Cardiovascular Flashcards Preview

Auburn ECC > Cardiovascular > Flashcards

Flashcards in Cardiovascular Deck (479):

Lidocaine class and MOA

1b: Na channel blocker (inactive state - depolarized), shortens action potential


Procainamide class and MOA

1a: fast Na channel blocker, slows phase 0, prolongs action potential


Atenolol class and MOA

Class II: beta1 blocker


Propranolol class and MOA

Class II: beta 1 & 2 blocker


Esmolol class and MOA

Class II: beta 1 blocker


Sotalol class and MOA

Class III: potassium blocker
Also beta blocker


Amiodarone class and MOA

Class III: potassium blocker
Also I, II, and IV


What is the most common primary cardiac tumor in dogs?

hemangiosarcoma (69%)


Aortic body tumors are most common in which breeds?

Boxer, Bostons, English bulldogs, and also German shepherd dogs


Capillary endothelium can be damaged by (6)?

1. Endotoxin
2. cytokines (TNFa, IL-6)
3. Arachidonic acid metabolites
4. complement components (C3a, C5a)
5. Vasoactive peptides (bradykinin, histamine)
6. chemokines (macrophage inflammatory protein 1 alpha)


What is the Gibbs-Donnan effect?

Describes the behavior of charged particles in solution separated by semipermeable membrane, which does not allow some particles to pass. For example, albumin is not permeable and its negative charge will attract cations like sodium.


What contributes the most to COP? What else contributes?

Albumin 65-80% of COP. Also: globulins, fibrinogen, hemoglobin, RBCs


Describe the activation of RAAS in detail.

Decreased renal blood flow & decreased Na deliver to distal portion of nephron--> renin release from macula densa--> angiotensinogen to angiotensin I--> angiotensin II (via ACE) in pulmonary vasculature


Effects of angiotensin II via RAAS system?

Increased thirst, vasoconstriction, cardiac and vascular remodeling and fibrosis, renal sodium & water retention, myocardial apoptosis, production of aldosterone


Effects of chronic sympathetic nervous system activation?

Adrenergic Rc downregulation, persistent tachycardia, increased myocardial oxygen demand, myocyte necrosis


Two main hormones that induce natriuresis, diuresis, and vasodilation?

Atrial natriuretic peptide (ANP)
B-type natriuretic peptide (BNP)
Both are increased in in dogs and cats with heart disease, roughly in proportion to disease severity


What is the function of ANP & BNP ?

To serve as a counter-regulatory system to RAAS and SNS, but ANP & BNP are overwhelmed in later stages of heart disease


What is the function of endothelin I?

Potent vasoconstriction produced by vascular endothelial cells in response to sheer stress, angiotensin II, and other various cytokines; alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes


Describe normal calcium ion handling

During systole calcium ions enter the myocardial cell; this triggers release of additional calcium ions from the main storage area of calcium (sarcoplasmic reticulum). Calcium stored in the SR flows through the ryanodine channel and binds to troponin C. Binding to troponin C causes SR contraction, then release of calcium from troponin C initiates relaxation cycle. Ca++ ions are then moved back into the SR


What happens to cells that have abnormal intracellular Ca distribution?

Electrical abnormalities, apoptosis, necrosis


What does the Frank-Starling mechanism state?

That an increase in the initial volume or pressure within a ventricle increases the strength of subsequent ventricular contractions. Up to a physiologic limit, preload and contractility are positively associated


What happens to the Frank-Starling curve during increased adrenergic drive?

Up and leftward; causes further improvement in cardiac performance


What happens to the Frank-Starling curve during disease?

Shifted down and to the right; contraction is less vigorous despite increased preload and fluid retention


What happens to the Frank-Starling curve with administration of diuretics?

Shifted to the left


What happens to the Frank-Starling curve with administration of arterial vasodilators?

Shifted upwards, decrease afterload, similar to positive inotropes


What happens to the Frank-Starling curve with administration of venous vasodilators?

Shifted leftward, decreased preload, similar to diuretics


What happens to the Frank-Starling curve with administration of positive inotropes?

Shifted upwards


What happens to the Frank-Starling curve with administration of mixed vasodilators?

Upward & leftward adjustment


Name and describe the 4 classes of heart failure

A- Healthy breeds at risk for developing heart disease (Maine Coons, dobermans >4 yrs)
B- Animals who are asymptomatic but have a murmur or arrhythmia, etc
B1= no signs of heart disease on echo or imaging
B2= signs of heart disease on echo or imaging
C- Animals with cardiac remodeling and current or historical signs of heart failure
D- Fulminant, severe CHF even at rest


Name the pulmonary and systemic pressures at which congestion may occur?

Pulmonary- >25 mm Hg
Systemic- >20 mm Hg


List management strategies in dogs with DCM and acute CHF

1. Minimize stress/ensure rest
2. Perform thoracocentesis PRN for pleural effusion
3. Provide O2 support
4. Administer furosemide 2-6 mg/kg IV then boluses
Administer 2% topical nitroglycerin 1-2 inches q 8
5. Treat life threatening arrhythmias
6. Sodium nitroprusside 2 mcg/kg/min until mean ABP 70 mm Hg
7. Dobutamine 2.5-5 mcg/kg/min
8. Other positive inotropes PRN


The PROTECT study found what regarding dobermans and DCM?

Administering pimobendan to dobermans with pre clinical DCM prolonged the time to onset of clinical signs and improved survival


DCM in some cocker spaniels is associated with what?

Low plasma taurine levels; supplementation with taurine and L-carnitine appears to improve myocardial function


List secondary canine myocardial disease categories and examples

1. Drugs/toxins (doxorubicin, catecholamines)
2. Canine X linked muscular dystrophy
3. Infiltrative (glycogen storage diseases)
4. Neoplasia
5. Ischemic
6. Metabolic (acromegaly, DM, hyperthyroidism, hypertension)
7. Nutritional (Taurine, L-carnitine, vitamin E)
8. Inflammatory (myocarditis)
9. Infectious (parvo, distemper, Lyme)


It is recommended to treat when you see ______ number of VPCs per 24 hrs in:

Dobermans: 50 VPC/24 hrs
Boxers: 100 VPC/24 hrs
In both: treat if couplets, triplets, R on T, clinical, etc


Treatment for AV myopathy (atrial standstill)?

Pacemaker- this improves short term outcome but most dogs will die of progressive myocardial failure


Poor px signs in dobermans with DCM?

Atrial fibrillation, bilateral CHF


Name 6 causes of secondary hypertension

Kidney disease
Diabetes mellitus
Hepatic disease
Chronic anemia


What is the mechanism of hypertension in patients with hyperadrenocorticism?

Glucocorticoids induce hepatic production of angiotensinogen, which results in an exaggerated response of the renin-angiotensin-aldosterone system


What is the mechanism of hypertension in patients with hyperthyroidism?

Secondary to the increased cardiac output caused by the effect of thyroid hormone on cardiac muscle


What are the four proposed mechanisms of hypertension in human patients with diabetes mellitus?

In type I, its thought to develop due to effects of diabetes on renal function

In type II, there are three mechanisms:
1. Hyperinsulinemia secondary to insulin resistance causes sodium and water retention and increased sympathetic activity.
2. Hypertrophy of vascular smooth muscle secondary to the mitogenic effects of insulin.
3. Elevations in insulin levels lead to increased levels of intracellular calcium which results in hyper-responsive vascular smooth muscle contraction and increased peripheral vascular resistance.


What is the mechanism of hypertension in patients with anemia?

Anemia leads to chronically dilated capillary beds. With resolution of the anemia, overcompensation of capillary constriction occurs, which results in an increase in peripheral vascular resistance.


What is hypertensive urgency and how should it be treated?

Marked elevation in blood pressure but the animal does not demonstrate clinical signs directly attributable to the elevation.

Blood pressure should be lowered in a gradual and controlled fashion by determining the underlying cause and starting treatment with an anti-hypertensive medication to lower the systolic blood pressure to 170 mm Hg or less, mean arterial pressure to 140 mm Hg or less, and/or diastolic pressure to 100 mm Hg or less.


What is hypertensive emergency and how should it be treated?

When the patient has a marked elevation in blood pressure as well as clinical signs directly attributable to hypertension.

Initial goal is to reduce mean arterial blood pressure by no more than 25% (within minutes to 1 hour), then if the patient is stable, to reduce blood pressure to 160/100 within the next 2 to 6 hours

Medications that may be used include amlodipine, sodium nitroprusside, hydralazine, enalaprilat, or nicardipine.


List possible sequela to infective endocarditis

CHF, IMPA, IMGN, thromboembolism, severe cardiac arrhythmias


With IE, what is exposed by damaged endothelium which triggers coagulation?

Extra cellular matrix proteins, thromboplastin and tissue factor


In IE, ___________ mediates the primary attachment of bacteria to the disrupted endothelium

Fibrinogen binding


In IE what triggers endothelial cell internalization and local proinflammatory and procoagulant responses?

Fibronectin binding


In IE inflammation induces endothelial cell expression of ________ that bind bacteria and fibronectin to the extra cellular matrix



In IE, how does fibrinogen promote the disease process?

Fibrinogen binding mediates the primary attachment of bacteria to the disrupted endothelium


In IE what is fibronectins role in perpetuating the disease process?

Fibronectin binding triggers endothelial cell internalization and local proinflammatory and procoagulant responses.


What are MSCRAMMS?

Microbial surface components recognizing adhesive matrix molecules- special receptors on bacteria which allow them to adhere to damaged valves


How is acute heart failure with IE different from normal CHF?

Due to acute nature, typically no left sided heart enlargement, fulminant pulmonary edema with alveolar flooding


What are 3 risk factors for thromboembolism in IE?

Mitral valve involvement, large mobile vegetative lesions more than 1-1.5 cm or increasing lesion size during antibiotic therapy


With CNS thromboembolism in IE what is the most common location and what are the results?

