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165 Cards in this Set

  • Front
  • Back
Cardiac muscle gets venous drainage via what vessel? (located where?)
Coronary Sinus (@ Right Atrium)

(remaining venous blood will drain directly into the heart chambers)
Cardiac muscle is mostly perfused during what period?
Diastole
Characteristics of LV Perfusion
10% of total perfusion @ Systole

(occurs thru LV capillaries)
Coronary Blood Flow reduction is Highest in which cells?

Occurs during what period?

Why?
LV Subendocardium myocytes

Systole

Greatest contraction occurs at the LV subendocardium, thus causing greatest compression of coronary vessels.
(thus reduction in coronary BF)
Cardiac Blood Flow Perfusion consumes what percentage of Cardiac Output?
5% of CO
Cardiac Myocytes have the highest consumption of?
O2
Coronary Perfusion Regulation is primarily controlled via what process?

What are the primary factors involved?

Other vasodilator effectors?
Other vasoconstrictor effectors?
Local Factors

Hypoxia & Adenosine (Vasodilators)

VD ==> NO & Alpha-adrenergics
VC ==> Beta-adrenergics
Vascular Blood Flow is proportional to?

Vascular Blood Flow is Inversely Proportional to?
(proportional to) ==> radius^4

(inversely proportional to) ==> Resistance
Decreased pH, Bicarb, & pCO2

(which one is compensatory)
Metabolic Acidosis

(pCO2 decrease is compensatory)
Increased pH, Bicarb, & pCO2

(which one is compensatory)
Metabolic Alkalosis

(pCO2 increase is compensatory)
Decreased pH
Increased Bicarb & pCO2

(which is compensatory)
Respiratory Acidosis

(Increased Bicarb)
Increased pH
Decreased Bicarb & pCO2

(which is compensatory)
Respiratory Alkalosis

(Decreased Bicarb)
DKA signs & symptoms
Metabolic Acidosis (ketoacidosis)

(DATA)
Dehydration
Altered Mental Status (confusion)
Tachypnea
Abdominal pain
Primary Tx for DKA
Insulin & Fluids
In treating DKA, Insulin increases & decreases what?
Increases Bicarb
(glucose uptake decreases lipolysis, thus decreasing ketones, which causes Bicarb increase)

Decreased Glucose
Decreased Potassium
(insulin causes Intracellular Shift of K+)
In treating DKA, Fluid hydration increases and decreases what?
Increase Sodium (Na+)

Decrease Osmolarity
Insulin causes intracellular shift of what ions?
Potassium
Opioid OD causes what respiratory change?

What pathology does this cause?
Hypoventilation

Respiratory Acidosis
Mineralocorticoids retains what?

Mineralocorticoids waste what?
(retains) Na+ & Water

(wastes) Postissum
Thyroxine causes what osmolar changes?

Thyroxine causes what fluid change?
Decreased Na+ & H2O

ECF expansion
What process has properties of NO Carrier Proteins & NO Saturation?
Simple Diffusion
What process has properties of Carrier Proteins & Saturation?
Facilitated Diffusion
Max & Min Pressures of:

- Right Atria
- Right Ventricle
- Pulmonary Artery
10 / 0

25 / 4

25 / 10
Max & Min Pressures of:

- Left Atria
- Left Ventricle
- Aorta
12 / 2

130 / 10

130 / 70
Which heart side has greater pressure?
Left side > Right side
ANP is produced by?

ANP released in response to?
Atrial myocytes

Hypertension & Hypervolemia
ANP functions?


Overall effect of ANP on CV properties
(ANP)

Arteriolar vasoDilation
Natretic/Diuretic
Prevents Renin

Decreased TPR
Resting membrane potential in Heart?

Resting membrane potential in Skeletal muscle?

