Unit 3 Flashcards
Cardiac output is determined mainly by
Venous return
CO= VR (Also CO = SV X HR)
SV = stoke volume HR = heart rate
Factors that influence VR
Body metabolism (local flow and autoregulation) - VR is a summation of all local blood flows
Age
Body size
Gender (heart size)
Factors affecting heart rate
Autonomic innervation
Hormones
Fitness levels
Age
Factors affecting stroke volume
Heart size Fitness levels Gender Contractility Duration of contraction Preload (EVD) Afterload (resistance)
Stroke volume =
SV = EVD - ESV
Cardiac index increases from age ___-___
It decreases after age
0 - 10ish
10ish
CO will match VR via the following mechanisms:
Frank sterling’s mechanism (effects force of contraction) Bainbridge Reflex (effects rate of contraction) SA node stretch (effects rate of contraction)
Normal CO limit (at rest)
5 L/min
Maximum CO it can achieve
13 L/min
Cardiac output curve demonstrates:
The effectiveness of cardiac function at different levels of right atrial pressure (which reflects venous return)
Hyper-effective heart causes (More than normal amount of CO)
Sympathetic stimulation
Hypertrophy
Hypo-effective heart causes (less than normal amount of CO)
Hypertension
Sympathetic inhibition
Any heart pathology
Factors that decrease peripheral resistance
These can cause:
Beriberi (Thiamin deficiency)
Arteriorvenous fistula
Hyperthyroidism
Anemia
Cause pathologically HIGH cardiac output
Abnormal connection between an artery and vein
Arteriovenous fistula
Inability to hold O2 in the blood
Anemia
Too much fluid in the cardiac sac
Cardiac tamponade
Cardiac factors that can cause pathologically low CO
Myocardial infarction
Severe valve disease
Myocarditis
Cardiac tamponade
Peripheral factors cause it pathologically low CO
Decreased blood volume (hypovolemia)
Acute venous dilation (SNS suppression)
Large vein obstruction
Decreased metabolic rate of tissues (hypothyroidism)
When cardiac output falls too low, it is called:
Circulatory shock
Venous return curve plateau is due to
Low atrial pressures leading to vein collapse
The higher the right atrial pressure, the _____ venous return will be
Less
Venous return curve- mean systemic filling pressure
The venous return becomes 0 when the right atrial pressure rises to mean systemic filling pressure
If first atrial pressure is in the negatives, what happens to venous return
Increases until it gets to plateau
What happens to CO when sympathetic stimulation increases
It increases as right atrial pressure increases
What happens to CO and VR curves during exercise? What happens to right atrial pressure?
Increase
Does not really change—- should never really change!!!!
If resistance increases, what happens to VR?
It decreases
What happens to VR if systemic filling pressure (Psf) increases?
It increases
Normal systemic filling pressure
7
2 ways to increase delivery (X) of a substance
Fick’s Principle
1- increase it’s concentration [x]
2- increase flow into a tissue (Q)
Equation of Fick’s principle
X = Q [x]
X = delivery
Q = flow into a tissue
[x] = concentration
Just know what calculation is for, don’t worry about the math
What does Fick’s principle calculate?
Cardiac output by solving for Q
Q = X/[x]
[x] can be measured by [x]art - [x]vein
How can you apply Fick’s principle?
By measuring oxygen uptake from the lungs, and blood gas measurements
If a tissue is metabolically active, it will have an increase demand for”
Oxygen
Most important determinant for how much blood flow is needed in a spot
Local-autoregulation
To maintain blood pressure when tissues require a lot of blood, ________ system steps in to help. Why?
Nervous
To increase heart rate via sympathetic NS (norepinephrine)
Sympathetic (norepinephrine) uses ______ receptors.
Which so adrenal (epinephrine) use?
Alpha
Beta
Mass sympathetic discharge increases:
HR and cardiac contractility
In mass sympathetic discharge, what happens to arterioles
They are contracted all over the body except muscles that are working, coronary blood vessels, and cerebral blood vessels
During mass sympathetic discharge, what happens to capacitance vessels and reservoirs?
