowmeter – inserted in the aorta – bad idea
Indicator dilution (dye such as cardiogreen)
Thermal dilution
Oxygen Fick Method
Fick Principle
The inhaled air has dumped 200ml of O2
The incoming blood has 160 ml/L of dissolved O2
The outgoing blood has 200 ml/L of dissolved O2
A difference of 40 ml of O2
The C.O. must be 5 Liters because 40 x 5 = 200 ml of O2
O2 Fick Problem
If pulmonary vein O2 content = 200 ml O2/L blood
Pulmonary artery O2 content = 160 ml O2 /L blood
Lungs add 400 ml O2 /min
What is cardiac output?
Answer: 400/(200-160) =10 L/min
I. Muscle Blood During Exercise
A. Can ≠ 20 fold during exercise.
B. Muscle makes up a large portion of body mass fi great effect on CO.
C. Resting blood flow = 3 to 4 ml/min/ 100 gm muscle.
D. Capillary density ≠s markedly.
E. Most blood flow occurs between contractions.
Blood flow to MM during exercise
Rest through MM: 3-4 ml/min in 100gm MM
In an athlete, during exercise, up to 50 -80 ml/min in 100 gm MM
Increases and decreases with each contraction
Blood vessels compressed during contractions
Ø O2 during exercise affects vascular smooth muscle directly by _______
Vasodilators (which ones?)
1. Adenosine
2. K+
3. Osmolality - esp. lactic acid, CO2
4. EDRF (nitric oxide) endothelial derived relaxing factor
5. Norepi release from sympathetic
A. Sympathetic release of norepinephrine (mainly a).
B. Adrenals release epinephrine (b and a) norepinephrine (a + a little b).
b receptors fi vasodilation mainly in muscle and the liver.
a receptors fi vasoconstriction in kidney and gut
Effects of AP on flow
A. MAP normally ≠s 20 - 80 mm Hg during exercise (F = DP / R)
B. ≠ DP fi ≠ F
C. ≠ MAP will also stretch the blood vessels and cause vasodilation
Coronary Circulation
I. Results of coronary artery disease (CAD)
A. 1/3 of all deaths in western affluent society due to CAD
B. 45% of all deaths are cardiovascular (only 22% cancer)
Risk factors for CAD which are not Reversible
1. Aging
2. Male Sex
3. Genetic Predisposition
Risk factors for CAD, those that are reversible
1. Cigarette smoking fi (Ø HDL and doubles chances of dying from heart attack)
2. ≠ BP fi vascular damage
3. Obesity - doubles mortality
4. Left ventricular hypertrophy
CAS RISK factors partiall reversible

1. ≠ Cholesterol or ≠ triglycerides (Øsaturated fat in diet fi Ø cholesterol)
2.Hyperglycemia or diabetes mellitus
3.Low levels of HDL

D. Others
1. Physical inactivity
2. Personality type
3. C-reactive protein
Normal coronary flow
225 ml/min
4-5% of C.O.
Phasic changes in coronary flow
During systole - less than 100 ml/min in left ventricular coronary cap.s
During diastole - back to normal
Less extreme change in rt. Vent. wall
Subendocardial vessels ________ compressed during systole
much more
Coronary blood flow regulated by local needs
A. Myocardial O2 consumption
B. Adenosine - related to Ø O2 and cell metabolism
C. Nervous stimuli (sympathetic) 1. Mainly affects epicardial flow (alpha)
2. Little effect of parasympathetics.
3. beta sympathetic increases
subendocardial flow
Coronary blood flow regulated by local needs
A. Fatty acid metabolism - 70% of cardiac energy source at rest (rather than carbs)
B. Glycolysis - during ischemia (lactic acid buildup from anaerobic resp -probably the source of pain during infarct)
C. During ischemia, ATP is degraded to adenosine and lost into circulation.
Within 30 minutes half of the cardiac intracellular adenosine is lost. Can’t be replaced in cells faster than 2% per hour. Lack causes cell death.
Atherosclerosis - cholesterol deposited _________
below the endothelium
Atherosclerosis - cholesterol deposited below the endothelium
Areas invaded by fibrous tissue
Calcium deposited, forming plaques
Plaque can break through endothelium and cause a thrombus from uneven surface and non-endothelial surface
Platelets accumulate.
Thrombus that occludes distally is an embolus.
Vessel spasm often follows
Smaller coronary arteries can and do anastomose, esp. over time.
Little or no flow to an area.
Local vessels dilate and become sluggish.
MM cells use the last of the O2.
Cells begin to die and leak fluid.
Damage is usually first to the subendothelial layer of tissue, since it is more compressed and less able to perfuse.
Death from occlusion
Decreased cardiac output (damaged wall area can’t contract and deliver stroke volume - more filling, more stretching)
Damming of blood in the pulmonary circulation, then pulmonary edema
Damming of blood in kidneys then they begin to fail - congestive symptoms
IX. Diagnosis of ischemic heart disease
A. Stress EKG
B. Thallium-201 perfusion
C. Cardiac catheterization
X. Treatment for ischemia
A. Ø Weight
C. Stop Smoking

