Cardiology

Front 1

Preload

Back 1

passive load that establishes the initial muscle length of the cardiac fibers prior to contraction

(left ventricular end-diastolic volume)

Front 2

after load

Back 2

sum of all loads against which the myocardial fibers must shorten during systole.

aortic impedance

arterial resistance

intraventricular pressure

mass and viscosity of blood in the great vessels

Front 3

contractility

Back 3

speed and shortening capacity at a given instantaneous load (ionotropy)

Front 4

diastolic compliance

Back 4

the ability to fill at a given diastolic pressure

Front 5

heart rate

Back 5

frequency of contraction

Front 6

ejection fraction

Back 6

end diastolic minus end systolic/end diastolic volume

most wildly used clinical indicator of LV function

Front 7

P wave

Back 7

atrial contraction (depolarization)

Front 8

QRS wave

Back 8

ventricular contraction (depolarization)

hides atrial repolarization

Front 9

T wave

Back 9

ventricular relaxation

Front 10

systemic vascular resistance =

Back 10

blood pressure/ cardiac output

Front 11

Blood pressure =

Back 11

= systemic vascular resistance (SVR) x cardiac output

Front 12

cardiac output =

Back 12

HR x stroke volume

Front 13

Thin filaments components

Back 13

G-actin (globular) polymerizes to form F actin (filamentous)

Tropomyosyin helps hold F-actin together

Front 14

Troponin complex

Back 14

Troponin T - binds tropomyosin, anchoring the troponin complex

Troponin C - binds Calcium

Troponin I - binds to actin, inhibiting actin-myosin interaction

Front 15

Thick filaments of muscle

Back 15

4 lights chains - structural role

2 heavy chains - each has biding site for ATP and a binding site for actin
also has ATPase activity/motor activity

Front 16

Sarcomere Organization

Z band

Back 16

Thin filaments bind to z line

Front 17

sarcomere organization

H zone

Back 17

middle of the sarcomere (z to z is one sarcomere)

Front 18

Sarcomere organization

M line

Back 18

thick bind to M line

Front 19

Muscle contraction

stages:

Back 19

Attachment

release

bend

force generation

Attachment

repeat

Front 20

muscle contraction

attachment

Back 20

ATP not present

get myosin head binding to actin

Front 21

Muscle contraction

Release

Back 21

ATP causes detachment of myosin head from actin

ATP causes a conformational change, myosin head loses affinity for actin

Front 22

muscle contraction

bends

Back 22

myosin head bends to original state

movement initiated by breakdown of ATP to ADP

bends towards Z line

Front 23

muscle contraction

force generation

Back 23

myosin head binds weakly to a new actin molecule (closer to Z line) only when calcium is present (calcium dependent)

phosphate is released, increasing the binding affinity, head returns to original position. As it returns, it pulls the thin filament along thick filaments (power stroke)

Front 24

Regulators of contraction:

Back 24

ATP

calcium

magnesium - requires ATPase activity

Na and channels

beta adrenergic receptors

Front 25

Cardiac muscle contraction

Back 25

action potential moves down T tubule

AP detected by DHP receptors that contain Ca channel

DHP opens to allow a small amount of extracellular Ca into the fiber

Ca binds to ryanodine receptors in the SR, opening SR to release large amount of calcium

Calcium release allows contraction of cardiac muscle

Front 26

Cardiac AP and calcium influx

Back 26

sodium initially flows in for AP

calcium then flows in, depolarization occurs

repolarization occurs with the outflow of potassium ions

Front 27

Function of intercalated disks

Back 27

attachments of cells to other cells

allows conduction of AP linearly

only found in cardiac muscle

Front 28

structure of intercalated disks

Back 28

(1) transverse component
major component is Fascia adherens - holds cells together to form fibers

(2) later component

each component has cell to cell junctions

fascia adherens

maculae adherens - help prevent cells from pulling apart under tension, in both components

gap junctions - major element of lateral component
provide ionic continuity among adjacent cardiac muscle cells, permit cardiac muscle cells to behave as syncytium

Front 29

SA node cells

Back 29

small
disorganized

no intercalated disks

slow depolarization in the late stage of each action potential

Front 30

AV node cells

Back 30

located in right atrium, near lower part of interatrial septum

small, few myofilaments, less organized, no intercalated disks

depolarize slowly (delay signal from SA node) - allows for delay in contraction of atria relative to ventricles....atria squeeze all the blood into the ventricles before ventricles contract

Front 31

Purkinje and bundle fibers

Back 31

from the AV node, transmit signal

transitional cells that end on myocardium

Purkinje cells - larger than cardiac muscle cells

large amounts of glycogen, few organized myofilaments

infrequent intercalated disks, frequent gap junctions

Front 32

Neural regulation of heart

Back 32

ANS -

parasympathetics - from vagus synapse on post synamptic in heart, terminate in SA/AV node

Para - use ACh to decrease HR

sympathetics from T1-T6

use NE to increase HR

Front 33

Sequence of heart contraction

Back 33

(1) SA node generates impulse
(2) AV node delays impulse
(3) impulse passes from atria to ventricles via the atrioventricular bundle of his (bundle to apex, and purkinje fibers to apex)

Front 34

Systole

Back 34

contraction

Front 35

diastole

Back 35

relaxation

Front 36

ventricular filling

Back 36

mid to late diastole

blood pressure low

Av valves open

then atrial systole

Front 37

ventricular systole

Back 37

atria relax

rising ventricular pressure results in closing of AV valves

isovolumetric contraction phase

ventricular ejection phase opens semilunar valves

isovolumetric relaxation occurrs

Front 38

Factors affecting stroke volume

Frank Starling Law

Back 38

(1)preload - amount ventricles are stretched by blood before contraction

increase SV with low heartbeat or exercise

decrease SV with extremely rapid HR or blood loss

(2) contractility - increase with some drugs/hormones...NE
decreased with acidosis, increased extracellular K, calcium channel blockers...

Front 39

depolarization of SA node process

Back 39

slow leak of calcium in, calcium released within the cell, potassium repolarizes cells

phase 0,3,4 only

Front 40

Sodium propagation of signal

Back 40

hits an L type calcium channel at teh bottom of the T tubule

allows calcium influx

calcium binds to ryanodine receptor on SR

calcium released within the cell

calcium binds to tropomyosin complex and shifts tropomyosin I (inhibitor) away from the myosin/actin binding site

myosin head interacts with actin

phosphate from hydrolyzed ATP is released, myosin head bends (get contraction)

calcium regulated, ATP dependent shortening of filaments

Front 41

cardiac cycle

Back 41

ventricle contracts - isovolumetric increase in pressure

when pressure equals aorta, aortic valve opens...ejection of blood

end of systole - myosin/actin dissociate

isovolumetric decrease in pressure

when pressure equal to atria, mitral valve opens

atria contract, ventricle full...repeat isovolumetric contraction

Front 42

Regulation of cardiac cycle by brainstem

Back 42

sympathetics - NE binds to beta 1 receptor...sends signals to increase sodium and calcium influx...causes an increase in depolarization (increased HR)

parasympathetics - ACh binds to muscaranic receptors and causes a decrease in Na/Ca...causes hyperpolarization

Front 43

Frank Starling Mechanism and preload

Back 43

if you stretch a muscle, you increase its performance

increase preload by aortic regurgitation

exercise - rapid relaxation and lower pressure increases stroke volume

valsalva - decreases

atrial fibrillation - decreases preload

Front 44

Frank Starling Mechanism and afterload

Back 44

afterload is the force that the ventricle must overcome to eject blood (mean arterial pressure) or aortic valve/outflow tract resistance

higher afterload results in longer isovolumetric contraction and slower rate of muscle fiber shortening

Front 45

Frank Starling Mechanism and contractility

Back 45

change in end systolic pressure volume relationship

increased contractility results in a greater stroke volume at any given preload or afterload

Front 46

CHF physiology

Back 46

rest: ventricle can still get low enough pressure to fill

exercise: can't relax as well...ventricle can't get low enough pressure, atrial pressure must increase

to improve stroke volume, must have higher end diastolic pressure

results in higher Left Atrial pressure, which results in pulmonary congestion, pulmonary congestion causes shortness of breath, shortness of breath increases disability

Front 47

CHF pathology

Back 47

usually starts with myocardial insult

myocardial dysfunction - reduced system perfusion

hemodynamic defense systems activated (normally suppose to be transient)...get altered gene expression, apoptosis, remodeling

Front 48

Hemodynamic defense systems

Back 48

(1) Sympathetic - NE

(2) rennin angiotensin

(3) aldosterone

Front 49

Sympathetic as hemodynamic defense

Back 49

NE

binds beta/alpha receptors

organs - cardiovascular, adrenal gland

cardiac - increase in automaticity, contractility, afterload, myocyte death

Front 50

Renin angiotensin as hemodynamic defense

Back 50

Angiotensin II

organs - kidney, lungs, cardiovascular

increases afterload and preload, myocyte hypertrophy

Front 51

Aldosterone as hemodynamic defense

Back 51

aldosterone

organs - kidney, heart

causes cardiac fibrosis

Front 52

Staging of CHF

Back 52

(a) high risk but no structural changes in heart

(b) structural changes without syndrome

(c) syndrome controlled by therapy

(d) syndrome uncontrolled despite therapy

Front 53

CHF symptom staging

Back 53

1 no limitation of activity

2 mild limitation improves with slowing down

3 marked limitation improves only with rest

4 severe limitation or symptoms at rest

Front 54

CHF types

Back 54

(1) diastole - thick non functioning heart, unable to fill

(2) systolic CHF - thin, large dysfunctional heart, unable to pump and unable to fill

Front 55

Diastolic CHF

Back 55

no change in heart volume

unable to fill

concentric hypertrophy of myocytes

near normal stroke volume

normal end diastolic volume

steep diastolic pressure preload volume

Front 56

Systolic CHF

Back 56

unable to fill and unable to pump

increase in heart volume

eccentric hypertrophy of myocytes

steep diastolic pressure preload volume

low stroke volume

high end diastolic volume

Front 57

Organization of the heart wall

Back 57

(1) endocardium - endothelial cells over connective tissue
collagenous connective tiisue
simple squamous epithelial cells on surface

(2) myocardium - cardiac muscle

(3) epicardium - connective tissue with blood vessels and nerve fibers, covered by layer of mesothelial cells

Front 58

endocardium

Back 58

endothelial cells over connective tissue

collagenous connective tissue

simple squamous epithelial cells on surface

Front 59

myocardium

Back 59

cardiac muscle with small amounts of connective tissue

richly vascularized

Front 60

epicardium

Back 60

connective tissue with blood vessels and nerve fibers

covered by layer of mesothelial cells

contains nerve bundles, larger blood vessels, and large fat deposits

Front 61

fibrous skeleton of the heart location and function

Back 61

(1) where ventricles/atria met

(2) where great vessels arise

function (a) extends partially into interventricular septum to anchor valves

(b) eletrically isolates right atrium from ventricles

Front 62

gross structure of valves

Back 62

form as extension of the endocardium

leaflets of collagenous tissue covered by endothelium that is continious with tha tof the chambers and the great vessels

central fibrous sheet (lamina fibrosa) is formed by margining of fibroelastic supporting layers beneath the endothelium

cardiac muscle of the myocardium does not extend into the valve, the valves are passive structures

Front 63

histological structure of the valves

Back 63

spongiosa - atrial side, underneath the endothelium

fibrosa - forms the bulk of the dense connective tissue in the valve

ventricularis - the dense connective tissue with layers of collagen and elastic fibers

Front 64

Atrial cardiac cells

Back 64

contain endocrine granules filled with atrial natriuretic hormone

secrete hormone when overly stretched

increases excretion of water, sodium, and potassium by kidneys

decreases BP by inhibitin rennin secretion and aldosterone secretion

Front 65

vascularization of cardiac muscle

Back 65

enter through epicardium

form many anastomoses

Front 66

Structure of blood vessels

Back 66

(1) tunica intima - closest to lumen.

