congestive heart failure Flashcards
Where is the only vein-capillary-vein system located in the body?
hypothalamus
what part of the body holds the most blood at any given time?
VEINS!
What are things that contribute to resistance of w/in yo body
1) blood viscosity (effected by volume and # of RBC)
2) total blood vessel length
3) blood vessel diameter
what is the biggest contributor to minute-to min control of resistance in the vascular system?
Blood vessel diameter
R= 1/(r^4)
can the heart heal itself?
yes, but very slowly- only 1% of heart muscle cells are replaced per year
how are electrical currents spread w/in the myocytes?
via gap junctions
what does atrial natriuretic peptide do?
regulates the concentration of sodium in the extracellular fluid
What part of the heart does the sympathetic fibers innervate?
the entire heart muscle, and node cells
releases NE
**the receptors will also bind to the neuroendocrine hormone epinephrine from the adrenal gland
what part of the heart does the pSNS innervate?
the SA-AV node, released acetylcholine
what is the inherent rate of the SA node?
100 bpm, but it is moderated by the nervous system
what part of the heart conduction system has a .1s delay>
the AV node- allows the atrai to contract and totally fill the ventricles
What to the purkinje fibers do?
supply the papillary muscles-tell them to contract before the rest of teh ventricles to hlep prevent backflow through the valves
why is the refractory period for heart cells important?
long refraction means the cell won’t fire again until its last contration is almost relaxed away- lets its empty completely
arrhythmia
uncoordinated atrial and ventricular contractions caused by a defect in the conduction system.
Fibrillation
: a rapid and irregular (usually out of phase) contraction where the SA node is no longer controlling heart rate.
ventricular fib
is more life threatening. The ventricles pump ineffectively and without filling. If the heart’s rhythm is not rapidly reestablished then circulation stops and brain death occurs
ectopic focus
abnomral pacemaker that takes over the conduction system- usually bc it goes faster than the SA node
Extrasystole
premature conractions, can be atrial or ventricular
total block
ventricles beat at their intrinsic rate- too slow to maintain circulation
partial block
AV impulse isslow, but it does get through
coronlary ostia
openings to coronary vessels- blood falls back into them during dicrhotic notch- heart is the FIRST THING to get oxygenated b/c of these
Cardiac Output
amount of blood pumpled out of each ventricle in one minute
CO=HR X SV
what is the normal cardiac output?
5.25 L/min
what is the most common way your body varies CO?
Via heart rate
what are things that increase heart rate?
positive chronotropic factors
-sympathetic NS
what are things that decrase heart rate?
PSNS
negative chronotropic factors
what is SV?
the diff bw end diastolic volume (after ventricles have completely filled) and end systolic volume (after ventricles have completely emptied)
what is the average amount of blood that gets pumped out?
60% of blood that was in the chamber (avg 70 ml)
inotropy
how wll the heart is working - muscle contractions
Starlings Law and SV?
the critical factor controlling SV is PRELOAD
preload
degree to which the cardiac muscle cells are stretched before they contract
is there an optimal Length/tension for preload?
yes! you want maximal force generation
-underextension limits force, but overextension leads to inefficient pumping
what is the most important factor in causing increased preload?
the amount of blood inthe ventricles by the end of diasole
what is the amount of blood in the ventricles controlled by?
venous return and the amount of time b/w ventricular contractions (diastole)
** anything that incrases venous return or slows heart rate increases EDV
Frank-Starling mechanism
the higher the EDV, the higher the SV
But there is a limit to how high the SV will go. at some pt, increased EDV doesnn’t help much
think-larger EDV =stronger contraction= lareger SV w/ same amount of residual volume
how can the ventricle be emptied better for increased SV?
“squeez force” contract dat shit
How does the SNS control stroke volume?
by increased the force of each ventricular contraction at any given SV
What is Ejection Fraction
expressed as a %- normally avgs btw 50-75 %
EF=SV/EDV
what can EF measure?
contractility via SV
*increased contractility=increased EF
preload definition?
is proportional to the amount of ventricular myocardial fiber stretch just before systole (EDV).
Preload ~ Starling’s “length”
afterload definition?
pressure that the ventricles must overcome to force open the aortic and pulmonary valves.
Afterload ~ how much tension the heart must create to do its job (systemic high bp ex)
what is the ideal situation for the heart to work its best?
high preload and low afterload
what can increase afterload?
anything that increases systemic or pulmonary arterial pressure (ex. HTN)
do arteries need to be more elastic or compliant?
Elastic! they are often called pressure reservoirs bc of their elastic recoil
they need to keep the pressure high
Veins: more elastic or compliant?
they need to be more compliant
-higher the compliance ofa structure, the more it can be stretched w/o a corresponding increased in pressure
V vs P: vein and artery
at low pressures, venous compliance is 10-20 times greater than arterial compliance, but arterial and venous compliance are similar at high pressures
is pulmonary pressure higher or lower than systemic pressure?
LOWER!
what would happen if pressure to the lungs when way up?
