Unit 3 Flashcards
Cardiac output it determined mainly by ___________
Venous return
What are the factors that influence Venous return?
Body metabolism (local flow and autoregulation)
______ is a slow process of plaque formation where large quantities of cholesterol become deposited beneath the endothelium, scar tissue forms (fibrosis) and then calcifies (plaque)
Atherosclerosis
Partial or total blockage of coronary arteries leads to _______
Ischemia (lack of blood flow)
________ is a sudden process which occurs due to a thrombus or an embolus
Acute coronary occlusion
______ is a penetrating atherosclerotic plaque can cause a blood clot to form which quickly occludes an artery
Thrombus
** when this breaks away, it is then called an embolus
_______ is a thrombus that has broken loose for th site of origin and flows to another site where it lodges
Embolus
***leads to acute coronary occlusion
_________ is an attempt by the body to restore blood supply to ischemic tissue
Collateral circulation
During plaque formation, _______ may occur during plaque development
Angiogenesis
After _______ angiogenesis is too slow to restore blood flow acutely, however _______ of collateral vessels may resent some cardiac muscle death
After acute occlusion; vasodilation
Ischemic heart disease includes what 4 forms?
Angina pectoris
Coronary artery disease
Myocardial infarction
Sudden cardiac death
What does angina pectoris mean?
Chest pain
What are the types of angina pectoris?
Chronic stable angina
Unstable angina
______ is often a prelude to MI if not treated
Angina
_________ angina is where pain comes along during activity and is released at rest
Chronic stable angina
______ angina where chest pain comes and goes and doesnt seem to be related to anything
Unstable angina
Myocardial infarction results from an _________
Acute coronary occlusion
The muscle has ________ blood flow and the area affected ceases to function and may die during myocardial infarction SP’s
Little or no blood flow
Myocardial infarction most commonly affects the __________
Left ventricle
What are the causes of death due to MI
- decreased cardiac output
- pulmonary edema and kidney failure
- fibrillation
- cardiac rupture (rare)
Decreased CO can cause death due to MI when more than ______ of the left ventricle is infarcted (no blood flow) OR when _________ exacerbates the decrease in CO
40% of the left ventricle is infarcted
Systolic stretch exacerbates the decrease in CO
Pulmonary edema and kidney failure results from_____________ and can clean to death from an MI?
Result from the backlog of blood in the body’s venous system
______ is a chaotic pattern of contraction in the ventricles
Fibrillation
Fibrillation may result from:
- leakage of ______ from infarcted area
- formation of an _______
- _______ reflexes
- bulging weka muscle sets up __________
K+; injury current; sympathetic reflexes; circus movement
The anatomy of an infarcted is made up of a _____ area and a ____ area
Central area and peripheral area
Central area made up of _______
Peripheral area made up of ______
**anatomy of an infarct
Dead cardiac myocytes
Non-functional but living myocytes
Recovery from MI:
Dead fibers are replaced by _______
Nonfunctional fibers either ____ or ______ depending on if the color is dissolved or collateral circulation is adequate
Normal tissue ______ overtime to compensate for tissue loss
Scar tissue; die or recover; hypertrophies
What are some life style modifications for treatment for ischemic heart diseases?
Lose weight
eat a diet low in Saturated fat and cholesterol
Exercise
What are other treatments for ischemic heart diseases?
Nitroglycerin Beta blockers TPA (tissue plasminogen activator) Bypass surgery Angioplasty
What is the definition of congestive heart failure?
Failure of the heart to pump enough blood to satisfy the needs of the body
Heart failure is characterized by ________ and ______
Reduced cardiac output and damming up of the venous circulation
Heart failure is due to either ______ dysfunction or a _______ dysfunction
Systolic; diastolic
Which dysfunction is more common in congestive heart failure, systolic or diastolic?
Systolic dysfunction
________ is progressive loss of contractile funciton of the heart muscle
Systolic dysfunction
_________ is the inability of heart to expand to fil the ventricles properly
Diastolic dysfunction
Heart failure can also be classified as R or L sided. What are the 4 causes of left heart failure?
Ischemic heart disease
Hypertension
Valve diseases
Myocardial diseases
** these diseases cause left ventricle to hypertrophy and/ or dilate
What does left sided CHF lead to?
Pulmonary congestion and edema
Decreased renal perfusion leading to water and salt retention
What are the symptoms of a left sided CHF?
Dyspnea, orthopnea and cough
What are the causes of R heart failure?
Left sided heart failure Cor pulmonale (heart problem likely secondary to a lung problem, ex: cystic fibrosis)
Pure R sided heart failure leads to what 4 things?
