Heart Failure Flashcards
Mean Arterial Pressure
average pressure in the systemic circulation.
indicator of how much force needed to move blood around the body
Intrathoracic Pressure & Venous return
Intrathoracic Pressure impedes venous return to the heart as it increases opposing pressure on veins and can occlude vessels
Systolic blood pressure
arterial blood pressure during ventricular contraction
Diastolic blood pressure
arterial blood pressure during ventricular relaxation
Cardiac output
total volume of blood ejected from the left ventricle per minute
determined by: stroke volume x heart rate
Stroke Volume
total volume of blood ejected from left ventricle per contraction
determined by preload, afterload, and contractility
Frank-Starling Mechanism
states that within limits, increased preload (stretch) increases contractility.
this is due to the optimal arrangement of sarcomeres when stretched
Preload
wall tension placed on the ventricular at the end of diastolic filling.
determined by central venous volume
increased preload = increased stroke volume
Contractility
force of contraction during systole.
increases stroke volume independent of preload/afterload
Afterload
force heart has to work against during systolic contraction.
determined by peripheral vascular resistance and ventricular wall tension.
increased afterload = decreased stroke volume
End Systolic Volume
blood volume remaining in ventricles after systole.
End Diastolic Volume
blood volume in ventricles at the end of diastolic filling.
end systolic volume + diastolic filling
determines preload
Heart rate and Preload
Increased heart rate decreases amount of diastolic relaxation between contractions
Reduced end diastolic volume causes reduced preload
Wall Tension & Wall Thickness
wall tension = opposing force of the wall of a blood vessel
wall thickness = diameter of the vessel wall
there is an inverse relationship between wall tension & wall thickness.
increased thickness = decreased tension
Determinants of muscle contraction
Calcium
ATP
Oxygen
Na+/K+ pump
Electrical Conduction System
SA Node –> AV Node (delayed) –> AV Bundle (delayed) –> Purkinje Fibers
Atrial Kick
during atrial contraction, the atria eject the remaining bit of blood from atrial chambers –> ventricles
Cardiac performance
affected by work demand of heart and ability of coronary perfusion to meet metabolic demand
Inotropy Factors
factors that alter muscle contraction
can be positive (promote contraction) or negative (inhibit contraction)
Vasoconstrictors
Angiotensin II
Catecholamines (mainly norepinephrine)
ADH
Prostaglandins - released by arachidonic pathway
Serotonin - released by clotting platelets
Vasodilators
Nitric Oxide - released by endothelial cells Natriuretic Peptides Histamine - mast cells + basophils Bradykinin Ace-i ARB
Common Causes of Heart Failure
Coronary Artery Disease Hypertension Myocardial Infarction Dilated Cardiomyopathy Valvular Heart Disease Pulmonary disorders (Right-sided HF)
Ejection Fraction
percentage of blood ejected from the heart during systole
calculated by stroke volume / end diastolic volume
Heart Failure EF
equal to or under 40%
Heart Failure Definition
functional or structural impairment of the heart causing inadequate cardiac output to meet metabolic demand
caused by heart not pumping properly or filling properly
HF Compensatory Mechanisms
Frank-Starling Law --> increased preload SNS activation RAAS activation Natriuretic peptides Myocardial remodeling
Pathology of Ventricular Hypertrophy
initially is effective as a compensatory mechanism.
concentric hypertrophy over time decreases contractility due to arrangement of sarcomeres + reduces ventricular lumen
increased wall thickness = decreased wall tension therefore reducing contractility and increases metabolic demand of heart
Angiotensin II functions
vasoconstrictor stimulates adrenal medulla to rls aldosterone stimulates PPG to rls ADH stimulates rls of norepinephrine increase thirst response
Aldosterone functions
Increase sodium reabsorption –> increase water retention
Increase potassium excretion
stimulate fibroblast activity in myocardium
Antidiuretic Hormone functions
aka vasopressin
increases water reabsorption
vasoconstrictor
Natriuretic Peptides
ANP –> rls by atrial cells
BNP –> rls by ventricular cells. biomarker for heart failure
released in response to stretch
promote excretion of sodium and water
vasodilator
Types of Heart Failure
Right-side vs. Left-side Diastolic vs. Systolic Reduced Ejection Fraction vs. Preserved Ejection Fraction Acute vs. Chronic Biventricular
S/S of Left Sided HF
Wet cough Reduced ejection fraction Hemoptysis SOB Dizziness, light-headedness Fatigue - gets worse throughout day Hypoxemia --> hypoxic tissue injury Orthopnea Proxysmal Nocturnal Dyspnea Inspiratory crackles
S/S of Right Sided HF
Distended Jugular Vein Peripheral edema Upper abdominal pain Hepatomegaly, splenomegaly Reduced appetite Nocturia
Normal BNP levels
<100 pg/Ml
Normal EF
> 50%
Pleural Effusion
fluid build in in the pleural cavity
Calcium Efflux mechanisms
1) Active calcium pump (req ATP)
2) Sodium-calcium exchanger
Medication classes used for heart failure
Diuretics
Ace-i
Angiotensin II Receptor Blockers (ARB)
Cardiac Glycosides
Spironolactone
potassium sparing diuretic
onset: unknown
peak: 2-3 days
duration: 2-3 days
Spironolactone mechanism
competitive antagonist
blocks aldosterone receptors on the distal convoluted tubule
prevents reabsorption of sodium while saving potassium and hydrogen ions
Captopril
ace inhibitor side fx: chronic dry cough onset: 15-60 min peak: 60-90 min duration: 6-12 hours
Captopril mechanism
antagonist?