Middle cerebral artery, brain ischemia and possible ischemic necrosis (if persistent)


What is the pathognomonic lesion of IE on echo?

Hyperechoic, oscillating, irregular shaped mass adherent to, yet distinct from the endothelial cardiac surface


What are the major Duke modified criteria to diagnose IE in dogs?

1. Positive echo - Vegetative lesion, erosive lesion, abscess2. New valvular insufficiency3. >mild AI in absence of SAS4. Positive blood cultures: >2. Or > 3 with common skin contaminant.


Duke minor criteria to diagnose IE in dogs

1. Fever 2. Medium to large breed > 15 kgs3. SAS4. Thromboembolic disease5. IMPA or IMGN6. Positive blood culture not meeting major criteria 7. Bartonella serology >1:1024


What constitutes a definitive diagnosis of IE?

Pathology of the valve, 2 major criteria or 1 major and 2 minor criteria


What constitutes a possible diagnosis of IE?

1 major and 1 minor criteria or 3 minor criteria


What constitutes an unlikely diagnosis of IE?

Other diagnosis made, signs resolved in <3 days with tx


What are the most likely bacteria to cause IE?

Staphylococcus (aureus, intermedius, coagulase positive and negative), Strep (canis, bovis, and beta hemolytic) and e.coli


List 7 less likely but possible causes of IE

Enterococcus, enterobacter, erysipelothrix rhusiopathiae, pasteurella, proteus, pseudomonas, corynebacterium


Where on the action potential does lidocaine work?

Depresses phase 0 in abnormal tissue (no effect in normal tissue), little effect on sinus rate, AV conduction, or action potential duration and refractoriness


List possible sequela to infective endocarditis

CHF, IMPA, IMGN, thromboembolism, severe cardiac arrhythmias


With IE, what is exposed by damaged endothelium which triggers coagulation?

Extra cellular matrix proteins, thromboplastin and tissue factor


In IE, ___________ mediates the primary attachment of bacteria to the disrupted endothelium

Fibrinogen binding


In IE what triggers endothelial cell internalization and local proinflammatory and procoagulant responses?

Fibronectin binding


In IE inflammation induces endothelial cell expression of ________ that bind bacteria and fibronectin to the extra cellular matrix



In IE, how does fibrinogen promote the disease process?

Fibrinogen binding mediates the primary attachment of bacteria to the disrupted endothelium


In IE what is fibronectins role in perpetuating the disease process?

Fibronectin binding triggers endothelial cell internalization and local proinflammatory and procoagulant responses.


What are MSCRAMMS?

Microbial surface components recognizing adhesive matrix molecules- special receptors on bacteria which allow them to adhere to damaged valves


How is acute heart failure with IE different from normal CHF?

Due to acute nature, typically no left sided heart enlargement, fulminant pulmonary edema with alveolar flooding


What are 3 risk factors for thromboembolism in IE?

Mitral valve involvement, large mobile vegetative lesions more than 1-1.5 cm or increasing lesion size during antibiotic therapy


With CNS thromboembolism in IE what is the most common location and what are the results?

Middle cerebral artery, brain ischemia and possible ischemic necrosis (if persistent)


What is the pathognomonic lesion of IE on echo?

Hyperechoic, oscillating, irregular shaped mass adherent to, yet distinct from the endothelial cardiac surface


What are the major Duke modified criteria to diagnose IE in dogs?

1. Positive echo - Vegetative lesion, erosive lesion, abscess2. New valvular insufficiency3. >mild AI in absence of SAS4. Positive blood cultures: >2. Or > 3 with common skin contaminant.


Duke minor criteria to diagnose IE in dogs

1. Fever 2. Medium to large breed > 15 kgs3. SAS4. Thromboembolic disease5. IMPA or IMGN6. Positive blood culture not meeting major criteria 7. Bartonella serology >1:1024


What constitutes a definitive diagnosis of IE?

Pathology of the valve, 2 major criteria or 1 major and 2 minor criteria


What constitutes a possible diagnosis of IE?

1 major and 1 minor criteria or 3 minor criteria


What constitutes an unlikely diagnosis of IE?

Other diagnosis made, resolved in


What are the most likely bacteria to cause IE?

Staphylococcus (aureus, intermedius, coagulase positive and negative), Strep (canis, bovis, and beta hemolytic) and e.coli


List 7 less likely but possible causes of IE

Enterococcus, enterobacter, erysipelothrix rhusiopathiae, pasteurella, proteus, pseudomonas, corynebacterium


Where on the action potential does lidocaine work?

Depresses phase 0 in abnormal tissue (no effect in normal tissue), little effect on sinus rate, AV conduction, or action potential duration and refractoriness


What does a positive deflection in an EKG signify?

the sum of the heart's electrical impulses was moving toward the positive electrode at that time


What does a negative deflection in the EKG signify?

the sum of the heart's impulses was moving away from the positive electrode


T/F: impulses traveling perpendicular to the heart can cause a deflection in the EKG?



What is excitation-contraction coupling?

Ca influx during phase 2 of cardiac cell activation triggers the intracellular release of more Ca from the sarcoplasmic reticulum. The increase in free intracellular Ca leads to contraction.


What are the functions of troponin I and C?

I: inhibits cross-bridge formation during diastole when intracellular Ca is low. When Ca is available it activates troponin C

C: Binds to troponin I to reduce its inhibitory effect which allows interaction between adjacent actin and myosin filaments


Describe the Frank-Starling relationship

As end-diastolic volume (preload) increases, the volume with each contraction increases

Diastolic stretch of the sarcomeres increases the myofilament Ca affinity


True or false: Contractility depends on the amount of free intracellular Ca available


It also depends to some degree on ATP availability


Describe what happens with calcium in the myocyte at the end of systole

Ca influx stops, the sarcoplasmic reticulum actively takes up Ca. Some Ca is transported out of the cell via a membrane Na/Ca exchange and Ca pump mechanisms


What is the normal canine resting cardiac index (CO/body size)?

3.1-4.7 liters/minute/m^2


What percentage of the end-diastolic volume is ejected with each contraction of the heart?



What determines the stroke volume?

SV is directly related to the level of myocardial contractility and preload, and inversely related to afterload


Chronic increases in ventricular volume stimulate what changes in the sarcomeres?

It stimulates the formation of new sarcomeres in series, lengthening the myofibers and creating a larger ventricle of normal wall thickness aka eccentric hypertrophy


Chronic increases in systolic pressure stimulate what changes in the sarcomeres?

It stimulates formation of new sarcomeres in parallel, increasing myofiber diameter and ventricular wall thickness aka concentric hypertrophy


What is responsible for the generation of the S1 heart sound?

Vibration associated with closing and tensing of the AV valves (when ventricular pressure exceeds atrial pressure)


What is responsible for the generation of the S2 heart sound?

Vibrations associated with the closing of the semilunar valve (ventricular pressure drops below that in the associated great artery)


What is responsible for the generation of the S3 heart sound?

Accentuated low-frequency vibrations associated with the end of early diastolic filling. It is most likely to be heard in animals with LV dilation and failure.

It is sometimes called the ventricular gallop sound.


What is responsible for the generation of the S4 heart sound?

It is associated with blood and tissue oscillations at the time of atrial contraction. It may be heard with an abnormally stiff or hypertrophied LV.

It is sometimes called the atrial gallop sound.


What is diastasis and what determines the duration of diastasis?

It is the slow filling phase of the ventricles (after the rapid filling phase that happens with the opening of the AV valves).

Duration depends on heart rate.


Describe the effects of sympathetic stimulation on beta receptors

Contractility is increased as more Ca enters the myocytes and more Ca is released from the sarcoplasmic reticulum. Relaxation is also accelerated via reduced troponin affinity for Ca as well as accelerated SR reuptake of Ca.

Sympathetic stimulation of the Sa node hyperpolarizes the cells and activates and inward flux of Na and K which causes faster spontaneous diastolic depolarization


Describe the layers of the heart from outside to inside

Parietal pericardium-->visceral pericardium (epicardium)--> myocardium--> endocardium


T/F: the RV wall thickness is approximately 1/4 of the thickness of the LV wall

false- RV is 1/3 LV thickness


What helps facilitate conduction through the RA and LA to the AV node once the SA node has fired?

specialized fibers called internodal pathways


What is it about the AV node that makes it have a slower conduction?

AV nodal cells are small and branching; this allows time for atrial contraction before ventricular activation


Where do electrical impulses go after the AV node?

bundle of His


T/F: conduction is fast through the His bundle and into the RBB & LBB?



Which part of the heart is activated by the RBB?

right ventricular free wall


How many branches of the LBB? What does each one activate?

3 branches:
1. septal fascicle
2. posterior fascicle- conducts to ventrocaudal aspect of LV wall
3. anterior fascicle- craniolateral LV wall


Where do purkinje fibers transmit their electrical pulses?

ventricular myocardium


T/F: the duration of cardiac action potential is longer than that of noncardiac tissues?



Describe the 2 types of cardiac action potentials

1. Fast response- atrial and ventricular muscle cells, purkinje fibers
2. Slow response- SA and AV nodal cells


What is the normal resting membrane potential for myocardial cells?

-90 mV... this means that inside the cell is negative compared with the outside of the cell


For each major electrolyte (Na, Ca, K) state whether the concentration is higher outside the cell or inside the cell

Na- higher outside
Ca- higher outside
K- higher inside


Which electrolyte is the most permeable into the resting sarcolemma?

K+- it tends to diffuse outward along its concentration gradient thru K specific chanels


What is responsible for maintaining the normal resting membrane potential?

the electrogenic Na, K-ATPase pump, which moves 3 Na ions out for every 2 K ions in


Describe the cardiac action potential

Phase 0=influx of Na
Phase 1= brief partial repolarization
Phase 2=Ca influx
Phase 3=K efflux


What is the effective refractory period?

period of time from phase 0 until membrane potential reaches -50 mV during phase 3; a time when the cell cannot be reexcited


What is the relative refractory period?

a stronger than normal stimulus may elicit another action potential but velocity may be slowed b/c partial Na channel inactivation


Describe the effects of vagal (parasympathetic) stimulation on the heart

Vagal innervation to the heart is mainly localized to the SA and AV nodes. Vagal stimulation slows the SA node rate by reducing the slope of diastolic depolarization via and acetycholine-activated outward K current.


