Cardiovascular Pathology I

The period of ventricular contraction is called what

systole

The period of ventricular relaxation is called what

diastole

The quantity of blood returning to the heart during diastole is called what

preload

• Diastolic wall stress

• Related to venous pressure

Impedance to ventricular emptying is called what

afterload

• Systolic wall stress

• Related to systemic blood pressure

What is the heart’s job?

• Pumps blood through the vascular system

• The heart is doing a good job if it meets the

  cardiac output demands of the body.

What if the body demands a greater output?

The heart and vascular system will employ mechanisms to compensate and meet those demands.

Compensatory mechanisms of the cardiovascular system to meet output demands what

• Intrinsic cardiac responses

• Systemic responses

Compensatory mechanisms of the cardiovascular system to meet output demand: Intrinsic cardiac responses what do we see

– Dilation

– Hypertrophy

Compensatory mechanisms of the cardiovascular system to meet output demand: Systemic responsesresponses what do we see

– Increase heart rate and peripheral resistance

– Redistribution of blood flow

– Venular constriction

– Increase blood volume

Cardiac dilation increases what

• Increases chamber volume

  • allows it to exapnd and welcome more blood into the ventricles: typically a trasient response

Transient compensatory response to what

• increases in workload/preload

• Chronic volume overload → dilation + hypertrophy

Increases contractile force (Frank- Starling’s Law) what does that mean

• more stretching there will be a point for greater contractile force

What do we mean by chronic overload (volume)

transitory theres both dilation also the heart will then grow to try and hypertrophy to meet those needs

Cardiac hypertrophy response to

– Increased physiologic demand

– Diseases causing chronic pressure/volume overload

Reversible increase in the mass but not

• number of cardiomyocytes

– Increases number of sarcomeres

Remember cardiac myocytes dont under go what

hyperplasia only hypertrophy

Which has a Increase in mass; no increase in ventricular volume, concetric or eccentric

Concentric

Which has a Chronic pressure overload/increased resistance to eject blood, concetric or eccentric

Concentric

Which has a Increased systolic stress, concetric or eccentric

Concentric

Which has a Increase in mass + increase in ventricular volume, concetric or eccentric

Eccentric

Which has a Chronic volume overload/increased preload, concetric or eccentric

Eccentric

Which has a Increased diastolic stress, concetric or eccentric

Eccentric

How does concentric under Cardiac hypertrophy does the sacromeres are positioned

Sarcomeres added in parallel

How does eccentric under Cardiac hypertrophy does the sacromeres are positioned

Sarcomeres added in series

Congenital Cardiac Disease Young animals with

• Cardiac murmur

• Polycythemia

• Cyanosis

• Congestive heart failure

What is Congenital Defects:

Abnormal formation of cardiovascular system

What are the consequences of Congenital Cardiac Disease

• Shunting of blood

• Obstruction to flow

What are the consequences of Congenital Cardiac Disease for shunting of blood

– Abnormal connections of right and left parts of the circulation

What are the consequences of Congenital Cardiac Disease for Obstruction to flow

– Abnormal stenoses of (or near) valves, abnormal “connections” causing intramural or extramural obstructions to flow

What are the results for Congenital Cardiac Disease

Result: Cardiac dilation or hypertrophy or both

Congenital Shunts at the Left to Right shunt what happens

• Oxygenated blood from left side goes through the lungs a second time

• Do NOT get cyanosis

Congenital Shunts at the Right to Left shunt what happens

• Poorly oxygenated blood from the right heart bypasses the lungs

• DO get cyanosis

Direction of the shunt can vary depending on

size and/or duration

Three major arteriovenous connections are

– Atria, ventricles, great vessels

Failure to fully close leads to what in (left to right) shunting

pathology

• Atrial septal defect

• Ventricular septal defect

• Patent ductus arteriosus (PDA)

For dogs with (left to right) shunting what do we see

PDA

For ox, horse, sheep with (left to right) shunting what do we see

VSD, ASD

For pig and cat with (left to right) shunting what do we see

rare

The duet arteriles is there normally in the fetus ?

bypasses the lungs not breathing the air

in the ventricular septal defct where is the shunt located and do we see cynatotic

• left to right shunt

• no cyanotic

in the patent ductus arterioles where is the shunt located and do we see cynatotic

• left to right shint

• no cynanotic

Clinical correlates of left to right shunting

• Severity of disease depends on amount of shunting

• Chief complaints: none, exercise intolerance, syncope, dyspnea, sudden death

• PE findings: murmur to heart failure

Congenital Heart Disease a right to left shunt or left to right shunt

Right to Left Shunts

What is the pathogensis of Congenital Heart Disease (R to L)

– Portion of blood bypasses the pulmonary circulation  poorly oxygenated blood enters the systemic circulation  Cyanosis

What are examples of Congenital Heart Disease (R to L)

– Large/chronic PDAs, VSD

– Tetralogy of Fallot

– Transpositions of Great Arteries

– Persistent truncus arteriosus

What is occurring in Patent Ductus Arteriosus (PDA)