(2) tunica media - middle layer with elements oriented circumferentially

(3) tunica adventitia - outermost layer with elemeents ordered longitudinally

Front 67

Tunica intima

Back 67

closest to lumen

endothelial cells oriented along direction of blood flow

endothelium with basal lamina

internal elastic membrane

variable subendothelial connective tissue

substanital in elastic arteries

smooth muscle cells produce the collagen and elastic fibers

Front 68

tunica media

Back 68

middle layer with elements oriented circumferentially

smooth muscle

variable amount of elastin and collagen

dominant layer in arteries

Front 69

tunica adventitia

Back 69

outermost layer with elements ordered longitudinally

collagenous fibers and a few elastic fibers

major component in veins with significant smooth muscle

contains vaso casorum and nervi vascularis in large vessels

Front 70

endothelium

Back 70

provides smooth, low resistance surface for flow

cell bound by junctional complexes and may have pinocytotic vesicles

secrete factors that maintain smooth muscle

can be activated by cytokines to express cell adhesion molecules that allow WBC to stick

Front 71

atherosclerotic plaque

Back 71

occupies tunica intima and expands it

contains connective tissue fibers, smooth muscle cells, lipid containing macrophages, necrotic material, cholesterl clefts

Front 72

tunica media

Back 72

shows greatest variation and structural specialization

large elastic arteries - media in concentric layers of elastic and smooth muscle

muscular arteries - have prominent media of smooth muscle (circumferential) bounded by internal and external elastic laminae

arterioles - few layers of smooth muscle, very responsive to vasoactive stimuli

elastic arteries - intima is longitudinally oriented with subendothelial connective tissue

Front 73

general structure of muscular arteries

Back 73

sparse endothelial connective tissue

prominent internal elastic membrane

prominent smooth muscle in t. media

longitudinally oriented, incomplete lamellae connective tissue in t. adventitia

Front 74

arteriole structure

Back 74

smallest branches of arteries

start of microvascular system

intimate endothelial cells with basement membrane

t. media has 1-2 layers of smooth muscle, smooth muscle becomes discontinous

t. adventitia is insignificant

small lumen relative to thickness of vessel wall

prominent endothelial nuclei

Front 75

venules

Back 75

postcap -> collecting -> muscular venules

large lumen compared to vessel thickness

post cap - site of migration of leukocytes out of blood stream and into peripheral tissue

regulated by factors produced by endothelial cells and cells outside of circulation

Front 76

medium veins

Back 76

irregular profile, larger lumen, thinner walls

more distinct t. intima, media and adventitia

sparse subendothelial connective tissue beneath endothelial cells

adventitia thicker than media

smooth muscle cells in media and adventitia

Front 77

vein valves

Back 77

in small/medium

develop as inelastic extensions of the t. intima but covered by endothelial cells

Front 78

structure of large veins

Back 78

t intima thin

t media circumferentially oriented smooth muscle cells, fibroblasts, and collagenous fibers

t adventitia thickest layer, prominent bundles of smooth muscle separated by connective tissue

Front 79

microvasculature structure

Back 79

capillaries arise from metarterioles

smooth muscle in t. media is discontinous form precapillary sphincters

contraction and relaxation of these sphincters regulates blood flow

pericytes help regulate capillary diameter

Front 80

microstructure of capillaries

Back 80

thin walls to permit exchange

capillary wall - endothelial cells, basal lamina covers pericytes, scattered contractile cells (pericytes)

endothelial cells make contact without gap junctions (selective permeability barrier)

Front 81

capillary types

Back 81

(1) continuous - form tight junctions
movement of material requires carried mediated transport in pinocytotic vesicles...
muscle, never, connective tissue

(2) fenestrated capillaries - contain fenestrae bridged by diaphagms of extracellular material
basal lamina is continuous
pancreas, intestines, endocrine glands, renal glomeruli

Front 82

sinusoids

Back 82

discontinuous capillaries

large diameter, thin walled

large fenestrae without diaphragms, gaps between endothelial cells, little basal lamina

greater amount of transport

found in bone marrow, liver, spleen, lymphoid organs

Front 83

blood flow and capillaries

Back 83

thorough fare channels bypass capillary beds - no sphincters

contraction of precap sphincters directs flow from bed to AV shunts or other way around

blood flow - greatest total cross sectional area, lowest velocity

velocity of flow depends on total cross sectional area, not individual diameters

Front 84

Portal systems

Back 84

vein or artery between to beds

hepatic portal system, hypothalamic-hyphophyseal portal system, kidney efferent arterioles carry blood from glomerulus to peritubular capillaries

Front 85

capillary exchange

Back 85

hydrostatic pressure drives fluid out of caps

highest on arterial side
bulk flow in on venule side

protein stays in, water/oxygen/glucose out

Co2, N wastes, water move in

Front 86

lymphatic capillaries

Back 86

single layer of endothelial cells with an incomplete basal lamina

endothelial cells overlap partially but have intercellular spaces for access to lumen

no fenestrae or tight junctions

anchoring elements terminate on abluminal plasma membrane

more fluid in tissues means higher extracellular hydrostatic pressure, forcing fluid into lymph

small/medium have closely spaced valves to ensure one way flow

flow maintained by muscle contractions

Front 87

lymph drainage areas

Back 87

(1)Rt side - above diaphragm, rt side head/neck..rt upper arm

drains into rt subclavian

(2) left - left head/neck arm. lower body

temporarily stored in cistern chyli

thoracic duct carries lymph to left lymphatic duct

drains into left subclavian

Front 88

Transcytosis

Back 88

process by which molecules are transported from blood plasma across endothelial wall

Front 89

Pathogenesis of Artherosclerosis

Back 89

(1)LDL/VLDL binds to charged proteoglycans instead of normally leaking back out to blood

(2)oxidized lipidsinduce the endothelial cells to begin producing adhesion molecules (selectins, VCAM1 and MCP1)

(3)selectins allow monocytes and T cells to roll along surface and invade arterial wall

(4)monocytes become macrophages and begin producing pro-inflammatory cytokines that attrct more cells to invade wall to consume lipids

(5) macrophages also produce oxidizing agents that modify LDL/VLDL

(6)SR-A receptor binds to modified lipids

Front 90

macrophage to foam cell

Back 90

LDL endocytosed

goes to lysosome

chopped into fragments

fragments are effluxed to HDL or
make into cholesterol esters

Esters build up in cell = foam cell

Front 91

role of PDGF in artherosclerosis

Back 91

produced by macrophages

tells smooth muscle cells to migrate from t. media to intima

begin producing fibromuscular cap

Front 92

T cell cytokines and smooth muscle cells

Back 92

cytokines inhibit smooth muscle cell proliferation and collagen production

destabilize plaque

Front 93

fate of macrophage foam cells

Back 93

some die and relase contents within the intima

activates neighboring macrophages to produce more pro-inflammatory cytokines

Front 94

plaque rupturing

Back 94

macrophage foam cells secrete MMP that breaks down collagen

foam cells tend to concentrate at edges of plaque...destabilizing edges

rupture interrupts the anti-thrombogenic endothelial cell surface and causes platelet aggregation

Front 95

major risk factors for atherosclerosis

Back 95

age

male gender

Front 96

primary risk factors for atherosclerosis

Back 96

high LDL

low HDL

hypertension

cigarette smoking

diabetes

Front 97

secondary risk factors for atherosclerosis

Back 97

obesity

sedentary life style

Front 98

Role of female sex hormones in atherosclerosis

Back 98

progesterone and estrogen given after menopause increase risk of stroke, breast cancer with no affect on CHD

estrogen given close to menopause reduces risk atherosclerosis

unknown: protective if given at time of menopause

if estrogen is only reason for less atherosclerosis in women

Front 99

Primary prevention for atherosclerosis

Back 99

reduction of LDL and plaque = primary prevention

most cholesterol comes from synthesis (not diet)

statin drugs reduce LDL and reduce initial event for CHD

Front 100

secondary prevention for atherosclerosis

Back 100

stabilize plaque

aggressive lowering of plasma cholesterol concentrations stabilizes plaque and reduces risk of rupture

Front 101

HDL and atherosclerosis

Back 101

HDL mediates cholesterol efflux
binds to macrophage ABCA1 and ABCG1 transporters

reverses cholesterol transport

Anti-inflammatory by reducing expression of adhesion molecules (p-selectin, VCAM1) on endothelial cells

stimulates nitric oxide production which stimulates vasodilation

Front 102

Resistance to blood flow

Back 102

vessel length

blood viscosity

and RADIUS

Front 103

resistance in vessels in series vs parallel

Back 103

series - changing resistance of one vessel, dramatically changes over all resistance

parallel - changing one vessel has little effect on total resistance

Front 104

parasympathetic

Back 104

preganglionic long, synapse near organ

Neurotrans = ACh
Receptor = nicotinic

postganglionic are short

NT = ACh
receptor = muscarinic

Front 105

Parasympathetic nervous in cardiovascular

Back 105

vagal fibers innervate the heart...originate in the dorsal vagal nucleus/nucleus ambiguous

have tonic tone - always on

vagal efferents from medulla travel to SA (rt vagal) and AV (left vagal)

Front 106

sympathetic nervous system

Back 106

preganglionic fibers are short

NT = ACh
receptor = nicotinic

postganglionics are long

NT= NE
receptor = Alpha/beta adrenergics

Front 107

Sympathetics in cardiovascular system

Back 107

adrenergic control of heart and blood vessels originates in medulla

spontaneous activity - always on

increases HR and contractility

Front 108

Neural control of circulation

Arterial baroreflex - sympathetics

Back 108

carotid sinus and aortic arch

stretch receptors

fire rate increases with increased pressure (stretch)

respond to mean pressure, changes in pulse pressure, and pressure over time

very sensitive to small changes

Front 109

BP neural projections in the medulla

Back 109

initially project to nucleus solitarius

then go to either (1)depressor center - caudal ventrolateral medulla (CVLM) and decreases BP

or go to (2)pressor center - rostral ventrolateral medulla (RVLM) and increase BP

CVLM inhibits RVLM

Front 110

parasympathetic baroreflex

Back 110

tonically active...arise in dorsal vagal/ambiguous

(1)excitatory connection to dorsl motor nucleus of vagas (DMN X) and the nucleus ambiguous (NA)

(2)inhibitory projections directly on end organs

Front 111

Cardiopulmonary reflexes

Back 111

stretch receptors in the heart - particularly atrium

relate blood volume

increase in blood volume leads to increased sympathetic activation and diuresis

Front 112

Chemoreceptor reflexes

Back 112

monitor oxygen, CO2 and H+

peripherally located in carotid and aortic body

also centrally in medulla

Regulate: respiratory activity to maintain normal pH, pO2 and pCO2

send to nucleus solitarius

Front 113

Humoral control

Back 113

(1) catecholamines

(2)Renin-Angiotensin-Aldosterone System

(3)Vasopressin

(4)Atrial natriuretic peptide

Front 114

Humoral control

catecholamines

Back 114

released by adrenal medulla (epinerpherine and NE)

stimulates renin release and subsequently AngII and aldosterone

Front 115

humoral control

renin angiotensin aldosterone system

Back 115

regulates blood volume and pressure (long term)

kidney main organ

regulated by: sympathetics, renal artery hypotension, decreased sodium

mechanism: renin converts angiotensinogen to A1, A1 becomes A2. A2 modulates many cardiovascular events

stimulates muscle mass in ventricles
stimulates vasoconstriction
stimulates thirst
stimulates aldosterone - kidney retains fluid