They contract to increase mean systemic filling pressure
a result of mass sympathetic discharge
Increase in arterial pressure
What can cause increase in anterior pressure? (AKA BP)
Which causes higher BP?
Stress
Whole body exercises.
Stress— there is little muscle activity so there is no vasaodilation, so higher BP
Increase arterial pressure increases:
Blood flow directly and indirectly (stress-relaxation of arteries decreases peripheral resistance.)
Average blood flow at rest
3-4 ml/min/100g of muscle tissue
When skeletal muscle contracts, what happens?
Muscles shorten and widen. They squish the blood vessels.
This causes the blood flow go down
Average blood flow during exercise
50-80 ml/min/100g of muscle tissue
Left coronary artery and branches supply
The anterior and left lateral portions of the left ventricle
Right coronary artery and branches supplies
Most of the right ventricle and posterior part of the left ventricle
During systole, coronary blood flow (INCREASES/DECREASES)
What about diastole?
Systole decreases
Diastole increases
Blood vessels on outside of the heart.
Epicardial coronary arteries
Cardiac arteries within the heart that cannot be seen on the outside
Subendocardial arteries
What arteries in the heart are affected more by the “squish” effect? Impacted more by pressure
Subendocardial arteries
Local autoregulation of coronary blood flow is determined by
Local muscle cells’ metabolism; most likely by adenosine secretion in presence of low O2
Some epicardial arteries contain ______ receptors. Why?
Alpha 1 vasoconstrictor receptors
Thought to help prevent backflow during heavy exercise in the epicardial arteries
Coronary mostly contain _________ receptors
Beta2 adrenergic receptors, so general tendency is vasodilation
Parasympathetic coronary innervation
Very little direct innervation.
Though since Ach slows heart rate, autoregulation leads to decreased blood flow
Structure of the blood brain barrier
Continuous capillaries- endothelial cells with tight junctions and lack fenestrae - low amount of vesicular transport
Astrocyte foot processes
Pericytes
Function of the blood brain barrier
Low permeability to most water soluble substances
Blood brain barrier needs special carrier systems to transport:
Glucose, amino acids, etc
% of the hearts energy is derived from fatty acids at rest
70
When must the heart rely more on glucose/glycolysis? What can this cause?
Under anaerobic or ischemic conditions.
Results in lactic acid which can cause pain
How is adenosine made? What happens with this in the cardiac cell?
ATP degrades to ADP -> AMP -> Adenosine
Diffuses out of the cardiac muscle cell and is a potent vasodilator
Excessive loss of adenosine can lead to:
Cardiac muscle death
About 1/2 of the heart’s adenosine can be lost in”
30 min of ischemia
A slow process of plaque formation
Artherosclerosis
In artherosclerosis, what happens to cholesterol
Large quantities become deposited beneath the endothelium, scar tissue forms (fibrosis), then calcifies (plaque)
Partial or total blockage of coronary arteries leads to:
Ischemia
A sudden process with Thrombus and/or embolus
Acute coronary occlusion
A penetrating artherosclerotic plaque that can cause a blood clot to form which quickly occluded an artery
Thrombus
A thrombus that has broken loose from the site of origin and flows to another site where it lodges
Embolus
Congestive heart failure
Failure of the heart to pump enough blood to satisfy the needs of the body
Heart failure is characterized by:
A reduced cardiac output and damming up of the venous circulation
Heart failure is due to:
Either systolic OR diastolic dysfunction
Progressive loss of contractile function of the heart muscle.