Trauma to smaller vessels of the lungs;
inflammation and repair;
narrowing of these vessels as they heal;
increased resistance of blood flow to the lungs.
systolic pressure
max pressure at Systole
diastolic pressure
min pressure at diastole
pulse pressure
systolic-diastolic
what is MAP?
Diastolic + 1/3 of the pulse pressure
what are you hearing when you listen to someones bp?
turbulence- a little blood can get through. so when it goes under diastolic pressure- there will be no sound of turbulence bc vessel is completely open
arterioles
smallest arteries- their function is controlled by neural, hormonal, and local chemicals
- muscularis!
- change their diameter via autoregulation
what are some local controls of arterioloar radius?
pH
- if an organ becomes morme metabolically active, its CO2 increased and O2 decreases
- resulting pH change leads to the dilation of the arteriolies
and vice versa
continuous capillaries?
most common and allow passage of fluids and small solutes
-skin and muscle
fenestrated capillaries
more permeable to fluids and solutes than continuous capillaries
- allow more rapid transfer of substances
- kidneys, intestins, endocrine
sinusoidal caps
leaky- allows large molecules to pass btw the blood and surrounding tissues
-liver, bone marrow, lymphatics
at what part of the capillary does osmotic pressure have more of an effect?
the distal end! bc blood is more concentrated there
what are the two main roles of lymphoid tissues?
- house and provide a proliferation for lymphocytes
2. give a surveillance site to examine and clean the lymph fluid
venous system: componenets?
3 main layers (tunics)
veins also have less smooth muscle and elastin than arteries
-veins also highly distensible- called “capacitance vessels”
what is the blood pressure in veins?
15 mmgh
what helps veins move blood back to the heart?
- respiratory pump
2. muscular pump
heart failure
inadequate pump function of the heart, which leads to congestion resulting from a back up of fluid in the lungs and peripheral tissues
what are the general etiologies of left heart failure?
1) inappropriately lrge workload on the heart
2) restricted ability of the heat to fill
3) loss of heart muscle cells
4) poor ability of myocytes to contract
wwhat can cause the restricted ability of the heart to fill?
pericardial dz, Mitral stenosis, infiltrative “fibrotic” heart dz (amyloid)
what can cause the loss of heart muscle cells?
cells died in heart attack
what can decrease the myocytes ability to contract?
poisons, infxns, mutuations of myocyte protines
what can cause an increased workload on the heart?
valves that regurg- M/A
pushing against too much systemic pressure
- HTN
- AS
- asymmetric septal hypertrophy
what happens in systolic left heart dysfuction?
pressure-volume line shifts to the right
- ventricle stops pumping out earlier (at a higher pressure reading) than is normal
- isovolumetric relaxation hit faster than normal
- reduced EF
how does your heart try to compensate for this? (systolid L heart dysfxn)
1) increase LV volume by increasing the overall size of the LV via muscle mass and chamber size
* gives the LV more “contents” to push out
more ways your heart compensates for systolic L heart dysfxn?
1) improve contractility by pumping catecholamines (epei or dopamine) “diggin deep”
3) improving preload (just shove more in there)
diastolic left heart failure
diastolic curve shifts to the right
-ventricle reaches a max pressure that it can handle at a lower volume than normal
**the ventriculare hypertrophy that initially can make the heart pump better in systole can eventually lead to dysfxn in diastole
symptoms of right-sided heart failure
-dependent edema
-JVD
-abdominal distention
-hepatomegaly
splenomegaly
-anorexia, N
-weight gain
-nocturnal distress
left sided heart failure sx
dyspnea
- tachypnea
- crackles in lungs
- dry hacking cough
- paroxysmal noctural dyspnea
what is a common cause of right heart failure?
chronic lung dz
cor pulmonale (enlargement of the right ventrical due to high BP in the lungs)
how does Right heart failure lead to left heart failure
- normally, the interventricular septum is usually bowed toward the thinner walled and lwoer pressure right ventrilce
- when R V pressure increases relative to the left, the IV septum can bow to the left and prevent efficient filling of hte LV
- lead to even More pulm congestion
what does SOB happen with heart failure?
1) pulmonary source (lung dz)
2) Right heart source (enlarged liver presseing agains diaphragm limiting lung volume)
3) left heart source
(decreased ability to pump blood has led to pulmonary edema)
ventricular hypertrophy: concentric growth
even grown of a ventrical w/o overall enlargment- wall of ventricle are thickened and volume is diminished
*sarcomeres added in parallel (increase width)
ventricular hypertrophy: eccentric growth
even growth of a ventricle w/ heart enlargment
- ventricle size and volume both increase
- increase myocyte cell lenthg
- more rapid change
what is concentric hypertrophy causes by?
HTN, aortic constriction
what is eccentric hypertrophy caused by?
valve dz
JVD
right sided heart failure
what is the classic wave form of JVP?
a, c, and v
a=atrial wave
c=contraction (ventricular wave)
v=filling wave
what are RF for CHF?