inhibits ACE-i activity thereby preventing the conversion of angiotensin I to angiotensin II
promotes vasodilation, decreased sodium reabsorption, decreased release of aldosterone
Angiotensin II effects
major vasoconstrictor -> increases blood pressure
promotes release of ADH from PGH
promotes release of aldosterone from adrenal medulla
increase sodium reabsorption in the kidneys
increases thirst sensation
decreases baroreceptor sensitivity
Losartan
angiotensin II receptor blocker used when ACE-i are contraindicated onset: 6 hours peak: 3-4 weeks duration: 24 hours
Losartan Mechanism
prevents angiotensin II from binding to receptors on smooth muscle –> promotes vasodilation
lowers blood pressure
Bisoprolol
selective beta-1 blocker
onset: 1-4 hours
peak: 2-4 hours
duration: 24 hours
Andrenergic receptors
cell membrane receptors that bind with catecholamines
Beta-1 Receptor Locations
heart
kidneys
fat cells
Bisoprolol Mechanism
prevents epinephrine from binding with beta-1 receptors on the myocardium
reduces contractility, decreases heart rate, promote diastolic filling, reduce O2 demand
reduces cardiac output (decrease work of heart)
decreases renin production by juxtaglomerular cells
Digoxin
cardiac glycoside requires a loading dose onset: 50min-2 hours peak: 2-6 hours duration: 2-4 days
Digoxin mechanism
beta-1 agonist
inhibits the sodium-potassium pump, increasing sodium –> increasing intracellular calcium
promotes increased contractility –> increased cardiac output
increases refractory period at sa/av nodes –> decreased heart rate
Inotropy
agent that affects the force of muscular contractions. can be positive or negative
positive = increase contraction
negative = decrease contraction
Positive inotropic agents
Digoxin
Calcium
BNP
brain natriuretic peptide released from ventricular cells in response to overstretching biomarker of heart failure <100 = normal >400 = heart failure likely
Normal hemoglobin levels for women
117-155 g/L
Normal hemoglobin levels in men
140-173 g/L
Heart Failure Treatment
fluid restrictions (1.5 L/day) daily weigh-ins restrict salt restrict fatty food exercise with rest periods medication tertiary prevention
Recommended Salt for HF Patients
2000 mg/day
Recommended activity levels
30 min of moderate activity daily
Acute cardiac symptoms
chest pain
shortness of breath
dizziness/light-headedness
HF Weight guidelines
no more than 4 lbs in 2 days or 5 lbs in 1 week
Aim of Heart Failure Medication Treatment
Increase preload
Increase contractility
Decrease remodeling
Decrease afterload
Which kidney cell produces renin
juxtaglomerular cells
First Line HF treatment
vasodilators (ACE-i, BNP, ARB) diuretics b-1 antagonists diuretics HCN blockers
Second Line HF treatment
Cardiotonic agents (digoxin) positive inotropic agents
Calcium efflux
sodium-calcium exchanger (3 Na+ for 1 Ca++)
exchange depends on voltage of plasma membrane
positive = more calcium ENTERS cell
negative = more calcium EXITS cell
Proxysmal nocturnal dyspnea
SOB that occurs during sleeping due to fluid accumulation in lungs –> wakes up the patient
HF Diagnostics
Blood tests - check for BNP levels Chest Xray - look at heart size ECG Exercise stress test Angiogram Echo - measures EF
5 Areas of HF
Coronary (Perfusion) Valvular Percardium Myocardium Electrical
Types of cyanosis
Central
Peripheral
Central cyanosis
caused by hypoxemia
decreased O2 in arterial blood
Peripheral cyanosis
caused by tissue consumption of O2
reduced cardiac output, vasoconstriction
Types of cardiomyopathies
dilated
hypertrophy
restrictive
Dilated cardiomyopathy
all four heart chambers dilate
impacts systolic and diastolic function
ventricle walls thin –> decreased contractility
diluted lumen –> excessive preload
Hypertrophic cardiomyopathy
concentric hypertrophy –> narrows lumen
impairs contractility due to overcrowding of sarcomeres
decreases diastolic filling due to narrow ventricular lumen
Restrictive cardiomyopathy
fluid in pericardium/fibrosis decreases cardiac compliance
impairs diastolic filling
