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Medicine 1 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Preload vs. Afterload

A
  • Preload – The level of stretch in the relaxed muscle immediately before it contracts
  • Afterload – The force that the muscle must generate during contraction or the resistance the LV must overcome to circulate blood
  • Increased Preload = Increased Ventricular Filling = Increased SV
  • Increased afterload = increased preload
  • More blood left in the ventricle added to preload – activates Frank-Starling mechanism
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2
Q

Stoke volume, Cardiac output, venous return

A
  • Stroke Volume: volume of blood pumped out with each contraction of the heart
    • Actual volume of whats there
    • Ejection fraction is just the percentage
  • Cardiac Output : volume of blood pumped out by the heart per minute
  • Venous Return : volume of blood returning to the heart via the veins per minute
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3
Q

Compents of stroke volume

A
  • Three components of SV = contractility, preload, and afterload
    • Low CO = low forward flow which gives symptoms of fatigue, weakness, and shortness of breath
  • Relationship between preload, afterload and cardiac output is the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling law/mechanism
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4
Q

Ejection fraction

A
  • Ejection Fraction (EF) is the percentage of blood that is pumped out of your heart to the body with each heartbeat
  • Normal is 50-75%
  • Systolic Dysfunction occurs when the EF falls below 50%
  • Measured by Echo, Nuclear stress test or Cardiac MRI
  • Normal = LVEF 50% - 70%
  • Dysfunction:
    • Mild: LVEF 40-49%
    • Moderate: LVEF 30-39%
    • Severe: LVEF < 30%
  • One of the ways we identify heart failure is to measure the percentage of blood that is pumped out of the heart during each beat.
  • That percentage is called the ejection fraction or pumping function.
  • In a normal heart, 50%–70% of the blood is pumped out during each beat.
  • People with heart failure, due to a problem with their heart’s ability to squeeze blood out, have an ejection fraction of less than 40%.
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5
Q

Defining Heart Failure

A
  • Heart failure is a progressive condition in which the heart has lost the ability to pump enough blood to the body’s tissues, because of poor contraction or poor relaxation.
  • Once you have it, you have it. Theres no going back
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6
Q

Types of Heart failure

A
  • Systolic vs diastolic
  • Left vs right
  • HFpEF vs HFrEF
  • Acute vs chronic
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7
Q

Systolic heart failure

A
  • (Pump Problem)
    • Inability of heart to contract enough to provide blood flow forward to the body.
    • Problem of Contraction and Ejection of Blood
  • Heart muscle is weakened and can’t squeeze as well - less blood is pumped out of the ventricles
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8
Q

Diastolic heart failure

A
  • Filling problem
    • Inability of left ventricle to relax normally resulting in fluid backing up to the lungs
    • Involves a thickened and stiff LV muscle
    • Problem with heart relaxation and filling with blood
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9
Q

Left Sided heart failure

A
  • A big heart does not mean more efficient, means less efficient
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10
Q

Right sided heart failure

A
  • Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure. LHF –>** **RHF
  • Elevated right-heart filling pressures right atrium and ventricle – without evidence of pulmonary congestion.
  • Less common to have RHF only.
  • Causes of RHF:
    • Cor Pulmonale, Chronic PEs, COPD, Cystic Fibrosis.
    • Pulmonary HTN – Sarcoidosis
    • Fibrotic Lung diseases
  • If you see that the right side of the heart is really big and the left is normal and theres no pulmonary disease, that’s really rare à this is pulmonary HTN and this is right sided heart failure
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11
Q

HFrEF

A
  • HFrEF (EF <40%) <= Systolic HF
    • Heart Failure REDUCED Ejection Fraction
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12
Q

HFpEF

A
  • HFpEF (EF >50%) <= Diastolic HF
    • Heart Failure PRESERVED Ejection Fraction
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13
Q

