General aspects of CV diseases. Clinical aspects of Heart Failure

Question 1

What is the CV system comprised of?

Answer 1

Heart- pump and endocrine

Vessels- diameter and integrity

Blood- vol, viscosity, O2 carrying (PCV, Hgb, pH)

Question 2

What id CV insufficiency and what are the 2 main causes

Answer 2

CO is not sufficient enough to deliver the required amount of O2 to the tissues

1. Heart failure (can lead to central shock)
2. Periph circ failure= periph shock

Question 3

Periph circ failure: causes and compensatory mechanisms

Answer 3

Decreased BV and dilatoin of vessels!!

Acute compensatory reaction: symp alarm reaction- vasoC of non-vital organs, incr HR and contraction

Tre`tment: REPLACE blood vol

Question 4

Heart failure:

Answer 4

primarily due to HD and secondary due to the cardiac changes (often induced by the HD)

1. Phys and haemodynamic
2. Neurohormonal
3. Inflamm- cytokines and FR’s

Question 5

Phys/ haemodynamic aspects of HF

Answer 5

Preload

Afterload

Contractility

HR

Distensibility

Synch of beats (rhythm)

Question 6

Frank-Sterling law

Answer 6

Preload!!

Incr length of myocytes– incr sensitivity of myofibrils to Ca– incr amount of Ca released for SR

The greater the venous return- the greater the contraction required to pump it

PAtho: overdilation- because the venous return is too high– congestion in venous system– at this point the cobtractility does not increase anymore.

The P in the LV will transfer to the L atrium– puml veins– pulm edema

P in RV– ascites

Question 7

Leplace Law

Answer 7

Afterload (the P the heart must overcome to open Aorta and pump blood)

Incr in wall thicknedd to overcome an incr in P

Incr ejection P is caused by a decreased volume

Tension should be high (using O2 and E) during dilation of the wall, even if arterial P is normal

Training hypertrophy- does not induce increased wall stress

Question 8

Distensibility

Answer 8

Depends on the cardiac muscle itself e.g if there is hypertrophy OR if there is anything compressing the heart e.g fluid in the pericardium

Results: DECREASED left ventricular vol i.e diastolic filling i.e preload

Question 9

Preload

Answer 9

Stretch of myocytes

It increases

Leads to congestion and an increased O2 demand (is this because the myocytes are stretching more therefore require more O2??)

Question 10

Afterload

Answer 10

Increases at beginning, the decreases.

Hypertrophy which requires more O2.. always detrimental

Question 11

Contractility

Answer 11

Increases!!

Higher O2 and E demand

Question 12

HR

Answer 12

Increases and then decr.

Correlates with SV because if there is more blood to be pumped then will beat faster. But if v high (above 180)- could mean that there is not enough time for diastolic filling

Question 13

Distensibility

Answer 13

Increases!! is always patho- there is an increased O2 and E demand

Question 14

Rhythm

Answer 14

Decreases (sunch of heart beats)

Question 15

Top priorities in compensation of HF

Answer 15

Sustain BP in vital organs (brain heart and kidneys)

Sustain BP in other organs

Keep preload low!!! i.e keep venous P low

Question 16

Neurohormonal comp process (4)

Answer 16

Incr HR but decr diatolic filling and coronary flow

incr myocardial activity/contraction- leads to hypertrophy and incr O2 and E demands

Periph vasoC… but incr afterload

Incr blood vol- RAAS which incr preload, it is our third priority to keep this low– patho overcompensation (because the cells detect a decr in BP-salt and water reabs to incr circ vol, alsoc vasoC)

Question 17

Neural compensation

Answer 17

baroreceptors Detects decr in BP– Incr symp tone!!!!- if chronic baroreceptor stim then down reg of beta1 especially

Later AT2 also incr symp

+ ino, lsuio and chrono tropic

VasoC

Arrhythmias

Incr renin

Decr parasymp

Question 18

RAAS

Answer 18

Na and H2O reabs

K excretion

VasoC

Incr symp tone

Local: myocardial fibrosis, apoptosis and necrosis, hypertrophy

Cardiac remodelling (is this because of Aldosterone?)- ECM production

Arrhythmias

Question 19

Progression of Cardiac failure (8)

Answer 19

permanent activation of RAAS

Incr HR

Incr O2 and E demand

Rhythmic disorders

FR’s

Inflamm mediators

Endotoxins to break down aldosterone e.g when there is liver failure

ET-1 release from endothel and myocard- receptors at endocardial layer and in valves— vasoC and hypertrophy

Question 20

Chronic HF- inflamm process, what causes fibrosis, necrosis and apoptosis?

Answer 20

AT 2

Aldosterone

Catecholamines

Endothelin

Question 21

What do the inflamm mediators IL 1.6 and TNF alpha do in chronic heart failure

Answer 21

Locally: necrosis and muscle damage

Systemically: cardiac cachexia, catab, alter carb digestion

Decr contractility

Hypertrophy, fibrosis

Incr synth of iNO (FR)

Question 22

Inflamm mediators thta are heroes and their role

Answer 22

Loss of Na and H20

VasoD

1. ANF, BNF
2. Bradykinin
3. NO
4. PG

Question 23

Inflamm mediators that are the villains and their role

Answer 23

VasoC

NA and H2O reabs

Cytotoxic

1. AT2
2. Aldosterone
3. Endothelin
4. IL-6
5. TNF alpha
6. Homocysteine
7. Endotoxins
8. FR’s
9. NA

Question 24

What are responsible for cardiac remodelling?