D. Walking not isometrics (≠ BP)
E. Nitroglycerin
F. Digitalis only if congestive heart failure present
G. b blockade
H. Coronary bypass
E. Angina pectoris
1. Probably due to glycolysis and lactic acid
2. Exacerbated by exercise
H. Coronary bypass
1. 1% mortality
2. Patency of grafts is 75% after 2 to 3 years.
3. fi Relief of angina in 85% of patients
Causes of cardiac failure – failure to pump
A. Myocardial infarction – decreased contractility from diminished coronary flow
B. Heart valve damage
C. Pulmonary embolism
D. Anemia
E. Myocarditis
F. Hypertension - severe
G. A-V fistula and Beriberi (high output failure)
H. External pressure around heart
Acute responses to cardiac failure
Reduced C.O.
Damming of blood in the veins

≠ Sympathetics (start 6 sec. max at 30 sec.) improve damaged heart function
≠ MSFP due to venoconstriction
Chronic responses to cardiac failure
A. Renal Na and H2O retention
≠ Blood volume and Øvenous resistance from distended veins
1. Sympathetic constriction of afferent arterioles fi Ø GFR and Ø Urinary Output
2. AngioII release fi Na retention
3. ALDO release (from AngioII and ≠K+) fi Na retention
Up to a point, increases in fluid volume is good in maintaining pressures and delivering O2
ADH release fi H2O retention
- Ø MAP initially then returns to normal
B. Cardiac recovery (repair of muscle)
Compensated heart failure (several days to a week)
1. Normal C.O.
2. ≠ RAP
3. Ø Cardiac reserve – poor response to exercise
4. ≠ HR
5. Pale skin
6. Sweating also with nausea
7. dyspnea from pulmonary fluid
8. Weight gain from fluid retention
9. Orthopnea – inability to breathe unless upright
Decompensated heart failure
A. Causes: Primarily fluid retention
1. Fluid retention causes overstretched sarcomeres.
Decompensated heart failure
2. Edema of heart muscle
3. Longitudinal tubules of sarcoplasmic reticulum fail to accumulate enough Ca++.
4. Norepi in sympathetic nerves Øs
B. Treatment of Decompensated Failure
B. Treatment of Decompensated Failure
1. Diuretics along with…
2. Ø Na and water intake
3. ACE inhibitor
4. Digitalis - like drug. cardiac glycosides (increase Ca++ conc inside cardiac MM cells)
5. Breathe O2
6. Heart transplant
Left Heart Failure
Rt Hrt continues to pump into pulmonary circ w/ normal pressures. Lft hrt is unable to empty completely and fluid collects in lungs because of the over filling of pulm cap.s
A. ≠ LAP
B. Pulmonary vascular congestion
C. Pulmonary edema
D. AP may be normal
E. CO may be normal
Left Heart Failure
During left heart
failure a relatively
large amount of
blood transfers from
the systemic
circulation into the
pulmonary circulation
and causes a big
increase in LAP
circulation has
small volume
and capacitance
has large volume
and capacitance
Right heart failure
A. Greater Ø in C.O. than left failure
B. Peripheral congestion over time – not acutely - as a result of kidney fluid retention
Right Heart Failure
During right heart
failure only a small amount
of blood transfers from
the pulmonary circulation to the systemic circulation.
This causes a small increase in RAP fi adrop in cardiac output.
Systemic circulation has large volume
and capacitance
Pulmonary circulation hasm small volume and capacitance
Cardiac shock – Cardiogenic shock
A. C.O. is very low – all tissues suffer
B. Ø C.O. fi Ø AP fi Ø coronary flow fi weak heart fi Ø CO
C. immediate transfusions
D. Treatment of cardiac shock
1. Digitalis
2. ≠ AP use digitalis and dobutamine (a and b stimulation)
3. Give volume expander
4. Dissolve blood clot if this is cause (streptokinase or plasminogen activator)
Acute pulmonary edema
A. Ø C.O.
B. ≠ pulmonary blood volume
C. Ø PaO2 fi peripheral vasodilation fi ≠ venous return fi ≠pulmonary cap. pressure fi more and more edema
D. Listen for rales - also chest x-ray
Renal effects in heart failure
Decreased GFR – from reduced art pressure and symp vaso constriction
Activation of renin - angiotensin system
(Which drops aff arteriole pressure even further & reduces Na and water excretion and ups fluid retention)
Angiotensin (and higher plasma K+) then trigger aldosterone release from the adrenal cortex
Higher salt ions stimulate ADH release – even more fluid retention
Atrial Natriuretic Factor helps by increasing salt and water excretion from the kidneys