What is responsible for the variation in heart rate seen with a sinus arrhythmia?

It is related to reflexly-mediated fluctuations in vagal tone associated with the respiratory cycle.

Increase in HR occurs with inspiration, and decreases with expiration.


What is the major source of energy for the heart?

Fatty acids


What is the equation for coronary blood flow?

(Aortic pressure - coronary sinus pressure) / coronary vascular resistance


What direction does coronary flow move within the heart?

From epicardium to endocardium (because the majority of major coronary arteries lie on the surface of the heart).


During what phase of the cardiac cycle does most coronary flow occur?

During diastole (lower intraventricular pressure allows flow)


What are the consequence of inadequate coronary blood flow?

It promotes myocardial ischemia which leads to replacement fibrosis. This contributes to diastolic dysfunction (inability to relax the ventricles) and can be seen in diseases such as HCM and SAS.


What determines blood flow through any part of the circulation?

Blood flow is directly dependent on the driving pressure and inversely dependent on vascular resistance.

Q = Change in P / R

Q is blood flow, P is pressure, R is resistance


The pressures at which location determine the change in pressure for both systemic and pulmonary circulation?

Systemic change in pressure is calculated from the difference between aortic pressure and right atrial pressure. This averaged over time is equal to Mean Arterial Pressure (MAP).

Pulmonary change in pressure is calculated from the difference between pulmonary arterial pressure and left atrial pressure.


Resistance in the systemic circulation is generally less than in the pulmonary circulation.

Resistance in the pulmonary circulation is generally less than in the systemic circulation. This allows perfusion of the lungs at relatively low pressures.


According to Poiseuille's law, what determines resistance?

Resistance is inversely proportional to vessel radius to the fourth power, and directly proportional to blood viscosity.


What does laminar flow mean?

Blood flowing in smooth vessels forms layers (streamlines) that slip over each other. Flow is faster towards the center of the vessel, while the outer layers drag against the vessel wall.


What factors promote turbulent flow?

High flow velocity (ventricular outflow obstruction)
Low blood viscosity (anemia)
Wide vessel diameter
Sudden change in vessel diameter or direction
Pulsatile flow


What is Reynold's number?

It is a measure of the tendency for turbulence to occur. Numbers over a critical level (~2,000) are likely to be associated with an audible murmur.


Name several causes of an under circulation pattern in the lungs

Severe dehydration
Obstruction to RV inflow
Right sided CHF
Tetralogy of Fallot


Name several causes of an over circulation pattern in the lungs

Left-to-right cardiac shunts
Other hyper dynamic states


What effect does enlargement of either ventricle have on the orientation of the caudal vena cava radiographically?

It pushes the caudal venal cava - heart junction dorsally, which results in a more horizontal caudal vena cava orientation


True or false: The caudal vena cava should have a similar diameter to that of the descending thoracic aorta


The size of the vena cava does change with respiration however


What conditions can result in a widening of the caudal vena cava?

RV failure
Cardiac tamponade
Pericardial constriction
Other obstruction to right heart inflow


What conditions can result in a narrowing of the caudal vena cava?

Poor venous return
Pulmonary overinflation


Name several conditions that can result in an alveolar lung pattern

Lung lobe torsion


What findings may be seen radiographically in conjunction with cardiogenic pleural effusion?

Wide caudal vena cava


What is the most sensitive radiographic view for identifying pneumothorax?

The lateral view

The lung border appears separated from the diaphragm and dorsal thoracic wall; the heart shifts toward the dependent lung and looks elevated off the sternum


On which view (DV or VD) can you most easily identify a pneumothorax?

Pneumothorax is best seen on the DV as the air rises to the widest (most dorsal) part of the thorax


True or false: The cardiac silhouette is best visualized on the DV view in a patient with pleural effusion


Its better visualized on the VD view as the fluid collects at the dorsal aspect of the thorax. This view may cause more respiratory compromise however.


What determines the magnitude of a deflection in an ECG?

The angle between the lead axis and the direction of the myocardial activation wave. As the angle between the lead and the activation wave increases (approaches 90 degrees), the ECG deflection in that lead becomes smaller.


If the deflection in the ECG is positive, in what direction is the myocardial activation wave traveling?

Towards the positive pole of the lead


What does the P wave represent?

Atrial muscle activation


What does the PR interval represent?

Duration of atrial muscle activation, conduction over the AV node, bundle of His, and Purkinje fibers


What does the QRS complex represent?

Ventricular muscle activation


What does the ST segment represent?

Period between ventricular depolarization and repolarization (phase 2 of the action potential)


What does the T wave represent?

Ventricular muscle repolarization


What does the QT interval represent?

Total time of ventricular depolarization and repolarization


The standard limb lead system records electrical activity in what plane?

The frontal plane (similar to that seen on a VD radiograph)
Left to right and cranial to caudal currents are recorded


How do you determine the heart rate on an ECG?

Count the number of complexes within a 3 or 6 second period and multiple by 20 or 10 respectively

At 25 mm/s 30 blocks equals 6 seconds

At 50 mm/s 60 blocks equals 6 seconds


What structures are better visualized on a thoracic DV as opposed to a VD view?

hilar area and caudal pulmonary vessels


What structures are better visualized on a thoracic VD as opposed to a VD view?

lung disease, small volume pleural effusion


What type of radiographic considerations/technique should be used for cardiac evaluation (kVp, mAs)

high kVp, low mAs


List some artifacts that occur during expiration on chest radiographs?

increased lung opacity, larger heart, diaphragm overlapping caudal heart border, pulmonary vessels difficult to delineate


T/F: displacement of the heart into the right hemithorax could be a normal variant?



Normal VHS for most dogs? Dogs with long thorax? Short thorax?

Most dogs 8.5-10.5
Short thorax: 11
Long thorax: 9.5


Normal VHS for cats?



How do you objectively measure the cardiac dimensions on a VD/DV radiograph in cats? What is the normal value?

Similar to the VHS- compare the mean short axis cardiac dimension with the thoracic spine starting at T4 on the lateral view. Normal is 3.4-3.5 (up to 4)


List some differentials for generalized cardiomegaly on radiographs

DCM, mitral and tricuspid insufficiency, pericardial effusion, PPDH, intrapericardial mass, VSD or ASD, PDA, systemic hypertension, athletic heart, hyperthyroidism, acromegaly, AV vistula, chronic anemia, intracardiac mass, intrapericardial fat


Where is the LA located on lateral and VD/DV thoracic radiographs?

Lateral: dorsocaudal aspect of the heart, with the auricular appendage extending cranially
VD/DV: caudal heartbase, with auricle at 2-3 o clock


How does LV enlargement manifest on lateral and VD/DV thoracic radiographs?

Lateral: taller heart, elevation of tracheal bifurcation
VD/DV: enlargement located at 2-6 o clock position


What does RA enlargement do to the cardiac silhouette on radiographs?

Lateral: bulge of cranial heart border
VD/DV: bulging in 9-11 o clock position
*difficult to differentiate from LV enlargement**


What does RV enlargement do to the cardiac silhouette on radiographs?

Lateral: increased widening and convexity of cranioventral heart border
VD/DV: reverse D appearance; widening at 6-9 o clock


T/F: a wavy, undulated aorta is always abnormal in geriatric cats?

False- usually normal variant


Where is the MPA located on lateral and v/d radiographs?

Lateral: overlaps trachea at cranial heart base (difficult to visualize)
VD/DV: 1-2 o clock position


Where would a ductus bump be located on VD radiographs?

2-3 o clock area


How do you objectively assess cranial pulmonary vessel size on thoracic XR?

on lateral view measure where vessel crosses proximal 1/3 of 4th rib. The vessels should be 0.5-1x the diameter of this part of the rib


How do you objectively assess caudal pulmonary vessel size on thoracic XR?

on the VD view compare the vessel to the 9th rib where they cross; they should be 0.5-1x the size of this part of the 9th rib


Describe the different murmur grades

I- very soft heard in quiet surroundings after listening intently
II- soft, easily heard
III- moderate intensity
IV- loud, no precordial thrill
V- loud, palpable precordial thrill
VI- very loud, can be heard without stethoscope, precordial thrill


what "shape" of murmur does AV valve insufficiency usually have?

plateau-shaped or holosystolic; begins at S1 and is uniform throughout systole


List some causes of functional murmurs

anemia, fever, high sympathetic tone, hyperthyroidism, peripheral AV fistulae, hypoproteinemia, athletic heart, extreme bradycardia


Describe the typical characteristics of functional murmurs

soft to moderate intensity, crescendo-decrescendo, left heart base PMI


At what age do puppy innocent murmurs typically disappear?

4-6 months


T/F: the intensity of a MR murmur caused by valve dz is related to severity?



What disease causes a murmur that is loudest at the left base and becomes louder as cardiac output or contractile strength increases?

ventricular outflow obstructions


which disease can occasionally cause a murmur that can be heard over the skull?

subaortic stenosis- heard best at low left base and radiates up the aortic arch to the right base and carotid arteries


T/F: most murmurs heard on the right cvhest wall are diastolic in nature?

false- most are holosystolic, plateau shaped with the exception of SAS murmurs


What is the most common cause of diastolic murmurs in dogs and cats? What are some less common causes?

aortic regurgitation from bacterial endocarditis = most common
Others= ventricular septal defect, congenital malformation, degenerative aortic valve disase


DDX for continuous murmur ?

