Westminster-Heart Function

Front 1

C.O. in a young healthy male =
C.O in a young healthy female =

Back 1

5.6 L/min
4.9 L/min

Front 2

Control of C.O. by venous return

Back 2

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

Front 3

CO is proportional to _____

CO is proportional to _____

Back 3

tissue O2. use.

1/Total Peripheral Resistance when AP is constant.

Front 4

High C.O. From low peripheral resistance

Back 4

Beriberi – vit. B deficiency (esp. B1)
AV shunts
Hyperthyroidism – metabolism h
Anemia – reduced viscosity and reduced O2 delivery

Front 5

Normal C.O. can increase up to _________ before the heart becomes the limiting factor

Back 5

13 L/min (2.5 times normal)

Front 6

High C.O.

Back 6

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

Front 7

Intrapleural pressure (IPP) shifts cardiac output because it affects atrial filling

Back 7

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.

Front 8

Measurement of cardiac output

Back 8

Electromagnetic flowmeter – inserted in the aorta – bad idea
Indicator dilution (dye such as cardiogreen)
Thermal dilution
Oxygen Fick Method

Front 9

Fick Principle

Back 9

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

Front 10

O2 Fick Problem

Back 10

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

Front 11

I. Muscle Blood During Exercise

Back 11

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.

Front 12

Blood flow to MM during exercise

Back 12

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

Front 13

Ø O2 during exercise affects vascular smooth muscle directly by _______

Back 13

vasodilation.

Front 14

Vasodilators (which ones?)

Back 14

1. Adenosine
2. K+
3. Osmolality - esp. lactic acid, CO2
4. EDRF (nitric oxide) endothelial derived relaxing factor
5. Norepi release from sympathetic

Front 15

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

Back 15

++++++

Front 16

Effects of AP on flow

Back 16

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

Front 17

Coronary Circulation

Back 17

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)

Front 18

Risk factors for CAD which are not Reversible

Back 18

1. Aging
2. Male Sex
3. Genetic Predisposition

Front 19

Risk factors for CAD, those that are reversible

Back 19

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

Front 20

CAS RISK factors partiall reversible

Others?

Back 20

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

Front 21

Normal coronary flow

Back 21

225 ml/min
4-5% of C.O.

Front 22

Phasic changes in coronary flow

Back 22

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

Front 23

Subendocardial vessels ________ compressed during systole

Back 23

much more

Front 24

Coronary blood flow regulated by local needs

Back 24

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

Front 25

Coronary blood flow regulated by local needs

Back 25

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.

Front 26

Atherosclerosis - cholesterol deposited _________

Back 26

below the endothelium

Front 27

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.

Back 27

xxxxxxx

Front 28

Infarction

Back 28

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.

Front 29

Death from occlusion

Back 29

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
Fibrillation

Front 30

IX. Diagnosis of ischemic heart disease

Back 30

A. Stress EKG
B. Thallium-201 perfusion
C. Cardiac catheterization

Front 31

X. Treatment for ischemia

Back 31

A. Ø Weight
B. Ø BP
C. Stop Smoking

D. Walking not isometrics (≠ BP)
E. Nitroglycerin
F. Digitalis only if congestive heart failure present
G. b blockade
H. Coronary bypass

Front 32

E. Angina pectoris

Back 32

1. Probably due to glycolysis and lactic acid
2. Exacerbated by exercise

Front 33

H. Coronary bypass

Back 33

1. 1% mortality
2. Patency of grafts is 75% after 2 to 3 years.
3. fi Relief of angina in 85% of patients

Front 34

Causes of cardiac failure – failure to pump

Back 34

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

Front 35

Acute responses to cardiac failure

Back 35

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

Front 36

Chronic responses to cardiac failure

Back 36

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)

Front 37

Compensated heart failure (several days to a week)

Back 37

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

Front 38

Decompensated heart failure

Back 38

A. Causes: Primarily fluid retention
1. Fluid retention causes overstretched sarcomeres.

Front 39

Decompensated heart failure

Back 39

2. Edema of heart muscle
3. Longitudinal tubules of sarcoplasmic reticulum fail to accumulate enough Ca++.
4. Norepi in sympathetic nerves Øs

Front 40

B. Treatment of Decompensated Failure

Back 40

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

Front 41

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

Back 41

A. ≠ LAP
B. Pulmonary vascular congestion
C. Pulmonary edema
D. AP may be normal
E. CO may be normal

Front 42

Left Heart Failure

Back 42

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

Front 43

Pulmonary
circulation has
small volume
and capacitance

Back 43

xxxxx

Front 44

Systemic
circulation
has large volume
and capacitance

Back 44

xxxxx

Front 45

Right heart failure

Back 45

A. Greater Ø in C.O. than left failure
B. Peripheral congestion over time – not acutely - as a result of kidney fluid retention

Front 46

Right Heart Failure

Back 46

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

Front 47

Cardiac shock – Cardiogenic shock

Back 47

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

Front 48

D. Treatment of cardiac shock

Back 48

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)

Front 49

Acute pulmonary edema

Back 49

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

Front 50

Renal effects in heart failure

Back 50

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

Front 51

Acute Pulmonary edema in late stage heart failure

Back 51

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

Front 52

Treatment of acute pulmonary edema

Back 52

1. Tourniquets on all extremities to sequester blood
2. Bleed patients
3. Furosemide or diuretics
4. Breathe O2
5. Digitalis
6. Bronchodilator

Front 53

Cardiac reserve – maximum% increase in C.O above normal

Back 53

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.

