Heart Failure- Lecture Flashcards
Congestive heart failure by definition is _
Congestive heart failure by definition is the inability of the heart to pump blood throughout the body, leading to congestion and decreased perfusion
Systolic heart failure means _
Systolic heart failure means loss of contractile strength which results in low ejection fraction
* Failure of the left ventricle
Diastolic heart failure is _
Diastolic heart failure is a problem filling the heart; our ejection fraction will often be normal
High output heart failure means that _
High output heart failure means that our cardiac output exceeds metabolic demand
Uncompensated heart failure is _
Uncompensated heart failure is when symptoms are worsened or exasterbated
* Precipitating factors: infection, arrhythmias, high salt diet, hypertension, MI
Systolic heart failure most commonly results from _ or _
Systolic heart failure most commonly results from cardiomyopathy or ischemic heart disease
Systolic heart failure –> low ejection fraction –> high EDV –> hypoperfusion to organs including the kidney –> ?
Systolic heart failure –> low ejection fraction –> high EDV –> hypoperfusion to organs including the kidney –> compensatory activation of the sympathetic nervous system and renin release from the juxtaglomerular apparatus
* Increased levels of renin, angiotensin, and aldosterone
* Vasoconstrictive effect of angiotensin II causes increased peripheral resistance
* Mineralocorticoid effects of aldosterone causes fluid retention and metabolic alkalosis
Diastolic heart failure is a problem of decreased _ and is most commonly a result of _
Diastolic heart failure is a problem of decreased compliance and is most commonly a result of hypertrophy
In diastolic heart failure, ejection fraction will be _ and EDV will be _
In diastolic heart failure, ejection fraction will be normal and EDV will be normal
(True/False) Normal BNP excludes congestive heart failure
True; Normal BNP excludes congestive heart failure
Name 3 cardinal signs of right heart failure
Right heart failure:
1. Distended jugular veins: due to elevated right atrial pressure
2. Hepatomegaly: due to elevated IVC pressure
3. Peripheral edema: due to elevated capillary bed pressure
If a patient has edema but clear lung sounds; they most likely have (left/ right) heart failure
If a patient has edema but clear lung sounds; they most likely have right heart failure
Three cardinal signs of left heart failure
Left heart failure:
1. Pulmonary rales (“crackles”): elevated pulmonary capillary pressure (from high LVEDP)
2. S3 or S4: increased LV pressure, decreased compliance
3. Orthopnea: increased venous return
Orthopnea is _
Orthopnea is breathlessness when lying flat
* Waking up at night from orthopnea is called paroxysmal nocturnal dyspnea
Patients with hypertrophy will have _ ECG findings
Patients with hypertrophy will have big, spikey S waves in V1 and big, spikey R waves in V5 and V6
What causes paroxysmal nocturnal dyspnea?
Paroxysmal nocturnal dyspnea occurs when the excess fluid below the waist has a chance to travel back up to the lungs after lying down
Describe the pathway of fluid build up in right heart failure
Fluid accumulates in RV –> RA –> IVC and SVC –> Systemic veins –> includes liver
Hepatomegaly, ascites, and even cirrhosis of the liver can all result from (left/right) sided heart failure
Hepatomegaly, ascites, and even cirrhosis of the liver can all result from right sided heart failure
Normal CVP/ JVP is _
Normal CVP/ JVP is less than or equal to 7 mmHg
* It is either only barely visible above the clavicle or not visible at all
Draw a pressure volume loop that represents a decrease in contractility
We see a decrease in the End Systolic Pressure Volume Relationship slope
* Decreasing contractility will also decrease stroke volume
Explain the change to the variables in LaPlace as we compensate for heart failure
When we are in systolic heart failure, our LVEDV is very large –> this means radius is big in Laplace equation –> Pressure * radius / 2 * wall thickness –> to try to prevnent wall stress from getting to large we will increase the wall thickness
Ultimately we compensate for large LVEDV by increasing wall thickness which is why the heart hypertrophies
Heart failure begins with a change in _
Heart failure begins with a change in contractility
* Contractility decreases –> higher preload is required to increase stroke volume via Frank-Starling Mechanism –> hypertrophy –> remodeling
Define pathological and physiological hypertrophy
- Physiological hypertrophy involves an addition of myofibrils (sarcomeres) in parallel aka due to development, pregnancy, exercise
- Pathologic hypertrophy involves an addition of myofibrils (sarcomeres) in parallel aka concentric hypertrophy due to pressure loading; involves fibrosis and sometimes cardiac dysfunction
Explain cardiac dilation in the context of heart failure
Patients with dilated cardiomyopathy or myocardial infarctions will experience cardiac dilation aka addition of myofibrils (sarcomeres) in series which is called eccentric hypertrophy
* Some patients who have concentric hypertrophy can experience remodeling to cardiac dilation
* Involves fibrosis, myocyte death, cardiac dysfunction (MI)
Explain the role of SNS involvement in heart failure
The body responds to the decreased perfusion in the organs by increasing SNS –> this acts on B1 receptors to increase heart rate (chronotropy) and contractility (inotropy) –> NE also acts on receptors in the kidney to increase renin release and promote fluid retention
* Note that NE also activates venous alpha1 receptors to vasoconstrict –> decrease venous compliance and increase venous return
Acutely, SNS compensation is adaptive and can improve cardiac output in a heart that has impaired contractility; what is the problem long term?
The heart is not designed to withstand this kind of SNS activation long term
* Chronic beta stimulation will lead to eventual downregulation of B1 receptors
* We also end up putting too much oxygen demand –> myocardial injury
* We end up with energy starvation, cardiomyocyte death, ventricular arrhythmias, fibrosis
Ultimately NE and E are great for acute responses but are toxic with sustained exposure
What is the problem with activating RAAS in heart failure?
We are increasing RAAS with the hopes of helping our cardiac ouput; however, our contractility is still crap and we are still not perfusing well
* Decreased CO decreases renal perfusion which turns on RAAS –> cycle just continues –> negative feedback is disrupted
After myocardial insult we get cardiac remodeling with involves _
After myocardial insult we get cardiac remodeling with involves:
* Big cardiomyocytes
* Cardiomyocytes that have less myofibrils, abnormal Ca2+
* Apoptosis and necrosis
* Fibrosis
* Poor heart function
* Heart failure –> death
When we triage heart failure we want to know _ and _ to determine how to treat (outpatient, inpatient, ICU)?
When we triage heart failure we want to know cardiac ouput and pulmonary capillary wedge pressure (volume status) to determine how to treat (outpatient, inpatient, ICU)?
* Poor cardiac output = cold patient = ICU
* Warm and dry patient = outpatient
* Warm and wet patient = inpatient diuretics needed
Diuretics can have beneficial hemodynamic effects through _ which helps alleviate the symptoms of HF without decreasing _
Diuretics can have beneficial hemodynamic effects through decreasing preload (LVEDV) which helps alleviate the symptoms of HF without decreasing stroke volume
Which heart failure therapies reduce mortality?
Reduce mortality:
* ACE inhibitors
* ARBs
* ARNIs
* Aldosterone inhibitors
* Beta blockers
* Sglt2 inhibitors
Digoxin is an old school medication that was often used with the intension of _ ; it works via _ mechanism
Digoxin is an old school medication that was often used with the intension of increasing contractility ; it works via Na/K ATPase inhibition –> this blocks the ability of Na/Ca2 antiporter to extrude calcium
