Unit 1 Cardiac physiology Flashcards
What is the number one cause of death
Cardiovascular disease
What are the major underlying cause of ischemia
Atherosclerosis
White Thrombus
Red Thrombus
Artery spasm
What pathway promotes thrombosis
Inflammatory pathways
What is thrombosis responsible for
Myocardial infarction
Strokes
What leads to atherogenesis
Blood cholesterol
What body system can modulate inflammation
The nervous system
What are the mechanisms in Hemostasis
Vascular spasm
Formation of platelet plug
Blood coagulation
Fibrous tissue growth
What causes Vascular constriction associated with traums
Neural reflexes
Local myogenic spasm
Local Humoral factors
What is responsible for the majority of the vascular constriction
Myogenic spasm
What type of vascular constriction is important in smaller vessels
Humoral factors (Thromboxane A2 from platelets)
What is released from platelets that causes vascular constriction
Thromboxane A2
What is found in the platelet cell membrane that initiates clotting
Thromboplastin
What happens when platelets contact a damaged area
1) Swell
2) move to surface
3) Granules release
4) Secrete ADP, Thromboxane A2
What is Thromboxane A2
Vasoconstrictor
Potentiates but not essential for granule release
What is the half life of platelets
8-12 days
What prevents platelet aggregation
Endothelium
What does the endothelium produce
PGI2 (procyclin) Factor VIII (Clotting)
What is Procyclin
Vasodilator
suppresses release platelet granules
Limits platelet extension
How does Aspirin and Ibuprofen work in the clotting cascade
Prevent the production of Thromboxane A2 and Prostacylin by blocking fatty acid cyclooxygenase
What do anticoagulants do
Prevents clots from forming
What causes lysis of clots
Plasmin (from plasminogen)
What are exogenous activators of plaminogen
Streptokinase
tPA
What is the reason tissues are damaged in an infarction
Reperfusion
What causes the damage in reperfusion
free radicals are generated when pressure on tissues are relieved and perused with blood
What is Collateralization
The ability to open up alternative routes of blood flow to compensate for a blocked vessel
What is the extrinsic mechanism in blood coagulation
Chemical factors released by damaged tissues
What is the intrinsic mechanism in blood coagulation
components in blood and trauma to blood or exposure to collagen
What chromosme is the hemophilia gene on
X
What clotting factor defect is most common in hemophilia cases
Factor VIII (85%) Factor IX (15%)
What clotting factors are made in the liver
I II VII IX X
What prevents the liver from making clotting factors
Warfarin
Cumadin
How does Warfarin and Cumadin prevent the liver from making clotting factors
By blocking action of Vitamin K
What is the key step in clotting
Conversion of Firbinogen to firbin
What is required to convert Fibrinogen to fibrin
Thrombin
What is Antiphospholipid antibody syndrome
An autoimmune disorder where the body makes antibodies against phospholipids in cell membranes (causes abnormal clotting)
What does Homocysteine do
Can irritate blood vessels –>Atherosclerosis
turn cholesterol into Oxidized LDL
Make blood more likely to clot
How can you reduce the amount of Homocysteine in blood
Increasing the intake of Folic Acid
What age are agglutinins produced
2-8 months
when do antibody titers in blood peak
age 10
What is the universal donor
O-
What is the universal acceptor
AB+
How can hemolysis cause kidney failure
Hemoglobin precipitates and blocks renal tubules
how many antigens are there in the Rh blood typing system
6
C D E
c d e
What is the most common and most antigenic antigen with respect to Rh+ blood
D antigen
What happens if someone is lacking the D antigen
they are Rh-
If you put Rh+ blood in a person with Rh- blood, how long does it take for the Rh antibodies to develop and cause Hemolysis
2-4 months
What is Erythroblastosis Fetalis
agglutination and hemolysis of the fetus’ RBC by the mothers anti Rh agglutinins
what do macrophages convert hemoglobin into
Bilirubin (Jaundice in Erythroblastosis Fetalis)
What is the most common cause of Erythroblastosis Fetalis
Mom = Rh- Dad = Rh+ Fetus = Rh+
When do symptoms of Erythroblastosis Fetalis occur
2nd (3%) and 3rd (10%) trimester of the pregnancy
After a child is born with Erythroblastosis Fetalis how long does it take for anemia to set in
1-2 months
What is caused when bilirubin precipitates into the brain during Erythroblastosis Fetalis
Mental impairment (Kernicterus)
What is the treatment for Erythroblastosis Fetalis
Replace neonates blood with Rh- blood
How can Erythroblastosis Fetalis be prevented
Rh immunoglobulin globulin administer to mother at 28 weeks gestation
what does Rh immunoglobulin globulin do
Suppress immune response to D antigen in fetal RBC’s that may cross placenta or enter moms circulation
