A&P 2: Cardio

right AV valve

tricuspid valve

left AV valve

bicuspid/mitral valve

right SL valve

pulmonic valve

left SL valve

aortic valve

blood pressure

systolic/diastolic (mmHg)

systole

“ventircular systole”

ventricles are contracting

diastole

“ventricular diastole”

ventricles are relaxing/filling

systole:

AV valves are ___; SL valves are ___

closed; open

diastole:

AV valves are ___; SL valves are ___

open; closed

pulse pressure equation

(systolic bp) — (diastolic bp)

mean arterial pressure (m.a.p.) equation

(diastolic bp) + (1/3)(pulse pressure)

S1 sound

“lubb”

what happens at S1?

AV valves are closing

S2 sound

“dubb”

what is happening at S2?

SL valves are closing

valvular stenosis

when a valve should be open, doesn’t open all the way (narrow)

valvular insufficiency/regurgitation

when a valve should be closed, doesn’t close all the way (blood flows backwards

systolic murmurs

aortic stenosis

pulmonic stenosis

mitral regurgitation

tricuspid regurgitation

systolic murmurs (condensed)

SL valve stenosis

AV valve regurgitation

diastolic murmurs

aortic regurgitation

pulmonic regurgitation

mitral stenosis

tricuspid stenosis

diastolic murmurs (condensed)

SL valve regurgitation

AV valve stenosis

Aortic valve

(1) right 2nd intercostal space on the sternal border

(aortic stenosis)

Pulmonic valve

(2) left 2nd intercostal space on the sternal border

Erb’s point

(3) left 3rd intercostal space on the sternal border

(aortic regurgitation)

Tricuspid valve

(4) left 4th intercostal space on the sternal borde

Mitral valve

(5) left 5th intercostal space, mid-clavicular line

epicardium

outermost layer of the heart

myocardium

middle layer of heart wall (thickest)

endocardium

covers internal surface of the heart and external surface of valves

cardiac muscle

striated

arranged in sarcomeres

cells connected with intercalated disks

“pacemaker of the heart”

SA node

heart conduction

1. SA node

2. AV node

3. AV bundle (bundle of his)

4. R + L bundle branches

5. purkinje fibers

electrical events

depolarization

repolarization

mechanical events

contraction

relaxation

electrical events ___ mechanical events

precede (come before)

vagus nerve (CN X)

sends parasympathetic innervation to the heart; slows down heart

ectopic pacemaker

when SA node is impaired, another pacemaker will take place

(AV node default)

patent foramen ovale

foramen ovale (between R+L atria) fails to close after birth

atrial septal defect

postnatal heart still with opening between R+L atria

ventricular septal defect

intraventricular septum incompletely formed

tetralogy of fallot

“cyanotic heart defect”

ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, overriding aorta

ECG segment

period of time in between waves and complexes

“flat” on the isoelectric line

ECG interval

period of time that includes waves and complexes

“not flat”

cardiac output equation

CO = (stroke volume) X (heart rate)

stroke volume equation

SV = (end diastolic volume) — (end systolic volume)

chronotropic agents

change heart rate

positive chronotropic agents

increase heart rate

(thyroid hormone, caffeine, nicotine, cocaine)

negative chronotropic agents

decrease heart rate

(parasympathetic activity, beta-blocker drugs)

ionotropic agents

change stroke volume; alter contractility (force of contraction)

positive ionotropic agents

increases contractility by increasing Ca2+

negative ionotropic agents

decreases contractility by decreasing Ca2+

cardiac cycle

1. atrial systole/atrial contraction (diastole)

2. isovolumetric ventricular contraction (systole)

3. ventricular ejection (systole)

4. isovolumetric ventricular relaxation (systole)

5. ventricular filling (diastole)

plasma

liquid matrix of blood (water, plasma proteins, other solutes)

formed elements

cells and cell fragments (rbc, wbc, platelets)

hematocrit

percentage of formed elements in the blood (viscosity)

cyanotic heart defect

low levels of oxygen in systemic circulation (blueish tint in skin, hypoxia)

acyanotic heart defect

abnormal blood flow but enough oxygenated blood is present in systemic circulation

hematopoesis

how we form all blood cells (formed elements)

occurs in red bone marrow

hemostasis

1. platelet plug (primary)

2. coagulation cascade (secondary)

3. fibrinolysis - weeks later fibrin mesh dissolves

coagulation cascade (last 3 steps)

3rd to last: factor X —> Factor Xa

2nd to last: prothrombin —> thrombin

last step: soluble fibrinogen —> insoluble fibrin

coagulation disorders

hemophelia A (messes with intrinsic pathway)

hemophelia B (messes with intrinsic pathway)

vitamin K deficiency (vitamin k important for coagulation)

WBC: neutrophil (granulocyte)

first responder

WBC: eosinophil (granulocyte)

parasites/allergies

WBC: basophil (granulocyte)

histamine/heparin/IgE

WBC: monocyte (agranulocyte)

macrophage/dendritic cell

WBC: lymphocyte (agranulocyte)

T, B, NK cells

reticulocytes

immature red blood cells

hemoglobin

RBC protein that binds to oxygen allowing RBCs to carry oxygen through the blood

(2 alpha + 2 beta chains)

1 hemoglobin can bind up to 4 oxygens

Hba1C

hemoglobin that is glycolated

(hyperglycemia = elevated HbA1C)

myoglobin

serves as an oxygen reserve in muscle tissue (higher affinity for O2)

antigen

surface proteins on cells, capable of causing an immune response

antibodies

proteins made by the immune system, circulate in the plasma, and they bind to specific antigen

blood type A

antigen on the RBCs: A antigen

antibodies in the plasma: anti-B atibodies

blood type B

antigen on the RBCs: B antigens

antibodies in the plasma: anti-A antibodies

blood type AB

antigen on the RBCs: both A + B antigens

antibodies in the plasma: neither anti-A nor anti-B antibodies

blood type O

antigen on the RBCs: neither A nor B antigens

antibodies in the plasma: both anti-A + anti-B antibodies

Rh-positive

D-antigen on RBCs

no anti-D antibodies

Rh-negative

NO D-antigen on RBCs

will make anti-D antibodies (after first exposure to Rh positive blood)

receiving the wrong type of donor blood

transfusion reaction - agglutination (clumping) + hemolysis (destroyed)

hemolytic disease of the newborn

Rh negative mother carries Rh positive fetus

microcytic anemia (mcv < 70)

ex. iron deficiency anemia

macrocytic anemia (mcv >110) — megaloblastic

enlarged cells, impaired DNA synthesis

ex. vitamin B9 (folate) deficiency; vitamin B12 (cobalamin) deficiency

macrocytic anemia (mcv >110) — non-megaloblastic

cells are rounder, problem with RBC formation in bone marrow

ex. chronic alcoholism

normocytic anemia (70<mcv<110)

normal size, don’t have enough functional RBC

ex. sickle cell anemia