Systolic dysfunction
Inability of heart to expand enough to fill the ventricles properly
Diastolic dysfunction
Which congestive heart failure is more common
Systolic dysfunction
Heart failure care also be classified as:
Left sided or right sided
Causes of left heart failure:
These cause:
Ischemic heart disease
Hypertension
Valve diseases
Myocardial diseases
This cause the left ventricle to hypertrophy and/or dilate
Left sided CHF leads to:
Pulmonary congestion and edema
Decreased renal perfusion leading to water and salt retention
Symptoms of CHF
Dyspnea (feeling of not getting enough air)
Orthopnea (Breathing effected differently depending on different positions)
Cough
Causes of right sided heart failure
Left sided heart failure
Cor pulmonale (heart problem secondary to a lung problem. So lungs started this, like cystic fibrosis)
Pure right sided heart failure leads to
Systemic and portal vein congestion
Hepatomegaly and spenomegaly
Peripheral edema
Kidney congestion leading to water and salt retention
What happens to a patient in severe CHF
The pt will manifest with both right and left heart failure symptoms
Acutely damaged heart, CO output at 4mmHg right atrial pressure
2ish l/min
If the heart is not too damaged from CHF, whaat happens to the excess fluid retention
It actually helps cardiac output by increasing venous return. (Compensated heart failure)
What happens w/ excess fluid in a heart severely damaged by CHF
Retention can overwhelm the heart and lead to severe edema and death (decompensated heart failure)
Aspects of compensated heart failure
CO will be normal
Right atrial pressure is ELEVATED
NO further renal salt and water retention occurs
Heart MAY recover over weeks and months
Aspects of decompensated heart failure
Excessive fluid retention
Overstretching of the heart (weakens it further)
Pulmonary edema (w/ decreased oxygenation)
Renal failure
Right atrial pressure at critical cardiac output level for normal fluid balance
This indicates decompensated heart disease.
5-11 mm Hg
Caused by fluid retention raising the rt atrial pressure over a period of days
The kidney needs a min CO of ______ L/min for normal fluid balance
5
Renal contribution to progressive decompensated heart failure:
Decreased _____ _____
Activation of:
Decreased glomerular filtration
Activation of renin angiotensin-aldosterone system
What hormone may slow the progression of heart failure
Atrial natriuretic hormone
Max percentage that the CO can increase above the normal level
Cardiac reserve
Cardiac reserve for normal adult
300-400%
Cardiac reserve for athlete
500-600%
Cardiac reserve for moderate coronary artery disease
150-200%
Cardiac reserve for compensated heart failure
As little as 0%
Cardiac reserve for decompensated heart failure
Less than 0%
1st heart sound (__)
Closure
Duration
Pitch
S1 Closure of AV valves Duration of .14 seconds Lower pitch “Lub”
2nd heart sound (__)
Closure
Duration
Pitch
S2
Closure of semilunar valves
.11 seconds
Higher pitch
“Dub”
3rd heart sounds
Happens during:
Caused by:
Frequency
During middle third of diastole Caused by inrushing of blood into ventricles Low frequency (may be audible)
4th heart sound
During:
Caused by:
frequency:
During atrial systole
Caused by inrushing of blood
Very low frequency—- very unlikely to hear without any machines
Range of sounds that can be heard is between:
This is in relation to:
40-520 cycles/second
Threshold of audibility
Where is auscultation of aortic area checked?
2nd rt intercostal space
Where is auscultation of pulmonic area checked?
2nd left intercostal space
Where is auscultation of Erb’s point checked?
3rd left intercostal space
Where is auscultation of tricuspid area checked?
5th left intercostal space
Where is auscultation of mitral area checked?
5th intercostal space at mid-clavicular line
Erb’s Point
Spot to hear the best sounds.
