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Physiology > Cardiovascular Physiology Rapid Review > Flashcards

Cardiovascular Physiology Rapid Review Flashcards

1
Q

Systole

A

Heart contracts and blood is ejected
Blood pressure is greatest during systole.
In Ventricular systole, ventricles pump blood to the blood vessels. Atrial systole, atria pump blood into relaxed ventricles

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2
Q

Diastole

A

Heart relaxes and fills with blood. Blood pressure is lowest during diastole

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3
Q

Pulse Pressure

A

Difference between the systolic and diastolic pressures

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4
Q

Valves of the heart

A

Mitral valve - AV valve that prevents backflow from the left ventricle into the left atrium
Tricuspid valve - AV valve that prevents backflow from the right ventricle into the right atrium
Semilunar valves: aortic and pulmonic, prevent blood from flowing back into ventricles during ventricular diastole. Aortic separates left ventricle from aorta. Both valves have three cusps.

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5
Q

Heart sounds

A

S1 - closure of AV valves
S2 - closure of semilunar valves
S3 - ventricular gallop (early to middle diastole, during rapid ventricular filling)
S4 - Atrial gallop (late diastole, atrial contraction against a stiffened ventricle)

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6
Q

S3 sound

A

Ventricular gallop, may be caused by a sudden limitation of ventricular expansion. Normal in children and young adults, but may be caused by rapid ventricular expansion associated with regurgitation of blood across an incompetent valve, which increases the rate of ventricular filling during diastole (in adults; aortic regurgitation)

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7
Q

S4 sound

A

Heard in late diastole, caused by atrial contraction against a stiffened ventricle. Indicates cardiac disease. Indicated decreased ventricular compliance (the ventricle does not relax as easily) which is commonly associated with ventricular hypertrophy or scarring. An S4 is almost always present after an acute MI.

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8
Q

Describe ventricular pressure changes

A

Ventricular pressure gradually increases in volume during diastole, which causes the ventricular pressure to increase
Atrial contraction causes a slight “hump” before systole in the final phase of ventricular filling.
The AV valves close when systole begins and the ventricular pressure is greater than the atrial pressure.
Isovolumetric contraction - Pressure continually builds until the ventricular pressure exceeds that of the aorta or the pulmonary artery.
The semilunar valves open.
Blood is ejected into the circulation.
Semilunar valves close when the pressure inside the ventricles is less than that of the aorta and pulmonary artery.
Isovolumetric Relaxation - Pressure decreases (same volume of blood, muscle relaxes)
When interventricular pressure is less than atrial pressures, AV valves open again, and ventricular filling of diastole begins.

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9
Q

Cardiac Output

A

Volume of blood pumped out of the heart each minute.
Product of heart rate and stroke volume.
Used to assess cardiac performance
5 L/minute in healthy adult (70 Bpm * 70 mL/beat)
Can also be measured using whole body oxygen consumption

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10
Q

Fick Principle

A

Oxygen consumption by the body is a functino of the amount of blood delivered to the tissues (cardiac output, CO) and the amount of oxygen extracted by the tissues (arteriovenous oxygen difference):

CO = oxygen consumption / (oxygen concentration in arteries - oxygen concentration in veins)

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11
Q

Stroke Volume

A

Volume of blood ejected from the ventricle during ventricular systole
Determines Pulse Pressure
SV = EDV (End diastolic volume) - ESV (End systolic volume)

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12
Q

Ejection Fraction

A

Percentage of blood in the ventricle at the end of diastole that is pumped into the circulation with each heartbeat.

SV (stroke volume) / EDV (End diastolic volume)

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13
Q

Determinants of Stroke Volume

A

Preload, Contractility, and Afterload

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14
Q

Preload

A

Degree of tension (load) on the ventricular muscle when it begins to contract (Volume of blood within the ventricle at the end of diastole) (venous return)

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15
Q

Frank-Starling relationship

A

Length-tension relationship of the heart theory

Increased ventricular wall tension associated with increased EDV stretches ventricular myocytes and results in a greater overlap of actin and myosin filaments, which causes more forceful contractions

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16
Q

Second theory of why an increased EDV increases SV

A

The contractile apparatus of cardiac myocytes becomes more sensitive to cytoplasmic calcium as the myocytes are stretched under conditions associated with increased preload

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17
Q

Contractility

A

Measure of the forcefulness of contractions at any given preload (independent of myocardial wall tension at EDV)

Inotropic state of the heart

(Drugs, sympathetic excitation, and heart disease may affect contractility)

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18
Q

What affects contractility?