What is another name for Erythroblastosis Fetalis
Hemolytic disease of the Newborn
How are heart muscles arragned
Striated, irregular columns with 1-2 centrally nuclei
What is the word used to describe the nature of heart muscles
Syncytium, they work together
How to heart muscles work together
Intercalated discs provide low resistance pathways
How long is the average action potential
.2 - .3 seconds
What happens to the ions during an action potential
Na+ increase during depol
Ca++ increase during plateau
K+ increase during repol
What happens to Na+ during cardiac action potential (depol + repol)
Depolarization: Increase
Repolarization: decrease
What happens to Ca++ during cardiac action potential (depol + repol)
Depolarization: Increase
Repolarization: Decrease
What happens to K+ during cardiac action potential (depol + repol)
Depolarization: Decrease
Repolarization: Increase
What are the fast channels in cardiac muscle
Na+
What are the slow channels in cardiac muscle
Ca++/Na+
What cardiac channels are operational during depolarization due to the SA node
Ca++/Na+ (slow channels)
What is the result of only having the slow channels (Ca++/Na+) open during depolarization
Depolarization time is increased
What causes passive ion movement across cells
Concentration gradient
Electrical gradient
Membrane permeability
When cardiac muscles are at rest what channels are open and what ones are closed
Closed: Na+ and Ca++/Na+
Open: K+
What happens to the contractile strength of cardiac muscle is the Na+/K+ pump is inhibited (Ca++ increases in cell)
Contraction strength increases
What is the ratio of Na+ to K+ that is pumped from the Na+/K+ pump
3 Na+ out
2 K+ in
Can cardiac muscle be stimulated during the absolute refractory period
no
Can cardiac muscle be stimulated during the Relative refractory period
Yes, it requires a supra-normal stimuls
When does the absolute refractory period occur
During plateau
When does the relative refractory period occur
During repolarization
What protects ventricles from supra-ventricular arrhythmias
Av node and Bundle
What is the pacemaker of the heart
the SA node
What channels does the SA node open
Slow (Ca++/Na+)
What is overdrive suppression
Drive a self-excitatory cell at a rate faster than its own inherent rate, suppressing its automaticity
What is it called when cells is excited faster than its inherent rate, suppressing its automaticity
Overdrive suppression
What happens to cycle length as heart rate increase
Cycle length decreases as HR increases
What is Systole
Isovolumetric Contraction
What is Distole
Isovolumetric Relaxation
at resting heart rate what is greater (in time) Systole or Distole
Distole
As HR increases what happens to Systole and Distole
Both shorten, Distole shortens more than Systole
What is EDV
End Diastolic volume (volume in ventricles at end of filling)
What is ESV
End Systolc volume (volume in ventricles at the end of ejection)
What is EDV-ESV
Stroke Volume (Volume ejected by ventricles)
What is the Ejection fraction
% of EDV ejected
What is a normal ejection fraction
50-60%
What are the different Artial Pressure waves
A wave
C wave
V wave
What is the A wave
Atrial contraction
What is the C wave
Ventricular contraction
What is the V wave
Atrial filling
How do valves function
Open with fwd pressure
Close with Bwd pressure
What are the two AV valves
Mitral
Tricuspid
What are the two semilunar valves
Aortic
Pulmonic
What valves have a strong construction
Semilunar valves
What is it called when a valve does not open fully
Stenotic
What is it called when a valve does not close fuly
Insufficient/leaky
What is it called when a valve makes vibrational noise
Murmurs
What is going on when there is a heart murmur during systolic phase
Aortic+pulmonry stenosis
or
Mirtral + Tricuspid insufficiency
What is going on when there is a heart murmur during diastoic phase
Aortic + pulmonary Insufficiency
or
Mirtal + tricuspid stenosis
What is the Law of Laplace
As ventricular radius increases, wall tension increases
What happens to the force of ventricular contraction when tension on ventricular walls increases
Contraction Force increases
If left ventricle is larger than the right, which ventricle will need to generate more tension to match the other
The left ventricle because it is larger and needs to fill more to generate the same tension
What is the problem with having large ventricles
The heart will need to consume more energy and oxygen in order to have a strong contraction
What does Chronotropic mean
Anything that affects heart rate
What is Dromotropic
Anything that affects conduction velocity
What in Inotropic
Anything that affects strength of contraction
What is Frank-Starlings law of the heart
The heart will pump all the blood that returns to it without allowing excessive damming of blood in veins