Aortic Murmur heard during systole
Aortic stenosis
Aortic Murmur heard during diastole
Aortic regurgitation
Mitral Murmur heard during systole
Mitral regurgitation
Mitral murmur heard during diastole
Mitral stenosis
Type of murmur that is continuous, although louder during systole
Patent ductus arteriosus
Circulatory shock
Generalized inadequacy of blood flow throughout the body to the extent that the body tissues are damaged
Cardinal features of circulatory shock inculde:
Decrease in CO
Decrease in BP
In circulatory shock, body tissues, including the CV system, begin to:
Deteriorate leading to death within hours or days.
it is self perpetuating
Causes of circulatory shock via cardiogenic shock
MI
Toxicity
Valve dysfunction
Arrhythmias
Something is wrong with the heart
Factors that decrease venous return, causing circulatory shock
Diminished blood volume
Decreased vascular tone
Venous obstruction
Stages of circulatory shock
Non-progressive
Progressive
Irreversible
Non-progressive stage of circulatory shock
Compensated stage- where the body’s own compensatory mechanisms will lead to recovery without outside help
Progressive stage of circulatory shock
Where shock becomes self-perpetuating until death- is reversible with treatment
Irreversible stage of circulatory shock
Severe shock that is refractory to treatment
Types of circulatory shock
Hypovolumic / hemorrhagic shock
Neurogenic shock
Anaphylactic shock
Septic shock
Shock characterized by decreased systemic filling pressure and therefore decreased venous return. CO and BP then also decrease
Hypovolumic/hemorrhagic shock
Hypovolumic/hemorrhagic shock- Non-progressive/compensated stage
What happens at 30 sec?
10 min-1hr?
1-48 hours?
30 sec- Baroreceptor reflexes (increase SNS response)
Within 10 min to 1 hour- Reverse stress-relaxation response
Renin-angiotensin system activation
Vasopressin (ADH)
Within 1-48 hrs- Absorption of water from interstitial spaces
Increased thirst.
Progressive stage of hypovolumic/hemorrhagic shock
Hallmarked by progressive deterioration of the CV system (positive feedback loops)
Progressive stage of hypovolumic/hemorrhagic shock features:
Cardiac depression Vasomotor failure (CNS depression) Blockage of small vessels “slugged blood” Increased capillary permeability (late) Release of toxins Cellular deterioration Acidosis (carbonic and lactic acid)
Review slide 64
Review slide 64
Irreversible stage of hypovolumic/hemorrhagic shock:
Too much tissue damage
Too many destructive enzymes and toxins have been released into the tissues
Too much acidosis
Depletion of high-energy phosphates in the body (creatine phosphate, ATP)
Other former of hypovolumic shock other than hemorrhagic
Intestinal obstruction
Severe burns
Dehydration (sweating, diarrhea, vomiting, nephrotic kidney disease)
Neurogenic shock-
Hallmarked by:
Causes
Hallmarked bu an increased vascular capacity (loss of vasomotor tone)
Causes- Deep general anesthesia
Spinal anesthesia
Brain damage
Shock caused by an allergic response to an antigen in the circulation
Anaphylactic shock
In anaphylactic shock, basophils and mast cells release:
This causes:
Histamine
Venous dilation
Arteriole dilation
Increased capillary permeability
Blood poisoning, AKA
Septic shock
Septic shock is caused by
A blood borne bacterial infection in which the bacteria has been disseminated throughout the body
Damage of septic shock is due to
Infection itself, or due to bacterial endotoxin release
Features of septic shock
High fever,
Vasodilation
Sludging of blood
Disseminated intravascular coagulation
Treatment of shock
Blood or plasma transfusion
Dextran
Sympathomimetic drugs
Oxygen therapy
Glucocorticoids
RBC, AKA
Erythrocytes
RBC lack:
Nucleus, ER, mitochondria
Size of RBS
8 micrometers in diameter
They are biconcave discs
Concentration of RBC in the blood
Approx 5 million/cc
RBC contains
Hemoglobin (O2 transport. And buffer)
And
Carbonic anhydrase
Process of making blood cells
Hematopoietic
Hematopoiesis takes place:
Bone marrow at birth- mostly axial skeleton
Hematopoeisis involves what cell types?