Front 116

humoral control

vasopressin

Back 116

released by posterior pituitary

acts at kidney

(1) increases fluid reabsorption
(2)vasoconstriction

Front 117

humoral control

atrial natriuretic peptide

Back 117

stored atrial myocytes

released by stretch and Ang2

counter balances RAAS by vasodilation and fluid release

Front 118

vasodilator reserve

Back 118

difference between basal and maximal flow

Front 119

AV O2 difference

Back 119

measure of oxygen extraction between arterial and venous sides

small differences suggest that additional oxygen can be extracted without greatly increasing flow

Front 120

active hyperemia

Back 120

increase in blood flow in response to metabolic demand

Front 121

reactive hyperemia

Back 121

blood flow increase in response to brief periods of ischemia

Front 122

Tissue Factor control of vasculature

Back 122

originate in surrounding tissue or paracrine cells

vasodilator or constrictor

interact with endothelium or smooth muscle

Front 123

endothelial factors and circulatory control

Back 123

endocrine, paracrine, or autocrine

physical factors - shear stress

may act on endothelial or on smooth muscle

vasodilator/constrictor

Front 124

myogenic response

Back 124

originates within the smooth muscle of arteries/arterioles

occur in response to sudden change in pressure

increased pressure, smooth muscle constricts to preserve vascular resistance and diameter

Front 125

vasodilators

Back 125

NE, PE, O2

Front 126

special circulations

Back 126

(1) coronary

(2)cerebral circulation

(3)skeletal muscle

(4)cutaneous blood flow

(5)splanchnic circulation

(6) renal circulation

(7) pulmonary circulation

Front 127

special circulation

coronary

Back 127

major vessels lie on epicardial surface = low resistance

branches dive into myocardim - act as regulators

Pulsatile perfusion - diastolic flow...compressive forces high during systole so not a lot of flow during systole

large vasodilator reserve

highly regulated by tissue metabolism (adenosine)

little oxygen extraction reserve

Front 128

special circulation

cerebral circulatoin

Back 128

circle of willis

rigid structure so in flow must equal out flow

endothelium has tight junctions and a basement membrane = BBB

blood flow tightly coupled to oxygen demand

predominant control of cerebral circulation is determined by local factors (CO2)

Front 129

special circulation

skeletal muscle

Back 129

blood flow to satisfy metabolic demand

vascular anatomy is highly organized - capillaries can be recruited if high demand

type of exercise changes blood flow - sustained contraction (reactive hyperemia) vs phasic (active hyperemia)

control: myogenic tone

muscle contraction can occlude vessels

metabolites - can override sympathetic control of vascular tone

Front 130

special circulation

cutatenous blood floow

Back 130

primary function = maintain body temp

regulation is neural

regulation at deeper AV anastomoses

Neural control: tonic sympathetic vasoconstriction

Raynaurds syndrome - too much constriction (ischemia, cold hands)

Front 131

special circulation

splanchnic circulation

Back 131

receives large portion of blood volume

can redistribute blood elsewhere (compensatory adjustments) if blood loss

neural control: sympathetic innervations of arterioles and veins

high resting sympathetic vasoconstriction tone

Front 132

special circulation

renal circulation

Back 132

receives relatively high blood flow but is constant

primary function - salt and water balance...long term BP control through blood volume

anatomy: two capillary segments in series...glomerular and peritubular

important for filtration and reabsorption


strong auto-regulation

doesnt respond to sympathetic stimulation

Front 133

special circulation

pulmonary circulation

Back 133

(a) pulmonary - supplies blood to alveoli for gas exchange

dervived from RT ventricle

low resistance, low pressure

hypoxia causes vasoconstriction to preserve blood flow to functional alveoli

(b) bronchial
derived from aorta

nutritive flow to trachea and bronchial structures

Front 134

Epidemiology of PAD

Back 134

8-12 million Americans
chronic process evolving over several decades

M=F

Front 135

Area most commonly affected in PAD

Back 135

abdominal aorta

lesion area greater in women

greater in smokers

pain when stenosis >75%

Front 136

PAD presentation

Back 136

gradual onset

exertional aching pain, cramping, tightness, fatigue

occurs in MUSCLE GROUPS not joint

reproducible pain (exact same amount of exercise every time)

resolves with rest

Front 137

Types of claudication

Back 137

(1) intermittent arterial claudication

(2) spinal neurological or pseudo claudication

(3) venous claudication

(4) arthritic claudication....good days/bad days

Front 138

pseudoclaudication

Back 138

musculosketal disease

location in the same place

pain similar

but problems still occur at rest

good days bad days

pain doesnt go away with standing

Front 139

lifestyle consequences of claudication

Back 139

functional ability similar to NYHA class III CHF

Front 140

Buerger's Disease vs atherosclerotic disease

Back 140

athero - have cardiovascular risks

smoking common in both

men = women

location - aorto iliac, coronaries, carotids

phlebitis - very rare

Front 141

thrombosis vs embolism in claudication

Back 141

embolism - 70%

sudden, no distal pulses, no collaterals, frequently bilateral

source: cardiac
atheroemboli
paradoxical - DVT

thrombosis - 30%
distal pulses, collaterals,
origin - aneurysm
arterial occlusive disease - hyper coag state or atherothrombosis/buerger's disease

Front 142

Atheromatous embolization

Back 142

causes of thrombembolus

trauma, invasive procedures

legs most common site (then kidneys)

blue toe sign

livedo reticularis

Front 143

risk factors for PAD

Back 143

Age
diabetes
smoking

lipids: high triglycerides
low HDL

family hx in young

Front 144

Ankle Brachial Index (ABI)

Back 144

= lower extremeity systolic/brachial systolic

use highest brachial

lowest calculated ABI for diagnosis of PAD

Front 145

Non-invasive evaluation of lower extremity circulation

Back 145

(1) ABI

(2) Resting segmental pressures

(3) resting pulse volume recordings

(4) Exercise testing

(5) Duplex utrasound

(6) Transcutaneous oximetry

Front 146

Sites of extremity atherosclerosis

Back 146

any bifurcation in arteries

CFA, SFA, profunda femoris
tibial, peroneal
aorto-iliac

Front 147

Major collateral pathways in legs

Back 147

(1) lumbar aortic branches (aortic disease)

(2) internal iliac system and pelvic circulation (CIA disease)

(3) circumflex femoral arteries (CFA disease)

(4) profunda femoris (SFA disease)

(5) geniculate arteries (PA disease)

Front 148

Leriche's Syndrome

Back 148

focal occlusive disease of distal aorta and proximal iliac

findings - small caliber abdominal aorta
multiple periaortic adhesions

calcified atherosclerotic plaque and thrombosis

operation - aorto iliac endarderectomy; aorto bi iliac bypass

Front 149

Post op for all PAD patients

Back 149

BP control
130/80 for renal and diabetics
140/90 for others

lipid control

diabetes control

smoking cessation

platelet control

Front 150

Plavix vs aspirin platelet control in PAD

Back 150

plavix

Front 151

Medical intervention for PAD

Back 151

exercise

smoking cessation

cilostazol - improves claudication, but dont use with heart failure

MAO: inhibits PDE III
blocks platelet aggregation, blocks thrombosis, vasodilation of collaterals

Front 152

Cilostazol

Back 152

improves caludication
dont use with CHF patients

MAO: inhibits phosphodiesterase III
blocks platelet aggregation, blocks thrombosis, vasodilation of collaterals

Front 153

Surgical intervention for PAD

Back 153

better improvement of clinical symptoms

Front 154

screening for PAD

Back 154

any patient with exertional leg pain

>50 with risk factors

>40 with strong risk factors

all patients over 70

Front 155

Renin in renal stenosis

Back 155

less blood flow, release Renin

Renin converts angiotensinogen to A1

ACE converts A1 to A2

A2 causes:

vasoconstriction
renal sodium retention
aldosterone secretion
LV Hypertrophy, remodeling, endothelin release
sympathetic nervous activation

Front 156

Unilateral renal stenosis and renin

Back 156

abnormal kidney activates RAAS

contralateral has increased perfusion, increases sodium excretion

net effect: plasma renin elevated

Front 157

bilateral renal stenosis and renin

Back 157

both activate renin

impaired sodium, water retention

once volume adequate get steady state: plasma renin is normal

patient is hypertensive

Front 158

clinical implications of renal stenosis

Back 158

paroxysmal hypertension - marked spikes in BP

treatment resistant hypertension

hypertensive nephropathy

renal failure

flash pulmonary edema

accelerated cardiovascular disease

Front 159

children with renal lesions

Back 159

correctable before 10 yo

Front 160

prevalence of adults with hypertension

Back 160

24% have renal vascular disease

older and BP>110 and renal insufficiency = more likely to have stenosis

Front 161

causes of renal stenosis lesions

Back 161

(1)atherosclerosis - 75%

(2) fibromuscular dysplasia - 20% and in younger people

(3) miscellaneous

Front 162

fibromuscular dysplasia

Back 162

(1) medial fibroplasias - 85%
more common in women

(2) intimal fibroplasias - 5%
focal and in children

arteries affected:
renal
carotid
iliac

can have aneurysms

Front 163

tests for reno-vascular disease

Back 163

(1) functional -

rapid sequence excretory urography

peripheral plasma renin

isotopic renography

(2) anatomic

angiography
MRI/MRA/CTA

Front 164

isotopic renography

Back 164

measures filtered radioactive tracer before and after ACE inhibitor

angiotensin II maintains GFR in kidney with renal stenosis via increased vasoconstriction in efferent arteriole

ACE inhibitor reduces synthesis of A2, diminishes efferent arteriole vasoconstriction and thus a decreased GFR

therefore less uptake of filtered radioactive tracer after ACE inhibitor

Front 165

when to intervene in renal stenosis

Back 165

severe

bilateral

rapidly deteriorating renal function

normal distal renal artery

Front 166

visceral ischemic syndromes: mesenterics

acute vs chronic

Back 166

acute - sudden onset
usually artery occlusion

mesenteric vein occlusion - more likely to cause gangrene of bowel

non-obstructive mesenteric ischemia - no lesion, large portion threatening to die off...just enough ishcemia to cause potential death

chronic - due to atherosclerosis

Front 167

incidence of mesenteric ischemia

Back 167

mesenteric artery occlusion - 75%

thrombus - 65%
embolus - 35%

mesenteric vein occlusion - 15%

non-obstructive mesenteric ischemia - 10%

Front 168

risk factors for mesenteric ischemia

Back 168

age >60

atrial fibrillation

CHF

recent MI

clotting disorder

hypercoaguable

hypOvolemia

Front 169

embolus vs thrombosis in visceral ischemia

Back 169

embolus - sudden onset
paucity of physical findings - extreme pain out of proportion

bowel evacuation

cardiac embolic risk

thrombosis -
insidious abdominal pain
systemic toxicity

Front 170

mesenteric vein occlusion

Back 170

insidious, diffuse abdominal pain

vague prodromal period
nausea, vomiting, distention
hypovolemic cardiovascular collapse

causes:
secondary
infection
clotting disorder
inflammatory bowel disease

Front 171

NOMI

Back 171

spasm of blood vessel in bowel

Front 172

chronic mesenteric ischemia

Back 172

fear of food
weight loss
post-prandial (after eating) abdominal pain

Front 173

dx of ischemic visceral syndromes

Back 173

CT
angiography
duplex

Front 174

tx of ischemic visceral

Back 174

can use local medical

embolus - surgery to remove

Front 175

survival of visceral ischemia

Back 175

remote organ dysfunction - systemic inflammatory response
main reason for death
renal insufficiency
hepatocellular dysfunction

survival - 20% in five years

Front 176

venous anatomy of legs

Back 176

deep system - within muscle and fascia

superficial system - drains into the deep

perforators connect the two

Front 177

vein wall

Back 177

has some components as an arterial wall (intima, media, adventitia)

muscular layer (media) not prominent in veins

Front 178

venous physiology

Back 178

post capillary blood collects in venules, drains into larger veins

superficial drains to deep

Front 179

vein valves

Back 179

allows flow towards larger tracts

prevent back flow

often found at junction and perforators

reduce column heihgt of blood to reduce STATIC PRESSURE

Front 180

hydrostatic pressure in veins

Back 180

static pressure of fluid column

transmitted right atrial pressure
overall volume status
thoracoabdominal pressure