Why difference important?
- 90 mV

-75 mV

Higher Negative Vm in cardiocytes means larger stimulus required to excite cells, thus preventing arrythmias
Phase 2 Plateau stage involves what kind of channels?
L-Type Calcium Voltage-gated channels
MCC of Palpitations is?
Anxiety
Atrial Fibrillation signs & symptoms
(CIITA)

Conscious w/
Irregularly Irregular Tachy-Arrythmia
Atrial Fibrillation is the Most Common what?
Chronic Arrythmia
Acute, isolated episodes of Atrial Fibrillation can be seen with what conditions?
Alcohol Binging ("Holiday Heart Syndrome")
Increased Sympathetic tone
Pericarditis
Atrial Fibrillation has what EKG findings?
(ATRI-al fibrillation)

Absent P wave
Tachycardia
R-R variability
Irregularly irregular QRS
Prolonged-QT is associated with what marked property?

Prolonged-QT predisposes to what condition?
Markedly increased HR

Torsade De Pointes
(unique V-tachy)
Prolonged-QRS has a normal what?
Normal HR
MCC of Prolonged-QRS?
BBB
High-QRS-Voltage
(aka - High Voltage of Precordial Leads)
- has what QRS characters
No irregularities
High-QRS-Voltage
(aka - High Voltage of Precordial Leads)
- indicates what condition?
- usually due to what condition?
Ventricular Hypertrophy

Prolonged, Untreated HTN
Absent P-wave
Tachycardia
R-R variability
Irregularly irregular QRS
Atrial Fibrillation
Absent P-wave
Bradycardia
Normal QRS
3rd degree AV block

(aka - Complete AV Block)
Absent P-wave
Bradycardia
Abnormal QRS
(prolonged, abnormal shaped QRS)
Pacemaker @ Below AV (purkinje)
Inspiration causes what pressure change?
Decreased Intrathoracic Pressure
Cardiac Failure stimulates what compensatory physiological mechanisms?
Sympathetics
&
RAAS
Renin is made by what cells?

Cells are located where vascularly?
JGA cells

Afferent arteriole (of renals)
Angiotensinogen is made where?
Liver
ACE is made by what cells?
Pulmonary Vascular ENDOThelium
ACE functions? x2
Converts Angiotensin I to Angiotensin II

Breaks down Bradykinin
Aldosterone is made by cells where?
Zona Glomerulosa
(of adrenal cortex)
Aldosterone is produced in response to what signals?
Angiotensin II
&
Hyperkalemia
PV LOOP

How does Infusion of Normal Saline change the vascular volume?

How does this affect SV?

How does this affect the PV Loop?

What other pathologies cause same events to PV LOOP?
Increases PRELOAD

Increase SV

Increases Width to the right

Any fluid overload scenario
(i.e. - Renal Failure, HF, NS infusion)
PV LOOP

Loss of myocardial cells cause what changes in terms of CV function?

How does this affect the SV?

How does this affect the PV Loop?

Is this a systolic or diastolic dysf(x)?
Decrease Contractility
(b/c less myocytes to contract)

Decrease SV (thus less EF)

Decreases Width from left

Systolic
(systolic is cardiac contraction)
(diastolic is cardiac innervation)
Upon entering cells via voltage-gated L-type Calcium channels, Ca2+ will bind to what receptor on the SR?
Ryanodine receptors
Cardiomyocyte relaxation occurs by Ca2+ efflux via what 2 transporters?
1.) Ca2+ ATPase

2.) Na+/Ca++ Exchanger
(does not require ATP)
What molecule acts as an INDIRECT contributor for Ca2+ efflux in cardiomyocyte relaxation?

This molecule binds what?

What is the effect of this binding?
Calmodulin

Binds Ca2+ ATPase

Removes intracellular Ca++ by hydrolyzing ATP
During normal Diastole, when the Mitral Valve is open, what 2 pressures are nearly equal?
LAP ~ LVP
(or LAEDP ~ LVEDP)

(due to minimal resistance btw LA & LV)
What variable can used in the measurement of LAEDP (LAP)
PCWP

(Pulmonary Capillary Wedge Pressure)
Under what pathology would PCWP (or LAEDP) be significantly elevated relative to LVEDP?

(PCWP or LAEDP >> LVEDP)
Mitral Stenosis

(thus marked increased resistance btw LA & LV, with LAP being much greater)
Short Acting BALANCED Vasodilator?
Nitroprusside
Nitroprusside affects Preload how?