A

Drugs, sympathetic excitation, and heart disease

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19
Q

Afterload

A

The pressure or resistance against which the ventricles must pump blood (including systemic blood pressure) and any obstruction to outflow from the ventricle (such as stenotic aortic valve

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20
Q

If Afterload increases, SV ____.

A

decreases

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21
Q

Laplace equation

A

Rho = P x r / 2h, where rho = wall tension, P = intraluminal pressure, r = intraluminal radius, and h = wall thickness

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22
Q

Stroke work

A

Measure of the mechanical work performed by the ventricle with each contraction

Composed of Pressure-volume work and Kinetic energy work

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23
Q

Pressure-volume work

A

work used to push the SV into the high-pressure arterial system and is equal to the systemic arterial pressure multiplied by the SV

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24
Q

Kinetic energy work

A

Supplied by ventricular contraction that is used to move the ejected blood at a certain velocity

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25
Q

Increased venous return _____ preload.

A

Increases

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26
Q

Venodilator examples

What is the effect?

A

Nitroglycerine, isorbide dinitrate

They lower venous return and right atrial pressure.

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27
Q

What increases venous return?

A

Exercise and venoconstriction

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28
Q

Effect of inspiration on pressures in the heart

A

Increases venous return (increases abdominal pressure and decreases inteathiracic pressure, increases venous pressure gradient)

Additional: P2 happens after A2 because it takes longer to eject the increased volume of blood in the right atrium (split S2 sound)

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29
Q

What would cause a wide S2 split?

A

Pulmonic stenosis

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30
Q

What would cause a constant S2 split? ( regardless of inspiration?)

A

Atrial septal defect

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31
Q

What would cause splitting without inspiration (and maybe no splitting with)?

A

Aortic stenosis

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32
Q

What are the four phases of the ventricular pressure-volume loops?

A

Phase I: ventricular filling in diastole. (Opening of the mitral valve and the beginning of ventricular filling)
Phase II: Isovolumetric contraction (onset if systole and closure of the mitral valve)
Phase III: ejection period (aortic valve opens, (pressure in the left ventricle exceeds those in the aorta), then aortic valve closes when pressure in aorta > left ventricle)
Phase IV: isovolumetric relaxation (immediately after closure of aortic valve, but no blood is flowing into the ventricle from the ateia because the pressure in the atria still exceeds the pressures in the atria. Ventricular volume dows not change. Then AV valves open in phase I.)

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33
Q

What are the atrial pressure changes during the cardiac cycle?

A

Slight pressure increase (a wave) caused by atrial contraction.
Large pressure increase (c wave) caused by isovolumetric ventricular contraction and inward bulging of the AV valves.
Rapid reduction in pressure (x descent) caused by initiation of the ventricular ejection phase (“vacuum effect”)
Gradual pressure increase (v wave) caused by atrial filling (after closure of the AV valves)
Gradual pressure decrease (y descent) caused by ventricular filling after opening of the AV valves.

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34
Q

What is a Swan-Ganz catheter?

A

It evaluates left atrial pressure. The catheter is inserted into a peripheral vein and threaded through the venous circulation until it becomes wedged in one of the small branches of the pulmonary artery

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35
Q

Effects of Aortic Stenosis

A

Increase in afterload, which decreases the stroke volume and decreases the cardiac output.

There is increased interventricular pressure to overcome the significant afterload produced by the stenotic valve.