Causes of Acute Decompensation of HF

A
  • Noncompliance with diet or therapy
  • Sepsis, Acute Illness (coxsackie, HIV, Influenza).
    • Once this person gets over the sepsis, they can go back to having normal heart function and can be completely fine
  • New onset arrhythmias (A. Fib)
  • Pulmonary Embolus
  • Anemia
  • Pregnancy
  • Hyper/hypothyroidism
  • Acute Coronary Syndrome
  • Uncontrolled hypertension
  • Toxins: Alcohol, cocaine
  • NSAIDS
  • Holiday Heart
  • Valvular dysfunction
  • Idiopathic
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14
Q

Chronic HF risk factors and causes

A
  • CAD - most prevalent
  • Cigarette smoking/ Nicotine Use
  • Hypertension
  • Obesity
  • Diabetes
  • CKD
  • Cardiotoxins
    • Alcohol, Cocaine, Cancer chemotherapeutics.
  • Valvular heart disease
    • Rheumatic Fever
  • Structural heart disease
    • Dilated Cardiomyopathy
    • Hypertrophic Cardiomyopathy
  • May develop over time (HTN, Alcohol, cocaine, CKD)
  • RF’s lead to the structural disease
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15
Q

Epidemiology of HF

A
  • 20% of hospital admissions for those over 65yo
  • About 5.1 million people in the United States have heart failure.
  • 1 in 5 have a lifetime risk of developing HF.
  • One in 9 deaths in 2009 included heart failure as contributing cause.
  • About half of people who develop heart failure die within 5 years of diagnosis.
  • Heart failure costs the nation an estimated $32 billion each year. This total includes the cost of health care services, medications to treat heart failure, and missed days of work.
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16
Q

Prevalence of HF

A
  • Men > Women
  • Increases with age
  • Every ten years of your life, something works a little bit less or takes a little bit longer to work à same with your heart
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17
Q

Pathologic Progression of Heart Failure

A
  • Neurohormonal Stimulation = RAAS system – how does this get activated?
    • Renal hypoperfusion - release of renin - produces Angio 1 - produces Angio 2
  • What does Angio 2 then do?
    • causes BP increase & release of aldosterone –> which then causes Na & H20 retention = increase preload/ volume.
  • Now there is a pump that isn’t working well with more volume to push. So is the heart able to do more or less??
  • It does less - decrease cardiac output!
  • Angiotensin II also stimulates cardiac cell growth, stimulates hypertrophy.
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18
Q

Pathophysiology of HF - neurohumoral feedack

A
  • Understand the Renin-Angiotensin-Aldosterone System
  • Sympathetic nerves
  • Compensatory mechanisms….ultimately make HF worse!
  • Understanding this serves as rationale for drug therapy
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19
Q

Angiotensin II

A
  • stimulates cardiac cell growth which leads to Hypertrophy
    • Angiotensin II also stimulates cardiac cell growth, stimulates hypertrophy.
    • This slide presents some examples of adverse remodeling. You’ll see the normal heart at the top. This might be the Stage A patient, the hypertensive or diabetic patient who has not yet developed a structural abnormality of the heart. For example, this may be the hypertensive patient who has not yet developed left ventricular hypertrophy or the coronary artery disease patient who has not yet had a myocardial infarction.
    • There are really two pathways for adverse remodeling. One is a hypertrophic pathway and the other a dilated pathway. So in response to chronic pressure overload, one may progress to concentric left ventricular hypertrophy associated with normal cavity size but a stiff ventricle and diastolic dysfunction and ultimately the onset of diastolic heart failure, or one may go down the pathway of progressive LV dilation and dysfunction associated with the development of a globular heart with systolic dysfunction with mitral regurgitation, and ultimately the onset and progression of symptomatic heart failure as well.
20
Q