Front 181

muscle pump in veins

Back 181

hydrodynamic pressure

calf muscles surround deep veins and the muscles are covered in fascial linings

muscle contraction increases the compartment pressure and forces blood out of the deep veins

valves prevent back flow to superficial system...propel blood to deep veins

Front 182

pathophysiology of venous disorders

Back 182

(1) valve failure - increased column height increases static pressure

(2) obstruction

(3) thromboembolus

effects: additional valve failure
capillary bed - edema inflammation
chronically - get structural changes and inflammation of surrounding tissue

Front 183

varicose veins

Back 183

genetic component
valve incompetence - saphenofemoral, saphenopopliteal, perforators

pain, aching sensation

Tx. compression stocking, elevation, removal of varicosities and any reflux

Front 184

Telangiectasias - spider veins

Back 184

same proces as varicose veins but on small scale

symptoms - cosmetic, occasional pain

tx - exclude larger vein reflux injection sclerotherapy, laser

Front 185

skin changes with venous stasis

Back 185

lipodermatosclerosis

pgimentation - hemosiderin deposition

eczema

ulceration - often perforating vein

gaiter area - common site

Front 186

management of varicose veins

Back 186

aggressive compression

elevation

antibiotics and debridement when infected

skin grafts

Front 187

DVT

risk factors

Back 187

local effects and embolization

age

prior hx

trauma

malignancy

exogenous estrogens

obesity

surgery - hip, knee, pelvic

malignancy - sometimes get DVT many years later get a malignancy

Front 188

DVT dx, hx, pe

Back 188

warmth, redness

homan's sign

d-dimer labs

imaging is the best...venous duplex

Front 189

DVT sequlae

Back 189

local - swelling distal
long term potential for dysfunction (morbidity)

systemic - postphlebitic syndrome or thrombo-emboli (mortality)

Front 190

DVT prevention/tx

Back 190

mechanical compressors

pham - anticoags

tx. anti coags and compression socks

Front 191

Phlegmasia Cerulea Dolens

Back 191

limb threatening extensive venous trhombosis

often associated with cancer

limb threatening, need emergency surgery

Front 192

lymphatic disorders

Back 192

extensive interstial fluid enters lymphatic capillaries

have valves too, usually fail

drainage dependent on compression forces

80% drain into left chest

Front 193

lymphedema

Back 193

protein rich

interstial volume overload

failed lymph drainage

Front 194

edema

Back 194

increased interstial fluid volume

Front 195

primary lymphedema

Back 195

inherent defect within lymph conduits

Front 196

secondary lymphedema

Back 196

acquired damage to lymph conduits

Front 197

types of primary lymphedema

Back 197

(1) congenital - milroy's disease

(2) lymphedema praecox - most common <35 yo
usually unilateral, adolescent women
hypoplastic lymphatics

(3) lymphedema tarda - congenitally weakened lymphatics event triggers onset >35 yo

Front 198

secondary lymphedema

Back 198

obstruction

most common in the world = filariasis

most common in US = treatments from other malignancy

Front 199

skin changes with lymphedema

Back 199

fibrosis

hyperkaratotic

Front 200

tx for lymphedema

Back 200

no cure

elevation minimal effect

exercise helpful

compression with massage

manual lymph drainage

Front 201

Stroke -

Back 201

focal neurlogical deficit related to neuronal cell death with signs and symptoms lasting greater than 24 hrs

Front 202

TIA

Back 202

a focal neurological deficit with signs and symptoms lasting less than 24 hrs

Front 203

risk factors for stroke

Back 203

Hypertension - most major modifiable risk factor

increasing age

cardiovascular disease: atrial fibrillation

smoking

carotid stenosis

Front 204

stroke etiology

Back 204

ischemia - 80%
embolism - major cause

hemorrhage - 20%

Front 205

stroke pathophysiology

Back 205

cardiac most common source - atrial fibrillation

atherothrombotic carotid stenosis

lacunar infarcts - diabetes and hypertension

Front 206

atherothrombotic stroke

Back 206

major cause of preventable stroke

carotid disease

vertebrobasillar disease

hypotension - watershed strokes

Front 207

carotid disease and stroke

Back 207

anatomy - disease of the carotid bulb
rich source of emboli
embolic risk related to plaque burden

predominantly atherosclerotic

other causes - fibromuscular dysplasia

arthritis - takayasu's
giant cell arthritis

dissections

radiation

Front 208

risk factors of carotid disease and stroke

Back 208

advanced age

cigarette smoking

HYPERTENSION

cardiovascular disease

hyperlipidemia

Front 209

carotid disease stroke presentation

Back 209

TIA

amaurosis fugax

completed stroke

vertebrobasillar symptoms

Front 210

TIA presentation

Back 210

contralateral paresis

contralateral numbness

aphasia

Front 211

Amaurosis fugax

Back 211

temproary ipsilateral monocular visual loss due to embolization of retinal artery or branches

visual field defect

not scotomas or floaters

Front 212

dx of carotid disease

Back 212

carotid duplex

CTA arteriography

MRA

Front 213

carotid disease natural hx

Back 213

depends on presentation

asymptomatic

symptomatic - 2 year stroke risk of 15-30%

Front 214

carotid disease tx

Back 214

secondary prevention/medical management

hypertension, smoking lipid, diabetes, antiplatelets

Front 215

surgical recommendations for carotid disease

Back 215

based on severity of stenosis and symptoms

(a) optimal medical therapy without revascularization in symptomatic patients with <50% stenosis

(b) medical when asymptomatic in patients <60% stenosis

(c) carotid endarterectomy plus medical in symptomatic 50-99% stenosis

(d) endarterectomy plus medical in asymptomatic 60-99% stenosis and low perioperative risk

Front 216

vertebrobasilar disease

Back 216

embolization or low flow

symptoms - dizziness, vertigo, diplopia, blurred vision, ataxia, drop attacks

epidemiology - much less common than carotid disease

Front 217

risk factors for vertebrobasillar disease

Back 217

`age

smoking

cardiovascular disease

Front 218

symptoms of vertebrobasilar disease

Back 218

more common from flow related phenomena

systemic hypotension, brady/tachy. autonomic dysfunction/compression

Front 219

arteries potentially affected in vertebrobasillar disease

Back 219

innominate

subclavian

vertebral

carotid

Front 220

presentation of vertebrobasillar

Back 220

dizziness

vertigo

diplopia

blurred vision

ataxia

Front 221

vertebrobasillar and precipitating factors

Back 221

need to know

problems when head turning?

problems when rising/standing?

problems when using upper extremities?

Front 222

dx of vertebrobasilar

Back 222

pulse examination of upper extremity blood pressures

duplex - transcranial doppler

imaging

Front 223

tx of vertebrobasilar

Back 223

hypertension management

smoking

lipid, diabetes, antiplatelet agents

increase pressure to basilar
- subclavian or vertebral artery

Front 224

tx of extracranial occlusive disease with global hypoperfusion

Back 224

treat anterior carotid disease first

Front 225

Giant cell arteritis (temporal arteritis)

Back 225

temporal headaches

jaw claudication

polymyalgia rheumatic

amaurosis

constitutional symptoms

dx temporary artery biopsy

tx corticosteroids

Front 226

carotid artery dissections

Back 226

spontaneous

traumatic

can lead to pseudoaneurysms

Front 227

aneurysm

Back 227

focal dilation of an artery involving an increase in diameter of at least 50% as compared to expected diameter

true - have the vessel layers

false - have none of vessel wall layers

Front 228

aortic aneurysms

Back 228

75% of all aneurysms

male> female

atherosclerotic

below renals

Front 229

pathogenesis of aortic aneurysms

Back 229

(1)smooth muscle

(2)matrix proteins - elastin, collagen
decreasing matrix concentrations from proximal to distal aorta

(a) elastin - load bearing protein
(b)collagen - safety net...resists AAA rupture

(3) up regulation of matrix metalloproteinases

(4) infection - chlamydia
(5) autoimmune/inflammation
(6) genetic

Front 230

Epidemiology of AAA

Back 230

3-10% of people over 50yo

Front 231

risk factors for AAA

Back 231

elderly white males...peak at 80yo

M>F

white>AA

Front 232

presentation of AAA

Back 232

asymptomatic

occasionally feel pulsation

Front 233

rupture of AAA symptoms

Back 233

most symptomatic

abdominal or back pain

most palpable

Front 234

dx of AAA

Back 234

imaging

ultrasound or CT

angiography not good for screening...use CTA more often

Front 235

AAA screening

Back 235

males >65

smokers

family hx

Front 236

risk of AAA rupture

Back 236

larger

>4 cm, screen every 6 months

5.5 cm surgery suggested

Front 237

when to do surgery for AAA

Back 237

>5.5 cm diameter

life expectancy is greater than 2 years

balance rupture risk, operative risk, life expectancy

Front 238

co-morbidities of AAA

Back 238

coronary artery disease

pulmonary disease

renal failure

Front 239

complications of AAA repair

Back 239

early - MI

late - graft infection

Front 240

Aortic Dissection

Back 240

non radiating chest pain

separation of aortic wall layers by extra luminal blood...usually through tear in intima

blood may circulate between aortic lumen and abnormal channel

uncommon clinical event

survival low

Front 241

risk factors for Aortic dissection

Back 241

male>female

location - ascending in 50-55yo
descending aorta 65-70yo

chronic systemic hypertension

aortic diseases

bicuspid aortic valve

trauma

cocaine

pregnancy

rebound from abrupt discontinuation of beta blocker therapy

Front 242

Marfan syndrome

Back 242

hereditary connective tissue disorder

auto dominant

defect in fibrillin 1

affects skeleton, heart, major vessels, lungs, eyes

get dilation of aorta

Front 243

DeBakey classification of Aortic Dissection

Back 243

type 1 - starts at valve goes all the way down

type 2 - just valve

type 3 - descending aorta

Front 244

Tx of aorta dissection

Back 244

ascending - surgery + medical control of bp (beta blockers)

descending - control with medical therapy for BP (beta blockers)