Parvus et tardus (weak and late)

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36
Q

Sound associated with stenotic aortic valve

A

systolic ejection murmur

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37
Q

Aortic Regurgitation

A 
Increases the stroke volume but not the effective stroke volume
Decreases the cardiac output
Increased preload
Diastolic pressure reduced
Widened pulse pressure

Aortic valve allows backflow into left ventricle

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38
Q

Things that can widen pulse pressure

A

ionotrophy increases systolic pressure
Aortic regurgitation decreases diastolic pressure
Atrioventricular fistula decreases diastolic pressure

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39
Q

Things that can lead to aortic regurgitation

A

Ehler’s Danlos syndrome, Marfan Syndrome, endocarditis, syphilitic aortitis

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40
Q

Mitral Stenosis

A

Increase in left atrial pressure
Increases in pulmonary venous pressure
Hydrostatic pressures in the pulmonary veins and capillaries also become elevated, causing net transudation of fluid into the pulmonary interstitium
Once the left atrial pressure exceeds 30-40 mm Hg, the compensatory capacity of the lymphatics is overwhelmed and fluid begins to accumulate in the lungs
Causes dyspnea and reduced exercise capacity
mitral commissurotomy (mitral valve repair) can treat
Rheumatic fever most common cause of mitral stenosis

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41
Q

Most common cause of mitral stenosis

A

Rhematic fever

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42
Q

Mitral Regurgitation

A

Backward flow of blood into left atrium during early systole
Reduced forward flow cardiac output
Elevated left atrial pressures and volumes
Left ventriular volume overload (due to the additional preload imposed on the left ventricle by the addition of the regurgitated blood to the normal venous return)
In actue settings, severe and even fatal pulmonary edema may develop (occurs with rupture of papillary muscle in an MI (of Right coronary artery))
In chronic settings, the left atrium has had time to enlarge and become more compliant and the pulmonary lymphatics have had time to augment their function (caused by ischemic cardiomyopathy); fatigue and weakness, heart-failure-like symptoms

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43
Q

What causes mitral regurgitation?

A

MI (Right coronary artery)
Ischemic cardiomyopathy
Mitral valve prolapse (asymptomatic)

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44
Q

Sound laminar blood flow makes

A

none

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45
Q

Reynold’s number

A

Re = 2rvp/n

Where r = radius of the vessel, v = velocity of flow, p = density of the fluid, and n = viscosity of the fluid

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46
Q

What is coronary blood flow dependent on?

A

rate of blood flow within the coronary arteries, length of diastole, diastolic perfusion pressure, and vascular resistance of the coronary arteries

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47
Q

Left ventricular blood flow is largely _____ on the length of time spent in diastole. Right ventricular blood flow is largely _____ of the time spent in diastole.

A

dependent,
independent

(compression of coronary vessels during left ventricular systole)

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48
Q

When will an aortic stenosis murmur occur?

A

Throughout systole (between S1 and S2)

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49
Q

When will an aortic regurgitation murmur occur?

A

In early diastole, decreases in intensity throughout diastole

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50
Q

When will a mitral stenosis murmur occur?

A

Diastole

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51
Q

When will a mitral regurgitation murmur occur?

A

Throughout systole

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52
Q

What is the driving force for coronary blood flow?

A

The diastolic perfusion pressure

53
Q

What does an intra-aortic balloon pump do?

A

It inflates during diastole and increases the aortic back pressure and the diastolic perfusion pressure, which improves coronary blood flow, cardiac function, and increases cardiac output. (It is inserted into the distal thoracic aorta)

54
Q

Substances that cause vasodilation

A

adenosine, hydrogen ions, and potassium

55
Q

Diseases that decrease arterial oxygen content

A

anemia and chronic obstructive pulmonary disease

56
Q

Main determinants of myocardial oxygen demand

A

Heart rate (proportionally more time spent in systole when HR increases, which increases cardiac workload and therefore increases myocardial oxygen demand, but supply is compromised)
Myocardial wall tension
Contractility

57
Q

Effect of hypertrophy

A

Increase in muscle mass due to increased afterloads reduces wall tension but increases the myocardial oxygen requirement

58
Q

When does angina occur?