Front 54

I. 1st Heart Sound

Back 54

. A-V valves close and taut valves and chordae tendinae themselves vibrate
B. Louder than second sound
C. Low pitch

Front 55

II. 2nd Heart Sound

Back 55

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

Front 56

III. 3rd Heart Sound

Back 56

A. Very low pitch
B. Caused by inrushing of blood into ventricles

Front 57

IV. 4th Heart Sound

Back 57

A. Atrial contraction late in diastole
B. impossible to hear with stethoscope except in hypertensive patients with a thick left ventricle

Front 58

Rheumatic valvular lesions

Back 58

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

Front 59

Dynamics of Streptococcal Damage to Heart Valves

Back 59

Streptococcus
Ø
release of M antigen
Heart valve cell with M antigens attached
Antibody formed against combination
Complement damage to heart valves

Front 60

Aortic stenosis

Back 60

Pressure in Lft Vent can rise to 300mmHg
Nozzle effect into aorta and subsequent vessels
Produces a ‘thrill’

Front 61

Aortic stenosis

Back 61

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)

Front 62

Aortic Stenosis Murmur

Back 62

s1-during systole

Front 63

Aortic Stenosis Hemodynamics

Back 63

Severe turbulance in the root of the aorta
Sound is loud and harsh
Can sometimes be heard without a stethoscope

Front 64

Hemodynamics of aortic stenosis

Back 64

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.

Front 65

Aortic regurgitation

Back 65

Normal systolic sound, but murmur during diastole
A “blowing” murmur

Front 66

Mitral stenosis

Back 66

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

Front 67

Mitral Stenosis Hemodynamics

Back 67

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

Front 68

Hemodynamics of mitral stenosis

Back 68

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

Front 69

Mitral regurgitation murmur

Back 69

A. “Blowing” murmur heard throughout systole - high pitch
B. Best sound heard over l. atrium (too deep); must be heard over l. ventricle.

Front 70

Mitral Regurgitation Hemodynamics

Back 70

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

Front 71

Hemodynamics of mitral regurgitation

Back 71

1. ≠ LAP can lead to pulm. edema
2. CO falls more if rt. heart fails
3. ≠ L. atrial volume can lead to atrial fibrillation

Front 72

Aortic Regurgitation Murmur

Back 72

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

Front 73

Aortic Regurgitation Hemodynamics

Back 73

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

Front 74

Diagnosis of Murmurs

Back 74

ECG axis deviation showing hypertrophy
Echocardiogram
X-ray
Catheterization
Stethoscope or phonocardiogram

Front 75

Persistent patent ductus

Back 75

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

Front 76

Interventricular Septal Defect

Back 76

Pan systolic murmur unless hole closes during contraction

Front 77

Interatrial Septal Defect

Back 77

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

Front 78

Tetrology of Fallot

Back 78

*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

Front 79

Causes of defects

Back 79

Commonly caused by exposure of the pregnant mother to viruses in the first trimester- esp. German measles
Can also be hereditary

Front 80

Shock

Back 80

Due to severely reduced C.O. (cardiogenic)
infarction
toxin release
valve dysfunction
Arrhythmias

Or reduced venous return
usually low blood volume (hypovolemic)
can be decreased vascular tone
or obstruction of flow

Front 81

Circulatory shock- inadequate C.O. to meet tissue needs.

causes

Back 81

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

Front 82

Compensated – non progressive

Back 82

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

Front 83

Progressive Shock - deteriorates

Back 83

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

Front 84

Acidosis in shock prevents glycolysis. Irreversible stage is postponed by Fructose 1,6 diphosphate.

Back 84

Glucose
Ø
Glucose 6-phosphate
Ø
Fructose 6-phosphate
Ø phosphofructokinase - blocked by acidosis
Fructose 1,6 diphosphate
System converts to anaerobic

Front 85

Loss of high energy phosphate reserves

Back 85

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

Front 86

Hypovolemic

Back 86

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

Front 87

Neurogenic shock

Back 87

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

Front 88

Anaphylactic Shock

Back 88

Antigen-antibody reaction releases histamine and causes vasodilation + cap. permeability increase – fluid into interstitium
drop in venous return
arteriole dilation
Therapy:
Sympathomimetic, glucocorticoids

Front 89

Septic shock - septicemia

Back 89

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

Front 90

tx for shock

Back 90

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