First Aid - Cardiology - Anatomy And Physiology

Front 1

What is contained in the carotid sheath?

Back 1

VAN

internal jugular vein (lateral)
common carotid artery (medial)
vagus nerve (posterior)

Front 2

What are the 2 coronary arteries?

Back 2

right coronary artery (RCA) - acute marginal artery (supplies RV) and often posterior descending artery (supplies posterior septum)

left main coronary artery - gives off left anterior descending (supplies apex and AV septum) - also left circumflex artery - supplies posterior left ventricle

Front 3

What are the AV and SA nodes commonly supplied by?

Back 3

RCA

Front 4

right dominant heart vs. left dominant heart

Back 4

80% people are right dominant - the RCA supplies the PDA

20% of people are left dominant - the LCX supplies the PDA

Front 5

What is the most common location for a coronary artery occlusion?

Back 5

LAD - which supplies the anterior intraventricular septum - called the widow maker

Front 6

When do coronary arteries fill during?

Back 6

diastole

Front 7

What can enlargement of the most posterior part of the heart cause?

Back 7

left atrium is the most posterior part of the heart - if it enlarges it can cause dysphagia (from compression of esophageal nerve), horseless (compression of recurrent laryngeal -

Front 8

What happens to CO during exercise?

Back 8

initially increases because of increased SV. After prolonged exercise CO increases because of increased HR

Front 9

What happens if the HR gets too fast?

Back 9

person will have decreased CO - because of decreased filling during diastole (ex. ventricular tachycardia)

Front 10

CO =

Back 10

SV x HR

SV = EDV - ESV
Fick's Principle
CO = rate of O2 consumption/(arterial O2 content - venous O2 content)

Front 11

mean arterial pressure =

Back 11

2/3 diastolic pressure + 1/3 systolic pressure

MAP = CO x total peripheral resistance (TPR)

Front 12

Pulse pressure =

Back 12

systolic pressure - diastolic pressure

pulse pressure is proportional to the stroke volume

Front 13

What affects stroke volume?

Back 13

contractility, afterload, preload

Front 14

What increases contractility?

Back 14

- catecholamines (increased activity of Ca2+ pump in sarcoplasmic reticulum)
- increased intracellular calcium
- decreased exracellular sodium (decreased activity of Na+/Ca2+ exchanger)
- digitalis (increased intracellular sodium, resulting in increased Ca2+)

Front 15

What decreases contractility?

Back 15

- B1 blockade
- heart failure
- acidosis
- hypoxia/hypercapnea
- non-dihydropyridine Ca2+ channel blockers

Front 16

What increases stroke volume?

Back 16

pregnancy, anxiety, exercise

Front 17

What is the SV in a failing heart?

Back 17

decreased

Front 18

Myocardial O2 demand is increased by what?

Back 18

increase in afterload, increase in contractility, increased heart rate, increased heart size (increased wall tension)

Front 19

preload is what?

Back 19

end diastolic volume

Front 20

afterload is what?

Back 20

mean arterial pressure = 2/3 diastolic pressure + 1/3 systolic pressure

mean arterial pressure = CO x TPR (total peripheral resistance)

Front 21

what do venodilators do?

Back 21

decrease preload - decrease return to the heart

ex. nitroglycerin

Front 22

What do vasodilators do?

Back 22

decrease afterload (arterial)
ex. hydralazine

Front 23

What increases preload?

Back 23

exercise (slightly), increased blood volume (overtransfusion), and excitement (sympathetics).

Preload pumps up the heart

Front 24

The force of contraction is related to what?

Back 24

the initial length of cardiac muscle fiber (preload)

Front 25

What increases and decreases the contractile state of the myocardium?

Back 25

increases: sympathetic stimulation, catecholamines, digitalis

decreases: pharmacologic depressants, loss of myocardium (MI)

Front 26

EF = what?

Back 26

EF = SV/EDV

EF = (EDV-ESV)/EDV

it is a measurement of the ventricular contractility

normal EF > 55%

Front 27

Normal EF is what?

Back 27

> 55%

Front 28

change in pressure = what?