Nitroprusside affects Afterload how?

Nitroprusside affects SV how?
Decreases

Decreases
(to same extent as Preload b/c Balanced)

No change in stroke volume
(b/c equal decreases btw preload & afterload)
In acute hemorrhage, what is the initial compensatory physiological response once the blood loss is significant (~ >10%)

If the hemorrhage persists Massively and Chronically, then what can it lead to?
Sympathetics

Hypovolemic shock
In what pathology is the Sympathetic response stimulation MAXED out?

Why clinically relevant?
HYPOVolemic SHOCK!

Vasopressors are of little & temporary benefit.
In Hypovolemic Shock, what is the primary treatment?
Crystalloid FLUIDS

(i.e. - Normal Saline)
Infusion of crystaloid fluids (i.e. NS) in treating Hypovolemic Shock, causes what volume changes?

This volume change causes what change in cardiomyoctes?

Thus causing what change in CV properties?
Increased PRELOAD
(due to incr. intravascular volume)

Increases ventricular
END-DIASTOLIC
SARCOMERE LENGTH

Thus, increased CO & SV
Aortic Arch Baroreceptors have what afferent nerve?

Baroreceptors at the Bifurcation of the Common Carotid Artery (@ Carotid Sinus) have what afferents?
Vagus (CN X)

Glossopharyngeal (CN IX)
(aka: Hering nerve, Carotid sinus nerve)
What CN nucleus does the afferents of the Baroreceptors @ Aortic Arch & Carotid Sinus travel to?

(what part of brain is that?)
Solitary Nucleus

(of Medulla)
External Pressure on the Carotid Sinus (Carotid massage) stimulate the baroreceptor afferents how?

How does this affect vascular radius?
Increase it's Firing rate
(baroreceptors act as if Systemic BP increased)

VasoDILATION
External Pressure on the Carotid Sinus (Carotid massage) manifest on to the patient with what signs?
Bradycardia
HYPOTension
Syncope (possibly)
What is the most important mediator of Coronary vasoDILATION of LARGE Arteries?
Nitric Oxide (NO)
What is the most important mediator of Coronary vasoDILATION of SMALL Arteries?
Adenosine
(byproduct of ATP metabolism)
Nitric Oxide (NO) is synthesized by what cells?

NO is synthesized from compounds?

Via what enzyme?
Endothelial cellls

Arginine & O2

endothelial NO Synthase (eNOS)
NO vasodilates large vessel coronary by relaxing SM via what Secondary messenger system?
G-Protein --> cGMP

messenger system
What is the significance of the Autonomic Nervous system on Coronary Blood flow?
Very Little Effect (teeny tiny effect)

(alpha-adrenergics = vasodilates)
(beta-adrenergics = vasoconstricts)
Conservation of Mass equations x2
Qin = Qout : for Q = V x A
(V=Velocity & A = XS area)

Mass(in) = Mass(out) : for M = VD
(V= Volume & D=Density)
Coronary BF occurs primarily at what period?
Diastole

(b/c @ systole, open Aortic Valve partially blocks coronary & contracting myocytes compress coronary)
What is the most important factor when considering Coronary BF?
Duration of Diastole
During Exercise, what happens to the Diastolic Duration?

What compensatory event occurs to preserve the metabolic needs of the heart?
Decreases
(and w/ increased HR cause hypoxia)

Adenosine (vasodilator released)
During Diastole with Exercise, Adenosine has what effects on BF & Resistance of coronary arteries?
(vasodilator, so)

Increase coronary BF
Decrease coronary Resistance
During Exercise, what is the Limiting Factor for coronary BF?
Diastolic Duration
EXCITATION-COUPLING

- depends on what electrolyte properties for Skeletal muscle

- depends on what electrolyte properties for Smooth muscle
INTRACellular Pool of Ca2+ (in SR)

EXTRACellular Influx of Ca2+
EXCITATION-COUPLING

- Extracellular Calcium enters muscle in which muscle type?

- Enters cells via what receptor?
Smooth muscle & Cardiac muscle

Voltage Gated Ca++ Channels
(skeletal muscles don't have this)
EXCITATION-COUPLING

- For Skeletal muscles, what event initiates AP?