Answer 24

ANS

RAAS

Inflamm mediators

Question 25

Macroscopic changes of cardiac remodelling

Answer 25

Concentric hypertrophy: muscle thickens but lumen is normal, P overload, seen with US Eccentric hypertrophy: dilation of lumen, muscle may be thinner, vol overload

Question 26

Microscopic changes of cardiac remodelling

Answer 26

Apoptosis, necrosis, fibrosis Cellular uncoupling

Question 27

Function/elctrophysio of cardiac remodelling

Answer 27

Ion channels and in communication Incr number of receptors? Ca mechanisms and therfore the contractility is altered- impacts systolic and diastolic function, maybe arryhtmias (both of which can be diagnosed with US)

Question 28

Heart disease and its relationship with circ failure

Answer 28

Failure is usually a result of severe heart disease, but can have heart disease without failure!

Question 29

5 major aspects of HF

Answer 29

Disfunction of myocard Failed pump action Failed. diastolic distension Brady, tachycard and arryhthmias Hyperkinetic

Question 30

Causes of failed pump (sytolic, mechanical) action of the heart

Answer 30

P overload- stenosis Vol overload: valves disoreder, infusion OD, periph ateriovenous shunt

Question 31

Causes of hyperkinetic (this is v high out[ut circ)

Answer 31

Gravidity Fever Anaemia Hyperthyroidism- v high HR in cats

Question 32

Left-sided heart failure

Answer 32

pulm edema Cats only: acc of modified transufate/chylous in the thorax Congestion is BEHIND the L side: goes from ventricles- atria- pulm veins--- in lungs hydrostatic P\> oncotic P--- pulm edema-- dyspnoea and the suffocation!

Question 33

Signd of L sided HF

Answer 33

Tachypnoea Mixed dyspnoea Pulm edema- progressive cough Pleural fluid in cats Cerebral hypoxia- Adam Stokes breathing Prerenal azotemia

Question 34

R Sided HF \*rare in cats\*

Answer 34

Ascites ALWAYS!! +/- pleural/pericard fluid Modified transudate, chylous SC fluid Heptatomegaly

Question 35

Signs of R sided HF

Answer 35

Distension of jugular vein- + reflux test Congested abd organs (liver) ASCITEs pleural fluid

Question 36

Main diseases causing HF in cats and dogs

Answer 36

Dogs: ENDOCARDOSIS/ mitral valve disease, then cardiomyopathy In cats number 1 is cardiomyopathy

Question 37

ACVIM staging of heart failure

Answer 37

A) High risk but no identifiable structural disorder B1) Asymptomatic with no evidence of remodelling B2) Asymptomatic WITH cardiac remodelling \*note in B they have the disease but not failure\* C) Past/current clinical signs of HF associated with structural HD D)Have end-stage disease and clinical signs of HF- refractory to the standard therapy

Question 38

Treatment of HF: decreasing the preload i.e the venous return

Answer 38

Diuretics VenoD's- nitrates, PIMOBENDAN

Question 39

Treatment of HF: Decreasing afterload

Answer 39

Only for category D!! because would cause hypotension so only use in refractory cases!! Arterial Dilators: Amlodipine and Hydralazine VenoD - PIMOBENDAN!

Question 40

Treatment of HF: Increasing contractility

Answer 40

Calcium sensitizers: Digoxin and pimobendan

Question 41

Digoxin

Answer 41

Inhibits the Na/K pump Be careful as is proarrhyth!! because in small doses has beta adrenergic stim and causes hypokalaemia Maintains baroreceptor function and decr adren overlaod Narrow TI Is used to treat supraventric arrhythmias

Question 42

Pimobendan

Answer 42

Calcium sensitizer, PDE inhib, veino and vasoD, relaxation Indications: * ALWAYS CHF!! * DCM preclinical state * MMVD preclinical stae if heart dialted Give PO or IV

Question 43

Treating CHF in an emergency

Answer 43

Must confirm the diagnosis!! O2 Decr preload: IV diuretics, pimobedan Decr afterload Incr contractility: pimobendan, dobutamine Sedate: ACP or but Treat life-threatening arrhythmias

Question 44

Treating a chronic CHF case

Answer 44

Furosemide (smallest effective dose) Pimobendan Prevent the neuroendocrine overcomp ( byt the RAS aldosterone escape?) ACE-1, spironolactone Supplement K and B-vits Decr HR: beta or Ca channel blockers Treat ventric arryhtmias: sotalol or amiodarone

Question 45

Treating CHF severe refractory case

Answer 45

All as for chronic CHF +++ Restrict salt Give diuretics parenterally! and use a combo Incr Pimobedan Amlodipine Sildenafil- for pulm hyperT Hydralazin (small dosage)