Back 28

change in pressure = Q x R

(similar to V = IR)

Front 29

What does resistance =?

Back 29

R = 8nl/(pi r^4)

n = viscosity
l = length
r = radius

as the radius decreases the resistance increases a lot!

Front 30

What is an example of resistance in parallel?

Back 30

Systemic circulation with the aorta

Front 31

What is an example of resistance in series?

Back 31

blood flow within individual organs

Front 32

What is viscosity most dependent on?

Back 32

hematocrit

viscosity increases with:
- polycythemia
- hyperproteinemic states (multiple myeloma)
- herediary spherocytosis

Front 33

What does a pressure gradient do?

Back 33

drives flow from high pressure to low pressure

Front 34

How does resistance, length, viscosity, and radius all affect each other?

Back 34

resistance is proportional to viscosity and length and inversely proportional to the radius

Front 35

What accounts for the most resistance in the blood?

Back 35

arterioles - regulate capillary flow

Front 36

What is the operating point of the heart?

Back 36

Where venous return and CO are equal

Front 37

What are the 4 phases of the left ventricle?

Back 37

MV closes - isovolumetric contraction (period of highest O2 consumption) - AV opens - systolic ejection - AV closes - isovolumetric relaxation - MV opens - rapid filling (period right after mitral valve opens) - reduced filling (period just before mitral valve closure)

Front 38

S1

Back 38

Mitral and Tricuspid valve closure

Front 39

S2

Back 39

Aortic and pulmonary valve closure

Front 40

S3

Back 40

rapid filling - after S2- in early diastole during rapid ventricular filling phase. Associated with increased filling pressures and more common in dilated ventricles (normal in children and pregnant women)

Front 41

S4

Back 41

usually pathologic

stiff left ventricle - so left atrium must kick to get more blood into the left ventricle - happens late diastole

*Associated with ventricular hypertrophy

Front 42

What are the waves in the JVP?

Back 42

upstrokes: a,c,v
downstrokes: xy

in order:
a - atrial contraction increase in pressure
*MV closes
c- RV contraction (tricuspid valve bulges into the atria causing increased pressure)
x - relaxation of the right atria
v - filling of the right atria from the veins
y - opening of TV - blood flows form RA to RV - decreased pressure in RA

Front 43

What is S2 splitting? What is normal splitting?

Back 43

The the aortic valve closes before the pulmonary valve

normal splitting: When you breath in decrease in intrathoracic pressure - more blood returns to the heart so pulmonary valve closes even later (to accommodate for the increase in blood volume) - the aortic valve closes earlier because less blood to the left side of the heart (held up in the lungs)

Front 44

What is wide splitting? What do you see it in?

Back 44

pulmonic sound is always very delayed

see in conditions that delay RV emptying (pulmonic stenosis, or right bundle branch block)

- have exaggerated splitting regardless of breath

Front 45

Fixed splitting

Back 45

seen in ASD

shunt present that causes blood to flow from the left side of the heart through the right - so increased flow through the pulmonary valve regardless of the breath, pulmonary closure is greatly delayed

Front 46

Paradoxical splitting

Back 46

seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block). The valve sounds are reversed - P2 closes before A2 - when inspire - loose splitting (P2 takes longer)

Front 47

What are the listening posts of the heart?

Back 47

'Are People That Mean'

Aortic (right 2nd intercostal space): systolic murmur: aortic stenosis, flow murmur, aortic valve sclerosis
Pulmonary (left 2nd intercostal space) systolic murmur: pulmonic stenosis, flow murmur (ASD)
Ticuspid (left 4th intercostal space): pansystolic murmur: TR, VSD
diastolic murmur: TS, ASD
Mitral (left 5th intercostal space): systolic murmur: MR
diastolic murmur: MS

Front 48

murmur in ASD

Back 48

commonly a pulmonary flow murmur (from increased flow through the pulmonary valve) and a diastolic rumble (increased flow across tricuspid); blood flow across the actual ASD does not cause a murmur because no pressure gradient. Murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery

Front 49

holosystolic blowing murmur

Back 49

MR or TR

mitral: loudest at the apex and radiates to the axilla. enhanced by maneuvers that increase TPR (squatting, hand grip) or LA return (expiration). MR is often due to ischemic heart disease, mitral valve prolapse or LV dilation.
tricuspid: loudest at tricuspid area and radiates to right sternal border. enhanced by maneuvers that increase RA return - inspiration. TR is due to RV diltaion or endocarditis.