Front 245

clinical manifestations of aortic dissection

Back 245

sharp pain

doesnt radiate

hypertensive

diastolic murmur

Front 246

dx of aortic dissection

Back 246

imaging - CT, MRI

Front 247

peripheral and visceral aneurysms

Back 247

femoral - most common false aneurysms

popliteal - most common true aneurysm

popliteal - tend to be limb threatening...more likely to thrombose of embolus then rupture
more likely atherosclerotic

male>female

strongly associated with aneurysms elsewhere in body

Front 248

popliteal vs femoral aneurysm

Back 248

popliteal - most common true anuerysm

usually atherosclerotic


femoral - more common false aneurysm

both more likely to embolus/thrombos then to rupture

Front 249

visceral aneurysms

Back 249

splenic artery most common

biggest concern is rupture

increased risk with pregnancy

diameter 2-3cm

Front 250

BP =

Back 250

(left ventricle end diastolic volume - left ventricle end systolic volume) x HR x SVR

depends on:

how full at end of diastole

how empty at systole - strength of contraction, difficulty in ejecting blood

heart rate

resistance in vasculature

Front 251

alpha 1 receptors

Back 251

peripheral and splanchnic vasculature in smooth muscle

few in heart muscle

stimulation: contraction of smooth muscle = vasoconstriction

Front 252

alpha 2 receptors

Back 252

peripheral and splanchnic vasculature

fewer than alpha 1

in smooth muscle, cause contraction

on presynaptic neurons, has negative feedback so less NE released with stimulation....net effect = less effect of future drugs

also present in CNS causes sedation and pain relief

Front 253

beta 1 receptors

Back 253

cardiac tissue

inotropic effect - increased contractility

chronotropic effect - increased HR

lusitropic effect - relaxes faster in systole

peripheral - causes smooth muscle relaxation/vasodilation....minor role

presynaptic receptors: causes positive feedback...increases enhanced release of future stimulus

Front 254

beta 2 receptors

Back 254

cardiac tissue - much more beta 1 though

ratio of beta 1 to beta 2 increases in CHF (lose beta 1s)

same effect as beta 1:
inotropic
chronotropic
lusitropic

peripheral - minor vasodilation

bronchial smooth muscle - causes bronchodilation/relaxation

Front 255

dopamine receptors

Back 255

cardiac tissue: 2 types
minimal effect but what it does is:

iontropic

CHRONOTROPIC

splanchnic vasculature- causes vasodilation...major role of dopamine receptors

CNS

Front 256

vasopressin receptors

Back 256

peripheral vasculature - marked vasoconstriction

splanchnic vasculature - marked vasoconstriction

Front 257

beta receptor complex:

Back 257

drug binds to receptor

receptor interacts with G protein

G protein interacts with intracellular bound adenylcyclase

adenylcyclase converts ATP to cAMP

cAMP activates numerous cascades...one activates a phosphorylase that binds to calcium channels

increaess amount of calcium that can come in, this increases amount of SR released calcium

get strong contraction, also allows for calcium to get pumped out faster so relaxation faster

phosphodiesterase degrades cAMP

Front 258

preload manipulation

Back 258

can't measure directly

increase: give fluids

alpha agonists in low doses

Front 259

afterload manipulation

Back 259

left ventricle end systolic volume

not measured = amount coming out of ventricle and resistance to pumping out

estimated with Hx and PE

rx: vasodilators

ACE inhibitors, nitroprusside
PDE inhibitors

Front 260

contractility manipulation

Back 260

also part of end systolic volume

not measured

estimated by hx and PE

= force generated by LV

Rx. inotropes
give beta
PDE inhibitors

Front 261

HR manipulation

Back 261

chronotropy

easily measured

at high rates, cant fill fast enough

rx. chronotropes
beta, atropine, aminophyline, pacemaker

Front 262

SVR manipulation

Back 262

vascular resistance

not measured, calculated

rx. vasoconstrictors - alpha and vasopressin

Front 263

epinepherine

Back 263

beta effects predominate (has some alpha at higher doses)

inotropic and chronotropic (Beta)

use - sepsis, cardiogenic shock

Front 264

dobutamine

Back 264

inotrope with vasodilator (reduces afterload)

beta mostly

increases contractility and HR

vasodilates and reduces afterload

Use - MI

Front 265

norepinephrine

Back 265

alpha effects - overwhelming vasoconstrictor

some beta high doses

use - sepsis helps support heart in high doses

Front 266

phenylephrine

Back 266

pure alpha, but weak

vasoconstriction and increased SVR

mild sepsis, hypotension

Front 267

dopamine

Back 267

use for renal support

beta and alpha at very high doses

one drug, every receptor

Front 268

vasopressin

Back 268

intense vasoconstriction, no alpha or beta

use - severe sepsis

Front 269

phosphodiesterase inhibitors

Back 269

vasodilators and inotropes

augements beta stimulation

smooth muscle relaxation

keeps cAMP around longer

Front 270

MI pathology general

Back 270

chronic - coronary atherosclerosis

acute - changes in plaque

Front 271

Dx of MI

Back 271

coronary arteriogram

Front 272

Acute symptoms of MI

Back 272

unstable angina

Non ST- elevation myocardial infarction

ST elevation myocardial infarction

Front 273

Acute Coronary syndromes

Back 273

result from diminished coronary perfusion relative to demand

usually a hemorrhagic rupture of a fat laden, unstable atheroma with development of an occlusive platelet thrombus

plaque rupture exposes interior to blood (1) platelet aggregation (2) coagulation thus get thrombus formation

Front 274

MI pathology specific

Back 274

Initially, a sudden change occurs in the morphology of an atheromatous plaque - intraplaque hemmorrhage, ulceration, or fissuring
Platelets are exposed to subendothelial collagen and necrotic plaque contents, leading to adhesion, activation, and aggregation of platelets. This leads to buildup of platelet mass which gives rise to emboli or potentiates occlusive thrombosis.
Simultaneously, tissue thromboplastin is released, activating the extrinsic pathway and fibrin deposition.
Adherent activated platelets release thromboxane A2, serotonin, and platelet factors . These predispose to coagulation, favors vasospasm, and adds to the bulk of the thrombus.
The thrombus evolves to become occlusive(often within minutes).

Front 275

uncommon MI pathology

Back 275

erosion of endothelium exposing interior plaque

vasospasm from cocaine

emboli from left atrium

Front 276

factors affecting MI plaque rupture

Back 276

Sudden changes in intraluminal pressure or tone
Bending and twisting of an artery during each heart contraction
Lipid content of plaque
Thickness of fibrous cap
Plaque shape
Mechanical injury

Front 277

myocardial response to coronary occlusion

Back 277

Get ischemia in region supplied
Starts at subendo and progresses to epicardium
Get anaerobic glycolysis…leads to inadequate production of ATP and accumulation of noxious breakdown products

Eventually get necrosis
In absence of reperfusion – hypoxia and noxious metabolites leads to impaired ventricular function…predisposing to lethal arrhythmias
Get transient diminished diastolic relaxation, abnormal systolic contraction, abnormal wall motion, diminished stroke volume

Front 278

dx of MI

Back 278

With symptoms of ischemia
ECG
Pathological Q waves

Front 279

presentation of MI

Back 279

Acute onset of chest pain radiating to left arm and neck, shortness of breath

Atypical chest or epigastric discomfort

Front 280

risk factors for MI

Back 280

Hypertension
Smoking
High ldl, low hdl
DM
Family hx
Sedentary lifestyle
Obesity
Age

Front 281

cardiac markers for MI

Back 281

Detection in plasma released by injured myocardium
Troponin most specific
Can use CK-MB
AST, LDH
Look at MB to CK, peaks early
LDH peaks late
Troponin peaks a few days after MI

Troponin and CK don’t begin evaluating until at least 4 hrs

Troponin correlated with outcome

Front 282

ECG findings in MI

Back 282

ST elevation
T waves get very high..earliest sign of injury
Ongoing injury will get ST elevation
Thought to be persistent occlusive disorder…no flow restored

Non ST Elevation MI
More likely to have multivessel CAD
Prior MIs
Diabetes

Front 283

fields of coronary arteries

Back 283

LAD – anterior, spetum/anteroseptum, anterolateral

L Circumflex – lateral or posterior

RCA – inferior

Front 284

Prognosis of MI

Back 284

Early – presence of arrhythmias

Late – determined by left ventricular function

Front 285

complications of MI

Back 285

Arrhythmias

CHF
Cardiogenic shock

Pericarditis

Scar or ventricular aneurysm

Front 286

CHD epidemiology in women

Back 286

leading cause of mortality

major cause of disability - 55% over 75yo

prevalence equal with men at 40-59yo

Front 287

Gender differences in MI

Back 287

Men younger

Women less likely to undergo cardiac workup when presenting with chest pain

Non-invasive studies have decreased sensitivity and specificity in women

Higher in hospital stay

Worse long term mortality

Women have more risk factors

Women have higher silent MI

Women have atypical pattern for angina such as neck/jaw pain, dyspnea or fatigue

Front 288

coronary artery disease risk factors

Back 288

Hypertension

Diabetes mellitus - relative risk increases with heart disease

Dyslipidemia

Smoking

Age (men >45 women >55)

Family hx

Front 289

obesity in women and MI

Back 289

increasing problem in the US

women started fatter, getting fatter

looking at wast circumference to hip
higher ration, higher risk of CHD

Front 290

Smoking and women with MI

Back 290

women smoke less than men

but still risk factor

Front 291

guidelines for LDL in MI

Back 291

<160 with 0-1 risk factors

<100 with >2 risk factors

<70 with CHD

Front 292

C reactive protein and CHD in women

Back 292

CHD - sensitive marker for inflammation

associated with CHD

statins will reduce

Front 293

Alcohol risk vs benefit in MI in women

Back 293

drinking less than 2 a day is slightly beneficial in no risk factors

>1 risk factors, even better improvement

>2 drinks, increases risk in women

Front 294

gender differences in risk factors

Back 294

Diabetes much stronger predictor in women than men

High triglycerides worse for women

Physical inactivity more prevalent in women

Smoking may be stronger

CRP levels higher in women

Front 295

Sex hormones in women with MI

Back 295

estrogen - modifies lipid, arterial vasodilation, clot formation

progesterone unclear

HERS study: HRT was associated with increase in invasive breast cancer without CAD benefit


increased stroke and PE

Front 296

types of atherosclerosis lesions

Back 296

fatty streak - innocuous, small, intracellular fat in intima

atheroma - raised, lipid center

fibrous plaque - innocuous, intimal scar...problem when it ruptures

Front 297

Atheroma

Back 297

sites: intimal, may involve media
arteries - aorta and its major branches

elements: necrotic center of extracellular lipid
fibrous cap - in contact with blood

proliferation cells - myofibroblasts


complications: within plaque - ulceration, fissuring
thrombosis - often caused by ulceration

medial damage - causing aneurysms

hemorrhage into plaque

calcification

insidious: usually asymptomatic until 75% stenosis

Front 298

atheroma effects and clinical complications

Back 298

Aortic branches: aneurysm, mural thrombus, rupture

Cardiac: infarct, ischemia, dysrhythmia, sudden death

GI: ischemia, infarction

Brain: infarction (Stroke), ischemia

Peripheral: ischemic atrophy, claudication and gangrene

Clinical complications of atherosclerosis:

Carotids and vertebral: cerebrovascular disease
Narrow, ulcerate, embolize, cause ischemia or infarct

Coronary arteries: ischemic heart disease
Narrow, ulcerate, or thrombose, causing ischemia, infarct, arrhythmia, heart failure

Peripheral arteries: PVD
Ischemia, gangrene, usually lower limbs or intestinal

Aorta: aneurysm, rupture, atheroembolism, mural thrombus with thrombembolism

Front 299

properties of ion channels

Back 299

selective but passive

unidirectional

Front 300

properties of exchanger channels

Back 300

selective and passive

exchanged based on differences in concentration...not necessarily 1 to 1, can change direction depending on relative gradients

Front 301

properties of pump channels

Back 301

selective and actively transport ions across membrane against concentrations or voltage gradients