PDA (most common), peripheral AV fistulae, aorticopulmonic window, ruptured sinus of Valsalva aneurysm


What does a gallop sound indicate in dogs and cats?

ventricular diastolic dysfunction


What does an audible S3 sound indicate in the dog/cat?

ventricular dilation with myocardial failure and poor compliance; may be the only abnormality in an animal with DCM


An S4 sound indicates what?

abnormal ventricular relaxation, increased ventricular stiffness


What causes a pericardial knock? What disease is it associated with?

early diastolic sound caused by sudden checking of ventricular filling by the restrictive pericardium; restrictive pericarditis


List some mechanisms causing syncope

acutely reduced cardiac output (decreased filling, arrhythmias), outflow obstruction, hypoxia, hypoglycemia, decreased vascular resistance


At what percentage of normal cerebral blood flow will syncope occur?

30-50% of normal CBF


Equation for cardiac output?



equation for cerebral perfusion pressure?



what is cough syncope?

syncope precipitated by coughing, more common in brachycephalic dogs or dogs with underlying airway disase or collapse; also chronic MMVD and marked LA enlargement


what is the mechanism behind cough syncope?

coughing-->increased intrathoracic pressure-->reduced venous return to heart-->reduced ICP-->reduced CPP
Can also cause vagally mediated bradycardia and vasodilation


How quick is the onset of action of furosemide? When do its effects peak? How long do the effects last?

Onset of action is 5 minutes

Effects peak by 30 minutes

Effects last 2 hours


Why are arteriolar vasodilators generally not used in patients with left ventricular outflow obstruction?

They can exacerbate the obstruction and worsen forward flow

Ex. Hypertrophic obstructive cardiomyopathy


How does nitroglycerin work?

It acts mainly on venous smooth muscle to increase venous capacitance and reduce cardiac filling pressure


Why is dobutamine preferred over dopamine for inotropic support?

It has a lesser effect on heart rate and after load. Dobutamine primarily stimulates B1 receptors, and has weak action on beta2 and alpha receptors


List 4 substances that are involved in local regulation of systemic vascular resistance

Vasodilatory substances: nitric oxide, histamine, prostacyclin, CO2

Vasoconstrictive substances: endothelin, thromboxane, thrombin


List 2 substances that are involved in systemic regulation of SVR

Catecholamines released from the SNS


List the 3 major categories of causes of hypotension

Reduction in preload
Reduction in cardiac function
Reduction in SVR


For reduction in preload resulting in hypotension, give the 2 main categories and examples of each

Hypovolemia: hemorrhage, severe dehydration, edema/cavitary effusion

Obstructive: GDV, mesenteric volvulus, caval/portal venous occlusion, pericardial effusion, severe pleural space disease, PTE


For reduction in cardiac function resulting in hypotension, give the two main categories and examples of each

Primary: cardiomyopathy, valvular disease, tachy/brady-arrhythmias

Secondary: SIRS/Sepsis, electrolyte abnormalities, severe hypoxia, severe acidosis or alkalosis


Give 4 examples of diseases that case a reduction in SVR resulting in hypotension

Electrolyte abnormalities
Severe hypoxia
Severe acidosis or alkalosis
Drugs or toxins


What is the primary mechanism of reduction in SVR is SIRS/sepsis?

Vasodilation related to excessive production of nitric oxide from upregulation of induced nitric oxide synthase by assorted cytokines (IL-1beta, IL-6, TNF alpha)


Other than excessive production of NO, what other mechanisms have been proposed for reduction in SVR in SIRS/Sepsis?

Upregulation of ATP-sensitive potassium channels
Depletion of vasopressin stores
Vascular insensitivity to catecholamines


What is responsible for the initial hyperdynamic state seen in SIRS/Sepsis?

In the early stages of SIRS/Sepsis, the afterload reduction from arterial vasodilation actually results in increase CO


Describe the baroreceptor reflex system

Main moment-to-moment regulator of blood pressure

With decrease in BP, there is decreased stretch of baroreceptors (carotid sinus and aortic body), resulting in decreased stimulus to the vasomotor center of the medulla.

Results in increase in sympathetic and decrease in parasympathetic outflow

Shift in autonomic balance and release of catecholamines lead to vasoconstriction and increased HR and contractility


Describe the chemoreceptor reflex system

Originates in chemoreceptor organs (carotid and aortic bodies) in response to decreased in tissue oxygen tension, increase in CO2, or decrease in pH.

Increased signalling from chemoreceptors results in excitement of the vasomotor center and promotes sympathetic outflow.


Describe how the RAAS responds to hypotension

Decreased BP and blood flow to the kidneys results in activation of the RAAS.

Release of renin from the juxtaglomerular cells in response to decreased baroreceptor activity, sympathetic activation, or decreased tubular chloride as sensed by the macula densa.

Angiotensin II than causes vasoconstriction by direct (triggering vascular smooth muscle contraction) and indirect (stimulation of sympathetic activity and release of vasopressin) actions

Angiotensin II also promotes Na and water retention in the proximal tubule and alters GFR through preferential constriction of the efferent arteriole.

Aldosterone release from the adrenal cortex drives Na reabsorption and K excretion in the cortical collecting duct


How does vasopressin act to counteract hypotension?

Release of vasopressin from the anterior pituitary is regulated by changes in blood osmolarity.

In significant hypovolemia/hypotension, release of vasopressin can increase significantly independent of osmolarity (nonosmotic stimulation of ADH)

V1 receptors are activated which causes vasoconstriction and an increase in SVR (binds to the receptor that results in activation of phospholipase C, and release of Ca from the sarcoplasmic reticulum and vasoconstriction)

Activation of V2 receptors in the renal collecting duct promotes water retention (though insertion of aquaporins) to help support blood volume and preload


what is the equation for mean arterial blood pressure?

MAP= diastolic + [(systolic-diastolic)/3]


what is the most frequent cause of secondary hypertension?

kidney injury/failure


list diseases other than kidney disease that may cause secondary hypertension

hyperthyroidism, diabetes mellitus, hyperadrenocorticism, pheochromocytoma


list medications that can cause hypertension

glucocorticoids, cyclosporine, phenylpropanolamine, erythropoietin


what is the guideline for selection of a cuff for noninvasive BP measurement

dogs- 40% circumference of limb
cats- 30% circumference of limb


a study in anesthetized cats showed that doppler is closest to what BP value?

more closely related to MAP; routinely underestimated systolic BP by 10-15 mm Hg


which value of BP is the most accurate using oscillometric measurement? why?

mean; because mean is measured and systolic/diastolic are calculated using a built in algorithm


what is high definition oscillometry

a newer modality for blood pressure monitoring; performs real-time analysis of arterial wall oscillations to obtain pressure-wave amplitudes; systolic and diastolic pressure are measured instead of calculated


what is the reported range of detection for BP using HDO

5-300 mm Hg, even at 500 beats/min HR and arrhythmias


what is photoplethysmography

based on the "volume clamp" principle; it measures BP based on cuff inflation/deflation


t/f- photoplethysmography has been determined to be accurate in dogs/cats



explain how you prime/connect an arterial catheter tubing system for direct BP monitoring

connect arterial catheter to a semirigid tubing primed with hep saline from 0.9% NaCl + 1 unit heparin/mL; pump fluid bag to 300 mm Hg; place transducer at level of patient's heart


what 3 things are visible on a direct BP waveform

peak systolic pressure, diastolic pressure, and dicrotic notch


what does the dicrotic notch represent on the invasive BP waveform

closure of the aortic valve


what things can interfere with accurate direct BP monitoring/waveform

noncompliant tubing, catheter lodged against artery wall, clot formation, air bubbles present, catheter/tubing kinking


what is damping of the waveform

causes falsely low systolic and falsely high diastolic values


complications assoc with direct BP monitoring?

thrombosis, hematoma, infection, necrosis (espec in cats with cath >6-12 hrs)


what are the benefits of using telemetric blood pressure monitoring

you feed the catheter SQ into the femoral artery, allows free patient movement; handling and restraint don't affect the values


what is the cvp used to estimate?

RA pressure, which is equal to RV end diastolic pressure when the tricuspid valve is open; also gives a measure of relative ability of heart to pump the volume of blood that is returned to it


what size catheter is typically used for cvp monitoring

16 g or 19g although size of catheter has no effect on measurement of cvp


what is a normal cvp

0-5 cm H2O, although trends are most impt due to variaton


t/f- in foxhounds, a multiple linear regression equation can be used to estimate the CVP using diameter of CVC, hepatic vein and velocity of the v wave



during inspiration the cvp increases and during expiration it decreases

false; this would be true only for PPV


List all the positive waveforms of the CVP and what they represent

a wave-R atrial contraction
c wave- caused by bulging of tricuspid valve into RA as R ventricle contracts
v wave- increasing pressure from blood flowing into RA before tricuspid valve opens


list the negative waveforms/descents of the CVP and explain what they mean

x descent- decrease in atrial pressure during ventricular ejection
y descent- rapid emptying of R atrium and tricuspid valve opens


what are large c waves on the CVP waveform assoc with

tricuspid regurgitation


what CVP is assoc with edema formation or body cavity effusion

>16 cm h2o


a cvp <0 may represent?

hypovolemia due to fluid loss or vasodilation


a cvp >10 may represent?

volume overload, right CHF, pleural effusion


if a patient is hypovolemic, what will happen with a test bolus to the cvp?

transient increase toward normal or no change in cvp, rapid decrease back to baseline


if a patient is euvolemic what will happen to the cvp with a test bolus?

small increase of 2-4 cm h2o with return to baseline in 15 min


if a patient is hypervolemic what will happen to the cvp with a test bolus?

>4 cm h2o or large increase in cvp then slow return to baseline (>30 min)


contraindications to cvp measurement?

hypercoagulable state, increased ICP, coaglopathy


what does a pulmonary artery catheter measure? pulmonary wedge cath?

left ventricular preload; left atrial pressure equals LV end diastolic pressure when mitral valve is open

PAOP measures left atrial filling pressure


t/f- PAP and PAOP are best predictors of pulmonary edema secondary to fluid overload?



what is normal PAOP?

