Cardiac physiology

automaticity

tendency of a tissue to produce AP spontaneously

cells oriented along the current flow vs

cells arranged against the current flow

ballance between oxygen demand

and supply

angina pectoris

milder, reversible ischemia without necrosis of myocardium

classical angina pain

substernal, central, dull, diffuse may be precipitated by exertion and radiating to arm or jaw or epigastrium. Can be relived by rest or taking nitrates

MI = myocardial infarction (med) = heart attack (non

pain more severe, prolong duration, not relieved by rest or nitrates. Connected with autonomic upset

vasa vasorum

nutrient arteries of arterial wall (from adventitia)

aneurysm / aneurism

abnormal, irreversiblel dilatation in the wall of aorta

dissection of aorta

in Marfan syndrome also HA

fenestrations

small hall in endothelial cells

continuous capillaries

have pinocytic vesicles

fenestrated capillaries

in GIT, kidney, endocrine glands, pancreas; no pinocytic vesicles

sinusoidal capillaries

disscontinuous basal lamina and endothelium, no tight junction. Highly porrus capillaries. Limforeticular system - liver spleen, limph nodes, bone marrow, adrenal cortex.

vericose veins

żylaki

systolic BP

max pressure in the major artery when hearst is at the top of systole

diastolic BP

minimal pressure in the major artery when heart is at the end of diastole

a-v nipping (retina) in st II HA

ucisk naczyn tetniczych na zylne w HA II stopnia

arteriosclerosis

hardening of arteries w loss of elasticity

VCAM-1

vascular cell endothelial adhesion molecule

foam cells

lipid loaded macrophages and smooth muscles

claudication

chromanie przestankowe, when arteries fail to supply working muscles with extra blood (fail to dilate)

aneurysm

abnormal, localized, irreversible dilatation of any part of CVS

atherosclerosis

response to chronic injury to intima of large and medial size arteries where there is formation of FIBROFATTY intimal plaques

chrypka

hoarseness

stridor

inspiratory noises in major airways

autoregulation

maintenance of blood flow despite changes in perfusion pressure

syncope

transient loss of conciousness due to reduce blood supply to cerebral cortex (global cerebral hypoxia)

atopy

familiar tendency to develop IgE antibodies

heaving apex beat

falujący

sinus of Valsalva

dilated pocket in the root of aorta just above the valves. They are the origin of coronary arteries

tree bark appearance

kora drzewna wyglad aorty od srodka przy kile

culprit

winowajca

palpitations

unpleasant awareness of your heartbeat

dyspnoe

unpleasant awareness of breathing process

stenosis

valve fail to open fully and produces impedement to forward flow

regurgitation

valve fail to close properly during systole and there is problem of reversal flow

pink frothy sputum

różowa pienista wydzielina

malar flush

cyanosis look on the chicks in advanced stages fo MS due to static engorgement

cor pulmonaire

RVF due to PRIMARY pulmonary hypertension due to pulmonary disease, or vasculature of lungs

apex beat

outermost and lowermost area of pericardium where definite cardiac impulse can be felt. TIp of the LV touching the chest wall during every systole

apex beat - tapping (MS), heaving (AS), thrusting(AR)

soft, little tap/ strong contraction of LV and prolong/ Strong but short time

rheumatic fever (rheumatic fever)

postreptoccocal multi systemic, immune mediated, non-suppurative inflammatory disease characterized by inflammation of synovial membranes and joints, pericardium, myocardium, even endocardium, may produce chorea, in the skin produces erythema marginatum

pulsus paradoxus

where inspiratory fall in BP is more than 10 mmHg

Kussmaul's sign

failure of JVP to go down during inspiration It sometimes even go up. In Constrictive pericarditis and restrictive cardiomyopathy. Rather not in cardiac tamponade. Due to thick pericardium ITP cannot be transferred on to cardiac pressures.

heart failure

despite appropriate filling of the heart it fails to generate enough CO to meets minimal oxygen demands of the body tissues

preload

EDV - amount of blood that is present in ventricular cavity at the end of diastole

contractility

intrinsic health of myocardium

afterload

resistance against which ventricles have to generate CO

haevy and boggy lung in LVF

ciężkie i bagniste płuca (obrzęk płuc)

ortopnea

dyspnea that worsens on lying down

oozing fluid

sączący się

cardiac failure

complex, progressive clinical pathological syndrome characterized by failure of the heart to provide enough CO to peripheral tissues in spite of normal or enough normal filling preasures

diastole

ability of the ventricle to relax properly and accommodate enough EDV

Ischemic heart disease

group of clinical pathological syndromes which result due to imbalance between supply and demand to the myocardium

coagulation

soluble fibrinogen is converted into insoluble fibrin

thrombus

platelet with coagulation material on it

necrosis

morphological changes in the cell tissue which has been lethaly injured WHILE this tissue is still part of a living person.

heart failure

describe wide spectrum of clinical and pathophysiological conditions, ranging from asymptomatic systolic and diastolic dysfunction to life-threatening acute pulmonary edema and cariogenic shock

unstable angina

severe angina, of recent onset or with progressively increasing frequency or angina which is precipitated by progressively reducing excursion even at rest. Have unstable atheromteous plaque with thrombus formation. Not relieved by rest or taking nitrates

shock

clinical pathological condition in which CVS collapses and there is wide spread hypoxia to multiple tissues in the body

cardiac tamponade

clinical pathological condition in which there is increased amount of fluid in pericardial suck and it result with compression of both ventricles and unables the heart to relax properly

endotoxins

integral layer of G negative bacteria. Only released when bacteria dye. Its. a Lipopolysacharide (LPS). Not affected by heat. Non specific. General effects. No Ab produced if previous attack.

exotoxins

released by living bacteria by G neg and G positive as well. Its a protein. Destroyed by the heat. Specific to organs, target tissue. Ab produced if previous attack - immunity.

toxaid

exotoxin altered in such a way that will not produce disease but still trigger the immune system

empyema

localised collection of pus in an epithelial lined area

abscess

localised collection of pus