Both MR and TR can be due to rhematic fever

Front 50

What increases MR?

Back 50

things that increase TPR - squatting or hand grip

things that increase flow to LA - expiration

Front 51

What increases TR?

Back 51

inspiration (increases RA return)

Front 52

Crecendo-decrescendo murmur

Back 52

AS - systolic ejection murmur following ejection click (EC: due to abrupt halting of valve leaflets). LV > aortic pressure during systole. Radiates to carotids/apex.

Pulsus parvus and tarvus
can lead to syncope. Often due to age-related calcific aortic stenosis or bicuspid aortic valve

Front 53

Where does AS radiate?

Back 53

to the carotids

can see pulsus tardus and parvus

Front 54

holosystolic, harsh murmur

Back 54

VSD - it is the loudest at the tricuspid area

Front 55

Mitral prolapse

Back 55

late systolic cresendo murmur with midsystolic click (MC; due to sudden tension of chordae tendineae). Most frequent valvular lesion. Loudest at S2. usually benign. Can predispose to infective endocarditis. Can be caused by myxomatous degeneration, rhematic fever, or chordae rupture. Enhanced by maneuvers that increase TPR (squatting or hand grip)

Front 56

Aortic regurgitation

Back 56

immediate high-pitched blowing diastolic murmur. Wide pulse pressure when chronic; can present with bounding pulses and head bobbing. Often due to aortic root dilation, bicuspid aortic valve, or rheumatic fever

Front 57

Mitral stenosis

Back 57

following opening snap (OS; due to tensing of chordae tendineae). delayed rumbling late diastolic murmur. LA>LV pressure during diastole. Often occurs secondary to rhematic fever. Chronic MS can result in LA dilation. Enhanced by maneuvers taht increase LA return (expiration)

Front 58

machine like murmur

Back 58

PDA. Loudest at S2

Front 59

What is cardiac muscle contraction dependent on?

Back 59

extracellular Ca2+ - it enters the cells during plateau of action potential and stimulates calcium release from the cardiac muscle sarcoplasmic reticulum (calcium induced calcium release)

Front 60

Cardiac muscle vs. skeletal muscle

Back 60

cardiac muscle action potential has a plateau, which is due to Ca2+ influx
- cardiac nodal cells spontaneously depolarize, resulting in automaticity due to If channels
- cardiac myocytes are electrically coupled to each other by gap junctions

Front 61

Ventricular action potential

Back 61

phase 0: rapid upstroke - Na+ rushes into the cell to depolarize it
phase 1: initial repolarization - inactivation of Na+ channels and opening of K+ channels (K+ goes outside of the cell)
Phase 2: plateau - Ca+ channels open and Ca2+ goes into the cell - balances K+ going out of cell - Ca2+ triggers calcium release from sarcoplasmic reticulum and myocyte contraction
Phase 3: rapid repolarization - massive K+ efflux due to opening of slow K+ channels and closure of Ca2+ channels
Phase 4: resting potential = high K+ permeatiblity through K+ channesl

Front 62

when does myocyte contraction occur?

Back 62

during plateau phase - when Ca2+ rushes into the cell (causes more Ca2+ release from sarcoplasmic reticulum)

Front 63

pacemaker action potential

Back 63

occurs in the SA and AV nodes

Phase 0: upstroke - depolarization via opening of Ca2+ channels - Ca2+ goes inside cells (no fast Na+ channels) - results in a slow conduction velocity to prolong transmission from the atria to the ventricles
phase 2: absent
phase 3: Ka+ channels open - K+ goes outside the cell (repolarization) - Ca2+ channels close
phase 4: slow diastolic depolarization - membrane potential spontaneously depolarizes as Na+ conductance increases (If different from the INa in the myocyte). Accounts for autoaticity of SA and AV nodes.