Acute Pulmonary edema in late stage heart failure
Increased load on a weak lft ventricle
Increased damming in the pulmonary system
Increased cap hydrostatic press
Increased fluid in alveoli – reduction of O2 absorption
Further weakens heart pumping
Treatment of acute pulmonary edema
1. Tourniquets on all extremities to sequester blood
2. Bleed patients
3. Furosemide or diuretics
4. Breathe O2
5. Digitalis
6. Bronchodilator
Cardiac reserve – maximum% increase in C.O above normal
A. Any type of cardiac failure Ø reserve
B. If normal C.O. = 5 L/min and you can ≠ to 20 L/min; cardiac reserve = 15/5 * 100 = 300%
C. Low cardiac reserve test by exercise
1. Will cause dyspnea
2. Muscle weakness
3. increase in hrt rt.
I. 1st Heart Sound
. A-V valves close and taut valves and chordae tendinae themselves vibrate
B. Louder than second sound
C. Low pitch
II. 2nd Heart Sound
Aortic and pulmonary valves close and cause vibrations in themselves and in the adjacent arterial walls. They are tauter than the AVs and produce a higher pith
III. 3rd Heart Sound
A. Very low pitch
B. Caused by inrushing of blood into ventricles
IV. 4th Heart Sound
A. Atrial contraction late in diastole
B. impossible to hear with stethoscope except in hypertensive patients with a thick left ventricle
Rheumatic valvular lesions
Rheumatic fever initiated by group A hemolytic strep
Cause large hemorrhagic lesions on hrt valves
Big immune response and antibody production
Under normal conditions, mitral valves get the most wear and tear – so it’s the one most damaged by inflammation and infection
Aortic semilunar is 2nd in degree of damage
Valves become scarred, distorted and stenotic. Unable to close completely
Dynamics of Streptococcal Damage to Heart Valves
release of M antigen
Heart valve cell with M antigens attached
Antibody formed against combination
Complement damage to heart valves
Aortic stenosis
Pressure in Lft Vent can rise to 300mmHg
Nozzle effect into aorta and subsequent vessels
Produces a ‘thrill’
Aortic stenosis
A. 80% of patients are male
B. Diamond shaped - or crescendo and decrescendo - (some are fast ejection murmurs)
C. Pressure in vent. may reach 400mm Hg fi vent. hypertrophy
D. Very loud - can be felt with hand if severe
E. Repair with prosthetic valve or porcine valve (as in all murmurs)
Aortic Stenosis Murmur
s1-during systole
Aortic Stenosis Hemodynamics
Severe turbulance in the root of the aorta
Sound is loud and harsh
Can sometimes be heard without a stethoscope
Hemodynamics of aortic stenosis
1. L. ventricular hypertrophy
2. Repair of valve sometimes leads to regurgitation
3. Angina pain in severe stenosis
4. High mortality in surgery
5. Chronic ≠ in blood vol.
Aortic regurgitation
Normal systolic sound, but murmur during diastole
A “blowing” murmur
Mitral stenosis
A. Murmur heard in last 3rd of diastole
B. Described as a soft “thrill” over apex of heart at the end of diastole
Lft vent barely fills
Mitral Stenosis Hemodynamics
L.A. can only produce about 30 mm Hg, so there is little pressure in the ventricle. As L.V. slowly fills, a low frequency noise can be recorded but rarely heard
If it’s recorded, it’s at the end of diastole
Hemodynamics of mitral stenosis
1. CO and MAP do not Ø nearly as much as in aortic stenosis
2. ≠ Atrial volume can lead to atrial fibrillation
3. ≠ R. ventricle pressure could lead to r. vent. failure
4. ≠ LAP could fi pulmonary edema
5. L. ventricle normal
Mitral regurgitation murmur
A. “Blowing” murmur heard throughout systole - high pitch
B. Best sound heard over l. atrium (too deep); must be heard over l. ventricle.
Mitral Regurgitation Hemodynamics
Regurg in to L.A. during systole
Since L.A. is so deep in the chest, Mitral regurg is heard best over the apex of the L.V. by its resonation down through thr ventricle
Hemodynamics of mitral regurgitation
1. ≠ LAP can lead to pulm. edema
2. CO falls more if rt. heart fails
3. ≠ L. atrial volume can lead to atrial fibrillation
Aortic Regurgitation Murmur
A. Blowing murmur - high pitch
B. Listen over l. ventricle for best sound
C. Short murmur means blood flows back rapidly and is more severe
D. May have stroke vol. of 300ml with 70ml going to periphery and 230 leaking back
Aortic Regurgitation Hemodynamics
Blood jetting back into, now low pressure, L.V.