Systemic and portal vein congestion
Hepatomegaly and splenomegaly
Peripheral edema
Kidney congestion leading to alter and salt retention
If the heart is not too damaged, the exces fluid retention actually helps CO by __________ (________ heart failure)
Increasing venous return
Compensated heart failure
If the heart is severely damaged, the excess fluid retention can overwhelm the heart and lead to __________
Severe edema and death
***decompensated heart
What are the characteristics of compensated heart failure?
CO will be normal
RA pressure is elevated
No further Na and H2O retention occurs
Over the ensuing weeks and months, Heath may recover
What are characteristics of decompensated Heart failure?
Excessive fluid retention
Overstretching of the heart (weakens it further)
Pulmoary edema
Renal failure
Renal contribution to progressive decompensated heart failure due to what 3 things?
The kidney need a minimum CO of 5 L/min for normal fluid balance
Decreased glomerular flatiron
ANH (atrial natiruretic hormone
________ hormone may slow the progression of heart failure
Atrial natriuretic hormone (ANH)
First heart sound of S! Is due to _______. Duration of _____ and more of a ___pitch
Closure of AV valves
Duration fo .14 sec
Lower pitch
2nd heart sound of S2 is due to closer of the ________ for a duration of _______ and _____ pitch
Closure of semilunar valves
1.1 seconds
Higher pitch
Third heart sound is during _______ and caused by _______. ______ frequency
During middle third of diastole
Caused by inrushing of bloo into ventricles
Low (may be audible
Fourth heart sound is during _______ and caused by ______. _______ frequency
During atrial systole
Caused by inrushing of blood
Very flow frequency
Aortic area - ______ intercostal space
Pulmonic area -_______ intercostal space
Erbs point -________ intercostal space
Tricuspid area - ______ intercostal space
Mitral area - _____ intercostal space at mid clavicular line
Aortic area- 2nd right Pulmonic area -2nd left Erbs point- 3rd left Tricuspid area- 5th left Mitral area- 5th intercostal space at mid clavicular line
What heart murmurs are heard during systole? (2)
Aortic stenosis
Mitral regurgitation
What heart murmurs are heard during diastole
Aortic regurgitation
Mitral stenosis
What heart murmur is heard throughout (continuous) diastole and systole?
Patent ductus arteriosus
________ is generalized inadequacy of blood flow throughout the body to the extent that the body tissues are damaged
Circulatory shock
What are the two cardinal features of circulatory shock?
Decrease in cardiac output
Decreased blood pressure
______ is self-perpetuating
Circulatory shock
What are the factors that affect Venous return?
Diminished blood volume
Decreased vascular tone
Venous obstruction
What causes lead to cardiogenic shock?
MI
Toxicity
Valve dysfunction
Arrhythmias
What are the three stages of shock?
Non-progressive stage (compensated stage)
Progressve stage
Irreversible stage
__________ stage of circulatory shock, the body’s own compensatory mechanisms will lead to recovery without outside help
Non-progressive (compensated stage)
________ stage of circulatory shock where shock becomes self-perpetuating until death; is reversible with treatment
Progressive stage
_______ stage of circulatory shock that is severe shock that is refractory to treatment
Irreversible stage
_________ shock is characterize by decreased systemic filling pressure and decreased venous return.
CO ad BP then also decrease
Hypovolumic/hemorrhagic shock
Non-progressive/compensated stage
- within 30 seconds: _________
- within 20min to 1 hr: ____, ____, _____
- within 1-48 hours: ______, _____
Within 30 sec: baraoreceptor reflex (SNS response)
Within 10 min to 1 hr: reverse stress-relaxation response, Renin-angiotensin system activation, ADH
Within 1-48 hrs: absorption of water from interstitial tissues, increased thirst
What is hallmark of progressive stage of circulatory shock?
Hallmarked by progressive deterioration of the cardiovascular system (positive feedback loops)
What are the features of the progressive stage of hypovolumic/ hemorrhagic shock?
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)
Describe the irreversible stage of hypovolumic/ hemorrhagic shock
Too much tissue damage
Too many destructive enzymes and toxins have been released
Too much acidosis
Depletion of high-energy phosphates in the body (creatine phosphate, ATP)
What are other forms of hypovolumic shock OTHER than hemorrhagic shock?
Intestinal obstruction
Severe burns
Dehydration (sweating, diarrhea, vomiting, nephrotic kidney disease)
What is the hallmark of neurogenic shock?
Hallmaked by an increased vascular capacity ( loss of vasomotor tone)
What are the causes of neurogenic shock?