ATP used

in heart

increase intracellular potassium and decrease intracellular sodium/calcium

Front 302

myocyte ion concentrations at steady state

Back 302

K in

ca/Na out

negatively charged inside (proteins inside are negative) -90mV

Front 303

cardiac myocyte channels at rest

Back 303

Na closed
Ca closed
some K closed
some K open

cell is actively pumping Na/Ca out

K is leaking out passively

Front 304

Cardiac AP

Phase 4

Back 304

resting state

Na closed

Ca closed

K closed, some leaking out

-90mV

Front 305

Cardiac AP

Phase 0

Back 305

rapid depolarization of Na into cell

Front 306

Cardiac AP

Phase 1

Back 306

very brief

some transient outward current corrects for over shoot of depolarizing

Front 307

Cardiac AP

Phase 2

Back 307

plateau phase

calcium channels open - calcium into cell

Na closed

calcium takes long time to come in, the other receptors hold depolarized state

Calcium binds to SR, letting out more calcium

(Calcium activated calcium release)

Front 308

Cardiac AP

Phase 3

Back 308

repolarization

calcium channels close

Na closed

K only ones open

lose positive charge

get to -90mV

Front 309

QRS and cardiac cycle

Back 309

phase 0

Front 310

ST and cardiac cycle

Back 310

phase 2

Front 311

T wave and cardiac cycle

Back 311

phase 3

Front 312

Refractory periods of cardiac cycle

Back 312

(1)absolute refractory period

(2) effective refractory period

(3)relative refractory period

Front 313

Absolute refractory period

Back 313

all Na inactivated

Ca open

cell is completely inexcitable

Phase 2

cant make a new AP

Front 314

Effective Refractory Period

Back 314

absolute + part of phase 3

Na channels still closed

Some Ca channels closed - meaning they can reopen

any inducible AP will be too weak to propagate

Effectively cell is inexcitable

Front 315

Relative refractory period

Back 315

cell is beginning to repolarize

not at rest yet (in phase 3)

Na channels are still inactivated

Ca channels are mostly closed but some can be reopened

strong stimulus can induce an AP that will be lower in amplitude and slower in velocity...strong enough to propagate

Front 316

Automaticity

Back 316

ability of cell to generate a tone rhythm

in cardiac cells - phase 4 resting takes external stimulus to get to threshold

but some cells have inward leak of positive ions in phase 4 (pacemaker current - SA, AV, His/purkinje bundles

mostly sodium, some calcium

continueal leak of opsotive ions does bring cell to threshold, generating automatic rhythm

SA/AV so leaky cant actually get to -90 or even threshold

depolarization is driven by Ca channels because they do not have Na channels

Front 317

difference in nodal cell AP and cardiac AP

Back 317

phase 0 - slower in nodal

phase 1 - does not occur in nodal (no Na to overshoot)

phase 2 - Ca drive phase 0 instead

phase 3 - occurs normally

Front 318

autonomic nervous system on cardiac AP

Back 318

affect slope of phase 4 depolarization

sympathetic increase slope (epi) - mediated by calcium channels

parasympathetics decrease slope and slightly hyperpolarize at end of phase 3...mediated through calcium channels

Front 319

Atrial myocytes and current flow

Back 319

repolarize quickly

able to sustain rapid arrhythmias (refractory period)

Front 320

His, bundle, and purkinje and current flow

Back 320

ERP longer than atrial

transmit signal through ventricles

all basically same type of cells

transmit individual heart beat quickly

have more Na channels - each individual cell activates faster, plus more gap junctions, plus better gap junctions

Front 321

AV node and current flow

Back 321

some automaticity, but real purpose is to conduct SA node

moves slowly - protects from atrial fibrillation becoming ventricular fibrillation

Front 322

dromotropic

Back 322

alters current propagation

Front 323

sympathetic stimulation of cardiac cycle

Back 323

positive chronotropic, positive dromotropic

Front 324

parasympathetic stimulation of cardiac cycle

Back 324

negative chronotropic

negative dromotropic

Front 325

Bradyarrhythmias

Back 325

(1) failure to generate
SA node automaticity failure - ischemia, fibrosis, metabolic disorders

(2) failed impulse propagation
SA block - current blocked
AV block - physiologic or pathologic

His bundle block - infranodal

Front 326

Escape rhythms

Back 326

cells with normal automaticity - sinus node, AV node and his bundle, bundle branches, purkinje system

faster one wins

Front 327

normal sinus node beat

Back 327

60-100 bpm

Front 328

normal AV node/His bundle beat

Back 328

40-60 bpm

Front 329

normal bundle branches/purkinje system beat

Back 329

30-40 bpm

Front 330

ectopic atrial pacemakers

Back 330

40-90s

blurs line between normal and abnormal

usually not referred to as an escape rhythm

reliable rhythm

Front 331

AV node/His bundle (AV junction)

Back 331

junctional escape

good but less reliable, more easily suppressed

Front 332

Purkinje Network

Back 332

includes bundle branches

ventricular escape

not reliable, easily suppressed

Front 333

Tacharrhythmias

Back 333

mechanism: abnormal automaticity

triggered activity

reentry

(1) abnormal automaticity - ischemia or metabolic derangement transforms phase 4

activity of atrial or ventricular myocyte

(2) triggered activity

after depolarizations
had normal, then after you get something extra...if big enough get another depolarization

early - phase 3
can be self perpetuating
likely to get Torsades de Pointes - prolonged QT interval

delayed - phase 4
intracellular calcium overload
digoxin toxicity

(3) reentry

Front 334

Typical AV node reentry tachy

Back 334

normal: two pathways are present but during normal sinus rhythm wave fronts hit each other when cells are in refractory period so conduction is extinguished

slow pathway
fast pathway

abnormal: fast pathway is blocked
slow pathway continues past where it would normally be extinguished, if it arrives at the right moment, cells can be reactivated and AP loops back onto the slow pathway

unidirectional block
premature beat
beat comes in very soon after preceding beat

Front 335

atypical AV node reentry

Back 335

get block in slow pathway

fast pathway circles around, and signal reenters through fast pathway

Front 336

Wolff-Parkinson White syndrome

Back 336

accessory conduction pathway penetrates fibrous skeleton of heart

AV would be slow pathway

accessory would be fast pathway

Front 337

Atrioventricular reentrant tachycardia

Back 337

with a block in the accessory (fast pathway), signal goes down AV node and comes back up through accessory

Front 338

VT after MI

Back 338

primary mechanism of death from MI

scar becomes slow pathway

normal becomes fast

get reentry through infarct

Front 339

Class 2 antiarrhymthic drugs

Back 339

beta blockers

Beta 1 in heart
Beta 2 in vascular smooth muscle, bronchial smooth muscle

MOA: block catecholamines of ANS

(1)negative chronotropic effect - slow automaticity in sinus node and AV node by slowing phase 4

(2) negative dromotropic effect - slows velocity of conduction through AV node. slow ventricular response rate during atrial tachycardia

(3) negative inotropic effect

Types (a) cardioselective - beta 1 only
(b) non-selective - 1, 2 and some alpha

intrinsic sympathomimetic activity - block and stimulate beta receptors

adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 340

cardioselective beta blockers

Back 340

atenolol

metoprolol

esmolol

Front 341

atenolol

Back 341

class 2 antarrhymthmic

beta blocker

cardioselective


adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 342

metoprolol

Back 342

class 2 antarrhymthmic

beta blocker

cardioselective


adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 343

esmolol

Back 343

class 2 antarrhymthmic

beta blocker

cardioselective

adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 344

nonselective beta blockers

Back 344

propranolol

lebetalol - also block some alpha

carvedilol - also block some alpha

adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 345

propranolol

Back 345

class 2 antiarrhymthmic

non selective beta blocker

blocks 1 and 2

adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 346

lebetalol

Back 346

class 2 antiarrhymthmic

non selective beta blocker

blocks beta 1 and 2 and alpha


adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 347

carvedilol

Back 347

class 2 antiarrhymthmic

non selective beta blocker

blocks beta 1 and 2 and alpha

adverse: sinus bradycardia
AV block

can worsen patients who already have severe decompensated heart failure

Front 348

Class 4 antiarrhymthmic

Back 348

calcium channel blockers

Types - dihydropyridine (DHP)
non dihydropyridine (non-DHP)

diltiazem
verapamil

block Ca channels in heart (DHP)
only affect sinus and AV nodal cells (mostly AV)

effects: negative chronotropy - sinus node slowed down
AV - junctional escape shutdown

Negative dromotropy
effect on AV node: terminate reentry circuit

negative inotropy
contraindicated for patients with systolic heart failure

adverse:
too much negative chronotropy, dromotropy, inotropy
hypotension
peripheral edema
drug interactions

Front 349

diltiazem

Back 349

block Ca channels in heart (DHP)
only affect sinus and AV nodal cells (mostly AV)

effects: negative chronotropy - sinus node slowed down
AV - junctional escape shutdown

Negative dromotropy
effect on AV node: terminate reentry circuit

negative inotropy
contraindicated for patients with systolic heart failure

adverse:
too much negative chronotropy, dromotropy, inotropy
hypotension
peripheral edema
drug interactions

Front 350

verapamil

Back 350

Class 4
block Ca channels in heart (DHP)
only affect sinus and AV nodal cells (mostly AV)

effects: negative chronotropy - sinus node slowed down
AV - junctional escape shutdown

Negative dromotropy
effect on AV node: terminate reentry circuit

negative inotropy
contraindicated for patients with systolic heart failure

adverse:
too much negative chronotropy, dromotropy, inotropy
hypotension
peripheral edema
drug interactions

Front 351

digoxin

Back 351

form of digitalis, cardiac glycoside

positive inotrope: poisons Na/K pump
increases Na concentration inside cell
Na/Ca exchanger keeps more Ca in cell to balance
net: more calcium enter SR so more Ca released

Use: increases vagal tone

AV node primary target - no hypotension, mild positive inotrope
less effective than older drugs at slowing AV nodal conduction
narrow therapeutic index

adverse:nausea vomiting, visual disturbances (yellow, green halos)
high grade AV block along atrial tachycardias
ventricular tachy due to delayed afterdepolarizations
renal toxicity

Front 352

adenosine

Back 352

natural occurring substance
Give as rapid IV, very short half life
Bronchospasm in an asthmatic does not go away
Large doses can cause atrial fibrillation
Primary use:
To block AV node
Slight affect on sinus node
Terminate reentry rhythms that include AV node

Front 353

Class 1 antiarrhythmias

Back 353

Na channel blockers


Drug slows upstroke of phase 0
Prolongs QRS duration
Blockade of sodium channels: less available for conduction
Raise the threshold for initiation of action potential
Decrease slope of phase 4
Takes larger stimulus to excite each cell (larger threshold)
Slows or terminates automaticity
Effect on conduction:
Na channel blockade causes each cell to activate a bit more slowly
Cumulative effect is to slow conduction through the affected tissue

Use: convert unidirectional block to bidirectional block
Slow the slow pathway so much that it no longer conducts
Bad effect on reentry:
Slow either pathway just enough to make the reentry circuit virtually incessant

Don’t give to prior MI unless they have defibrillator

Front 354

Class 1 A:

Back 354

prolong QRS and QT

quinidine
procainamide
disopryamide

advese: Torsades de pointes

Front 355

quinidine

Back 355

class 1A antiarrhythmic

blocks Na channels

Major side effects: GI nausea vomiting
Diarrhea
CNS: cinchonism – confusion, visual, tinnitus
Autoimmune thrombocytopenia
Major interaction with digoxin

Front 356

procinamide

Back 356

Type 1A antiarrhythmic

Na channel blocker

IV only
Breakdown product = NAPA
Active metabolite
Metabolism depends on rate of acetylation
Blood level = check both procainamide + NAPA
Lupus-like syndrome

Front 357

disopyramide

Back 357

Type 1A antiarrhythmic

Na channel blocker

Strong anticholinergic effect – dry mouth, urinary retention, constipation, dry eyes
Negative inotrope – can use with hypertrophic cardiomyopathy