- For Smooth muscles, what event initiates AP?
Release of ACh

Influx of Ca2+
(via voltage-gated Ca++ channels)
EXCITATION-COUPLING

Can skeletal muscle cells self-depolarize?

Can smooth muscle cells self-depolarize?
No

Some can
(i.e. - GI, uterus, bladder, etc.)
EXCITATION-COUPLING

- what causes Ca2+ release in skeletal muscle cells?

- what causes Ca2+ release in smooth muscle cells?
ACh release & widespread depolarization

Ca2+-dependent-Ca2+-channel (of SR)
EXCITATION-COUPLING

- In skeletal muscle cells, intracellular calcium binds to what?

- In smooth muscle cells, intracellular calcium binds to what?
- Troponin C

- Calmodulin
EXCITATION-COUPLING

- Are T-tubules found in either skeletal muscle or smooth muscle cells?
only in skeletal muscle cells
EXCITATION-COUPLING

- what induces contraction in skeletal muscle cells?

- what induces contraction in smooth muscle cells?
- Calcium binding Troponin C

- Calcium binding Calmodulin
EXCITATION-COUPLING

- Calcium-TroponinC complex found in which muscle cells?

- what does it do to induce contraction?
- Skeletal muscle cells

- displaces tropomyosin so that Actin can bind Myosin
EXCITATION-COUPLING

- Calcium-Calmodulin complex found in which muscle cells?

- what does it do to induce contraction?
- Smooth muscle cells

- activates Myosin Light Chain Kinase
EXCITATION-COUPLING

- Myosin-Light-Chain Kinase is found in which muscle cell type?

- is activated by what?

- once activated, will do what?
- Smooth muscle cells

- Calcium-Calmodulin complex

- Phosphorylate Myosin
(allowing it to bind to Actin)
EXCITATION-COUPLING

- in order for contraction to occur after Myosin and Actin bind, what additional reaction must occur?
ATP hydrolysis

(of the ATP on Myosin)
EXCITATION-COUPLING

- Verapamil is what class drug?

- Verapamil can affect what muscles?
- CCB

- Cardiac & Smooth muscles
EXCITATION-COUPLING

- Verapamil MOA

- which muscle can it not effect?

- why?
- Blocks Voltage Gated Calcium channels
(so Ca2+ can not enter cell)

- can NOT affect skeletal muscles

- b/c skeletal muscle is not dependent on extracellular calcium
(its dependent on intracellular pool of Ca2+)
EXCITATION-COUPLING

- Verapamil has what effects on the vasculature radius?
Vasodilates

(by relaxing vascular smooth muscles)
Heart Failure (with repeated bouts of MI) will affect which cardiac property?
Decreased EF

(due to ischemic loss of myocytes)
S3 heart sounds are normal in?

S3 heart sounds are pathological in?

S3 heart sounds are associated with what heart pathology?
children

adults

LVHF
Describe S3 frequency.

Thus, should be auscultated how?
Low frequency (unlike S1 & S2)

Bell
S3 immediately follows what heart sound?

What PV Loop phase is this in?
S2

Rapid Ventricular filling
(soon after Mitral Valve Opens)
What pathophysiological process causes the S3 to be audible?
Blood rapidly rushing into
PARTIALLY-FILLED ventricles
or
STIFF ventricles
S3 is best heard at what location?

What conditions could enhance the audible nature of S3?
Apex

1.) Left Lateral Decubitus position
2.) Complete exhalation by pt
(to bring heart closer to wall)
What maneuvers would increase VR?

(thus increasing LV volume & pressure)
Valsalva RELEASE

Squatting
What maneuvers would decrease VR?

(thus decreasing LV volume & pressure)
Valsalva MANEUVER

Standing
Valsalva maneuver (or standing) is good for enhancing the audible sounds of what murmurs?