5-12 mm Hg


what else can be measured by a swan-ganz catheter besides PAP and PAOP?

cardiac output using thermodilution technique, RA pressure


what is normal cardiac output for dog/cat?

dog 125-200 ml/kg/min, cat 120 ml/kg/min


list other values that can be calculated with a pulmonary artery catheter

cardiac index, stroke volume, stroke volume index, systemic vascular resistance, pulmonary vascular resistance


complications assoc with pulmonary artery catheterization?

arrhythmias, damage to tricuspid/pulmonic valves, rupture of pulmonary artery, PTE


where is Scvo2 measurement taken? Svo2?

Scvo2= central vein such as vena cava or RA
Svo2= pulmonary artery


normal values for Scvo2 and Svo2?

Scvo2= >65%
Svo2= >75%


in a recent vet study looking at the best discrimators between survivors and nonsurvivors in dogs with severe sepsis or septic shock, what 2 values were the best?

base deficit and Scvo2


what are limitations to svo2 and scvo2 measurement?

hgb and SaO2 can affect them; if there is underlying defect in O2 extraction, the values can be normal or high despite oxygen debt


Name the types of vessels in order as they leave the heart and return to the heart

arteries -> arterioles -> capillaries -> venules -> veins


What types of vessels are referred to as conduits and why?

Because they have low and relatively unchanging resistance to flow


How does the structure of arterioles differ from arteries?

Arterioles have much thicker walls with more smooth muscle and less elastic material


What types of vessels are referred to as resistance vessels and why?

Because of their high and changeable resistance, this helps them to regulate flow through individual organs


True or false:
Capillaries can change their diameter, but less so than arterioles

They lack smooth muscle so cannot actively change their diameter


What types of vessels are referred to as exchange vessels and why?

They are composed of a single layer of cells separating them from the interstitium so solutes can diffuse through them


What types of vessels are referred to as capacitance vessels and why?

Peripheral venules and veins
They can distend and contain more than 50% of the blood volume


What percent of the blood volume can be contained in the peripheral venules and veins?

More than 50%


Describe the innervation of arterioles

Sympathetic nerves innervate arterioles
These nerves release norepinephrine at their endings and interact with alpha-adrenergic receptors on the smooth muscle cells to cause contraction and arteriolar constriction

These neural fibers provide the most important means of REFLEX control of vascular resistance and organ blood flow


True or false:
There is no important neural or local metabolic control of either arterial or capillary vessels



What is the equation for hematocrit?

Hct = cell volume / total blood volume


What are the conditions necessary to control the composition of the interstitial fluid?

1- Adequate blood flow though the tissue capillary
2- Controlled chemical composition of the arterial blood to be optimal for the interstitium
3- Short diffusion distance


What is the maximal distance between a cell and capillary?

10 um


Which organ receives the most of the arterial blood?

Kidneys (about 22%)


Define blood-conditioning organ

Systemic organ that receives blood flow that exceeds the amount of flow necessary to supply their nutrient need, and recondition the composition of blood (ex. lungs, kidney, liver, skin (heat))


Name 3 organs in which blood flows solely to supply the metabolic needs of the tissue (as opposed as blood-conditioning organ)?

Heart muscle
Skeletal muscles


What percentage of the oxygen supplied to the myocardium is consumed?



True or false: Active tension in the cardiac muscle cells is higher at very long muscle lengths

Active tension is at its highest point at an intermediate muscle cell length


What are the three mechanisms that explain the relationship between cardiac muscle length and tension

1) This relationship depends on the extent of overlap of thick and think filaments in the sarcomeres (at long lengths there might not be enough overlap and at short lengths, think filaments may overlap)

2) As muscle lengthens it has an increased sensitivity to calcium

3)After increasing the resting length of the cardiac muscle, there is an increase in the amount of calcium that is released with excitation, which leads to higher force


Where is the sensor for cardiac muscle length-dependent activation?

Within the troponin C molecule


Define isotonic contraction

A muscle shortens against a constant load


True or false, as muscle shortens, its inherent contractile potential increases

it decreases


What determines resting cardiac muscle length?



True or false, afterloaded cardiac muscle shortens less than non-afterloaded muscle



What is the most important physiologic regulator of cardiac muscle contractility?



How does epinephrine affects cardiac muscle contractility?

Norepi interacts with the beta 1 adrenergic receptor -> activation of the G-protein-cAMP-protein kinase A -> which phosphorylates the Ca2+ channel-> which increases the inward calcium current during the plateau of the action potential


What is a positive lusitropic effect?

Increased rate of relaxation of cardiac muscle

An example is norepinephrine causing phosphorylation of phospholamban on the SR Ca-ATPase pump, which leads to increased retrapping of calcium in the SR, and increased rate of relaxation


What is the staircase phenomenon (or treppe)?

A sudden increase in beating rate of the heart is followed by a progressive increase in contracticle force to a higher plateau


How do length-tension relationships of cardiac muscle fibers determine volume and pressure relationships of the ventricular chamber? (3 points)

1) An increase in ventricular volume causes an increase in ventricular circumference and therefore an increase in individual cardiac muscle cells -> extent of diastolic filling determines preload

2) At a given ventricular volume, an increase in the tension of individual cardiac cells causes an increase in intraventricular pressure

3) As ventricular volume decreases, a lesser total force is required by the muscle cells in the ventricular walls to produce a given intraventricular pressure


What is the Law of Laplace?

T = P x r

Total wall tension equals intraventricular pressure times the internal radius


What important implication does the Law of Laplace have for the heart?

Muscle cells in the ventricular wall have an easier job of producing internal pressure at the end of ejection (radius is small) than at the beginning of ejection (radius is large)

This is important in conditions like HCM and DCM


How does the voltage of the heart corresponds with the P, QRS T waves and its intervals.

P is atrial depolarization
PR interval to the conduction time to the atria and AV node
QRS complex to ventricular depolarization
QT interval to the duration of ventricular systole
T ventricular repolarization


What is the intrinsic rate

its the spontaneous electrical pacemaker activity, in the absence of outside influences. In humans about 100bpm. Its determined by how long it takes for the cells in the pacemaker (SA node) to spontaneously depolarize to the threshold level.


What are the main two outside influences on the automaticity of the SA

The autonomous nervous system: Sympathetic and parasympathetic.


what is the difference between chronotropic effect and dromotropic effect

Chonotropic effect are caused by factors that affect the HR.
Dromotropic effect is caused by factors that affect the conduction velocity (most notable at the AV node and can influence the duration of the PR interval


What are the processes that participate in the reduction of intracellular calcium that terminates the contraction

80% of the calcium is actively taken back up into the SR by action of Ca ATPase pumps
20% is extruded from the cell into the extracellular fluid either via the Na-Ca exchanger in the sarcolema or via sarcolemmal Ca ATPase pumps


What is the difference between Isomeric and isotonic contraction?

Isomeric: fixed length: maximum ability to develop tension
Isotonic: fixed tension: muscle shortens with its maximum possible velocity


What 3 things make cardiac muscle cell action potentials differ from those of skeletal muscle cells?

1. They can be self-generating
2. They can be conducted directly from cell to cell
3. They have long-duration, which precludes fusion of individual twitch contraction


What are three ions that are the most important determinants of cardiac trans-membrane?

1. Na (more concentrated in the interstitial fluid than intracellular)
2. Ca (more concentrated in the interstitial fluid than intracellular)
3. K (more intracellular than interstitial)


What are three general types of transmembrane protein structures that are involved in ion movement across the cell membrane?

1. Ion channels
2. Ion exchangers
3. Ion pump


What are 2 categories of cardiac cell action potentials, depends on “the speed of response”, and “the type of cells”?

1. Cardiac pacemaker-type cell, slow-response action potentials
2. Ordinary cardiac muscle cell, fast-response action potentials


With regard to fast-response action potentials, what are 3 periods and what’s the significance?

1. Absolute refractory period (during the most of the action potential, they cannot be stimulated to fire another action potential)
2. Relative refractory period (near the end of action potential, can be re-excited only by a larger-than-normal stimuls)
3. Supranormal, or vulnerable period (immediately after the action potential, transiently hyperexcitable)


True or false: During the resting phase, membranes are more permeable to K than Na or Ca. Therefore, the membrane potential are close to the potassium equilibrium potential (-90 mV) during this period



True or false: During initial depolarization phase of action potential, sudden increase in Na permeability causes rapid rising phase of fast-response action potential. Whereas, it’s an inward movement of Ca ions that cause slower rising phase of slow-response action potential.



What 5 improvements in cardiac performance are caused by the sympathetic nervous system?

1. Positive chronotropic effect
2. Decrease in cardiac action potential duration (minimizes the effect of high heart rate on diastolic filling time)
3. Positive dromotropic effect (increased rate of conduction of the action potential)
4. Positive inotropic effect
5. Positive lusotropic effect (increase in rate of cardiac relaxation)


True or false:
Fetal and newborn hearts rely primarily on fatty acids for ATP; whereas, adults derive their ATP from glucose and lactate

It is the opposite, adults derive 60-90% of ATP from fatty acids


What percentage of ATP is generated by fatty acids in the adult myocardium?



What is the end product of metabolism of glycogen, glucose, fatty acids, triglycerides, pyruvate and lactate? And what happens to this molecule?

The end product is Acetyl CoA
It enters the citric acid cycle (Krebs cycle) in the mitochondria, whereby through a process of oxidative phosphorylation it is degraded to carbon dioxide and water and the energy is converted to ATP


What characteristics of the heart are consistent with the fact that the majority of energy is derived from the aerobic pathways?

1. High number of mitochondria
2. Presence of high concentrations of oxygen-binding protein myoglobin within cardiac muscle cells


What does myoglobin do within cardiac muscle cells?

