Cardiovascular Flashcards
Layers of the Heart
Pericardium: fibrous covering around heart holding it in place, providing physical protection and a barrier to infection
Myocardium: muscular portion, forms walls of atria and ventricles
Endocardium: thin three layered membrane lining the heart
what is between the visceral and parietal layers
pericardial cavity, a portential space containing 30-50 mL of serous fluid. this minimizes friction as the heart contracts and relaxes. Also the site of pericarditis and hemopericardium
AV Valves
supported by papillary muscles, which project form the walls of the ventricals, and chordae tendineae, which attach to the valve.
Chordae tendineae
cordlke structures that support AV valves and prevent eversion into the atria during systole
Fibrous Skeleton
provides structural support and isolating force for electrical impulse
What happens when excess blood enters the heart
the atria is distended, excess blood is pushed back into the veins.
Cardiac cycle
Systole and diastole:
Sys: period in which ventricles contract.
Dias: ventricles relax and fill with blood.
electrical activity precedes mechanical events
Semilunar valves opening
signal the onset of the ejectrion period. sixty percent of stroke volume is ejected during the first quater of systole, 40% ejected during the next two quaters of systole
Closure of the AV valves
first sound, healds the onset of of systole
S2
blood from the large arteries flows back toward the ventricles, causing the aortic and pulmonic valves to snap shut
The last third of the cardiac cycle
atrial contraction and accounts for 20% of the filling of the ventricles
what is the difference between end diastolic and end systolic volumes
stroke volume
Cardiac output
the efficiency of the heart is measured by this. HR x SV = CO
Cardiac REserve
the maximum percentage of increase in CO above normal resting level
Preload
volume of blood pumped per heartbeat. largely determined by venous return
AFterload
the pressure it must generate to pump the blood out of the heart. systemic arterial pressures main source of afterload on the left heart.
Cardiac Contractility
the ability of the heart to change its force of contraction without changing its resting diastolic length
Frank-Starling mechanism
the change in preload. briefly an increase in venous return to the heart increases the filled volume of the ventricles, which stretches the muscle fibers thereby increasing their preload.
The greater the amount of volume of blood in the heart before contraction, the greater the volume of blood ejected from the heart
Changes in ventricular inotropy (contractility)
alter the rate of ventricular pressure development (heart failure)
Pulmonary circulation
moves blood throught he lungs and creates a link with the gas exchange function of the respiratory system. right heart, pulmonary artery carries venous blood. and pulmonary veins are the only ones that carry arterial. low pressure, low resistance, short system
Systemic circulation
all other tissues of the body. includes the coronary system. left heart, brain and tissues, veins from the lower body merge to form the inferior vena cava and those from the head and upper extremities form the superior vena cava.
Composition of blood vessels
Tunica externa- outermost layer. primarily loosely woven collagen fibers that protect the blood vessel and anchor it to surrounding structures
Tunica media: largely smooth muscle that constricts to control diameter
tunica intima: single layer of flattened endothelial cells. prevents platelet adherence and blood clotting
Venous System
veins are capable of enlarging and storing large quantities of blood. when blood is lost, veins constrict. valves prevent retrograde flow.
heat syncope
think of a sudden decrease in muscle support to venous system, after running or strenuous exercise. think of marathoners laying down after race
Microcirculation
the nutrient flow is blood flow through capillary channels designed for exchange of nutrients and metabolites. blood flow bypasses the capillary bed moving through an arteriovenous shunt which directly connects an arteriole and a vein.
Nonnutrient flow
does not allow nutrient exchange. common in the skin and are important for heat exchange and temperature regulation
blood pressure
stroke volume times heart rate times peripheral vascular resistance
Where does blood flow remain constant
the brain, heart, and kidneys
Angiogenesis
process of changing the amount of vascularity over a prolonged period of time
Collateral circulation
also a mechanisms for long term regulation of local blood flow. in the heart and other vital structures, anastomic channels exist between some smaller arteries that permit perfusion of an area by more than one artery. if the artery is occluded, anastomtic channels increase in size, allowing blood from a patent artery to perfuse an area
Vasodilator and vasoconstricot substanes
norepi/epi
antiotensin 2, histamine, serotonin
Autoregulation
of blood flow is mediated by changes in blood vessel tone due to changes in flow through a vessel or by local tissue factors. lack of oxygen, accumulation of tissue metabolites, hyperemia
Forces determining the movement of fluid
intracapillary fluid pressure, interstitial fluid pressure, plasma colloidal osmotic pressure, interstitial colloidal osmotic pressure.
Filtration
net fluid movement out of the capillary into the interstitial spaces.
absorption
net movement fromt he intertstitium into the capillary
Edema
Definition: exceess interstitial fluid in the tissues.
Causes: imbalances of any of the factors that control movement of water between the vascular compartment and the tissue spaces.
Disproportionate increase in capillary fluid pressure or permeability, decreased capillary colloidal osmotic pressure, or impaired lymph flow.
Regulation of systemic arterial blood pressure
baroreceptors or pressoreceptors are pressure sensitive receptors in the walls of blood vessels and ther heart. carotid and aortic baroreceptors are in areas between the heart and the brain
Arterial chemoreceptors
chemosensitive cells that monitor blood levels of o, CO2,and H and are in the carotid and aortic bodies
Humoral mechanisms
renin-angiotensin aldosterone system
Renin:
synthesized, stored and released by the kidneys. occurs with dec bp, ecv, or ec na concentration. converts inactive circulating plasma protein, angiotensinogen to angiotensin.
