Cardiac Physiology Flashcards
Which disease is the # 1 cause of death?
Cardiovascular Disease
Major underlying cause of ischemia I due to:
Atheroscerosis (plaquing)
Artery Spasm
Causes of Inflamation
High blood cholesterol (dyslipidemia)
recruitment &expression of pro-inflammatory cytokines
Inflammatory pathways promote:
Thrombosis
Thrombosis is responsible for:
MI & most strokes
The Nervous System can modulate
Inflammation
Hemostasis is:
Prevention of blood loss
Mechanisms of hemostasis:
Vascular Spasm
Formation of platelet plug
Blood coagulation
Fibrous tissue growth to seal
Vascular Constriction associated with:
Trauma
SNS induced constriction from pain is caused by:
Neural Reflexes
Responsible for most of the constriction
Local myogenic spasm
Local humoral factors include:
Thromboxane A2 from platelets (especially important in smaller vessels)
Platelets contain:
Contractile proteins (actin & myosin) Enzymes Calcium ADP & ATP Thromboxane A2 Serotonin Growth Factors
Platelet Cell Membrane Contains:
Glocoproteins (adhere to damaged area
Phospholipids containing platelet factor 3 (initiates clotting)
Mechanism of Platelet Activation:
When platelets contact damaged area they:
- Swell
- Irregular form w/ irradiating processes protruding from surface
- Contractile proteins contract causing granule release
- Secrete ADP, Thromboxane A2, & Serotonin
Thromboxane A2 is a/an:
Vasoconstrictor &
Potentiates the release of granule contents
Platelets are important in:
Minute ruptures
A lack of platelets is associated with:
Small hemorrhagic areas under the skin and throughout internal tissues
Platelets have a half-life of:
8-12 days
Platelets primarily eliminated by:
Macrophage action (mostly occurs in spleen)
On average there are ______platelets per ul
150,000-300,000
Role of Endothelium:
Prevents platelet aggregation
Produces PGI2
Produces factor VIII
PGI2’s role in endothelium:
Its a vasodilator
Stim. Platelet adenyl cyclase which suppresses release of granules
limits platelet extension
Factor VIII’s role in endothelium:
Clotting
Aspirin blocks:
Thromboxane A2 & prostacyclin production by inhibiting fatty acid cyclooxygenase which converts arachidonic acid to PGG2 & PGH2
Anticoagulants prevent:
Clots from forming via:
Chelators (tye up calcium)
Heparin (complexes w/ Antithrombon III)
Dicumarol (Inhibits Vit. K dependent factors; II, VII, IX, X aka Cumadin/ warfarin)
Dissolving clots that have already formed is called:
Lysis of Clots
The inactive form of plasmin which circulates in the blood
Plasminogen
Endogenous Activators of Plasminogen are found in:
Tissues, plasma, & urine
Exogenous Activators of Plasminogen:
Streptokinase
Tissue Plasminogen Activator (tPA)
Most of the frank tissue damage associated w/ infarction occurs via:
Reperfusion
Reperfusion associated w/
Formation of highly reactive oxygen species w/ unpaired electrons (free radicals)
Free radicals are generated when:
pressure on tissues relieved & again perfused w/ blood
The ability to open up alternate routes of blood flow to compensate for a blocked vessel
Collateralization
The formation of new blood vessels
Angiogenesis
Collateralization occurs via:
Angiogenesis
Vasodilation
SNS stimulation (may impede via vasoconstriction and/ or augment via the release of NPY)
Extrinsic mechanism of thrombosis:
Initiated by chemical factors released by damaged tissues
Intrinsic mechanism of thrombosis:
requires only components in blood trauma to blood exposure to collagen (or foreign surface)
Clotting Factors:
I - fibrinogen II - Prothrombin III -Thromboplastin IV - Calcium V - Proaccelerin VII - Serum prothrombin conversion accelerator VIII - Antihemphilic factor (A)
Clotting Factors Cont:
IX - Antihemophilic factor (B) X - Stuart factor XI - Antihemophilic factor (C) XII - Hageman factot XIII - Fibrin stab. Factor Prekallikrein High molecular weight kininogen Platelets
Hepatocytes (liver’s) role in clotting:
Liver synthesizes 5 clotting factors; I - fibrinogen II - Prothrombin VII - SPCA IX - AHF B X - Stuart factor
Hepatocytes (liver’s) role in clotting Cont.:
Coumarin depresses liver formation of II, VII, IX, & by blocking action of Vit K
Hemphilia is sex linked on the _____chromosome
X Chromosome
mostly men
85 % of Hemophilia cases occur due to a defect in:
Factor VIII
15 % of Hemophilia cases occur due to a defect in:
Factor IX
Key step to clotting is the conversion of:
Fibrinogen to fibrin which requires thrombin
Autoimmune disorder where the body makes antibodies against phospholipids in cell membranes
Antiphospholipid antibody syndrome
Antiphospholipid antibody syndrome causes ______ to form
Clots
Amino acid in the blood that may irritate blood vessels prompting atherosclerosis.