It can release its oxygen to the mitochondrial cytochrome oxidase system when intracellular oxygen levels are lowered


What percent of myocardial energy use is normally accounted for by the basal metabolism of the heart tissue?

And what percent is accounted for by muscle contraction?

25% for basal metabolism
75% for muscle contraction


What phase of the cardiac cycle accounts for the largest portion of total myocardial oxygen consumption?

Isovolumetric contraction


Are increases in the afterload or the stroke volume more costly to myocardial oxygen consumption?

Increased in the afterload


In terms of myocardial oxygen consumption, is it more efficient for the heart to work at a low heart rate and high stroke volume, or at a high heart rate and low stroke volume?

It is more efficient to work at a low heart rate
This is due to the energy required during the pressure development phase of the cardiac cycle, the less pressure developed and the less often pressure development occurs, the better.


3 condition of proper filling of the ventricles

1. Filling pressure of blood returning to the heart and atria
2. Ability of AV valves to open fully (not be stenotic)
3. Ability of ventricular wall to expand passively with little resistance (to have high compliance)


True or false: atrial contraction is initiated near the end of ventricular diastole, which causes P waves. At normal resting heart rate, atrial contraction is NOT essential for adequate ventricular filling.

True: Atrial contraction plays an increasingly significant role in ventricular filling as HR increases, because the time interval between beats for passive filling becomes progressively shorter with increased HR. Throughout diastole, atrial and ventricular pressures are nearly identical, and normal open mitral valve has very little resistance to flow and thus only a very small atrial-ventricular pressure difference is necessary to produce ventricular filling.


What is isovolumetric contraction phase and isovolumetric relaxation phase?

Both phase means that left ventricle is a closed chamber (both mitral valve and aortic valve are closed). Isovolumetric contraction phase: from mitral valve closure to opening of aortic valve when LV exceeds that in the aorta
Isovolumetric relaxation phase: from aortic valve closure to mitral valve opening (after aortic valve closure, intraventricular pressure falls rapidly as the ventricular muscle relaxes)


What is stroke volume?

The amount of blood ejected from the ventricle during a single beat. It’s equal to ventricular end-diastolic volume minus ventricular end-systolic volume. In normal condition, heart ejects only 60% of its end-diastolic volume.


True or false: At a resting HR, heart spend approximately ⅔ of cardiac cycle in diastole and ⅓ in systole.



What’s the major difference between the right and left pumps? (1) pressure, (2) stroke volume. And why?

Pressure developed by right side is considerably lower than those for the left side. Because the lungs provide considerably less resistance to blood flow than that offered collectively by the systemic organs


What is physiological splitting of the second heart sound?, and What are two factors that lead to this prolonged ejection time from the right ventricle?

Discrepancy that pulmonic valve usually closes slightly after the aortic valve.
(1) Inspiration-induced decrease in intrathoracic pressure, and increased filling of the right side of the heart. So this extra volume will be ejected, with a little extra time.
(2) Inspiration-induced decrease in pulmonary vascular resistance (increased pulmonary compliance), which reduces pulmonary artery pressure and right ventricular afterload. With reduced afterload, ventricular ejection can go on for a slightly longer period of time.


What is gallop rhythm?

S3 and S4 are not normally present. When they are present along with S1 and S2, produce what are called gallop rhythm.
S3 along with S1 and S2: ventricular gallop rhythm.
S4 along with S2 and S2: atrial gallop rhythm.


What is the mean electrical axis of the heart? How can we use it clinically?

It describes the orientation of the net dipole at the instant of maximum wavefront propagation during ventricular depolarization.

We can use it as an indicator of whether ventricular depolarization is proceeding over normal pathways.
It usually falls between 0 and +90 degrees


How would affect a left ventricular hypertrophy to the mean electrical axis.

It would produce a left axis deviation: when the mean electrical axis falls in the patient's upper left quadrant. Indicates physical displacement of the heart to the left.


What principle do the most accurate methods to measure cardiac output follow? Give the formula

Fick principle
Q = Xtc / ([X]a - [X]b)
Q: blood flow rate
Xtc: amount of substance consumed by the tissue in time
[X]a: arterial concentration of the substance
[X]b: mixed venous concentration of the substance


Where should we ideally collect the blood from to get mixed venous blood

Right ventricle or pulmonary artery


What substance/marker do we most commonly use with the Fick principle to measure cardiac output

O2, dye, heat (thermodilution)


What is cardiac index?

Cardiac output corrected for the individual's size


What are 3 imaging techniques to measure cardiac output?

- Echocardiography
- Cardiac angiography (radiopaque contrast medium and high-speed x-ray filming)
- Radionuclide ventriculography (radioactive isotope and measurement of radiation intensity changes over the ventricle)


What is the formula to define ejection fraction (EF)? What is the normal range?

EF = SV / EDV -55-80%-
SV: stroke volume
EDV: end-diastolic volume


How can we measure end-systolic pressure?

Obtaining arterial pressure at the point of the closure of the aortic valve (incisura)


How can we assess myocardial contractility using the LV end-systolic pressure-volume relationship?

By looking at the slope of the line joining the point on the LV pressure-volume loop at the closure of the aortic valve, and the point 0
Steep slope: increased contractility (decreased end-diastolic volume for the same pressure)
Flat slop: decreased contractility (increased end-diastolic volume for the same pressure)


What are the 3 things can be evaluated from ECG?

1. HR, 2. rhythm, 3. conduction characteristics


What's the significance of P, QRS, T wave, PR interval, QT interval?

P: atrial depolarization
QRS: ventricular depolarization
T: ventricular repolarization
PR interval: AV nodal transmission time (the time it takes for an action potential to spread through the atria and the AV node) = conduction from SA node through AV node to the ventricle
QT interval: duration of ventricular systole


True or false: in normal healthy status, PR interval is longer than QT interval

False: PR interval is usually shorter than QT interval. If PR interval is longer than QT interval: 1st degree AV block


True or false: during T wave, all the cells in the heart are in the resting state



True or false: PR interval is from beginning of P wave until the R wave

False: PR interval is from beginning of P wave until the beginning of QRS complex
PR segment? baseline portion of PR interval


True or false: QT interval is from the beginning of Q wave until the end of T wave

True. It's not from the peak of Q wave to the end of T wave


Describe Einthoven's triangle (3 location of electrode, i.e. lead 1 connect from A to B)

From RA to LA: lead 1
From RA to LL: lead 2
From LA to LA: lead 3


What is compliance when referring to the vascular system?

How much a volume changes in response to a given distending pressure


When listening to a doppler while taking a blood pressure how you determine the systolic and diastolic values?

Systolic: highest cuff pressure at which heart sounds are heard

Diastolic: cuff pressure at which heart sounds become muffled or disappear


What two major components affect the mean arterial pressure?

Cardiac output
Total peripheral resistance


How do you calculate MAP?

MAP = Diastolic pressures + 1/3 (systolic - diastolic)


How is pulse pressure calculated?

Pulse pressure = Systolic - diastolic


Why does pulse pressure increase with age?

Decrease in arterial compliance


True or false:
Changes in total peripheral resistance have little effect on pulse pressure

Because a change in total peripheral resistance causes parallel changes in both systolic and diastolic pressures


True or false
Blood flows most rapidly in the smallest total cross-sectional area or the capillaries

False, it does but the smallest total cross sectional area is the aorta, not the capillaries.


True or false
With laminar flow each layer goes at different velocity

True. Velocity is fastest along the central axis.


What are the peripheral and central venous pool ?

Peripheral: circulating blood contained within the veins of the systemic organs.

Central: is smaller. Blood in the great veins of the thorax and the right atrium


How does the blood pressure changes from the aorta to the capillaries

At the arch of the aorta is about 100mmHG and is similar within the arterial system.
It drops at the arterioles, where it loses the pulsatile nature.
At the capillaries the pressure is 25mmHg
It continues to decrease in the venules and veins.
The central Venous pressure is close to 0mmHg


What segment of the circulatory system regulates the peripheral vascular resistance.

The changes in the radius of the arterioles.


What is the total peripheral resistance

It is the overall resistance to flow through the entire systemic circulation. The resistance of every organ contributes to the total peripheral resistance.


How does histamine produce arteriolar vasodilation and tissue edema?

It produces arteriolar vasodilation via the cAMP pathway and tissue edema due to increased vascular permeability from separations in the junctions between the endothelial cells that line the vascular system


In terms of vasodilatory potency, which is more potent, bradykinin or histamine?

Bradykinin is 10 times more potent than histamine


What is the myogenic response when talking about arterioles?

Active constriction of the arteriole in response to passive distension produced by a sudden increase in the internal pressure of the arteriole


What is active hyperemia and how is it produced?

Change in blood flow to skeletal muscles in response to muscle exercise. It results from local metabolic vasodilatory feedback on arteriolar smooth muscle. Endothelial flow-dependent mechanisms may assist in propagating the vasodilation to larger vessels


What is reactive or post-occlusion hyperemia and what mechanisms are responsible for producing it?

Higher than normal blood that occurs transiently after the removal of any restriction that has caused a period of lower than normal blood blood flow.

Both local metabolic and myogenic mechanisms may be involved


What is autoregulation?

The ability of organs to keep their blood flow constant despite variations in arterial pressure


What mechanisms are responsible for the arteriolar vasoconstriction of the autoregulatory response and how do they work?

1) Local metabolic feedback: washout of metabolic vasodilator factors from the interstitium by the excessive initial blood flow

2) Myogenic response: increase in arteriolar tone stimulated by the increase in stretching forces that the increase in pressure imposes on the vessel walls


What is the tissue pressure hypothesis of blood flow autoregulation?

An abrupt increase in arterial pressure causes transcapillary fluid filtration and thus leads to a gradual increase in interstitial fluid volume and pressure.

The increase in extravascular pressure would cause a decrease in vessel diameter by simple compression.

This may be particularly important in organs such as the kidney and brain whose volumes are constrained by external structures


What are the purposes of the ability to make vascular diameter changes?