CAD, MI, smoking, HTN, obesity DM, valvular heart dz, cardiomyopathy
what is CHF
clinical syndrome characterized by abnormal retention of water and sodium
causes of diastolic HF
restrictive, infiltrative cardiomyopathies (amyloidosis, sarcoidosis), pericardial effusion, hypertrophic card, MI, HTN
systolic HF etiology
dialated cardiomopathies, MI, Ischemic heart dz, chronic HTN
high output HF
anemia, hyperthyroidism, AV fistula, Beriberi (thiamine deficiency) Paget dz
systolic dysfunction
HF w/ decreased or impaired EF (HFrEF)
<40%
diastolic dysfxn
diastolic HF w/ normal or perserved EF
HFpEF >50%
what does CFH affect?
left atrial pressure, CO
what are some PE findings of HF?
tachypnea, JVD, hepatojuglar reflux, pulm rales or crackles, wheezing, pleural effusion,
-lateral displacement of apical impulse
cyanosis, anasarca, hypotension, cheyne-stokes
ascites
anasarca
peripheral edema
what causes the S3 sound
oscillation of blood back and forth between the walls of the ventricles initiated by the inflow of blood from the atria.
what is the confusion and unconsciousness caused by in HF?
the decreased O2 to brain
when might one hear the S4 sounds?
diastolic HF
what are the predominant features of RHF?
anasarca and hepatomegaly
what cuases the cold and clammy skin associated with heat failure?
sympathetic activity
what is another randome x of HF
nocturia
what to expect BP wise
hypotension and narrow pulse pressure
BP can be high, normal , or low
diagnostic studies: labs
- anemia
- renal insufficiency
- hyper kalemia
- hyponatremia
- elevated liver enzymes
what is the most useful imaging study?
Echo- assess size and function of the chambers, valve abnormalities, pericardial effusion, shunting, and segmental wall abnormality
what would a chest xray show?
cardiomegaly, bilateral or right-sided pulmonary effusion, perivascular or interstitial edema, venous dilation and cephalization, alveolar fluid
what are kerley B signs?
horizontal lines less than 2cm long, commonly found in the lower zone periphery. These lines are the thickened, edematous interlobular septa. Causes of Kerley B lines include; pulmonary edema, lymphangitis carcinomatosa and malignant lymphoma, viral and mycoplasmal pneumonia, interstital pulmonary fibrosis, pneumoconiosis, sarcoidosis.
NYHA class I
cardiac dz but no limitations, asx
when is stress imaging or radionuclide angiography needed?
to assess the cause of severity of the dz
what other cardiac labs may be elevated?
BNP or N-termial pro-BNP may be elevated
creatine kinase mB and troponins should also be tested to evaluate for new MI
what is something taht should be looked at in older population that present w/ Hf?
thyroid test
Class II
Cardiac disease slight limitation with ordinary activities, symptoms with ordinary activities
Class III
Cardiac disease marked limitation; symptomatic with less than ordinary activities
Class IV
Cardiac disease inability to perform any physical activity without symptoms. Symptoms at rest
tx of HF-non-pharmacologic
progressive aerobic exercise,low-sodium diet, tobacco and alcohol stopping, stress reduction
initial pharmacologic methods
early initiation of ACE I
2cd: ARB, BB, aldosterone agonists
How does ACEI help?
decreases let ventricular wall stress, slows mycardial remodeling and fibrosis
BB?
improve EF, reduce Left ventricular dilation, and reduce the incidence of arrythmias
reduced EF heart failure?
systolic (enlarged ventricles fill w/ blood and pump out less than 40-50%)
non-reduced EF heart failiure
diastolic (stiff ventricles fill with less blood than normal- vetricles pump out about 60% of the blood, vut the amount may be lower than normal
what are some meds that cn worsen HF
NSAIDSNSAIDs Some anesthesia and chemotherapy meds TZDs CCBs Saxagliptin and sitagliptin Flecainide, disopyramide, sotalol, dronedarone Alpha blockers, minoxidil Itraconazole, ampho B
More meds that worsen HF?
Carbamazepine, pregabalin TCAs, citalopram, clozapine, lithium Bromocriptine, pergolide, pramipexole Albuterol, bosentan, epoprostenol TNF-alpha inhibitors Chloroquine, hydroxychloroquine
Stage A tx
high risk for HF but no damage or sx
*get yo house in order
Stage B tx
damage, but no sx
- ACEI or ARB (all pts w/ rEF)
- BB (all pts w/ rEF)
- statins
when can you use CCB?
preferably amlodipine- used only to tx associated angina or HTN
ARni?
sacubitril/valsartan
aRB + neprilsyn inhibitor
neprilysin- breaks down natriuretic peptides–> vasoconstriction
DI of arni
nsaids, K sparing diuretics, Lithium
ADRS of arni
hypotension,, hyperkalemia, cough, dizzy, renal failure
when aer IDCs indicated?
when EF falls below 35
when is biventricular pacing indicated?
resynchronize the heart when QRS becomes prolonged