Deep general anesthesia
Spinal anesthesia
Brain damage
_______ shock is an allergic response to an Ag in the circulation
(Due to a severe type 1 hypersensitivity reaction)
Anaphylactic
In ______ shock, basophils and mast cells release histamine which causes ______, _____ and _____
Anaphylactic
Venous dilation, arteriole dilation, increased capillary permeability
______ shock AKA blood poisoning that is causes by BLOOD BORNE bacterial infection in which the bacteria has been disseminated throughout the body
Septic shock
Damage during ______ shock is due to infection itself or due to bacterial ENDOTOXINS release
Septic shock
_______ shock has nothing to do with IgE, while ______ shock does
Septic shock; anaphylactic shock
______ shock features high fever, vasodilation, sludging of blood, disseminated intravascular coagulation
Septic
What are the treatments of shock? (5)
Blood or plasma transfusion Dextran Sympathomimetic drugs (epipen) Oxygen therapy Glucocorticoids
What are general characteristics of RBCs?
Lack nucleus, ER and mitochondria
Biconcave discs
Contains Hb
Contains carbonic anhydrase
Regulation of RBC is controlled by
Erythropoietin
Where is erythropoietin secreted from?
Kidneys
The kidneys secreted ________ in response to low oxygen levels in the blood
Erythropoietin
What are the factors that decrease oxygenation?
Low blood volume
Low Hb
Anemia
Poor blood flow pulmonary disease
______ carries oxygen and some CO2 in the blood
Hb
What is Hb composed of?
Heme and globin
Heme: iron containing protoporphyrin ring structure
Globin: polypeptide (alpha, beta or gamma delta
What are the most common type of Hb?
HbA-adult Hb- alpha2/Beta2
HbF- fetal Hb- alpha2/gamma2
Iron is absorbed from ______
GI tract
Iron binds to _______ to form transferrin
Aportrasnferrin
What is the function f transferin?
Carries iron in the blood
Iron is released to tissue which then bind to _____ to form ferritin
Apoferrin
______ is the storage form of iron in cells
Ferritin
When ferritin stores are maximized, a insoluble form of iron storage is ______
Hemosiderin
Iron is incorporated into ______
Heme
Iron loss occurs in what 3 things?
In feces
Bleeding
Menstrual loss
What is the average life span of RBCs?
120 days
Metabolism of RNC weakens so that: Cell membrane becomes \_\_\_\_\_\_\_ Membrane transport of ions \_\_\_\_ Heme iron goes into the\_\_\_\_\_\_ form \_\_\_\_\_\_ of proteins
Cell memabnr becomes less pliable
Membrane transport of ion decreases
Heme iron goes into the ferric form
Oxidation of proteins
RBCs rupture in the ______ or _______
Peripheral circulation
Especially in the spleen
Hb is broken down into _____ and ______ which then break down into _____ and ______
Heme and globin
Bilirubin and amino acids
What is the definition of anemia?
Deficiency of Hb
Classification based on RBC size. What are the different sizes?
Microcytic (MCV 80)
Macrocytic (MCV >100)
Normocytic (MCV 80-100)
Classifications based on Hb content: ______ and _____
Normochromic
Hypochromic
Low ______, _____ and _______ all indicate anemia
Red blood cell count
Hematocrit
Hemoglobin
________ indicates average cell size (microcytic, normocytic, macrocytic)
Mean corpuscular volume
______ and _______ indicates Hb content per cell (hypochromic, normochromic)
Mean corpuscular hemoglobin
mean corpuscular hemoglobin concentration
The completel blood count is useful but it cannot do what?
Detect abnormalities in shape of cells
What are the characteristics of cells in hemorrhagic anemia?
Normocytic
Normochromic
What are the characteristics in aplastic anemia
Generally normocytic
Normochromic
What are the characteristics of megaloblastic anemia’s?
Macrocytic, normochromic
What anemia is anemia of folate deficiency?
Megaloblastic anemia
What anemia is characteristic of anemia of B12 deficiency?
Megaloblastic anemia
What is characteristic of pernicious anemia?
Megaloblastic anemia
What are the characteristics of hemolytic anemia’s?
Normochromic, normocytic
Hereditary sperocytosis
Sickle cell anemia
Eyrthroblastosis
What are the characteristics of anemia of iron defiency?
Microcytic, hypochromic
What are symptoms common to anemia in general?
Fatigue
Weakness
Dizziness
Paleness of skin
In severe anemia what are the symptoms?
Fainting
Angina
Chest pain
Heart attack
_________ is high RBC count
Polycythemia
What is relative polycythemia?