• Large/chronic patency

• Pulmonary arterial hypertension  increased pulmonary vascular resistance > systemic vascular resistance  right ventricular hypertrophy  right to left shunt  cyanosis

• Eisenmenger physiology

Tetralogy of Fallot what are the steps

1. Ventricular septal defect

2. Pulmonic valve stenosis

3. Over-riding aorta

4. Right ventricular hypertrophy

What animal normal gets Transposition complexes

BOVIDS

What is Transposition complexes

Malposition or transposition of arterial trunks

• Examples: overriding aorta or pulmonary artery, partial transposition, complete transposition

What are Semilunar valves

– Stenosis (constriction) of

pulmonary artery, aortic valve,

or pulmonic valve

What are Atrioventricular valves

– Stenosis, insufficiency or both

For dogs what Valvular malformations is affecting them

pulmonic, subaortic stenosis

For pigs what Valvular malformations is affecting them

subaortic stenosis

For cat what Valvular malformations is affecting them

mitral or tricuspid dysplasia

For ox/horse what Valvular malformations is affecting them

rare

Clinical correlates of valvular malformations the severity, CF, and PE findings

• Severity of disease depends on the amount of stenosis or insufficiency

• Chief complaints: none, exercise intolerance, syncope, dyspnea, sudden death

• PE findings: murmur to heart failure

What are other Congenital Cardiac Diseases

– Pulmonic Stenosis

– AV Valve Dysplasia

– Valvular hematocysts

– Ectopic Heart

– Endocardial fibroelastosis

– Excessive moderate bands

Vascular anomalies occurs when

Persistent right fourth aortic arch

– Right 4th aortic arch becomes the descending aorta rather than left

– Ligamentum arteriosum entraps the esophagus

What are the clin signs for Vascular anomalies

regeneration

• the left 4th aortic arch becomes the descending aorta and got swithced, ligmation or tnsion ends up being entrapped

What are the Cardiomegaly 4 forms:

– Dilated

– Hypertrophic

– Restrictive

– (Unclassified-cats)

Cardiomegaly is based on what

based on heart weight, ventricular wall thickness measurements, and absence of a reason for morphologic change

What is occurring in Dilated cardiomyopathy (DCM)

Ventricles are enlarged (hypertrophied) and dilated (thin, flabby muscle)  all chambers

Systolic dysfunction (decreased contractile force)

What is causing Dilated cardiomyopathy (DCM)

The cause and pathogenesis is unknown

Dilated cardiomyopathy (DCM) is commonly seen in

Most commonly recognized cardiomyopathy of DOGS- *familial tendency in some breeds (Dobermans and Boxers)

What is occurring in Hypertrophic cardiomyopathy (HCM)

Left ventricle is hypertrophied +/- septum and right

Diastolic dysfunction (decreased ventricular volume and resistance to filling)

Hypertrophic cardiomyopathy (HCM) is commonly seen in

Most common primary cardiomyopathy of CATS

*Cats (Ragdoll and Maine Coon)- associated with an inherited mutations in myosin-binding protein C gene

Sequela of HCM in cats:“Saddle thrombus” occurs when

-Thromboembolus at the aortic trifurcation

-Thrombus formation in left atrium  dislodges and passes through the aorta (embolus)  lodges at the aortic trifurcation (thrombosis)  distal limb ischemia  5 Ps (pain, paresis, pulselessness, poikilothermic and pallor of hind limbs)

Restrictive cardiomyopathy (RCM) is less common in what animal

Less common, seen mostly in cats

Restrictive cardiomyopathy (RCM) is characterized by

Characterized by impaired ventricular filling

due to reduced ventricular compliance

what is the depositon of Restrictive cardiomyopathy (RCM)

Deposition of fibrous/elastic tissue to the

endocardium or excessive moderator bands

Restrictive cardiomyopathy (RCM) what happens to the vnetricles

Ventricles are usually normal in size but

atria are dilated

Cardiac Output (CO) is

volume of blood the heart ejects per minute

• CO = SV x HR

– SV = volume of blood the ventricle ejects per beat

To increase stroke volume: we must

• increase Myocardial Contractility

• increase preload

• decrease afterload

Stroke Volume with dilated cardiomyopathy (DCM) we must see

• decrease Myocardial Contractility

• increase preload

• increase afterload

• decrease Overall stroke volume

Stroke Volume with hypertrophic cardiomyopathy (HCM) we must see

• increase of Myocardial Contractility

• decrease prelaod

• no afterload

• decrease Overall stroke volume

Renin-Angiotensin System (RAS) Activated in response to low

CO

What is the goal of RAS

–Goal: Increasing blood volume

• Maintain systemic blood pressure  tissue perfusion

When we have a decrease in CO and a decrease in renal perfusion what will happen

its going to turn the system on so the kidney will secrete renin

renin turns into what

angiotensis that comes from the liver into the angiotensis I

AEF converts into what

angiotensin into angiotensin 2 the has a down stream affect (causes vasoconstricton of the peripheral blood vessels to increase BP)

• from here then activates the adrenal gland to sescrete aldosterone

• will also stimualte the pituiatry gland to serete ADH