A

When oxygen demand by the heart exceeds oxygen supply

59
Q

Causes of angina pectoris

A

Atherosclerotic narrowing of coronary vessels in CAD (increased resistance, decreased blood flow)
Spasm of the coronary arteries in Prinzmetal’s angina (reduces coronary blood flow so much that the pain may occur at rest)

60
Q

How does nitroglycerin relieve anginal pain?

A

Nitrates reduce wall tension generated during systole, reducing myocardial oxygen demand. They dilate both veins and arteries, which reduces perload and afterload. May also prevent vasospasm of coronary arteries by causing vasodilation

61
Q

Concentric hypertrophy

A

occurs in response to significant afterloads (systemic hypertension, aortic stenosis)
myocytes thicken (not proliferate
Decreased ventricular compliance (impaired diastolic ventricular filling, elevated filling pressures)

Pressure overload

62
Q

Hypertrophic cardiomyopathy

A

myocardial muscle hypertrophies without a physiologic stimulus. Often occurs asymmetrically with the cardiac septum exhibiting the most hypertrophy.
May cause left ventricular outflow obstruction, resulting in a systolic murmur
Can be so severe during intense exercise that syncope or sudden death occur (due to conduction defects)

63
Q

Eccentric hypertrophy

A

Volume overload

Occurs in response to increased preload (aortic regurgitation, mitral regurgitation)
Ventricular chamber increases in diameter, sarcomeres added to existing myocytes in series (elongates ventricle, does not appreciably thicken)
Decreases amount of tension on each sarcomere at end-diastole

64
Q

Idiopathic dilated cardiomyopathy

A

heart dilates without being volume-overloaded

Excessive alcohol use most common

65
Q

Electric signal pathway

A

SA node through Purkinje system and intercalated disks of myocytes.
SA node discharges at own inherent rate (80 times per minute)

66
Q

SA node depolarization

A

Fairly permeable to sodium ions, so membranes gradually depolarize at rest.
Voltage-gated calcium channels open, allowing slow current of calcium to enter cells and generate action potential
Calcium channels close spontaneously, potassium flows out of cells
(Resting potential is about -70 mV)

67
Q

Maximum diastolic potential

A

Most negative membrane potential of the SA node

If made more negative, heart rate slows (how vagus nerve works)

68
Q

Factors affecting heart rate

A

Lowering maximum diastolic potential lowers heart rate
Making nodal cells more permeable to sodium increases HR (less permeable decreases HR)
Catecholamines raise heart rate (from sympathetic excitation)
Raising threshold lowers heart rate

69
Q

Backup pacemakers

A

AV node not as permeable to sodium ions, does not spontaneously depolarize as rapidly

70
Q

Action potential in a cardiac myocyte

A

resting membrane potential is maintained at -90 mV. Sodium channels closed
Depolarization occurs when voltage-gated sodium channels open, sodium rushes into cell and causes membrane potential to become increasingly positive
Rapid efflux of potassium and cessation of sodium efflux repolarizes cell.
Calcium influx (balances potassium efflux) - responsible for long duration of cardiac myocyte action potential, initiaes contraction of cardiac myocytes.
Repolarization occurs by rapid efflux of potassium and cessation of calcium influx
Refractory period - sodium channels cannot open again. Prevents tetany and places an upper limit on heart rate (180-200 BPM)

71
Q

The force of contraction is proportional to the _____.

A

intracellular calcium level

72
Q

Sympathetic excitation

A

increases contractility by increasing the influx of extracellular calcium, causing a greater calcium-induced calcium release. It also speeds up reuptake of calcium

73
Q

Calcium channel blocking drugs

A

dilitiazem, verapamil
Have a negative inotropic effect on the heart (by preventing the influx of extracellular calcium during the cardiac action potential)
beneficial in patients with chronic heart failure (reduces myocardial oxygen demand and hypertension (reduces cardiac output)

74
Q

Digitalis (Digoxin)

A

A cardiac glycoside, has a positive inotropic effect on the heart

increases cytoplasmic calcium by inhibiting the sodium-potassium adenosine triphosphate pump, which increases intracellular sodium.