Aortic diastolic press. Øs rapidly

Over filling of ventricle can compress inner parts of heart and coronaries

L. ventricular hypertrophy
1. Aortic diastolic press. Øs rapidly
2. Filling of ventricle can compress inner parts of heart and coronaries
3. L. ventricular hypertrophy
Diagnosis of Murmurs
ECG axis deviation showing hypertrophy
Stethoscope or phonocardiogram
Persistent patent ductus
blood mixes from rt and lft heart - lower oxygenation
Before birth - high resistance to blood flow into lungs. As aortic O2 levels rise after birth, ductus smooth MM constricts
In kids, blood circulates back through lungs and lft heart repeatedly.
In adults, it can lead to cyanosis and pulmonary edema
Cardiac reserve and respiratory reserve falls
“machinery murmur”
Ligate it
Interventricular Septal Defect
Pan systolic murmur unless hole closes during contraction
Interatrial Septal Defect
A. Foramen ovale does not close
B. 1/3 of people do not have normal fibrotic closure of f. ovale, but ≠ LAP causes it to close
Tetrology of Fallot
*Pulm artery stenosis or pulm. valve stenosis
*Aorta over rides hole in the septum
*Equal systolic pressure in both ventricles - septal defect
*Enlarged rt. ventricle
Blue baby - blood does not flow through lungs enough
Surgery very helpful
Causes of defects
Commonly caused by exposure of the pregnant mother to viruses in the first trimester- esp. German measles
Can also be hereditary
Due to severely reduced C.O. (cardiogenic)
toxin release
valve dysfunction

Or reduced venous return
usually low blood volume (hypovolemic)
can be decreased vascular tone
or obstruction of flow
Circulatory shock- inadequate C.O. to meet tissue needs.

A. Ø Cardiac function curve
1. Myocardial infarction
2. Valvular disease
3. Arrythmias
4. Metabolic problems
5. Myocarditis
B. Ø Venous return
1. Ø Blood volume
2. Ø Vascular tone
Compensated – non progressive
Baroreceptors_ sympathetic output - powerful response
Arterioles and veins constrict except in coronary and cerebral vessels
_ Angio II - pressure up and decreased urine output
_ ADH – “
Reverse stress – relaxation response – blood vessels contact around diminished volume
Absorption of fluid into blood from G.I, interstitium, and caps
Progressive Shock - deteriorates
Cardiac shock – coronary circulation drops
Vasomotor center failure causes vascular dilation
Sludged blood - blockage in small vessels
Capillary permeability – from hypoxia
Endotoxin release – from gut flora or gram negatives anywhere
Cell damage – Na+ /K+ pumps fail, mitochondria fail, lysosomes open, hormones and enzymes fail, including Kreb’s and insulin
Tissue acidosis
Decreased urine output
Acidosis in shock prevents glycolysis. Irreversible stage is postponed by Fructose 1,6 diphosphate.
Glucose 6-phosphate
Fructose 6-phosphate
Ø phosphofructokinase - blocked by acidosis
Fructose 1,6 diphosphate
System converts to anaerobic
Loss of high energy phosphate reserves
ATP to ADP to (eventually) adenine.
Which is lost from the cell to interstitial fluid and converted to uric acid – which cannot re-enter cells
Replacement rate – in healthy cells is less than 2% per hour
One of the most damaging events in shock
3. Renal fluid loss from damaged kidneys
a. Diabetes mellitus
b. Diabetes insipidus
c. Excessive use of diuretics -
4. Cutaneous fluid loss
a. Burns - direct plasma loss
b. Perspiration (give saline)
5. Intestinal obstruction - plasma loss - bloated belly obstructs venous return increases cap permeablity and bloats further also plasma protein loss into belly
Neurogenic shock
Drug induced (O.D.)
1. Ingestion (barbituates)
2. deep anesthesia depresses vasomotor center
3. Ganglionic blockers in paravertebral
Brain damage esp. brain stem concussion/damage
Spinal injury, spinal anesthesia – blocks sympathetic if the anesthesia is high enough
Anaphylactic Shock
Antigen-antibody reaction releases histamine and causes vasodilation + cap. permeability increase – fluid into interstitium
drop in venous return
arteriole dilation
Sympathomimetic, glucocorticoids
Septic shock - septicemia
Peritonitis – from many causes
Spread of infection
Symptoms of severe infection
high CO, then drops
high fever
DIC and hemorrhage
loss of fluid through deteriorating capillary walls
tx for shock
Hypovolemia - volume expander
Whole blood, plasma, dextran (large polysaccharide solution unable to leave caps, but good transporter of nutrients)
Sympathomimetic drugs in neurogenic and anaphylactic shock – not in hemorrhagic shock – NN are already maxed
Glucocorticoids – increase contractility in late stage shock, stabilize lysosomes, inr. Glucose meatb in damaged cells
Morphine to block pain
Head down position, & O2