PHSC cells (Pluripotent hematopoietic stem cells)
CFU-S (Colony-forming unit-spleen)- (Myeloid stem cell)
LSC (lymphoid stem cell)
CFU-S cells can form
CFU-GM
CFU-B/CFU-E
CFU-M
LSC cells can form
T lymphocytes and
B lymphocyte
Genesis of RBC:
Proerythroblast
Reticulocyte
Erythrocytes
For regulation of RBC production, ______ is secreted by __________ in response to low O2 levels in the blood
Erythropoietin (EPO)
Kidneys
EPO stimulates:
EBC production in the bone marrow
Factors that decrease oxygenation
Low blood volume Anemia Low hemoglobin Poor blood glow Pulmonary disease
Hemoglobin composition
Heme- Iron containing protoporphyrin ring structure
Globin- Polypeptide, alpha, beta, gamma or delta
Most common types of hemoglobin
HbA - Adult Hg = Alpha2/beta2
HbF- Fetal Hb- Alpha2/Gamma2
Iron is absorbed from the:
GI tract
Iron binds to ________ to form:
Apotransferrin
Forms transferrin which carries the ion in the blood
Iron, leased to tissues, will bind to ______ to form:
Apoferritin
Forms ferritin which is the storage form of iron in cells
What happens when ferritin stores are maximized
An insoluble form of iron storage is hemosiderin
Iron excreted from plasma daily
0.6 mg
Amount of iron lost daily in menses
0.7 mg Fe
Dead hemoglobin enters _______
What happens here?
What is excreted?
Macrophages
Hemoglobin is degraded, free iron is released
Bilirubin is excreted
How is iron lost
In feces
Bleeding
Menstrual loss
Avg RBC life span
120 days
Why does the metabolism of RBS weaken?
So that: Cell membrane becomes less pliable Membrane transport of ions decreases Heme iron goes into the ferric form Oxidation of proteins
RBCs rupture where?
In the peripheral circulation, or especially in the spleen
What phagocytoses damaged RBC?
Kupffer cells
Hemoglobin is broken down into ____ and _____ which then break down into _____ and _______
Heme
Globin
Bilirubin
amino acids
Deficiency of hemoglobin
Anemia
Classification of anemia is based on
RBC size (Normocytic, Macrocytic, microcytic)
Anemia classification if based on
Hemoglobin content
Normochromic
Hypochromic
CBC, AKA
Complete blood count
What aspects of the CBC indicate anemia?
Low RBC, HCT (hematocrit), and HGB
MCV in CBC indicates
Average cell size
MCHC and MCH indicates
Hemoglobin content per cell
Problem with CBC
It cannot detect abnormalities in shape of cells
Types of anemia’s
Hemorrhagic
Aplastic
Megablastic
Cbl, aka cobalamin =
B12
Hemorrhagic anemia
Had a bleeding episode, so anemic until you have a transfusion or make new RBC
Blood cells lost- normocytic and normochromic
Aplastic anemia
Bone marrow not growing RBC- could be genetic, a drug that kills the bone marrow, etc
Generally normocytic and normochronic
Megaloblastic anemias
Macrocytic, normochromic
Anemia of folate deficiency
Or
Anemia of B12 deficiency
Pernicious anemia
Anemia B12 deficiency with special mechanism
Pernicious anemia
B12 and HC come together to bind,_______ is resp to transport the B12 into the blood
Intrinsic factor (IF)
An autoimmune disease keeping us from making intrinsic factor (IF), making it difficult to absorb B12
Pernicious anemia
Hemolytic anemia’s
Normocytic, normochromic
Shorter lifespan, so lose them faster
Hereditary spherocytosis
Sickly cell anemia
Erythroblastosis fetalis
Anemia of iron deficiency
Microcytic, hypochromic
Abnormal hemoglobin, causing Hemoglobin S
Shapes distorts in absence of O2`
Sickle cell anemia
Erythroblastosis fetalis
Mother with Rh- blood type with an Rh+ blood type baby. No problem bc moms blood and babies blood don’t mix.