Symptomatic relief in patients with heart failure

75
Q

Autonomic innervation of the heart - sympathetic

A

Adrenergic

Innervates nodal tissues, atria, and ventricles

Norepinephrine released from sympathetic nerves, binds to adrenergic receptors in the heart, resulting in increased heart rate (positive chronotropic effect) and increased contractility (positive inotropic effect)

76
Q

Receptor primarily responsible for mediating sympathetic excitation of heart rate and contractility

A

beta1-receptor

Beta-1- increases CAMP

77
Q

Beta-blocking drugs

A

metoprolol

antagonize beta1-receptors and can slow the heart rate and reduce contractility

78
Q

Autonomic innervation of the heart - parasympathetic

A

innervation of the heart is limited to the nodal tissues and the atria (none to the ventricles)

Acetylcholine released from parasympathetic nerves (vagus) binds to muscarinic receptors. Decreases heart rate by increasing the maximum diastolic potential, raising the action potential threshold and decreasing the rate of phase 4 depolarization in nodal cells

79
Q

Atropine

A

blocks the muscarinic receptors in the heart and increases heart rate. It is useful in treating patients with acute symptomatic bradycardia

80
Q

ECG leads

A

bipolar limb leads - I, II, III (vertical/frontal plane)
unipolar limb leads - aVF, aVR, aVL (vertical/frontal plane)
Precordial limb leads - V1-V6 (transverse plane)

81
Q

Normal EKG basics

A

P-wave corresponds to atrial depolarization
PR interval corresponds to impulse conduction through the AV node
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization

82
Q

Mean arterial pressure equation

A

MAP = cardiac output x total peripheral resistance

83
Q

Resistance equation

A

= 8nl/(pi*r^4)

n = viscosity, r = radius of the vessel, l = length of the vessel

84
Q

ECG abormality: ST segment elevation
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) Acute myocardial infarction

2) Prolonged repolarization

85
Q

ECG abormality: Split R wave
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) Bundle Branch Block

2) Depolarization of right and left bundle branches no longer occurs simultaneously

86
Q

ECG abormality: PR interval > 200 msec
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) Heart block

2) Excessive vagal outflow, drugs that slow atrioventricular conduction, or degenerative disease

87
Q

ECG abormality: Pathologic Q wave
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) “Transmural” myocardial infaction

2) Not listed in book

88
Q

ECG abormality: Deviation of mean QRS axis
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) Myocardial infarction or ventricular hypertrophy
2) Left ventricular hypertrophy in response to increased afterload (e.g., hypertension, aortic stenosis, or right ventricular hypertrophy in response to massive pulmonary embolism

89
Q

ECG abormality: Inverted T wave
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) Ischemia

2) Prolonged ventricular depolarization and ventricular ischemia from coronary artery disease

90
Q

ECG abormality: “peaked” T wave
Diagnosis: (1)
Possible Pathophysiology: (2)

A

1) hyperkalemia

2) not listed

91
Q

When vasomotor tone is normal, the majority of the body’s arterioles are ____.

A

at least partially constricted

92
Q

Medullary vasomotor center

A

Tonic sympathetic ouflow from this center maintains arterial pressure.
Involved in reflex regulation of blood pressure

93
Q

Sympathetic stimulation of vascular smooth muscle contraction is mediated by ____.

A

Alpha-1 receptors
Alpha-blocking drugs such as prazosin antagonize this receptor and inhibit vasoconstriction, thereby lowering blood pressure.
Prazosin can also cause orthostatic hypotension

94
Q

Baroreceptor reflex

A

Mechanoreceptors in the aortic arch and carotid sinuses fire action potentials to vasomotor center in brainstem when arterial blood pressure is higher. Medullary sympathetic ouflow is blocked and parasympathetic outflow is stimulated.
Causes arteriolar dilation and decreases sympathetic drive to the heart, decreasing the heart rate. Reduces firing frequency of the SA node.

Drop in blood pressure

If low blood pressure detected, baroreceptors fire less frequently, reduce inhibition of sympathetic outflow. Increase in cardiac output and peripheral vascular resistance acts rapidly to prevent a further decline in blood pressure.