Front 358

Class 1B antiarrhytmic

Back 358

Na channel blocker

lidocaine

mexiletine

Front 359

Lidocaine

Back 359

Class 1B antiarrhythmic

block Na channels

Shorten QT interval
Target ventricular cells, ischemic tissue
Lidocaine: IV only
Cleared by liver…careful with liver disease
With heart failure, liver doesn’t have good perfusion
CNS side effects: can be serious if levels get too high…confusion, seizures

Front 360

mexiletine

Back 360

Class 1B antiarrhytmic

Na channel blocker

Oral
Mixes well with other antiarrhythmics
Basically oral lidocaine…liver toxicity, cns

Front 361

Class 1C antiarrhythmic

Back 361

Na channel blockers


Flecainide

Propafenone

prolong QRS

no difference in QT

negative inotropes

Front 362

flecainaide

Back 362

Class 1c
Na channel blockers

Most potent Na channel blockers
Markedly decerase upstroke of phase 0
Clean durgs – no effect on K channels
No direct effect on QT interval
Can cause bad arrhythmias, but not Torsades

Negative inotropes – contraindicated in systolic heart failure
Primarily used for atrial arrhythmias (AFib)
accessory pathways

Side effects are common but not severe
Fatigue
Visual disturbances

Front 363

propafenone

Back 363

Class 1c

Na channel blockers

Most potent Na channel blockers
Markedly decerase upstroke of phase 0
Clean durgs – no effect on K channels
No direct effect on QT interval
Can cause bad arrhythmias, but not Torsades

Negative inotropes – contraindicated in systolic heart failure
Primarily used for atrial arrhythmias (AFib)
accessory pathways

Has beta blocking properties
Mild CNS symptoms – dizziness

Use dependence:
Na channel blocking drugs bind preferentially to open channels
More open, more being blocked
Means they are more effective at faster HR

Front 364

Class 3 antiarrhythmics

Back 364

K channel blockers

sotalol

dofetilide and ibutilide

amiodarone

dronedarone

Reverse use dependence:
Greater affect the slower HR
Less useful for Afib (good for prevention, not stopping)
Also means that bad arrhythmias usch as Torsades are more likely during slower HR if QT is prolonged
Prolong phase 3…lengthening refractory period
Torsades: more likely when
Too much drug
Hypokalemia
Bradycardia

Front 365

Sotalol

Back 365

class 3 antiarrhythmic

K channel blocker

Also has beta blocker activity
Cleared by kidney – renal toxicity
QT must monitored periodically

Reverse use dependence:
Greater affect the slower HR
Less useful for Afib (good for prevention, not stopping)
Also means that bad arrhythmias usch as Torsades are more likely during slower HR if QT is prolonged
Prolong phase 3…lengthening refractory period
Torsades: more likely when
Too much drug
Hypokalemia
Bradycardia
Use with patients with MI scar

Front 366

dofetilide and ibutilide

Back 366

Class 3
ibutilide = IV

convert Afib
torsades in 10%

dofetilide = oral

cleared by liver and KIDNEY
relatively safe for heart failure
Reverse use dependence:
Greater affect the slower HR
Less useful for Afib (good for prevention, not stopping)
Also means that bad arrhythmias usch as Torsades are more likely during slower HR if QT is prolonged
Prolong phase 3…lengthening refractory period
Torsades: more likely when
Too much drug
Hypokalemia
Bradycardia
Use with patients with MI scar

Front 367

Amiodarone

Back 367

Class 3

Safest antiarrhythmic drug for your heart, most dangerous for rest of body

Prolongs QT but rarely causes Torsades
Don’t need to monitor QT
Rarely causes Torsades

Almost never causes ventricular arrhythmias

Adverse:
Multiple toxicities require routine monitoring
Eyes – corneal deposits, optic neuropathy
Hypothyroidism – common easily remedied
Hyperthyroidism rare
Hepatic injury
Pulmonary toxicity –irreverisble but usually after several years (look at age of pt)
Skin photosensitivity – bluish
Interacts with warfarin

Has some properties of all antiarrhythmics
K, Na, Ca channel blockers

Front 368

dronedarone

Back 368

class 3 antiarrhythmic

Supposedly like amiodarone without toxicities

But need to monitor QT, torsades probably low

Interferes with creatinine secretion – raises serum creatinine level but renal function fine

Front 369

idiopathic necrotizing arteritis

Back 369

(1)Kawasaki's disease

(2) takayasu arteritis

(3) Thromboangiitis obliterans (Buerger's Disease)

Front 370

kawasaki's disease

Back 370

idiopathic necrotizing arteritis

young children under 5yo

high fever

enlarged lymph nodes

rash

10% get coronary artery autoimmune attack

weakens wall, get aneurysm or dilation

Front 371

Takayasu arteritis

Back 371

Thickening of aortic arch
Blindness, cns deficits, decreased pulses in upper extremities
Microscopic = giant cell artitis
Women most commonly affected

Front 372

Thromboangiitis obliterans (Buerger's Disease)

Back 372

Pain and ischemia in legs/arms
Relatively young men
Leads to gangrene
Genetic predisposition
Almost exclusively smokers
Inflammatory with thrombosis
Lesion – cellular thrombosis with inflammation

Front 373

Phlebitis: inflammation of veins

Back 373

Usually with thrombosis
Caused by injury
Pylephlebitis – portal vein…associated with appendicitis
Dural sinuses
Pulmonary veins in pneumonia

Examples: iliofemoral veins in puerperal sepsis
Hepato-veno-occlusive disease from chemo
Migratory thrombophlebitis – Trousseau Syndrome
Idiopathic trhombophlebitis

Front 374

Phlebothrombosis

Back 374

venous thrombosis without inflammation

Usually in deep veins or pelvic veins
Exact incidence uncertain
Pain, tenderness, swelling or may be symptomatic
Complications: pulmonary embolus – 50%
Clots usually form in relation to valve cusps, propagate upwards

Front 375

vericose veins

Back 375

Abnormal dilated, tortuous veins
Produced by prolonged increase in intraluminal pressure
Often in relation to injury or defect of the vein proximally
Sites: legs in estimated 20% of population
Clusters in families
Complications- inflammation, thrombosis, stasis dermatitis, ulceration of skin
No pulmonary embolism

Sites: perianal – hemorrhoids
Testis – varicocele
Esophageal varices hepatic cirrhosis, portal hypertension…can hemorrhage

Front 376

Atherosclerotic aneurysm

Back 376

Age: >50, males 5:1, relatively common
Location : abdominal aorta (97%)
Usually below renals, may involve iliacs, but may occur in thoracic aorta
Mechanism: atheromasmedial destruction, ulcerated plaques

Presentation: pulsatile abdominal mass or pain
Rupture causes pain, swelling and shock
Incidentally on x ray (calcified)

Complications: rupture (retroperitoneal hemorrhage)
Stenosis of ureter by pressure or fibrosis
Occlusion of aortic branch (renal, mesenteric)
Embolism
Rupture: related to size
Greater than 7cm 80% rupture
Use ultrasound for cut-off
Therapy: surgery

Front 377

syphilitic dissection

Back 377

Location: ascending thoracic aorta and arch
Mechanism: tertiary syphilis involves vasa vasorum causes vasculitis and medial damage of aorta
Presentation: dyspnea, stridor, dysphagia, cough, pain
Congestive heart failure due to aortic insufficiency
Aneurysm can compress esophagus
Causes: heart failure or hemorrhage
Therapy: surgery

Front 378

mycotic aneurysm

Back 378

Mycotic refers to any infection, not necessarily fungal
Mechanism: infection causes destruction of media
Complication: infarcts distally, septic or bland
Cause: sequel of infective endocarditis or endarteritis…can embolism to brain carrying infection

Front 379

dissecting hematoma of aorta

Back 379

Age: 40-60 males
Location: intimal tear in ascending aorta
Types: A: most common involves ascending aorta and may extend distally
B: begins distal to subclavian artery, extends distally – better prognosis than A

Mechanism: hypertension
Trauma
Creates false lumen
Presentation: 85% pain in chest or radiating to back
Usually normal or elevated blood pressure
May have MI
Therapy: anti hypertensives, surgery

Front 380

Stenotic lesions cause what kind of hypertrophy

Back 380

cause pressure overload, and myocardial hypertrophy = concentric hypertrophy

Front 381

regurgitant lesions cause what kind of hypertrophy

Back 381

volume overload, eccentric hypertrophy

Front 382

Rheumatic heart disease

Back 382

uncommon in Us

Front 383

most common valvular lesion in US

Back 383

aortic stenosis

Front 384

Aortic stenosis and bicuspid valve

Back 384

Bicuspid Aortic valves 1-2% population
Frequent cause of symptomatic aortic stenosis in young patients
Associated with other congenital abnormalities in 20% of cases
80% of coarctation patients have Bicuspid

Front 385

aortic stenosis etiology

Back 385

Young patient: think bicuspid
Male more than female
Old patient – think degenerative: MOST COMMON in older patients

Front 386

aortic stenosis symptoms

Back 386

Cardinal symptoms
Chest pain (angina)
Reduced coronary flow reserve
Increased demand – high afterload
Syncope
Dyspnea on exertion
Impaired exercise tolerance
Heart failure
GI bleeding possible

Front 387

classification of aortic stenosis symptoms

Back 387

Classification of AS severity
Normal aortic valve area 2-3cm
Mild AS >1.5cm
Moderate As 1.0-1.5 cm
Severe AS <1.0 cm

Front 388

when to treat aortic stenosis

Back 388

Asymptomatic patients – follow expectantly
Endocarditis prophalaxis
Survey with echo annually when severe AS or symptoms change

Surgery – severe and symptomatic AS
If need heart surgery (bypass, etc.) for another reason, replace even if asymptomatic

Front 389

aortic regurgitation causes

Back 389

Causes:
Bicuspid – coarctations and aortic root dilation
Infective endocarditis
Rheumatic heart disease
Radiation
Subvalvular causes (septal defects)
Etiologies:
Chronic: rheumatic disease
Congenital bicuspid
Myoxamtous disease
Marfan’s
Syphilis
Acute: dissection
Infective endocarditis
Traumatic

Front 390

symptoms of aortic regurgitation

Back 390

Chronic AR – asymptomatic for a long time
Symptoms – exertional dyspnea, orthopnea, PND
Syncope and angina are less common
Uncomfortable awareness of heart beat especially lying down

Front 391

aortic regurgitation PE

Back 391

PE – apical impulse diffuse
Tachycardia
Diastolic descrendo murmur, begins just after second heart sound at apex
S3 and S4
Severity of AR correlates with duration of murmur
Murmur best heard along RIGHT sterna border
Austin Flint murmur – apical rumble due to regurgitation trying to close mitral valve (valve normally trying to open)…blowing diastolic murmur

Bobbing of head
Capillary pulsations
Clubbing of fingers

Front 392

treatment for aortic regurgitation

Back 392

Dilated aortic root or mild LV dysfunction – class I indication for surgery
Don’t do surgery if: normal systolic and asymptomatic with Chamber size normal

Front 393

mitral valve stenosis etiology and prevalence

Back 393

Primarily result of rheumatic fever
Rarely congenital
Slightly female to male
Don’t see in the US much unless poor access to care

Front 394

mitral valve stenosis downstream affects

Back 394

IN crease in left atrial pressure, can cause increase in pulmonary congestion and edema
Dypsnea common
Mitral valve stenosis associated with diastolic murmur because of turbulence
Diastolic murmur always pathologic

Front 395

secondary concerns with mitral valve stenosis

Back 395

Increase in mitral valve gradient – causes shortened diastolic phase
As atria expand, can get loss in atrial ventricular synchrony….get atrial fibrillation
Likely to get strokes
Valvular atrial fibrillation high risk of strokes

