Cardiovascular

Hemostasis

stopping the flow of blood within a vessel

3 steps to clot formation

1. vascular spasm (constriction to reduce blood loss)

2. formation of the platelet plug (blockage of the injury site)

3. blood coagulation (formation of fibrin meshwork)

Platelet Plug Formation

prostacyclin production ceases in an injured vessel, and collagen protein reveals platelet binding receptors. Platelets then release thromboxane A2 and ADP to recruit more platelets to the site of vascular injury.

what causes thrombin formation?

Upon platelet aggregation, PF3 is secreted, which activates thrombin via the clotting cascade.

critical functions of thrombin (4)

1. autoactivation - positive feedback

2. conversion of fibrinogen to fibrin

3. activation of factor Viii (stabilizes fibrin meshwork)

4. platelet aggregation enhancement

Clotting Cascade requires...

Ca2+ and Vitamin K (liver)

Mechanisms to slow the clotting process

Antithrombin III (always present in blood. When it encounters thrombin it will inactivate it).

Thrombomodulin (present on endothelial cells, binds thrombin which activates protein C (which inactivates factors V and VIII)

Fibrin meshwork: inactivates thrombin itself.

thrombolysis mechanism

tissue plasminogen activator (t-PA) which activates plasminogen to plasmin (dissolving clot).

thrombolytics

t-PA: activates plasminogen to form plasmin, actively dissolving clots.

Common anticoagulants

- aspirin: inactivates COX enzymes to produce prostaglandins & thromboxane A2

- heparin: facilitates binding of thrombin to antithrombin III

- coumadin/warfarin: competes with vitamin K (required to form 4 clotting factors)

Risk Factors for Coronary Artery Disease (CAD)

high cholesterol ("LDL: bad cholesterol")

hypertension

diabetes

family history

smoking

obesity

gender

age (men over 45, women over 55)

markers (C-reactive protein)

General mechanism of plaque formation in CAD

cholesterol ("LDL") can deposit within vessels resulting in plaque formation. Inflammatory response leads to muscle thickening and formation of scar tissue. Damage to the vessel endothelium will result in thrombus formation (could become an embolus & stuck in heart, lungs, or brain)

Coronary artery disease treatment

angioplasty (balloon catheter to expand smooth muscle of vessel), may insert stent

coronary artery bypass graft (CABG) - circumvent occluded artery by grafting a vein

heart tissue exhibits the following characteristics

excitability

automaticity

conductivity

refractoriness

pulmonary circuit

carries blood to the lungs for gas exchange and returns it to the heart

systemic circuit

carries blood between the heart and the rest of the body and back to the heart

explain blood flow

GL!

Heart Valves

atrioventricular - tricuspid, bicuspid (mitral)

semilunar - pulmonary, aortic

How do valves open

greater pressure behind it \= opens

greater pressure in front \= closed

Layers of heart wall

epicardium (thin, outer covering)

myocardium (muscle layer of heart, spinal arrangement)

endocardium (thin innermost layer of smooth endothelium)

Intercalated disks

desmosomes (mechanical) and gap junctions (electrical)

pericardial sac

surround heart with fluid-filled sac

pericardium layers

fibrous - outermost layer of connective tissue that protects the heart and keeps it in place

serous

- parietal pericardium: attached to the fibrous pericardium, external layer

- visceral pericardium: part of epicardium, internal layer

Blood components

Plasma - 55%

buffy layer - 1%

RBC - 45%

What stimulates RBC production

Kidneys release erythropoietin which stimulates bone marrow to produce RBC

Characteristics of mature erythrocytes

-flexible

-enucleated + no mitochondria

-short life span around 120 days

-bioconcave

-old/damaged are phagocytosed in the liver, spleen, and marrow

Hemoglobin can bind to

4 oxygen molecules

AV nodal delay

pause between SA and AV node depolarization (and delay in contraction), allows more time for blood to be expelled from the atria into the ventricles.

Atrial Kick

contraction of atria allows 15% more blood to be pushed into the ventricles before ventricular contraction

two types of cardiac muscle cells

contractile (mechanical) and autorhythmic (responsible for initiation and conduction of APs that lead to contraction)

Why 2 action potentials?

contractile and autorhythmic cells have different membrane characteristic resulting in different action potentials.

Ventricular Action Potential

0: voltage gated Na+ channels open

1: voltage gated K+ channels open

2: voltage-gated Ca 2+ channels open

3: slow K+ channels open

4: only resting K+ channels open

Refractory period

cardiac muscle is unresponsive to electrical stimulation \= sufficient time for ventricular filling and emptying

SA node action potential

4: leaky Na+ channels

0: voltage-gated Ca 2+ channels open

3: voltage-gated K+ channels open

Autonomic stimulation by SNS

SNS bathes heart in NE, which increases the leakiness of sodium channels (increases slope of phase 4 in SA node action potential, increasing rate of depolarization) \= higher heart rate. Also, stronger contraction from increased Ca 2+ permeability

PNS stimulation of heart

decreases heart rate via input from vagus nerve to SA and AV nodes

How many leads in an ECG

12

types of leads

6 limb, 6 chest

limb leads

I, II, III, aVR, aVL, aVF

chest leads

V1, V2, V3, V4, V5, V6

how are deflections determined?

Current flowing toward the positive end of a lead produces a positive (upward) deflection of the ECG stylus.

sinus rhythm

P wave: atrial depolarization

QRS complex: ventricular depolarization

T wave: ventricular repolarization

why is atrial repolarization masked?

QRS complex

Normal segment lengths

PR segment: AV nodal delay (~0.1 sec)

PR interval: normally

ST segment: normally at zero deflection

ECG abnormalities

Wolff-Parkinson White syndrome

heart block

atrial flutter

atrial fibrillation

ventricular tachycardia

ventricular fibrillation

First degree heart block

PR interval \> 0.2 because conduction is slowed through AV node

third-degree (complete) heart block

no conduction through AV node

P waves occur independently of QRS complex

Heart block treatment

Automated Implantable Cardioverter-Defibrillator (AICD)

wolff-parkinson white syndrome

display sloped delta wave & shortened PR interval on an ECG. delta wave is a result of conduction through an accessory pathway. Treatment \= catheter ablation of accessory pathway.

V-tach

"conduction loop" where a ectopic ventricular focus fires and sets overall pace