95
Q

Pressure on the carotid sinuses can cause ____.

A

a rapid “compensatory” drop in blood pressure and syncope

96
Q

Side effect of prazosin (alpha-1 blocker)

A

increased orthostatic hypertension

97
Q

Cushing’s sign

A

When head injury causes significantly increased intracranial pressure that may activate the CNS ischemic response, decreasing blood flow to the medullary vasomotor center and causing hypertension.

Bradycardia develops

98
Q

CNS ischemic response

A

Sympathetic outflow from the vasomotor center is strongly stimulated.

99
Q

Metabolic mechanism of autoregulation

A

vasoactive compounds adenosine and lactic acid released

100
Q

Myogenic mechanism of autoregulation

A

Differential permeability of the vascular smooth muscle to extracellular calcium depends on the contractile state of the vascular smooth muscle cell

101
Q

Vascular compliance

A

ability of a vessel to withstand an increase in volume without causing a significant increase in pressure. Compliance = volume/pressure

Arteriosclerosis reduces compliance and raises arterial pressure (isolated systolic hypertension)

102
Q

Long-term control of blood pressure

A

With high blood pressure, kidneys remove water from blood stream using higher-than-normal glomerular filtration rate (diuresis)
Sodium also excreted.
Intravascular volume reduced, cardiac output reduced, arterial pressure brought down to normal.

Pressure natriuresis occurs with low blood pressure. Sodium and water are retained.

103
Q

Renin-angiotensin-aldosterone system

A

The macula densa (part of the juxtaglomerular apparatus in afferent arterioles) releases renin when there is reduced renal blood flow. This results in production of angiotensin II, which increases arterial blood pressure by stimulating expansion of the intravascular volume. It stimulates aldosterone secretion from the adrenal glands and stimulating renal sodium retention. Angiotensin II also stimulates systemic vasoconstriction, which increases arterial blood pressure by increasing TPR.

104
Q

Effect of renal artery stenosis and congestive heart failure

A

May activate the renin-angiotensin-aldosterone system because the kidney is underperfused

105
Q

What do ace inhibitors do?

A

They inhibit the production of angiotensin II. ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II.

They reduce blood pressure.
They prevent constriction of efferent arterioles

106
Q

What might NSAIDs do to the kidney?

A

Prevent vasodilation of the afferent arteriole and cause prerenal azotemia by decreasing blood flow

107
Q

ADH

A

Anti-diuretic hormone is secreted form the posterior pituitary. It regulates plasma volume and is secreted by hypothalamic osmoreceptos in response to either slight increases in plasma osmolarity or marked reductions in plasma volume

Stimulates water reabsorption by the collecting tubules of the distal nephron. Stimulates vasoconstriction.

108
Q

Bainbridge reflex

A

Increased venous return induces low-pressure stretch receptors to increase the heart rate, which increases cardiac output and renal perfusion (further increasing diuresis)
Atrial natriuretic peptide also promotes diuresis.

109
Q

Starling forces

A

interaction between plasma and interstitial hydrostatic and osmotic forces, determines net filtration pressure

Hydrostatic pressure of the capillary (Pc) (greater from arterial end, lower on venous end) (Edema occurs when hydrostatic pressure is abnormally elevated (venous obstruction can cause this))

Plasma oncotic pressure or plasma colloid osmotic pressure ( pi c) (Determined by serum albumin level. Hypoalbuminemia can cause edema)

Interstitial hydrostatic pressure (PIF)
(normally negative)

Interstitial oncotic pressure (pi IF) (proteins in the interstitium are usually lower than in the capillaries)

110
Q

Hemmorhage has what effect in regard to starling forces?

A

Lowers hydrostatic pressure, causes interstitial fluid to replace lost blood volume

111
Q

What can cause hypoalbuminemia?