- To efficiently distribute the cardiac output among tissues with different current needs (arterioles)
- To regulate the distribution of blood volume and cardiac filling (venules)


Where are vascular smooth muscle cells absent from?



What are the differences in anatomic and functional characteristics between smooth muscle cells and other skeletal or cardiac muscle cells?

1- Contract and relax much more slowly
2- Develop active tension over a greater range of muscle lengths
3- Can change their contractile activity as a result of action potentials or changes in resting membrane potential
4- May change their contractile activity in the absence of changes in membrane potential (changes in the Ca2+ sensitivity of the contractile machinery / contractility changes in the absence of change in intracellular free Ca2+ levels)
5- Maintain tension for prolonged periods at low energy cost
6- Can be activated by stretch
7- Filaments (actin and myosin) are not arranged in regular, repeating sarcomere units (no visible striation), but many travel obliquely or even traversely to the long axis of the cell
8- Actin filaments do not attach to Z-lines in the interior of the cell, but to '''dense bands''
9- Sequence of steps linking an increase free Ca2+ level to contractile filament interaction is different -> Ca2+ and calmodulin complex formation -> Activation of the myosin light-chain kinase -> Phosphorylation of the light-chain protein (cross-bridge head of myosin) -> cross-bridge formation and cycling
10- Lower resting membrane potentials [-40 ; -65 mV]


How are adjacent smooth muscle cells electrically connected?

Gap junctions similar to those found in the myocardium


What type of channel is predominantly responsible for the resting membrane potential of the smooth muscle cells?

''Inward rectifying-type K+'' channel = K+ move slightly more easily into the cell than out
''ATP-dependent K+'' channels = open when ATP level falls ---> important to match blood flow and metabolic state of an organ


What are the channels involved in depolarization? Repolarization? of the smooth muscle cells

Depolarization (inward flux of Ca2+): voltage-operated calcium channel (VOC)
Repolarization (outward flux of K+): delayed K+ channels, and calcium -activated K+ channels


What is Pharmacomechanical coupling?

Chemical agents (i.e. norepinephrine) can induce smooth muscle contraction without the need for a change in membrane potential.


What are the two mechanisms initiated by alpha1- agonists that cause intracellular Ca2+ levels to increase in the absence of a change in membrane potential in smooth muscle cells?

- Activated receptor may induce the formation of an intracellular ''second messenger'' (IP3) that open specific channels that release Ca2+ from the intracellular sarcoplasmic reticulum stores
- Activated receptor may open surface membrane receptor-operated channels for Ca2+ (influx)


What percentage of cardiac output do the splanchnic organs receive?



What percentage of oxygen do the splanchnic organs extract?



When the sympathetic nervous system is activated, what percent reduction in flow to the splanchnic organs can occur?

This results in a large amount of blood being returned to the central venous pool


True or false: Changes in renal blood volume are inconsequential to overall cardiovascular hemodynamics

Control of renal blood flow is important to overall cardiovascular function


How much of resting cardiac output does the skin receive?



What are venous plexuses and what is their function?

Interconnected veins
Heat transfer from the blood takes place across the large surface area


True or false:
Pulmonary blood flow is slightly less than cardiac output

Pulmonary blood flow = cardiac output


How does pulmonary vascular resistance compare to systemic vascular resistance?

Pulmonary resistance is 1/7th of total systemic vascular resistance


What effect do changes in pulmonary arterial pressure have on pulmonary vascular resistance?

An increase in pulmonary arterial pressure DECREASES pulmonary vascular resistance because pulmonary arteries and arterioles are less muscular and more compliant


What effect does hypoxia have on pulmonary arterioles?

Pulmonary arterioles constrict in response to hypoxia


What role do autnomonic nerves play in pulmonary vascular activity?

No major role
Physical and local hypoxic influences are more important


In the lungs is capillary hydrostatic pressure high or low?

It is LOW which promotes fluid reabsorption and prevents fluid accumulation in airways


What is the driving force for myocardial blood flow?

systemic arterial blood pressure, just as it is for systemic organs


True of false? increases in myocardial oxygen consumption must be accompanied by appropriate increases in coronary blood flow.

True. Because myocardial oxygen extraction cannot increase significantly from its high resting value.


What is the most important influence on coronary blood flow?

Myocardial oxygen consumption


Why coronary flow is lower during systole than during diastole, even though systemic arterial pressure (coronary perfusion pressure) is highest during systole?

Because of systolic compression and the associated collapse of coronary vessels (large force pressure is generated within the myocardial tissue during cardiac muscle contraction)


True or false? Myocardial infarcts occur most frequently in the epicardial layers of the right ventricle.

False. endocardial layers of the left ventricle. systolic compressional forces on coronary vessels are greater in the endocardial layers of the left ventricular wall than in the epicardial layer.


True or false? When the activity of the sympathetic nervous system increases, the coronary arterioles normally vasodilate rather than vasoconstric.

True. Because an increase in sympathetic tone increase myocardial oxygen consumption by increasing the heart rate and contractility.


What are the name of two factors designed to keep mean arterial pressure constant in cerebral blood flow?

total peripheral resistance and cardiac output


True or false? Cerebral blood flow decreases when arterial blood Pco2 rises.

False, Cerebral blood flow decreases when arterial blood Pco2 decreass.


True or false? Sympathetic and parasympathetic neural influecens on cerebral blood flow are minimal.



What determines where the cardiac function and venous function curves intersect?

Influences on the heart and on the peripheral vasculature

ie sympathetic tone, blood volume, etc


If a patient has an abnormally high central venous pressure what might the cardiac function and venous function curves look like?

Depressed cardiac function curve (left shift), right shifted venous function curve, or both


What conditions cause an abnormally high CVP?

CHF, fluid overload


If a patient has an abnormally low central venous pressure what might the cardiac function and venous function curves look like?

Elevated cardiac function curve (right shift) or left shifted venous function curve


What conditions cause an abnormally low CVP?

Most often caused by left shift of venous function curve either due to low blood volume or lack of venous tone


What physical exam finding might indicate increased CVP?

Jugular venous distension and pulsation


What is central comand? How does it affect BP?

Is the response from the cerebral cortex to lower brain centers during physical exercise.
Mean art BP and RR increases during exercise


How dosuperficial and deep pain affect BP

Superficial or cutaneous causes a raise in BP
Deep from viscera or joints causes a decrease on sympathetic tone, increase on parasympathetic and a serious decrease in BP


Where is the temperature regulation controlled?

In the hypothalamus. It controls the sympathetic activity to cutaneous vessels ansd thus skin blood flow.


How does a raise in BP affects the UOP, how does the body compensates a raise in BP?

The UOP changes the total fluid volume. An increase in BP, increases UOP which reduces the fluid and blood volume, this reduces cardiac output thus reduces BP


T/F: Peripheral vascular adjustments associated with arterial baroreceptor reflex take place primarily in organs with strong sympathetic vascular control.



What's general function of cardiopulmonary receptors?

Sensing the pressure (or volume) in atria and the central venous pool. Increased CVP cause receptor activation by stretch, which elicits a reflex decrease in sympathetic activity.


T/F: cardiopulmonary baroreceptors normally exert a tonic excitatory on sympathetic activity.

False: inhibitory, not excitatory.


Which receptors are responsible for increase RR and MAP in condition of low PO2 and high PCO2?

Arterial chemoreceptor (located in carotid arteries and aortic arch), central chemoreceptor (located somewhere in CNS)


T/F: gravity change the arterio-venous pressure difference at any one height level.

False: because gravity has the same effect on arterial and venous pressure.


Two major direct effects of the increased pressure in lower extremities due to gravity?

1. increase in venous transmural pressure distends compliant peripheral vein.
2. increase in capillary transmural hydrostatic pressure causes a tremendously high transcapillary filtration rate in the lower leg and feet.


What two forces are counteracting venous blood pooling and edema formation in the lower extremeties during standing?

1. skeletal muscle pump
2. vasoconstriction from sympathetic activation (is only marginally effective in ameliorating the adverse effects of gravity on the lower extremities)


Briefly explain orthostatic or postural hypotension

In long-term bed rest or zero gravity, patient become hypovolemic (by normal earth standpoint) which means substantial decrease in circulating blood volume. Upon standing, blood shift out of the central venous pool into peripheral veins, SV falls, and individual often becomes dizzy and may faint because of dramatic fall in blood pressure.


What is the normal intrapleural pressure at the end of expiration? inspiration?

-2 mmHg / -7 mmHg


What are the receptors involved in the sinus cardiac rhythm?

- Stretch of the airways receptors -> inhibition of the normal tonic vagal activity to the sinoatrial node -> transient increase in the heart rate
- Stretch of the low-pressure cardiopulmonary baroreceptors -> transient increase in the heart rate
-> Increased MAP -> Stretch of the high-pressure arterial baroreceptors -> Reflex adjustment (decreased sympathetic, increased parasympathetic)


How is the venous return affected by inspiration?

Increased venous return (decreased intrathoracic pressure)


How does respiration affect the venous return during exercise?

Deep and rapid breathing -> increased venous return


How does yawning affect the venous return?

More negative intrathoracic pressure -> increased venous return


How does coughing affect the venous return?

Increased intrathoracic pressure -> decreased venous return


How does vasalva maneuver affect the cardiovascular parameters?

- 1 (first heart beats)- Increased arterial pressure due to increased intrathoracic pressure
- 2 - Compensation: increased HR and peripheral vasoconstriction (decreased venous return due to increased intrathoracic pressure - distended peripheral veins (facial))
- 3 - End of maneuver: decreased intrathoracic pressure and BP, Venous return restores -> increased SV, CO, BP and decreased HR


How does positive pressure ventilation affect the venous return?

Increased intrathoracic pressure -> Decreased venous return
Increased RV afterload


What are the 2 direct effects of gravity on vasculature?