An increase in venous return causes an increase in what
Stretch of cardiac muscle fibers (increase Contraction force, and HR)
Stretching of the SA node will cause what
An increase of Ca++ and or Na+ permeability, thus increasing HR
What are some extrinsic influences on Cardiac muscle
Autonomic nervous system
Hormonal influences
Ionic influences
Temperature influences
What does the sympathetic NS do to the heart
Increase HR
Increase contraction str
Increase conduction velocity
What does the parasympathetic NS do the the heart
Decrease HR
Decrease contraction Str
Decrease conduction velocity
What is used to block SNS effects on the heart
Propranolol (Beta blocker)
What is used to block parasymp NS effects on the heart
Atrpoine (blocks muscarinic receptors)
What happens when the Parasym NS is blocked by Atrpoine
HR increase
Decreased contraction Str
Parasympathetic NS exerts what type of effect on the heart
Dominate inhibitory influence on HR
Sympathetic NS exerts what type of effect on the heart
Dominate stimulatory influence on contraction Str
Direct SNS influence on the heart uses what hormone. What percent of SNS influence is direct
Norepinephrine
85%
Indirect SNS influence on the heart used what hormone. What percent of SNS influence is indirect
Epinephrine and Norepinephrine from adrenal medulla
15%
If the SNS stimulates the left stellate ganglion, what is the result
Decreased Ventricular fibrillation threshold
Prolongation of QT interval
is the SNS stimulates the right stellate ganglion what is the result
Increased ventricular firbeilation threshold
What is the brainbridge reflex
Stretch on atrial wall + stretch receotors send signals to Medulla and increase SNS outflow
What is the Benzold-Jarisch reflex
Barroreceptors in LV send info to CNS via CN X due to occlusion of artery. Increase in LVP and LV volume
What do thyroid hormones do to the heart
Increase Inotropic
Increase Chronotropic
Increase COs by increasing BMR
What happens if K+ is elevated (2-3x normal)
Dilation and flaccidity of cardiac muscle
Decrease resting membrane potential
What happens if Ca++ is elevated
Spastic contrations
How are HR and body temp related
HR increases ~10 beats per 1 degree F in body temp
What happens to the contractile str when body temp increases
It will increase temporarily, but prolonged fever can decrease contractile str (exhaustion)
What happens to HR when body temp drops
Decreased HR and contraction STR
How much energy the heart utilizes is converted into heat
75%
if 75% of the energy the heart uses why is the rest of the energy used for
99% of the 25% is for pressurization of blood
1% of the 25% is for acceleration of blood
What does an EKG measure
Potential difference across the surface of the myocardium with respect to time
What is a normal HR
between 60-80
What is a Tachycardia
High HR (over 100)
What is a Bradycardia
Low HR (under 50)
What are the different intervals in a EKG
PR interval
P wave
QRS
T wave
What is the PR interval
the AV node Delay
What is the P wave on a EKG
Atrial depolarization
What is the QRS complex on a EKG
Ventricular depolarization
What is the T wave on a EKG
Ventricular depolarization
Where is atrial repolarization in an EKG
It is hidden in the QRS complex
On an EKG what node is the active electrode and what one is the reference
+ is Active
- is reference
What is a first degree AV block
Depolarization wave from atria to ventricle is delayed
What is a second degree AV block
Some depolarization wave pass other blocked (Dropped P wave with no QRS)
What is a third degree AV block
All depolarization waves from atria are blocked, no relation between P and QRS
How can you tell if there is hypertrophy in an EKG
Prolonged QRS
Axis deviation to side of problem
increased voltage in QRS
What happens to the myocardial blood flow during contraction
Blood flow become limited
During a contraction what heart chamber has the most impaired myocardial blood flow
Left ventrical
What does left coronary flow peak
at the onset of diastole
How much oxygen is taken from the blood by the myocardium at rest
70%
What direction are depolarization and repolarization in relation to eachother
Opposite
What does ischemia do to depolarization and repolarization
Prolongs Depolarization
Delays repolarization
What does the T wave look like in a EKG of someone who has ischemia
The T wave inverts from normal (opposite to direction of the ventricular depolarization)
What happens to cells in an infarction
Cell are no longer able to repolarize
What happens to the EKG when a patient has an infarction
Depressed baseline which appears an an elevated ST segment
What a preferred blood markers for myocardial injury
Troponins T and I
what is troponin
a contractile protein not found in serum