But also decreases audible murmurs of?
1.) Hypertropic Cardiomyopathy
2.) MVP

- Aortic Stenosis
Furosemide causes brisk diuresis, thus it will affect what heart sound and how?
S3 gets less audible
Amyl Nitrate Inhalation causes vasodilation and decreased BP, thus it will affect what heart sounds and how?
(same as valsalva maneuver)

Enhances murmurs of
- Hypertropic cardiomyopathy
- MVP

Decreases audible for:
- Aortic Stenosis
Verapamil is what drug class?
CCB
&
Class 4 Antiarrhythmic
Verapamil is used as Tx in what conditions?
(ASH)
Angina
SVT
HTN
Verapamil MOA for the heart

(include specific cells affected)
Blocks Voltage-gated Ca2+ channels

(at the SA & AV node)
Verapamil causes what changes in on the cardiac AP? (specify which AP phase)
Slows down
Phase 0 Diastolic Depolarization
Verapamil causes what physical changes in cardiac property?
Decrease HR (by decr. SA firing rate)

Decrease AV CV (by decr. AV firing rate)
Impulse conduction going from SA --> AV --> Ventricular myocardium occurs during what period?
Diastole

(myocyte contraction occurs @ systole)
Verapamil causes what physical changes in muscles & BV?
Smooth muscle relaxation
(thus vasodilation)
Which Antiarrythmic drugs INCREASE THRESHOLD POTENTIAL (the amt of depolarization needed to initiate AP)
Class IA
Class IB
Class IC
Which Antiarrythmic drugs SHORTENS AP
(via Na+ channel blockade)
Class IB
Which Antiarrythmic drugs PROLONG REPOLARIZATION?
Class IA
Class IC

Class III
Acutely, AV Fistulas cause what vascular effect?
Decrease TPR

(b/c it shunts blood from arteries to veins)
Over time, Chronic AV Fistulas compensate for decreased TPR by what 2 mechanisms?
1.) Sympathetic stimulation

2.) Renal Retention of Fluids
In Chronic AV Fistulas, the sympathetics stimulate what CV changes?
Increased CO, thus Increased VR
How does Acute AV Fistula cause a right shift on the VR curve?
It does not.

(Right shift on VR curve happens later on with Chronic AV Fistula)
In Chronic AV Fistula, how does the Sympathetics promote Right shift in VR curve?
Increase VR
In Chronic AV Fistula, how does the Renals promote Right shift in VR curve?
Renal Retention of Fluids

==> Increased Blood Volume
Chronic AV Fistula has what changes in:
- CO?
- MSP?
- TPR?
Increase
Increase

Decrease
CO & VR CURVES

- changes seen with Chronic AV Fistula
CO curve shifted Upward
(b/c increased CO)

VR curve shifted Right
(b/c increased MSP)

Slopes of both curves Increase
(b/c of decreased TPR)
CO & VR CURVES

- affects from Acute GI Bleed
loss of blood volume, so

Left shift of VR curve
CO & VR CURVES

- affects from Phenylephrine infusion
increases sympathetics, so vasoconstriction causing Increased TPR, thus

Downshift CO curve
Decreased Slope (CCW rotation) of VR curve
CO & VR CURVES

- what changes are seen with Anaphylaxis?
causes widespread vasodilation, so

Massively Decreased VR
CO & VR CURVES

- what changes are seen with MI
less myocytes, so decreased contractility, thus decrease EF, so decreased CO, so

Decrease in CO curve
WITHOUT Changes in VR Curve
CO & VR CURVES

- affects seen with Chronic Anemia
CO is increased to meet metabolic needs, so

Increased CO Curve Slope
CO & VR CURVES

- Isolated decrease in CO curve ONLY implies what conditions?
- Negative Ionotropic drugs
or
- Heart injury inhibiting contraction
(i.e. Myocardial Infarction)
CO & VR CURVES

- which curve illustrates Frank-Starling effect?
CO curve
CO & VR CURVES

- what is the value at the point when VR curve intersects the X-axis?
MSP
CO & VR CURVES

- TPR is presented by what on the curves?
VR curve Slope

(thus when TPR increases, slope decreases)
PV LOOP

- Right shift of Isovolumetric Contraction line (1-->2) implies what CV change?
Increased Preload

(increased EDV means increased EDP)
PV LOOP

- Left shift of Isovolumetric Relaxation line (3-->4) implies what?
Increased Contractility