- Increased venous transmural pressure -> distension of compliant veins
- Increased capillary transmural hydrostatic pressure -> increased transcapillary filtraton rate


What are the 2 main compensatory mechanisms for gravity?

- Reflex activation of sympathetic nerves (marginal effects)
- Skeletal muscle pump (contraction exels both venous blood and lymphatic fluid)


How does standing affect the blood volume?

Increased sympathetic activity -> fluid retention from kidneys


What are potential causes of altered diastolic properties in heart failure?

1) Decreased cardiac tissue passive compliance due to extracellular remodeling,collagen cross-linking, and extracellular matrix protein alterations
2) Increased myofibrillar passive stiffness due to alterations in titin
3) Delayed myocyte relaxation early in diastole due to slow cytosolic calcium removal
4) Inadequate adenosine triphosphate levels required to disconnect the myofilament cross-bridges rapidly
5) Residual, low grade cross-bridge cycling during diastole due to calcium leaking from the SR


What is cor pulmonale?

Right sided heart failure resulting from chronic pulmonary hypertension


Hypertension is associated with an increase or decrease in total peripheral resistance



What may cause the increase in total peripheral resistance from hypertension?

1) decrease in density of microvessels
2) pronounced structural adaptations that occur in the peripheral vascular bed
3) continuously increased activity of the vascular smooth muscle cells
4) an increased sensitivity and reactivity of the vascular smooth muscle cells to external vasoconstrictor stimuli
5) diminished production and/or effect of endogenous vasodilator substances such as nitric oxide


Name six treatments for hypertension

1) Restricted salt intake
2) Diuretic therapy
3) Beta-adrenergic blockers
4) ACE inhibitors
5) Angiotensin II receptor blockers
6) Alpha-adrenergic receptor blockers


How does a pulmonary embolus mimic hypovolemic shock?

Decreased left ventricular filling -> Decreased cardiac output (+ interferes with adequate gas exchange in the lungs)


What substances (exemples) mediate anaphylactic shocks?

Histamine, prostaglandines, leukotrienes, bradykinin


How does endotoxin induce vasodilation?

Endotoxin (lipopolysaccharide released from bacteria) -> induces formation nitric oxide synthase in endothelial cells, vascular smooth muscle and macrophages (inducible as opposed as constitutive) -> nitric oxide production


Give two potential causes for neurogenic shock

- Deep general anesthesia
- Deep pain


What are three mechanisms that stimulate sympathetic output during shock?

- Reduced arterial baroreceptor discharge
- Decrease in central venous pressure and/or volume
- Cerebral ischemia (when BP falls below 60 mmHg and brain blood flow falls / most intense of all activation of the activation of the sympathetic nerves)


What are the additional compensatory mechanisms to shock in addition to the autonomic nervous system?

- Rapid and shallow breathing -> respiratory pump promoting venous return
- Release of renin from the kidneys (sympathetic stimulation) -> angiotensin II which is a potent vasoconstrictor and promote thirst sensation / aldosterone which promotes renal sodium retention
- Increased level of vasopressin from the posterior pituitary gland in response to decreased firing of the cardiopulmonary and arterial baroreceptors
- Increased level of circulating epinephrine (sympathetic stimulation)
- Net shift of fluid from the interstitial space into the vascular space (decreased capillary hydrostatic pressure due to arteriolar constriction)
- Increased glyconeogenesis by the liver (epinephrine and norepinephrine) increasing BG, increasing extracellular osmolarity by as many as 20 mOsm -> net shift of fluid from the intracellular space to the extracellular space


Define heart failure

The hearts inability to meet the metabolic needs of the peripheral tissues, or instances when the heart can only do so in the presence of increased venous filling pressures


Name two of the most important neuro-hormonal systems in regards to heart failure

SNS (sympathetic nervous system) and RAAS (renin-angiotensin-aldosterone system)


Typical sigsn of low cardiac output

weakness, activity intolerance, hypothermia, depressed mentation


Inadeqaute tissue perfusioin results in which labratory abnormalities?

azotemia, oliguria, lactic acidosis


Name the primary trigger for activation of the RAAS

the heart's inability to provide normal renal perfusion


What induces renin release from the macula densa

decreased renal blood flow and sodium delivery to the distal portion of the neprhon


Renin converts ____ to produce ____

angiotensinogen to angiotensin 1


angiotensin 1 is rapidly converted to _____ by _______

angiotensin 2 by ACE (angiotensin-converting enzyme)


where is angioten 1 converted to angiotensin 2 by ACE?

pulmonary vasculature


list the maladaptive responses which result from angiotensin 2 in regards to cardiac injury

renal sodium and water retention, production of aldosterone, myocardial apoptosis, cardiac and vascular remodeling and fibrosis, increased thirst, and vasoconstriction


Name the main effector molecules of the SNS

Nor-epi and epi


In times of danger, the SNS has what effects through epi and norepi

increased HR, cardiac output, and increased blood flow to important stress response oprgans such as skeletal muscle


chronic activation of the SNS leads to what?

adrenergic receptor downregulation, persistent tachycardia, increased myocardial oxygen demand and myocyte necrosis


myocardial tissue produced what two main hormones that induce natriuresis, diuresis and vasodilation

ANP (atrial natriuretic peptide and BNP (b-type natriuretic peptide)


ANP and BNP are produced in response to what

myocardial stretch


reasons for loss of natriuretic peptide efficacy

natriuretic receptor downregulation , inappropriate or inadequate production, or increased peptide clearance or degredation


Endothelin 1 is a potent vaso (constrictor/dialator)



What produces endothelin 1

vascualr endothelial cells in repsonse to sheer stress, angiotensin 2 and other various cytokines


endothelin 1 works with angiotensin 2 to cause ______ and ______

vasoconstriction and increased cardiac afterload


Dogs and cats in heart failure have an elevated/decreased endothelin 1 level



In addition to its vascualr effects, endothelin 1 alters what else?

normal calcium cycling within muscle cells and is directly cytotoxic to myocardioctyes


what is the function of ADH (vasopressin)

increases re-absorption of free water within the renal collecting duct


how does vasopressin worsen heart disease?

the increase in fluid retention leads to fluid overload, congestive heart failure, and dilutional hyponatremia


In both humans and veterinary pateitns, dilutional hyponatremia is a marker of what?

severe neurohormonal activation and is a poor prognostic signs


name three signaling molecules that can cause cardiac hypertrophy

angiotensin 2, norepi, and aldosterone


What conditions cause concentric hypertrophy?

conditions that cause pressure overload such as systemic hypertension or subaortic stenosis


Pathophysiology of how concentric hypertrophy occurs

increased afterload triggers replications of sarcomeres in the parallel, resulting in an increase in the relative thickness of the ventricular walls


List some limitations of concentric hypertrophy

increased myocardial oxygen demand, endocardial ischemia, fibrosis, collagen disruption, injury to small coronary vessels, myocardial slippage, wall stress


Pathophysiology of myocardial remodeling in instances of volume overload

(mitral valve regurg, DCM, etc), sarcomeres replicate in series leading to elongation of myocytes and dilation of the ventricular chamber


Overall myocardial contraction pathway

During systole Ca enters myocardial cell which striggers release of additional Ca from the SARCOPLASMIC RETICULUM Ca from the SR flows through the RYANODINE channel and binds to TROPONIN C located on the ACTIN/MYOSIN complex.


The majority of Ca responsible for myocardial contraction comes from where?

the sarcoplasmic reticulum inside the cell


What receptor is responsible for Ca release from the sarcoplasmic reticulum



Once Ca has been released from the SR, where does it go?

Ca binds to troponin C on the actin molecule


Describe the pathophys pathway of myocardial relaxation

Ca ions are released from troponin C and sequestered back into the SR through the sarcoplasmic reticulum Ca ATPase (SERCA) channel. Other effector molecules such as PHOSPHOLAMBAN regulate the reuptake of Ca


After Ca is released from troponin, where does it go?

Back to the sarcoplasmic reticulum


what channel does Ca travel through to re-enter the SR?

Sarcoplasmic/endoplasmic reticulum Ca ATPase channel (SERCA)


Does phospholamban allow or inhibit the reuptake of Ca via the SERCA channel?



Myocyte mitochondria provided high energy phosphate molecules that fuel ...........

Ca pumps, ion pumps, sarcomeres contraction, sarcomeres relaxation, maintencance of the resting cell membrane potential, and propagation of the cardiac action potential


In heart failure, the heart preferentially uses what energy source and why?

glucose --> requries less oxygen to metaboilize than fatty acids


Define the Frank starling law

A mechanism which states that an increase in the initial volume or pressure within the ventricles increases the strength of the subsequent ventricular contraction


Excessive amounts of (preload/afterload) result in CHF



Classic example of diastolic heart disease

hypertoprhic cardiomyoiptahty in cats


Three things that affect ventricular compliance

1 - thickness of ventricular wall, 2- changes in cytoskeleton, 3 - function of the pericardium


TX of diastolic dysfunction

targeted at improving ventricular relaxation, increasing ventricular compliance, and alleviating existing pericardial disease


Class A heart disease

Patients at risk - no detectable cardiac disease (IE, dobermans, maine coon cats)


Class B heart disease

Patients with diagnostic evidence of heart disease


Class B1 heart disease

Patients with no radiographicor echocardiographic evidence


Class B2 heart disease

Patients with radiographic or echocardiogenic evidence


Class C heart disease

Pateints which have ben in heart failure


Class D heart disease

Patients with severe to debilitating heart disease even at rest


Pulmonary venous pressures greater than ____ and systemic venous pressures greater than ____ are sufficient to produce congestion that manifests are pulmonary edema, pleural effusion, ascites

Pulmonary >25mmHg, systemic >20mmHg


Common causes of left sides HF in dogs

mitral valve disease, DCM, PDA


Common causes of left sides HF in cats

hypertrophic or restrictive cardiomyopathy


common causes of right sided HF in dogs

DCM, degernative or congenital tricupside valve disease and pulmonary hypertension