Angiotensin 1 role in Blood pressure regulation
converted to 2 while blood is flowing through the lungs, catalyzed by angiotensin converting enzyme produced in the endothelium of lung blood vessels. functions in short term and long term blood pressure regulation. it is a vasoconstrictor. stimulates the adrenal gland aldosterone secretion, which contribute to long term regulation of blood pressure by increasing kidney salt and water retention.
Mean Arterial pressure
defined as the average pressure in a patients arteries during one cardiac cycle. better indicator of perfusion to vital organs.
most people need a MAP of at least 60, or greater to ensure full perfusion. 70-100 is normal.
((SBP+(2 x DBP))/3
Dyslipidemia
imbalance of the lipid components of the blood
lipoproteins
carry cholesterol and triglycerides to various tissues for energy utilization, lipid deposition, steroid hormone production, and bile acid formation
LDL
primary transport for cholesterol
HDL
facilitates reverse transport of cholesterol (carrying it back to the liver to be secreted as bile). 50% protein. exercise, moderate alcohol, and certain meds increase HDL. smoking, metabolic syndrome and excess alcohol decrease it
Hypercholesterolemia
240 mg/dl or greater.
Metabolic syndrome
defined as the presence of three or more of the following:
Elevated fasting blood glucose (or current treatment for diabetes)
Elevated blood pressure (or current treatment for hypertension)
Elevated waist circumference (country-specific norms) and increased abdominal fat deposits
Dyslipidemia reflected by increased blood triglycerides and/or decreased HDL cholesterol in the blood (or receiving current treatment for dyslipidemia).
Atherosclerosis:
hardening of the arteries characterized by the formation of fibrofatty lesions in the intimal lining of large and medium sized arteries.
Formation of Atherosclerosis:
Endothelial cell injury -> Migration of inflammatory cells -> Lipid accumulation (macrophages become foam cells, attach to lipids, apostosis of foam cells leave necrotic cell material and lipid in vessel wall -> Plague structure (superficial fibrous cap).
Risk for Atherosclerosis
hypercholesterolemia, elevated LDL. modified by dietary and lifestyle and medications. fmaily history, increasing age, and male sex.
Atherosclerotic Occlusive disease
sudden event that interrupts arterial flow to the affected tissues or organ
Raynaud disease and phenomenon
intense vasospasm of the arteries and arterioles in the fingers and less often the toes.
Disease: exposure to cold or strong emotions and is usually limited to the fingers. cause is unknown.
Phenomenon: associated with other disease states or konwn causes of vasospasm.
The 7 Ps of acute arterial embolism
pistol shot, pallor, polar, pulselessness, pain, paresthesia, paralysis.
Atherosclerotic Occlusive disease
PAD: 50% narrowing of the vessel before symptoms of ischemia arise. primary symptom is pain with walking (intermittent claudication)
Goals of treatment: 1. dec considerable CV risk 2. reduce symptoms.
Walking slowing to the point of claudication may be encouraged to increase collateral circulation.
Aneurysm
abnormal localized dilation of a blood vessel. true is bounded by a complete vessel wall and remains within the compartment.
likelihood of rupture correlates with the size.
Dissecting aneurysm
false aneurysm resulting from a tear in the intimal layer of the vessel that allows blood to enter the vessel wall, dissecting the layers to create a blood filled cavity
often occurs without evidence of previous vessel dilation. most common site is the ascending aorta. second most common: thoracic aorta.
pain is associated.
Venous circulation
1 way valves. superficial veins. deep venous channels. perforating, or communicating veins connect the two systems. blood from skin and sc tissues in the leg collects in superficial veins and is then transported across the communicating veins into deeper venous channels.
Varicose veins
dilated, tortuous veins, common, when flow in deep channels is impaired or blocked, most common cause is DVT. because there are no valves,
prolonged exposure to increased pressure causes venous valves to become incompetent.
Chronic Venous insufficiency
pathophysiologic condition of persistent venous hypertension on the structure and function of the venous system of the lower extremities. leads to tissue congestion, edema and eventual impairment of tissue neutrition. necrosis is caused.
Stasis Dermatitis
advanced venous insufficiency, impaired tissue nutrition causes stasis dermatitis, and stasis or venous ulcers. characterized by thin, shiny, bluish brown, irregularly pigmented desguamative skin.
most common cause of lower leg ulcers
Venous Thrombosis
presence of thrombus and the accompanying inflammatory response in the vein wall.
stasis of the blood, increased coagulability and vessel wall injury
Hypertension
primary risk factor for cardiovascular disease
primary or secondary. primary: clinical presentation without evidence of causative clinical condition
Risks for HTN
nonmodifiable fators.
modifiable: diet, blood lipids, tobacco, alcohol. fitness
Secondary hypertension
in response to another disease. may be corrected by surgery or meds. renal disease is the largest cause
Organ damage from HTN
heart, brain, kidneys, PAD, retinopathy, sexual dysfunction, can lead to a HTN emergency
Emergency: ongoing neurological, myocardial, hematological or renal target organ disease.
Urgency: target organ disease is likely if BP is not controlled
Orthostatic Hypotension
abnormal drop in BP on assumption of the standing position of at least 20 mm or a diastolic blood pressure of 10 mm HG
D-dimer
measurement of plasma d-dimer, a degradation product of coagulation factors that have been activated as the result of a thromboembolic event.
tests for amount of fibrin D-dimer int he blood. it is produced whenever fibrin is being actively degraded somewhere in the vascular system.
it is not the end point if positive, but mandates further testing to look for DVT/VTE.
positive can have support for further imaging and testing.
negative can be used to reliable exclude VTE.
Helical CT angiography
requires administration of radiocontrast medium. sensitive for the detection of emboli in the proximal pulmonary arteries.