Fusion causes valve to become more spherical – less efficient

Tightening of valve – get turbulent flow in atrium
Tend to clot
Clots found in atrial appendage likely to embolize to brain

Front 396

primary affects of mitral stenosis

Back 396

Consequences:
Reduced ventricular filling
Reduced stroke volume
Decreased cardiac out put
Stroke volume low enough may result in a reduction in aortic pressure

Front 397

mitral valve regurgitation

acute

Back 397

Acute – infective endocarditis
Myxomatous disease
Ischemic heart disease

PE: loud S4, heard best at apex, radiates to axilla

Front 398

mitral valve regurgitation

chronic

Back 398

Chronic – myxomatous disease (prolapsed)
Rheumatic heart disease
Annulo-aortic ectasia – dilated aortic root
Ischemia – kill papillary muscle

Chronic:
Leak into left atrium
Left ventricle volume load
Compensation – left ventricle dilates and hypertrophies
Increase in stroke volume
Left atrium dilates

Front 399

mitral valve stenosis PE findings

Back 399

PE:
Jugular venous distension – normal until late
Carotids – normal until late
Apex impulse – laterally displaced and hyperdynamic
Pan systolic murmur in apex, axilla right precordium or back

Front 400

mitral valve stenosis dx

Back 400

Dx: systolic displace of mitral leaflet into atrium of at least 3mm, mitral regurgitation
Can have prolapsed but no leak can be of little concern

Front 401

mitral valve stenosis tx

Back 401

Tx. Surgery if see signs of atrium/ventricle dilation

Front 402

normal changes in cardiovascular system with aging

Back 402

increased stiffness of the left ventricle and arteries, and decreased maximal heart rate and cardiac output during exercise

3. These normal age related changes reduce cardiovascular reserve capacity, and thereby lower the threshold for development of common cardiovascular diseases, and reduce the ability to adapt to them

Front 403

when does cardiovascular risk for women rise?

Back 403

5. Cardiovascular risk for women rises after menopause and becomes similar to men by age by 70

Front 404

cardiovascular disorders unique to elderly?

Back 404

diastolic heart failure

calcific aortic stenosis

Front 405

presentation of elderly with MI

Back 405

Atypical presentations: 1/3 of elderly
Confusion
Dyspnea
Lassitude
New onset of CHF
Syncope
Stroke
Increases with age and women

Front 406

gender differences in CHF

Back 406

women more likely to have normal ejection fraction heart failure

Differences in preserved vs reduced
PEF – old, women, coronary artery disease reduced, morbidity
Reduced – middle aged, men, CAD common, morbidity,

Front 407

venous insufficiency ulcer characteristics

Back 407

gaiter distribution

larger with irregular border

shallow with moist, granulating base

surrounding pigmentation and inflammation

tx. compression and elevation

Front 408

arterial insufficiency ulcer characteristics

Back 408

painful with punched out appearance

dorsum of foot or toes

surrounding skin pale or molted

poorly developed granulation tissue at wound base

little bleeding seen with probing or debridment

tx. revascularization

Front 409

neurotropic ulcer characteristics

Back 409

completely painless

bleed with manipulation

appear over pressure points of toe or foot

surrounded by acut and chronic inflammatory reaction

associated with longstanding diabetes with neuropathy

tx. meticulous wound and foot care, well fitting shoes

Front 410

arterial baroreflex vasconstriction

Back 410

Receptors are sensitive to stretch…aortic arch and carotid sinus
Graded response
firing increases with increased stretch
sensitive to stretch, pulse stretch, rate of change
small deviations result in large change in firing because it responds to slope of curve (slope of change, not absolute amount of change)

drop in pressure = less firing

How it works:
From baroreceptor to nucleus tract soliatirus to either(1) CVLM – depressor or (2) RVLM – pressor centers in medulla
Barorecptor input into NTS…NTS sends excitatory to CVLM..CVLM projects inhibitory signal to RVLM…get less output from pressor centers….low BP

Baroreceptor input into NTS…NTS decreases signal to CVLM, CVLM has decreased firing on RVLM..RVLM increases vasoconstriction and BP

Front 411

parasympathetic baroreflex of heart

Back 411

Cell bodies originate in dorsal vagal/nucleus ambiguous of medulla
Excitatory connection to dorsal motor nucules and nucleus ambiguous with secondary projections to sympathetic
Get increased parasympathetic firing and thus decreased on heart

Front 412

chemoreceptor control

Back 412

Regulate respiratory activity
(a) Peripheral receptors
Carotid and aortic bodies
Increased CO2, acid, decreased O2, and hypoperfusion
Sends info via NTS to medulla

Humoral Control:
Catecholamines:
Released by adrenal medulla
80% Epi, 20% NE
NE also from end of sympathetic
NE stimulates release of Renin

Front 413

receptor dependent vasodilators

local vascular control

Back 413

histamine

sub P

SE

ACh

Front 414

receptor independent vasodilators

local vascular control

Back 414

sodium

nitroprusside

NO donor

Front 415

vasocontrictors

Back 415

PE

NE
NPY coreleased with NE augments actions of NE

Angiotensin II

arginine vasopressin

NE, Epi

Endothelin

Increased PO2

Front 416

Special circulaitons

coronary

Back 416

compensate increased demand with increased flow

local factors predominate over neural

use adenosine (vasodilator)

Front 417

special circulation

cerebral

Back 417

local factors predominate over neural

Front 418

special circulation

skeletal muscle circulation

Back 418

local factors and hypoxia regulate flow

metabolites out compete sympathetic vasoconstriction

Front 419

special circulation

skin

Back 419

control by neural and physical factors most important

tonic sympathetic tonic

hot vs cold temps

Front 420

special circulation

splanchnic circulation

Back 420

reservoir of blood

use to redistribute blood as needed

neural control predominates

Front 421

special circulation

renal

Back 421

two capillary segments in series

strong autoregulation - depends on sympathetic tone

Front 422

special circulation

pulmonary

Back 422

two criculations

(1) pulmonary - hypoxia causes vasoconstriction to maintain proper perfusion ratios

(2) bronchial - maintain flow to trachea and bronchial structures

Front 423

MI of LAD

Back 423

anteroseptal LV

Front 424

MI of LCX

Back 424

lateral LV

Front 425

MI of RCA

Back 425

posteroseptal LV

Front 426

stages of MI

Back 426

early acute: 6-24 hrs

acute 1-6 days

organizing 1-3wks

Remote 3mos or more

Front 427

Early Acute MI

Back 427

6-24 hrs

thin wavy fibers, eosinophilia

pallor, patchy, hyperemia

Front 428

Acute MI

Back 428

1-6 days

obvious pale, yellow

necrotic myocytes

Front 429

organizing MI

Back 429

1-3wks

red-brown edge around pale center

granulation tissue, acute and or chronic inflammation

Front 430

remote MI

Back 430

3 mos or longer


firm, white, scar

collagen

Front 431

Transmural infarcts

Back 431

infarction of full thickness of ventricular wall

caused by severe CAD with acute plaque disruption and occlusive thrombosis

Front 432

subendocardial infarct

Back 432

limited to inner 1/3 to 1/2 of ventricular wall

diminished perfusion

Front 433

transmural infarct pathogenesis

Back 433

90% due to CA stenosis and disrupted plaques

significant plaques mainly in proximal CA

less common: vasospasm, PLT aggregation, emboli

complete vessel occlusion may not cause MI if sufficient collateral flow

Almost all IN LV

initial event - plaque disruption with thrombosis following

Front 434

subendocardial infarct pathogenesis

Back 434

diffuse CAD and global perfusion made transiently critical by increased demand, vasospasm, hypotension

disrupted plaque with overlying thrombus that lyses , thus limiting extent of MI

Front 435

Rupture of MI which stage?

Back 435

Acute more likely

Front 436

LV aneurysm of MI in which stage?

Back 436

organizing

Front 437

CHF of MI in which phase?

Back 437

early acute

Front 438

dysrhythmia of MI in which stage?

Back 438

early acute

Front 439

pericarditis of MI in which stage?

Back 439

organizing fibrous in remote

Front 440

chronic ischemic heart disease

Back 440

due to left heart failure

Pure RV failure tdue to intrinsic lung disease

major manifestations - portal, systemic and dependent peripheral congestion and edema and effusions

Front 441

Idiopathic dilated cardiomyopathy

Back 441

results from viral myocarditis or toxic myocarditis

male>female

african americans>caucasains

genetic predisposition

heart biopsy is not diagnostic

treat like CHF - beta blocker, angiotensin, aldosterone antagonist

Front 442

Viral myocarditis

Back 442

probably cause of idiopathic cardiomyopathy

coxsackie B most common agent

immunologic mechanism - develops weeks after original infection

enhanced susceptibility - animal studies...radiation, malnutrition, steriods, exercise, previous MI

tends to be more aggressive in infants and pregnant women

myocytes infiltrate heart

other: HIV, CMV, hepatitis
ricketsia
bacterial
spirochetal
protozal

Front 443

peripartum cardiomyopathy

Back 443

distinct type of cardiomyopathy related to pregnancy

clear relationship to recent pregnancy with high risk of relapse on subsequent pregnancies

embolic phenomena common

better prognosis

evidance of inflammation good prognosticator

Front 444

hypertrophic cardiomyopathy

Back 444

cardiac muscle disease characterized by abnormal hypertrophy, mainly involving ventricular septum

histology: myofibrillar disarray

functional abnormalities

outflow tract obstruction

diastolic dysfunction

atrial and ventricular arrhythmias

50% autodominant

thickening of septum impingnes on outflow tract. plus systolic anterior movement of mitral valve causing mitral regurgitation.

have decreased pressure in outflow tract and aorta

Front 445

Infectious pericarditis causative agents

Back 445

coxsackie, echo virus, and HIV

TB outside US

Front 446

non-infectious pericarditis causative agents

Back 446

idiopathic

neoplasm - metastatic lung, breast or primary mesothelioma

renal failure

Front 447

hypersensitive pericarditis causes

Back 447

collagen vascular disease - LUPUS, rheumatoid arthitis

drug induced

post MI

Front 448

Dx of pericarditis

Back 448

diffuse ST segment elevation in early stage

depresison of PR segment and T wave inversion in late stages

or eletrical alternans

Front 449

Dx of pericardial effusions

Back 449

CXR

ECG - low voltage

echo

Front 450

cardiac tamponade

Back 450

accumulation of fluid in the pericardial space leads to an increased pericardial pressure

increased pressure = cardiac compression and impaired diastolic ventricular filling....means decreased cardiac output

Front 451

clinical presentation of cardiac tamponade

Back 451

mimics heart failure

dyspnea on exertion and orthopnea

trachycardia, tachypnea

jugular venous distention

pulsus paradoxus - typically 10mm variation in systole exhale/inhale...greater than 10 then cardiac tamponade

Front 452

constrictive paricarditis

Back 452

results from dense fibrosis and adhesion of the parietal and visceral layers

creates rigid cause around heart

early ventricular filling is unimpeded but diastolic filling is subsequently abruptly reduced as a result of the ventricles fo fill secondary to the restraints imposed by a rigid, thickened, and calcified pericardium

Front 453

presentation of constrictive pericarditis

Back 453

right heart failure

weakness, dyspnea, orthopnea, anorexia

peripheral edema, hepatomegaly, splenomegaloy, ascites

prominent Y decent with jugular venous pressures

exaggerated filling of jugular with inspiration

effects end diastole when ventricle volume is higher

Front 454

non penetrating trauma and heart

Back 454

most commonly causes cardiac contusion - new arrhythmias and ECG changes

can have transaction of descending thoracic aorta