A

malnutrition or liver diease,

possibly nephrotic syndrome

112
Q

Starling equation

A

NFP = (Pc +Pi IF) - (P IF + pi c)
Net filtration pressure = hydrostatic pressure of capillary + interstitial oncotic pressure - ( hydrostatic pressure of the interstitial fluid + plasma oncotic pressure)

113
Q

Things that can cause edema

A 
Liver disease (less plasma protein results in lowered plasma oncotic pressure), 
inflammation (increased vascular permeability results in proteins in interstitial fluid and greater oncotic pressure in intersitial fluid), 
venous obstruction and heart failure (hydrostatic pressure increases in venous capillary), 
myxedema (more proteins in intersitial fluid increases oncotic pressure of interstitial fluid),
nephrotic syndrome (proteinuria results in less plasma protein and decreased plasma oncotic pressure)
114
Q

Heart failure definition

A

Any state in which cardiac output is inadequate to meet the body’s metabolic demands

115
Q

Systolic heart failure

A

“pump” failure, 2/3 of all heart failure
Impaired contractility (MI, chronic volume-overloaded states such as aortic or mitral regurgitation, dilated cariomyopathy)
Pathologic increases in afterload (hypertension and aortic stenosis)

Decrease in stroke volume and cardiac output

116
Q

Diastolic heart failure

A

1/3 of heart failure cases. Ventricular filling during diastole is impaired.

Reduction in ventricular compliance (left ventricular hypertrophy and hypertrophic cardiomyopathy (no relaxing), restrictive cardiomyopathy (deposition of substances within the myocardium causes fibrosis), or myocardial ischemia (oxycen supply not enough to support active diastolic relaxation)
Obstruction of left ventricular filling (mitral setnosis and cardiac tamponade (fluid accumulated in the pericardial space and opposes ventricular filling), restrictive pericarditis (scarring of pericardium limits ventricular expansion and filling))

117
Q

Cardiac tamponade

A

fluid accumulated in the pericardial space and opposes ventricular filling

118
Q

High-output heart failure

A

Caused by large arteriovenous fistulas or in thyrotoxicosis or sever anemia

119
Q

Compensatory responses to reduced cardiac output

A

Frank-Starling relationship
Myocardial hypertrophy
Neurohormonal activation

120
Q

Frank-Starling relationship

A

Reduced renal perfusion from reduced cardiac output activates renin-angiotensin-aldosterone system and expands plasma volume, which causes pulmonary edema and peripheral edema

121
Q

Myocardial hypertrophy

A

Increased myocardial wall stress leads to myocardial hypertrophy and results in increased myocardial oxygen demand, reduced ventricular compliance if concentric hypertrophy develops, and impaired contractility if eccentric hypertrophy develops

122
Q

Neurohormonal activation

A

Baroreceptors trigger this and cause a risk of arrhythmias and vasoconstriction in skeletal muscles produces weakness

123
Q

Signs of shock and their cause

A

Acidosis (tissue ischemia/hypoxia causes anaerobic respiration)
Pale, cool, moist skin (sympathetic-mediated peripheral vasoconstriction and sweating)
Rapid, weak pulse (reflex tachycardia in hypotension)
Reduced urinary output (decreased renal blood flow results in lower glomerular filtration rate)
and confusion (insufficient cerebral perfusion)

124
Q

Types of shock

A

Cardiogenic
Distributive (Spinal/neurogenic, septic, and anaphylactic)
Hypovolemic

125
Q

Cause of cardiogenic shock

A

Failure of the heart to pump effectively (ie reduced ejection fraction resulting in reduced cardiac output)

MI or viral myocarditis

126
Q

Cause of Distributive Spinal shock

A

spinal cord injury
Disrupts autonomic outflow from the spinal cord, which abolishes normal tonic stimulation of arteriolar contraction by sympathetic nerves

127
Q

Cause of distributive septic shock

A

Severe bacteremia
bacterial infection of blood leads to release of bacterial toxins and cytokines, which results in high fever and massive vasodilation and decreased vascular resistance

128
Q

Cause of anaphylactic shock

A

allergies, Massive IgE-mediated histamine release

129
Q

Cause of hypovolemic shock

A

Hemorrhage, vomiting, diarrhea, burns, dehydration

Hypovolemia leads to decreased venous return and decreased cardiac output

Physiology (11 decks)

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