When baby is born and placenta bleeds into the uterine wall. Some of the blood comes in contact with the moms immune system. Causes her to make anti-Rh antibodies.
Antibodies can cross the placenta and attack another baby
Hereditary sperocytosis
Non spheared blood cells
Symptoms of general anemia
Fatigue
Weakness
Dizziness
Paleness of skin
High RBC count
Polycythemia
What is real active to polycythemia
Intravascular volume depletion
- loss of fluid concentrates blood cells
Absolute polycythemia
Actual increase in RBC production
Primary polycythemia
Genetic defect involving bone barrow
Secondary polycythemia
Consequence of hypoxia, drugs, high altitude, sleep apnea, COPD, etc
2 most important blood groups antigens
ABO blood group- possible blood types
Rh (rhesus blood group)- gene located on chromosome 1
What happens if wrong blood types are mixed
An immune reaction takes place
During early childhood, we make antibodies against:
Gut bacteria that have similar antigens to the A and B, unless they are present on your own blood (self vs non-self principle)
So, type A RBC have antibodies against
B types
People only make anti-rh antibodies if:
They are Rh negative and they are exposed to Rh positive blood in their life.
Review slide 94 chart
Review slide 94
Most common blood type
O+
Rarest blood type
AB-
Hemostasis =
Prevention of blood loss
Steps of hemostasis
Vascular spasm
Platelet plug formation
Fibrin clot formation
Retraction
Vascular spasm
Constriction of blood vessels reducing the rate of blood loss.
What can cause vascular spasm?
Pain, vascular wall damage, or thrombocytes A2
Platelet plug formation
Activated platelets forming a weak plug
Fibrin clot formation (coagulation)
A series of clotting factors are involved in forming a clot
Retraction in homeostasis
“Shrinking” of a clot material to approximate edges of would together
Platelets are formed where?
In bone marrow from megakaryocytes
What do platelets contain?
Actin and myosin
What do platelets store?
Calcium
Platelets synthesize:
ATP, ADP, prostaglandins, fibrin-stabilizing factor, thrombocytes A2, and growth factors
Platelets have _____ ______ that stick to exposed ______
Surface glycoproteins
Collagen
Lifespan of platelets
12 days
Primary hemostasis-
Platelet plug formation
What happens when platelets encounter damaged blood vessel wall?
Platelets swell and send out pseudopods that stick to the vessel wall
After platelets swell and send out pseudopods that stick to the vessel wall, what happens?
Contractile proteins contract
This causes release of factors including ADP and thromboxane A2; these factors activate other platelets, and promote vascular spasm
What happens to newly activated platelets
They stick to the growing plug
Secondary hemostasis
Coagulation, clot formation
Platelet plugs are strengthened by the clotting process
Clotting factors for 2ndary hemostasis
1- Fibrinogen 2- prothrombin 3- Tissue factor 4- Calcium 5- label factor 6- obsolete factor 7- stable factor 8- anti-hemophilia factor 9- Christmas factor 10- Stuart-prower factor 11- Plasma thromboplastin 12- Hangeman Factor 12- Fibrin stabilizing factor
Hemostasis clotting cascade
Intrinsic and extrinsic pathways ——> common pathway
Final common pathway for clotting
Prothrombin
Activated by prothrombin activator
Ends with cross-linked fibrin fibers
Extrinsic pathway for clotting
Tissue trauma -> Tissue factor -> prothrombin activator
See slide 103
Slide 103
Review slide 104
Slide 104
Prothrombin time states:
The lower the concentration of clotting factors such as prothrombin, the longer it takes for blood to clot
What test is used to help detect and diagnose a bleeding disorder?
Prothrombin Time (PT)
Prothrombin time test can also be used to monitor:
How well an anticoagulation medication is working to prevent blood clots
Contraction of platelets tighten the clot and pull the edges of the wound together
Clot retraction
What are ways to prevent unwanted clotting?
Keeping an intact blood vessel wall
Glycocalyx
Thrombomodulin
What effect does glycocalyx have?