Loss of fluid concentrates blood cells (intravascular volume depletion)
What is an absolute polycythemia?
Actual increase in RBC production
What is absolute primary polycythemia?
Defect involving bone marrow results in increase in red cell production
(Genetic)
Polycythemia Vera, primary congenital and familial polycythemia
What is secondary absolute polycythemia?
Consequence of hypoxia or other problem which leads to an actual increase in RBC production
______= prevention of blood loss
Hemostasis
What are the steps of hemostasis?
Vascular spasm
Platelet plug formation
Fibrin clot (coagulation)
Retraction
________ - constriction of blood vessels reduces the rate of blood loss
Vascular spasm
_______ is due to pain, vascular wall damage or thromboxane A2
Spasm
_________- activated platelets form a weak plug
Platelet plug formation
__________ - a series of clotting factors are involved in forming the clot
Fibrin clot formation (coagulation)
________- shrinking of the clot material to approximate edges of clot together
Retraction
Where are platelets formed and from what?
Formed in bone marrow
From megakaryocytes
Platelets contain _____ and ______ and store _____
Contain actin and myosin
Store calcium
What do platelets synthesize?
ATP, ADP Prostaglandins Fibrin stabilizing factor Thromboxane A2 Growth factors
Platelets have surface _____ that stick to exposed collagen
Glycoproteins
Primary hemostasis - ____________
Platelet plug formation
What are the events that occur when platelets encounter damaged blood vessel wall?
- Platelets swell and send out pseudopods that stick out to the vessel wall
- Contractile proteins contract to cause release of factors including ADP and thromboxane A2
- Newly activated platelets stick to the growing plug
______ and _______ activate other platelets and promote vascular spasm
ADP and thromboxane A2
Secondary hemostasis (_____, _____) platelet plugs are strengthened by the _________
Coagulation, clot formation
Clotting process
Clotting factors: I: \_\_\_\_\_\_\_ II:\_\_\_\_\_\_ III:\_\_\_\_\_\_\_\_\_ IV:\_\_\_\_\_\_\_\_ VIII:\_\_\_\_\_\_\_ XIII:\_\_\_\_\_\_
I: fibrinogen II: prothrombin III: tissue factor IV: calcium VIII: antihemophilia factor XIII: Fibrin stabilizing factor
The intrinsic and extrinsic pathways of the clotting cascade both end with ______
Prothrombin (factor 1) common pathway
What starts the extrinsic clotting cascade?
Tissue trauma leads to tissue factor production
How does the intrinsic clotting cascade begin?
Blood trauma or contact with collagen
The lower the concentration of clotting factors such as _______ the longer it takes for the blood to clot
Prothrombin
___________ is a test used to help detect and diagnose a bleeding disorder
Prothrombin time test
_________ can be used to monitor how well an anticoagulant medication is working to prevent blood clots
Prothrombin time test
___________- contraction of platelets tighten the clot and pull the edges of the wound together
Clot retraction
What are the preventions of unwanted clotting?
Intact blood vessel wall
Glycocalyx- repels platelet s and clotting factors
Thombomodulin
_______ inhibits thrombin and activates anticoagulant protein C which inturn inactivates factors ____ and ____
Thrombomodulin; V and VIII
________ purpose is to limit the size of the clot
Anticoagulant
What are examples of anticoagulants
Heparin
Antithrombin
______ binds with _______ which binds to thrombin
Heparin; antithrombin
__________ is released by damaged tissues over time as they heal
Plasminogen activator (tissue plasminogen activator, TPA)
________ converts plasminogen to plasmin when the concentraiton of the activator is great enough
TPA (plasminogen activator
_________ digests away the fibrin clot
Plasmin
_________ can be used o digest thrombi (abnormal clots)
Plasminogen activator
What clotting factors are affected by vitamin K deficiency?
Factors II, VII, IX and X
*** require within K for their synthesis by the liver
_______ is the source of many clotting factors
Liver
___________ is caused by inheritance of a faulty factor 8 gene. It is an ___ -linked trait
Hemophilia; X-linked trait
________ is a lack of platelets (______ rash= red sports visible on the skin)
Thrombocytopenia
Petechial rash
What are the 4 bleeding disorders?
Vitamin K deficiency
Liver damage/ disease
Hemophilia
Thrombocytopenia
_______ are abnormal clots that form on roughed endothelial surfaces (arteriosclerosis, infection, trauma)
Thrombi
_______ are thrombi that have broken loose from their attachment and may age lodge elsewhere in circulation
Embolus
Unwanted clots may be dissolved clinically by administering _________
Plasminogen activator
What are the factors affecting heart rate?