Sympathetic activation

A
  • Cardiac stimulation – norepinephrine beta1 adrenoreceptors increases HR and inotropy (contractility)
    • Ventricular hypertrophy, arrhythmias, etc.
  • Peripheral vascular constriction – norepinephrine via alpha2 adrenoreceptors cause vasoconstriction
    • Arterial vasoconstriction maintains BP but, increases afterload
    • Venous vasoconstriction increases venous return (preload) in an attempt to maintain SV
  • Norepi not enough to restore normal inotropy d/t the ventricular dysfunction, and continues to stimulate the system, never getting back to NL.
  • Arterial and venous vessels richly innervated by sympathetic nervous system.
  • Increase venous pressure leads to pulmonary edema.
21
Q

Pathophysiology takeaways

A
  • Cardio-Renal syndrome
    • Important interactions between heart disease and kidney disease.
    • Bidirectional – Acute or chronic dysfunction in one system can lead to acute or chronic failure in the other.
  • Low CO = Fatigue, SOB, weakness.
    • Not all SOB from HF is d/t pulmonary edema
  • Kidneys Unhappy -> Causes Water Retention + Vasoconstriction -> Ventricular Hypertrophy => Heart Failure
  • Nor Epi β1receptors increase HR
  • Nor Epi α1receptors cause vasoconstriction
22
Q

Symptoms of HF

A
  • Orthopnea : Sleeping in a chair/ or on multiple pillows - Are you able to sleep lying flat? How many pillows?
  • PND (paroxysmal nocturnal dyspnea) - Ever wake up short of breath?
  • SOB / DOE - Exertional dyspnea/Decreased exercise tolerance: careful may be asymptomatic but, how much do they move around?
  • Fatigue
  • CP
  • Palpitations
  • Edema
  • Insomnia
  • Change in Exercise capacity
  • Poor appetite or recent weight gain ?
  • Abdominal distention/bloating? RUQ tenderness?
  • Sudden Cardiac Death
23
Q

Clinical presentation HF: physical findings

A
  • Vital signs and appearance: BP, HR (regular or irregular), pulsus alternans
    • Resting sinus tachycardia
    • narrow pulse pressure
    • diaphoresis or edematous
    • peripheral vasoconstriction
    • All 4 together are Indicative of decreased CO
  • Pulsus alternans alternating strong and weak pulses. The heart is using two beats. BIG preload full heart, strong squeeze, second beat weak fill, less preload, less force.
    • S3, S4
    • Murmur
    • Diminished S1
    • Parasternal Lift
    • Gallops
    • Enlarged/ sustained LV impulse
    • Hypotension
  • Crackles
  • Basilar rales
  • Cough
  • Narrow Pulse Pressure
  • JVD
  • Ascites
  • Peripheral Edema
  • Anasarca
24
Q

Workup HF: testing

A
  • Transthoracic Echocardiogram:
    • Ventricular function = EF!
    • wall motion, wall thickness, valve function, atrial enlargement
  • Chest X-ray: cardiomegaly, pulmonary edema
  • Kerley B Lines- short parallel lines at the lung periphery near the bases
  • Batwing or Butterfly shadow – enlarged hila and alveolar edema
  • Water bottle or boot shaped heart
  • Ultrasound of heart = echo (TTE)
  • EKG: arrhythmias, LVH, LAE, widened QRS complex.
25
Q

Echo

A
  • dilated cardiomyopathy with HF
    • The images are upside down in ECHO, just know that
26
Q

Kerley B lines on CXR

A

thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs

27
Q

Workup HF: select patients

A
  • REFERRAL
    • Labs for hemochromatosis, HIV, pheochromocytoma, scleroderma, amyloidosis, Sarcoidosis
    • Stress testing: Stress echo, Nuclear (Adenosine or Lexiscan) testing.
    • Cardiac MRI: Rarely done –Aneurysmal LV, Restrictive CMP vs. Pericarditis
    • Cardiac cath/ Angiogram: Strong suspicion of MI/ Ischemia
    • ICU Admit: Invasive hemodynamic monitoring for those in respiratory distress, renal decline, low BP’s, require parenteral agents
    • Endomyocardial biopsy: RARE! Only if a specific diagnosis would influence therapy.
28
Q

