General aspects of CV diseases. Clinical aspects of Heart Failure Flashcards
What is the CV system comprised of?
Heart- pump and endocrine
Vessels- diameter and integrity
Blood- vol, viscosity, O2 carrying (PCV, Hgb, pH)
What id CV insufficiency and what are the 2 main causes
CO is not sufficient enough to deliver the required amount of O2 to the tissues
- Heart failure (can lead to central shock)
- Periph circ failure= periph shock
Periph circ failure: causes and compensatory mechanisms
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
Heart failure:
primarily due to HD and secondary due to the cardiac changes (often induced by the HD)
- Phys and haemodynamic
- Neurohormonal
- Inflamm- cytokines and FR’s
Phys/ haemodynamic aspects of HF
Preload
Afterload
Contractility
HR
Distensibility
Synch of beats (rhythm)
Frank-Sterling law
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
Leplace Law
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
Distensibility
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
Preload
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??)
Afterload
Increases at beginning, the decreases.
Hypertrophy which requires more O2.. always detrimental
Contractility
Increases!!
Higher O2 and E demand
HR
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
Distensibility
Increases!! is always patho- there is an increased O2 and E demand
Rhythm
Decreases (sunch of heart beats)
Top priorities in compensation of HF
Sustain BP in vital organs (brain heart and kidneys)
Sustain BP in other organs
Keep preload low!!! i.e keep venous P low
Neurohormonal comp process (4)
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)
Neural compensation
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
RAAS
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
Progression of Cardiac failure (8)
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
Chronic HF- inflamm process, what causes fibrosis, necrosis and apoptosis?
AT 2
Aldosterone
Catecholamines
Endothelin
What do the inflamm mediators IL 1.6 and TNF alpha do in chronic heart failure
Locally: necrosis and muscle damage
Systemically: cardiac cachexia, catab, alter carb digestion
Decr contractility
Hypertrophy, fibrosis
Incr synth of iNO (FR)
Inflamm mediators thta are heroes and their role
Loss of Na and H20
VasoD
- ANF, BNF
- Bradykinin
- NO
- PG
Inflamm mediators that are the villains and their role
VasoC
NA and H2O reabs
Cytotoxic
- AT2
- Aldosterone
- Endothelin
- IL-6
- TNF alpha
- Homocysteine
- Endotoxins
- FR’s
- NA
What are responsible for cardiac remodelling?
ANS
RAAS
Inflamm mediators
Macroscopic changes of cardiac remodelling
Concentric hypertrophy: muscle thickens but lumen is normal, P overload, seen with US
Eccentric hypertrophy: dilation of lumen, muscle may be thinner, vol overload
Microscopic changes of cardiac remodelling
Apoptosis, necrosis, fibrosis
Cellular uncoupling
Function/elctrophysio of cardiac remodelling
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)
Heart disease and its relationship with circ failure
Failure is usually a result of severe heart disease, but can have heart disease without failure!
5 major aspects of HF
Disfunction of myocard
Failed pump action
Failed. diastolic distension
Brady, tachycard and arryhthmias
Hyperkinetic
Causes of failed pump (sytolic, mechanical) action of the heart
P overload- stenosis
Vol overload: valves disoreder, infusion OD, periph ateriovenous shunt
Causes of hyperkinetic (this is v high out[ut circ)
Gravidity
Fever
Anaemia
Hyperthyroidism- v high HR in cats
Left-sided heart failure
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!
Signd of L sided HF
Tachypnoea
Mixed dyspnoea
Pulm edema- progressive cough
Pleural fluid in cats
Cerebral hypoxia- Adam Stokes breathing
Prerenal azotemia
R Sided HF *rare in cats*
Ascites ALWAYS!!
+/- pleural/pericard fluid
Modified transudate, chylous
SC fluid
Heptatomegaly
Signs of R sided HF
Distension of jugular vein- + reflux test
Congested abd organs (liver)
ASCITEs
pleural fluid
Main diseases causing HF in cats and dogs
Dogs: ENDOCARDOSIS/ mitral valve disease, then cardiomyopathy
In cats number 1 is cardiomyopathy
ACVIM staging of heart failure
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
Treatment of HF: decreasing the preload i.e the venous return
Diuretics
VenoD’s- nitrates, PIMOBENDAN
Treatment of HF: Decreasing afterload
Only for category D!! because would cause hypotension so only use in refractory cases!!
Arterial Dilators: Amlodipine and Hydralazine
VenoD - PIMOBENDAN!
Treatment of HF: Increasing contractility
Calcium sensitizers: Digoxin and pimobendan
Digoxin
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
Pimobendan
Calcium sensitizer, PDE inhib, veino and vasoD, relaxation
Indications:
- ALWAYS CHF!!
- DCM preclinical state
- MMVD preclinical stae if heart dialted
Give PO or IV
Treating CHF in an emergency
Must confirm the diagnosis!!
O2
Decr preload: IV diuretics, pimobedan
Decr afterload
Incr contractility: pimobendan, dobutamine
Sedate: ACP or but
Treat life-threatening arrhythmias
Treating a chronic CHF case
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
Treating CHF severe refractory case
All as for chronic CHF +++
Restrict salt
Give diuretics parenterally! and use a combo
Incr Pimobedan
Amlodipine
Sildenafil- for pulm hyperT
Hydralazin (small dosage)