Front 64

What does the slope of phase 4 determine?

Back 64

phase 4 is when If (Na+) channels are open - the slope determines the heart rate. Ach decreases the rate of diastolic depolarization and decreases the heart rate. catecholamines increase the depolarization and increase the heart rate. Sympathetic stimulation increases the change that If channels are open

Front 65

What is the speed of conduction difference between the AV, SA node, bundle of His?

Back 65

purkinje>atria>ventricles>AV node

Front 66

What does the P wave represent?

Back 66

Atrial depolarization

Front 67

What does the PR interval represent?

Back 67

delayed conduction through AV node because of Ca2+ channels (should be less than 200 ms)

Front 68

What does the QRS complex represent?

Back 68

ventricle depolarization - should be less than 120 ms

Front 69

What does the QT interval represent?

Back 69

mechanical contraction of the ventricles

Front 70

What does the T wave represent?

Back 70

Ventricular repolarization - can be inverted after a MI

Front 71

What represents atrial repolarization?

Back 71

nothing - it is masked by ventricular depolarization

Front 72

ST segment

Back 72

isoelectric, ventricles depolarized

Front 73

What does the U wave represent?

Back 73

hypokalemia, bradycardia ( it is depressed segment after the T wave)

Front 74

What does the delay of firing between the SA and AV node allow for?

Back 74

filling of the ventricles

Front 75

Torsades de pointes

Back 75

ventricular tachycardia is shifting sinusoidal waveforms on ECG. Can progress to V-fib. Anything that prolongs the QT interval can predispose to torsades de pointes

Front 76

Congenital long QT syndromes

Back 76

usually due to defects in Na+ or K+ channels - can present with severe congenital sensorineural deafness (Jervell and Lange Nielsen syndrome)

Front 77

Wolff-Parkinson-White syndrome

Back 77

ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bundle of kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to delta wave. may result in reentry current leading to supraventricular tachycardia

Front 78

delta wave

Back 78

increase in voltage right before QRS segment - classic for wolff-parkinson-white syndrome

Front 79

irregularly irregular ECG

Back 79

Atrial fibrillation - chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes. Can result in atrial stasis and lead to stroke

Front 80

treatment for A-fib?

Back 80

B-blocker, Ca2+ channel blocker; prophylaxis against thromboembolism with warfarin (Coumadin)

Front 81

Holiday heart syndrome - risk of it?

Back 81

A-fib - risk of thromboembolism - from static blood in atria - risk of clots

Front 82

sawtooth pattern

Back 82

Atrial flutter - rapid succession of identical, back to back atrial depolarization waves. Try to convert back into sinus rhythm. Use class IA, IC, or III antiarrhythmics.

Front 83

treatment for Atrial flutter?

Back 83

IA, IC, or III antiarrhythmics

Front 84

AV block 1st degree

Back 84

PR interval is increased (greater than 200 ms). Asymptomatic

Front 85

AV block - 2nd degree - Mobitz type I (Wenckebach)

Back 85

Progressive lengthening of PR interval until a beat is dropped (a P wave not followed by QRS). Usually asymptomatic

Front 86

AV block 2nd degree - Mobitz type II

Back 86

Dropped beats that are not preceded by a change in length of PR interval. The abrupt, nonconducted P waves result in a pathologic condition. Often found as a 2:1 block, 2 P waves to 1 QRS complex. May progress to 3rd degree block

*normal PR intervals

Front 87

AV block 3rd degree

Back 87

atria and ventricles beat independently of each other, but both P and QRS are present. P waves bear NO relation to QRS complexes. Atrial rate is faster than the ventricular rate

Front 88

What can cause a 3rd degree AV block? What is the treatment?

Back 88

Lymes disease can cause it
treat with a pacemaker

Front 89

Ventricular fibrillation

Back 89

completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.

Front 90

What maintains the mean arterial pressure?