Autonomic innervation
Hormones
Fitness levels
Age
What are the factors affecting stroke volume?
Heart size Gender Contractility Duration of contraction Preload (EDV) Afterload (resistance)
CO will match VR via what 3 mechanisms?
Frank starling’s mechanism (effects force of contraction) Brainbridge reflex (effects rate of contraction) SA node stretch (effects rate of contraction)
The heart has a limit to the maximum CO it can achieve.
Normal (at rest) ________
Maximum _________
5 L/min
13 L/min
_______ demonstrates the effectiveness of cardiac function at different levels of RA pressure (which reflects _____)
Caridac output curve
VR
What causes a hypereffective heart?
Sympathetic sitmulation
Hypertrophy
What causes a hypo-effective heart?
Hypertension
Sympathetic inhibition
Any heart pathology
Pathologically LOW cardiac output can be due to ______ or _______ factors
Cardiac
Peripheral
What are the 4 cardiac factors that can lead to pathologically low caridac output?
Myocardial infarction
Severe valve disease
Myocarditis
Cardiac tamponade
What are the 4 peripheral factors that can lead to 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
In the venous return curve, that is the plateau due to?
Low atrial pressures leading to vein collapse
___________- the venous return becomes zero when the RA pressure rises to __________
Mean systemic filling pressure (both answers)
The steady ______ with changes in amount of sympathetic activity
RA pressure
_________ can be used to calculate CO
Flicks principle
Applying _______ by measuring oxygen uptake from the lungs and blood gas measurements
Ficks principle
In circulation during exercise, it is regulated locally via _______
Autoregulation
In circulation during exercise, regulation via the NS is controlled by ______ and ______
Sympathetic (norepinephrine) and adrenal (epinephrine)
Norepinephrine works via ______ receptors
Epinephrine works via ___ receptors
Alpha
Beta
Exercise results in mass __________
Sympathetic discharge
Mass sympathetic discharge during exercise results in what 3 things?
Increases HR and cardiac contractility
Arterioles are contracted all over the body (except coronary blood vessels and cerebral vessels)
Capacitance vessels and reservoirs contract to increase mean systemic filling pressure
Increase in arterial pressure during exercise is a result of what?
Mass sympathetic discharge
What are the 3 results of mass sympathetic discharge?
Increases HR and cardiac contractility
Arterioles are contracted all over the body except muscles that are working, coronary blood vessels and cerebral blood vessels
Capacitance vessels and reservoirs contract to increase mean systemic filling pressure
Who is more likely to have higher blood pressure, a stress induced individual or one in whole body exercise?
Stress induced individual would end up with higher blood pressure than whole body exercise because whole body exercise would result in vasodilation and stress induced will not compensate with vasodilation
What is the effect of rhythmic muscle contraction on blood flow?
When muscles are contracted you have less flow and when they are released you have more flow
Left coronary artery and branches- supplies the ______ and ________ portions of the left ventricle
Anterior and left lateral
Right coronary artery and branches- supplies most of the ___________ and _________ of the left ventricle
RV and posterior part of the left ventricle
Local autoregulation as determined by local muscle cells metabolism; most likely by _________ secretion in presence of low O2
Adenosine
Sympathetic coronary arteries contain mostly ________ receptors; therefore general tendency is ________
Beta androgenic
Vasodilation
Some pericardial arteries also contain _______ receptors, it is a thought that this helps to prevent backflow during heart exercise in the epicardial arteries
a1 (vasoconstrictor) receptors
What helps to prevent backflow during heavy exercise in the epicardial arteries?
Some epicardial arteries also contain a1 (vasoconstrictor) receptors
________- very little DIRECT innervation to coronary vessels
Parasympathetic
________ slows heart rate and contractility, autoregulation leads to ____________
Ach
Decreased blood flow
What is the structure of blood brain barrier?
Continuous capillaries
Astrocytes foot processes
Pericytes
__________ - endothelial cells have tight junctions and lack fenestrae, low amount of vesicular transport
Continuous capillaries
What is the function of blood brain barrier
Low permeability to most water soluble substances
Need special carrier systems to transport glucose, amino acids, etc.
_______ of the hearts energy is derived from fatty acids at rest
70%
Under anaerobic or ischemic conditions, the heart must rely more on _______.
Glucose/ glycolysis
ATP degrades to ADP-> AMP-> adenosine. ________ diffuses out of the caridac muscle cell and is a potent vasodilator
Adenosine
Excessive loss of adenosine can lead to _______
Cardiac muscle death
About ______ of the hearts adenosine can be lost in 30 min of ischemia
1/2