Homocysteine
Homocysteine levels can be reduced by taking
folic acid, B6 and B12
Produced 2-8 months after birth spontaneously
Agglutinins
Immediate Hemolysis in mismatched transfusions
less common
Delayed Hemolysis in mismatched transfusions
More common
Syncytium =
many acting as one
Intercalated discs create
low resistance pathways connecting cells end to end
Na+
Inc. at depol
Dec. at repol
Ca++
Inc. at depol
Dec. at Repol
K+
Dec. at DepolInc. at repol
Tetradotoxin blocks fast Na+ channels selectively changing a fast response into
a slow response
During resting membrane potential ______ and ____ are closed and ____ channels are open
Na+ and Ca++ closed
K+ open
If the Na+/K+ pump is inhibited, what accumulated?
Ca+
Ca+ accumulation in the cardiac cell _____contractile strength
Increases
Absolute Refractory Period
Unable to re-stim cardiac cell
Occurs during the plateau
Relative Refractory Period
Requires a supra-normal stimulus
Occurs during repol
Normal pacemaker of the heart
SA node
The SA node is:
less (-) at Er, has a leaky membrane to Na+ and Ca++, and contracts feebly
Cells of the AV node and perkinje system are under overdrive suppression by the
SA node
Delays the wave of depolarization from entering the ventricle
AV node
Allows the atria to contract slightly ahead of the ventricles
AV node
Slow conduction velocity due to smaller diameter fibers
AV node
AV node may act as a slower pacemaker in absence of
SA nodr
AS Heart Rate Inc, cycle length:
decreases
At a resting heart rate systole is ____diastole
During systole perfusion of the myocardium is restricted by the
contracting cardiac muscle compressing blood vessels
Isovolumic contraction and ejection
Systole
Isovolumic relaxation, rapid inflow, diastasis, atrial systole
Diastole
Volume of ventricles at the end of filling
End Diastolic Volume
Volume in ventricles at the end of ejection
End Systolic Volume
Volume ejected by ventricles
Stroke Volume
% of EDV ejected
Ejection Fraction (SV/EDV * 100)
Normal Ejection Fraction
50-60%
Stretch on the wall prior to contraction
Preload
Changing aortic BP during ejection of blood from the left ventricle
Afterload
Associated with atrial contraction
A wave
Associated with ventricular contraction
C wave
Associated with atrial filling
V wave
LV pressure > Aortic pressure =
Aortic Valve open
Aortic pressure > LV pressure =
Aortic valve closed
AV valves
Mitral and tricuspid
Semilunar valves
Aortic and pulmonic
Valve not opening fully
Stenoic
Valve not closing fully
Insufficient/leaky
Valve creates vibrational noise
murmor
Systolic Heart Murmur =
Aortic and pulmonary stenosis + mitral & tricuspid insufficiency
Diastolic Murmur
Aortic and pulmonary insufficiency + mitral & tricuspid stenosis
Both Systolic and Diastolic Murmur =
Patent ductus arteriosis combined valvular defect
Law of Laplace
At a given operating pressure as ventricular radius INC, developing wall tension also INC.
Anything that effects the heart rate
Chronotropic
Anything that effects conduction velocity
Dromotropic
Anything that effects strength of contraction
Inotropic
Within physiologic limits the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins
Frank-Starling Law of the Heart
Mechanism of Frank-Starling:
Increased venous return causes increased stretch of cardiac muscle fibers
Increased stretch of cardiac muscles causes:
An increase in cross-bridge formation, calcium influx, and stretch on SA node
When cardiac fibers are stretched and the force of contraction is increased, this is called
Heterometric autoregulation
3 methods of Heterometric Autoregulation:
Flow induced
Pressure induced
Rate induced
Flow induced means:
inc. stroke volume maintained as EDV dec.
Pressure induced means:
Inc. in aortic BP will Inc. force of contraction
Rate induced means:
Inc. HR will Inc. force “treppe”
Stretch on SA node will:
Increase Ca+/Na+ permeability, increases HR
Sympathetic innervation:
Increases HR, strength of contraction, and conduction velocity
Parasympathetic innervation:
Decreases HR, strength of contraction, conduction velocity