Back 90

decrease in MAP causes:
1) medullary vasomotor center senses decreased baroreceptor firing - increases sympathetic activity (B1: increases heart rate and contractility - increased CO, a1: venoconstriction, increased venous return - increased CO, also a1 causes arterial vasoconstriction - increased MAP
2) JGA senses decreased MAP (effective circulating volume) - increased renin release - RAAS system - (AT II - vasoconstriction - increased TPR, aldosterone increased blood volume - increased CO)

Front 91

What is released in a response to increased blood volume and atrial pressure?

Back 91

ANP from the atria - causes generalized vascular relaxation. Constricts efferent renal arterioles, dilates afferent arterioles. Involved in escape from aldosterone mechaism

Front 92

Where are baroreceptors located? What do they respond to?

Back 92

In the carotid sinus (respond to increases and decreases in BP via glossopharyngeal nerve to solitary nucleus of medulla) and aortic arch (respond only to increases in BP - via vagus nerve to medulla)

Front 93

What happens to baroreceptors during hypotension?

Back 93

decreased BP - decrease stretch on baroreceptors - decreased firing - causes increased sympathetic firing and decreased parasympathetic firing - vasoconstriction, increased in HR, contracitility and blood pressure - important response to hemorrhage

Front 94

What happens to baroreceptors during carotid massage?

Back 94

increased stretch - increased firing of receptors - decreased HR (trick the medulla to think that there is increased BP)

Front 95

What are the 2 types of chemoreceptors?

Back 95

1) peripheral - carotid and aortic bodies respond to decreased PO2 (<60 mm Hg), increased PCO2, and decreased pH of the blood
2) central - respond to changes in pH and PCO2 of brain interstitial fluid. Do not directly respond to PO2. Responsible for cushing reaction - increased intracranial pressure constricts arterioles - cerebral ischemia - hypertension (sympathetic response) - reflex bradycardia.

*cushing's triad: hypertension, bradycardia, respiratory depression

2) central

Front 96

cushing's reaction

Back 96

increased intracranial pressure constricts arterioles - cerebral ischemia - hypertension (sympathetic response) - reflex bradychardia

*cushing's triad: hypertension, bradycardia, respiratory depression

Front 97

What gets the largest share of systemic cardiac output?

Back 97

liver

Front 98

What gets the highest blood flow per gram of tissue?

Back 98

kidney

Front 99

Where is O2 extraction 100%?

Back 99

in the heart - increased O2 demand is met by increased coronary blood flow, not by increased extraction of O2

Front 100

What are the normal pressures in the heart?

Back 100

RA <5
RV <25/<5
PA <25/10
PCWP (LA pressure) <12
LV <130/10
Aorta <130/90

Front 101

What is PCWP?

Back 101

pulmonary capillary wedge pressure - an approximation of LA pressure

measured with Swan-Ganz catheter

Front 102

What is autoregulation?

Back 102

how blood flow to an organ remains constant over a wide range of perfusion pressures

Front 103

What does the heart do to autoregulate?

Back 103

local metabolites - O2, adenosine, NO

Front 104

What does the brain do to autoregulate?

Back 104

local metabolites - CO2 (pH)

Front 105

What does the kidneys do to autoregulate?

Back 105

myogenic and tubuloglomerular feedback

Front 106

What does the lungs do to auto-regulate?

Back 106

hypoxia causes vasoconstriction - so blood does not go to areas of the lung that don't have oxygen

Front 107

How does skeletal muscle autoregulate?

Back 107

local metabolites - lactate, adenosine, K+

Front 108

How does skin autoregulate?

Back 108

sympathetic stimulation most important mechaism - temperature control

Front 109

What is the starling equation?

Back 109

Pnet = Kf (Pc-Pi) - (pic - pii)

Front 110

What causes edema?

Back 110

edema - excess fluid outflow into interstitum commonly caused by:
- increased Pc (heart failure)
- decreased plasma proteins (decreased pi c; nephrotic syndrome, liver failure)
- increased capillary permeability (increased Kf; toxins, infection, burns)
- increased interstitial osmotic pressure (increased pi i; lymphatic blockage)