Blood Typing, Hemostasis, Cardiac Cycle, ECG, and Blood Pressure

Agglutination

Reaction when antibodies in a patient's blood react with antigens on transfused blood

Blood Type Compatibility

(Recipient receives packed RBCs with plasma removed):

Type A: Preferred: A

| Permissible (Emergency): A, O

Type B: Preferred: B

| Permissible (Emergency): B, O

Type AB: Preferred: AB

| Permissible (Emergency): AB, A, B, O

Type O: Preferred: O

| Permissible (Emergency): O

Type A:

A antigen, anti-B antibody

Type B:

B antigen, anti-A antibody

Type O:

No A or B antigens, both anti-A & anti-B antibodies (universal donor)

Type AB:

Both A & B antigens, no anti-A or anti-B antibodies (universal recipient)

Rh Factor:

Presence of Rh antigen (+ / positive); lack of Rh antigen (- / negative)

Erythroblastosis fetalis:

Occurs when an Rh- mother has an Rh+ fetus

Extrinsic pathway:

Activated by tissue damage

Intrinsic pathway:

Initiates clots by exposing platelets (in the blood) to collagen

Calcium ions (Ca2+):

Necessary for clotting

Thrombin:

Key enzyme that converts fibrinogen to fibrin

Plasmin:

Key enzyme that digests fibrin blood clots during fibrinolysis

Platelet aggregation inhibited by:

Nitric oxide, Prostacyclin, CD39

Platelet aggregation promoted by:

von Willebrand factor

Systole:

Ventricular contraction

Diastole:

Ventricular relaxation

Cardiac cycle timing:

Atrial systole begins immediately after the P wave; ventricular systole begins after the QRS complex

Stroke Volume (SV):

Amount of blood ejected per heartbeat (EDV - ESV)

Cardiac Output formula:

Stroke Volume × Heart Rate

Stroke Volume example:

If EDV = 120mL and ESV = 50mL, then SV = 70mL/beat

Resting heart rate:

Average is 75 beats/min (clinically acceptable: 60 - 100)

Tachycardia:

Heart rate higher than 100 beats/min

Bradycardia:

Heart rate lower than 60 beats/min

P wave:

Atrial depolarization

P-Q segment:

Atrial systole

QRS complex:

Ventricular depolarization

S-T segment:

Ventricular systole

T wave:

Ventricular repolarization

Conduction pathway order:

SA Node -> AV node -> AV bundle -> Bundle branches -> Purkinje fibers

Failure of SA node:

ECG lacking a P wave (nodal rhythm)

Ventricular tachycardia:

> 100 beats/min with wide, bizarre QRS complexes overshadowing P waves

Sinus tachycardia:

> 100 beats/min where a normal P wave precedes every QRS complex

Damage to AV node:

Multiple P waves on ECG

Cardiac muscle property:

Long absolute refractory period prevents tetanus

Sympathetic stimulation:

Norepinephrine released from sympathetic neurons increases heart rate

Sympathetic receptors:

Binds to beta-adrenergic receptors

Sympathetic effects:

Increases strength of myocardial contraction, conduction rate, and depolarization rate

Parasympathetic stimulation:

Acetylcholine released from the vagus nerve decreases heart rate

Parasympathetic receptors:

Binds to muscarinic receptors

Cardiac and vasomotor control centers:

Located in the medulla oblongata

RAAS Pathway:

Angiotensinogen -> Angiotensin I (via renin) -> Angiotensin II (via ACE)

Angiotensin II:

Raises blood pressure through vasoconstriction

ACE inhibitors:

Reduce vasoconstriction to lower blood pressure

ADH (Antidiuretic Hormone):

Stimulates water reabsorption in kidney; raises blood volume and blood pressure

Aldosterone:

Stimulates salt reabsorption in kidneys (water follows salt into blood)

Atrial Natriuretic Peptide (ANP):

Decreases blood pressure

Baroreflex monitors:

Baroreceptors in the carotid sinus and aortic arch monitor BP changes

Resting blood flow distribution:

Greatest blood flow to the GI tract

Maximal exercise blood flow distribution:

Up to 85% of blood flow to skeletal muscles

Blood vessel pressure:

Aorta has the highest pressure; large veins (SVC/IVC) have the lowest pressure

Nitric oxide:

Causes vasodilation

Epinephrine/norepinephrine:

Cause vasoconstriction in most vessels (alpha receptors), but vasodilation in skeletal/cardiac muscle vessels (beta receptors)

Vasodilation triggers:

Increased tissue CO2, decreased tissue O2, increased extracellular K+, increased tissue metabolism, histamine Fluid Balance and Shock

Capillary exchange:

Hydrostatic pressure > colloid osmotic pressure at arterial end; hydrostatic pressure < colloid osmotic pressure at venous end

Hydrostatic pressure:

Forces fluid out of the capillary

Colloid osmotic pressure:

Attracts fluid into the capillary

Body water distribution:

2/3 intracellular, 1/3 extracellular

Edema causes:

Lymphatic vessel blockage, high capillary hydrostatic pressure, increased capillary permeability to proteins (low albumin), hypertension

Hypovolemic shock:

Decreased blood volume

Cardiogenic shock:

Can result from myocardial infarction

Septic shock:

Infection causing dangerously low blood pressure

Vascular shock:

Due to widespread vasodilation

Anaphylactic shock:

Systemic allergen causing histamine release

Shock symptoms:

Decreased blood pressure, rapid pulse, cold and clammy skin

Venous return mechanisms:

Gravity, respiratory pump (deep inhalation decreasing thoracic pressure), skeletal muscle pump

Pulse measurement:

Superficial arteries (e.g., radial artery) can be palpated to measure pulse Respiratory System: Gas Exchange & Mechanics

Most oxygen transport:

Bound to hemoglobin in red blood cells

Most carbon dioxide transport:

As bicarbonate ions in blood plasma

Oxygen/CO2 in plasma:

Only a small percentage is dissolved directly in plasma

Simple diffusion:

Drives passive movement of O2 and CO2 across respiratory membranes

Expiratory Reserve Volume (ERV):

Extra volume forcibly exhaled after normal tidal expiration

Inspiratory Reserve Volume (IRV):

Extra volume forcibly inhaled after normal tidal inspiration

Total Lung Capacity (TLC):

Maximum amount of air the lungs can contain

Tidal Volume (TV):

Volume of air inhaled or exhaled in a normal resting breath

Vital Capacity (VC):

Maximum volume of air exhaled after maximum inhalation

Residual Volume (RV):

Air remaining in lungs after maximal expiration

Surfactant cells:

Produced by Type II alveolar cells

Surfactant function:

Lowers surface tension in alveoli to prevent collapse

Respiratory rhythmicity center:

Located in the medulla oblongata

Chemoreceptors:

Detect changes in blood levels of CO2, O2, and pH (located in medulla, carotid, and aortic bodies)

CO2 blood pH equation:

CO2 + H2O <-> H2CO3 <-> HCO3- + H+

Carbonic anhydrase:

Enzyme that facilitates the CO2 conversion reaction

CO2 impact on pH:

Increased CO2 drives equation right, increasing H+ ions and lowering blood pH

Respiratory acidosis:

pH drops below normal due to accumulated CO2 (hypoventilation)

Respiratory alkalosis:

pH rises above normal due to excessive loss of CO2 (hyperventilation)

Kussmaul's respiration:

Deep, rapid, labored breathing pattern often associated with severe metabolic acidosis

Hypoventilation effects:

Increases CO2 levels and decreases blood pH (acidosis)

Hyperventilation effects:

Decreases CO2 levels and increases blood pH (alkalosis)

Ventilation control:

Rising CO2 and falling blood pH stimulate respiratory centers to increase rate and depth

Bohr effect:

Decreased hemoglobin affinity for oxygen in response to lower pH/higher CO2, enhancing O2 unloading

Chloride shift:

Exchange of HCO3- exiting and Cl- entering RBCs in systemic capillaries to maintain electrical neutrality

Boyle's law:

Pressure of a gas is inversely proportional to its volume (P1V1 = P2V2)

Apnea:

Temporary cessation of breathing

Dyspnea:

Difficult or labored breathing / shortness of breath

Eupnea:

Normal, quiet, unlabored resting breathing