It repels platelets and clotting factors
What effect does thrombomodulin have?
Inhibits thrombin
Activated the anticoagulant “protein C” which in turn inactivates factors V and VIII
Purpose of anticoagulants
To limit the size of the clot
Types of anticoagulants
Heparin
Antithrombin
What does heparin bind with
Antithrombin
What does antithrombin bind with
Thrombin
What is heparin used in surgery for?
To prevent blood clots
Lysis of blood clots is done by
Plasminogen activator (tissue plasminogen activator, TPA)
Plasminogen activator is released by what?
By damaged tissues over time as they heal
Plasminogen activator converts _____ to _____.
When?
Plasminogen
Plasmin
When the concentration of the activator is great enough
What does plasmin digest?
Fibrin clot
Plasminogen can be used to:
Digest thrombi (abnormal clots)
Bleeding disorders
Vitamin K deficiency
Liver damage/disease
Hemophilia
thrombocytopenia
Factors that need vitamin K for their synthesis by the liver
Factors II, VII, IX, and X
What is the source of many clotting factors?
The liver
What causes hemophilia?
Inheritance of a faulty factor VIII gene.
It is an X-Linked trait
Lack of platelets (petechial rash = red spots visible on the skin)
Thrombocytopenia
Abnormal clots that form on roughened endothelial surfaces (atherosclerosis, infection, trauma)
Thrombi
Thrombi that have broken loose from their attachment and may large elsewhere in the circulation
Emboli
Unwanted clots may be dissolved clinically how?
By administering plasminogen activator
Nerves used for circulation regulation
Sympathetic (norepinephrine)
Adrenal (epinephrine)
Attempt by the body to restore blood supply to ischemic tissue
Collateral circulation
What happens in collateral. Circulation during plaque formation?
Angiogenesis may occur
What happens after acute occulsion of the collateral circulation?
Angiogenesis is too slow to restore blood flow acutely,
However, vasodilation os collateral vessels may prevent some cardiac muscle death
Ischemic heat disease includes:
Angina pectoris
Coronary artery disease
Myocardial infarction
Sudden cardiac death
Chest pain
Angina pectoris
2 types of angina
Chronic stable angina
Unstable angina
Angina is often a prelude to _____ if not treated
MI
Myocardial infarction results from
An acute coronary occlusion- muscle has little or no blood flow
What happens to the affected area of a MI?
It ceases to function and may die
MI most commonly affects what part of the heart?
Left ventricle
Causes of death due to MI:
Decreased cardiac output
Pulmonary edema and kidney failure
Fibrillation
Cardiac rupture
Decreased CO usually occurs when?
When more than 40% of the left ventricle is infarcted
Systolic stretch exacerbates the decrease in:
CO
How does MI cause pulmonary edema and kidney failure?
Results from the backlog of blood in the body’s venous system
Fibrillation may result from:
Leakage of K+ from infarcted area
Formation of an “injury current” (ischemic muscle cannot repolarize effectively)
Sympathetic reflexes
Bulging weak muscle sets up “circus movements”
Cardiac rupture happens (OFTEN/RARELY)
Rarely
An infarct area of the heart has a central area of:
And a peripheral area of:
Dead cardiac myocytes
Non-functional but living myocytes
Dead fibers from MI are replaced by what?
Scar tissue
What happens to nonfunctional fibers after recovery of MI?
They either die, or recover (if reversible) when clot is dissolved, or collateral circulation is adequate
What happens to scar tissue on the affected MI area over time?
It retracts (shrinks)
Normal tissue hypertrophied over time to compensate for tissue lost
Lifestyle treatments for ischemic heart disease
Lose weight
Eat a diet low in saturated fat and cholesterol
Exercise
Other treatments for ischemic heart diseases
Nitroglycerin (vasodilator)
Beta blockers
TPA (tissue plasminogen activator)
Bypass surgery
Angioplasty