(thus increases in EF & SV)
(decrease in ESV)
For Fick's CO equation, the Venous concentration of O2 is obtained from what vessel?
Pulmonary artery
Acutely, AV Fistulas cause what vascular effect?
Decrease TPR

(b/c it shunts blood from arteries to veins)
Over time, Chronic AV Fistulas compensate for decreased TPR by what 2 mechanisms?
1.) Sympathetic stimulation

2.) Renal Retention of Fluids
In Chronic AV Fistulas, the sympathetics stimulate what CV changes?
Increased CO, thus Increased VR
How does Acute AV Fistula cause a right shift on the VR curve?
It does not.

(Right shift on VR curve happens later on with Chronic AV Fistula)
In Chronic AV Fistula, how does the Sympathetics promote Right shift in VR curve?
Increase VR
In Chronic AV Fistula, how does the Renals promote Right shift in VR curve?
Renal Retention of Fluids

==> Increased Blood Volume
Chronic AV Fistula has what changes in:
- CO?
- MSP?
- TPR?
Increase
Increase

Decrease
CO & VR CURVES

- changes seen with Chronic AV Fistula
CO curve shifted Upward
(b/c increased CO)

VR curve shifted Right
(b/c increased MSP)

Slopes of both curves Increase
(b/c of decreased TPR)
CO & VR CURVES

- affects from Acute GI Bleed
loss of blood volume, so

Left shift of VR curve
CO & VR CURVES

- affects from Phenylephrine infusion
increases sympathetics, so vasoconstriction causing Increased TPR, thus

Downshift CO curve
Decreased Slope (CCW rotation) of VR curve
Verapamil is what drug class?
CCB
&
Class 4 Antiarrhythmic
Verapamil is used as Tx in what conditions?
(ASH)
Angina
SVT
HTN
Verapamil MOA for the heart

(include specific cells affected)
Blocks Voltage-gated Ca2+ channels

(at the SA & AV node)
Verapamil causes what changes in on the cardiac AP? (specify which AP phase)
Slows down
Phase 0 Diastolic Depolarization
Verapamil causes what physical changes in cardiac property?
Decrease HR (by decr. SA firing rate)

Decrease AV CV (by decr. AV firing rate)
Impulse conduction going from SA --> AV --> Ventricular myocardium occurs during what period?
Diastole

(myocyte contraction occurs @ systole)
Verapamil causes what physical changes in muscles & BV?
Smooth muscle relaxation
(thus vasodilation)
Which Antiarrythmic drugs INCREASE THRESHOLD POTENTIAL (the amt of depolarization needed to initiate AP)
Class IA
Class IB
Class IC
Which Antiarrythmic drugs SHORTENS AP
(via Na+ channel blockade)
Class IB
Which Antiarrythmic drugs PROLONG REPOLARIZATION?
Class IA
Class IC

Class III
Verapamil is what drug class?
CCB
&
Class 4 Antiarrhythmic
Verapamil is used as Tx in what conditions?
(ASH)
Angina
SVT
HTN
Verapamil MOA for the heart

(include specific cells affected)
Blocks Voltage-gated Ca2+ channels

(at the SA & AV node)
Verapamil causes what changes in on the cardiac AP? (specify which AP phase)
Slows down
Phase 0 Diastolic Depolarization
Verapamil causes what physical changes in cardiac property?
Decrease HR (by decr. SA firing rate)

Decrease AV CV (by decr. AV firing rate)
Impulse conduction going from SA --> AV --> Ventricular myocardium occurs during what period?
Diastole

(myocyte contraction occurs @ systole)
Verapamil causes what physical changes in muscles & BV?
Smooth muscle relaxation
(thus vasodilation)
Which Antiarrythmic drugs INCREASE THRESHOLD POTENTIAL (the amt of depolarization needed to initiate AP)
Class IA
Class IB
Class IC
Which Antiarrythmic drugs SHORTENS AP
(via Na+ channel blockade)
Class IB
Which Antiarrythmic drugs PROLONG REPOLARIZATION?
Class IA
Class IC

Class III