Tx diastolic HF

A
  • ​No consensus yet, ongoing studies
  • Systolic and diastolic BP should be controlled according to guidelines
  • Control their HR (Lower the better)
  • Diuretics should be used for relief of symptoms due to volume overload - THEY DON’T DO ANYTHING FOR MORBIDITY OR MORTALITY
  • Coronary revascularization is reasonable in patients with CAD that is symptomatic or demonstrable myocardial ischemia
  • Manage AF (atrial fibrillation) preferably rhythm control > rate control
  • Use of BB, ACE-I, ARB’s in those with hypertension is reasonable.
  • ARBs might be considered to reduce hospitalizations
  • Biggest sx of heart failure = SOB
  • Side effect of ACE inhibitors = cough
29
Q

Systolic HF tx: medications

A
  • Medication Types
    • Ace inhibitor (angiotensin-converting enzyme) – expands blood vessels which lowers blood pressure, neurohormonal blockade
    • ARB (angiotensin receptor blocker) – similar to ACE inhibitor – lowers blood pressure
    • Beta blocker – reduces the action of stress hormones and slows the heart rate
    • Digoxin – slows the heart rate and improves the heart’s pumping function (EF)
    • Diuretic – filters sodium and excess fluid from the blood to reduce the heart’s workload
    • Aldosterone blockade – blocks neurohormonal activation and controls volume
30
Q

Rationale for Medications

A
  • Improve Symptoms
    • Diuretics (water pills)
    • Digoxin
  • Improve Survival
    • Betablockers
    • ACE-inhibitors
    • Aldosterone blockers
    • Angiotensin receptor blockers (ARB’s)
  • If you see your weight increase 3 lbs in a day or 5 lbs in a week, increase diuretic to BID until weight comes down
31
Q

Lifestyle Changes for HF

A
  • Eat a low sodium low fat diet à sodium increases blood pressure, causes fluid retention
  • Lose weight - extra weight can put a strain on the heart
  • Stay physically active - exercise can help reduce stress and blood pressure
  • Reduce or eliminate alcohol and caffeine à alcohol and caffeine can weaken an already damaged heart
  • Quit smoking - smoking can damage blood vessels and make the heart beat faster
32
Q

Device therapy for HF

A
  • CardioMems (Abbott)
  • ICD and CRT Devices
    • (Boston Scientific, Medtronic, St Jude, Abbott, Biotronik…)
    • Pulmonary Artery Pressure Monitor
    • Prevention of HF admissions
33
Q

HF and sudden cardiac death

A
  • Your heart suddenly goes into a very fast and chaotic rhythm and stops pumping blood
  • Caused by an “electrical” problem in your heart
  • SCD is one of the leading causes of death in the U.S. – approximately 450,000 deaths a year
  • Patients with heart failure are 6-9 times as likely to develop sudden cardiac death as the general population
  • Sudden Cardiac Arrest is as scary as it sounds. It means that your heart suddenly starts beating very fast and quivers instead of beating in a regular and organized way. No blood gets pumped, and you will die unless you get treatment within minutes. We’ll talk more about treatments in a moment.
  • Unlike a heart attack, SCA is caused by an electrical problem in your heart.
  • SCA can strike without warning, and there are no symptoms.
34
Q

Device therapy for stage C systolic HF

A
  • (EF <35%)
    • ICD (Implantable cardiac defibrillator) recommended for primary prevention of sudden cardiac death (SCD) in patients with non-ischemic dilated cardiomyopathy (DCM) or ischemic heart disease at least 40 days post-MI with LVEF of 35% or less on chronic optimal therapy.
    • CRT (cardiac resynchronization therapy) aka Bi-ventricular pacing for those with EF of 35% or less and a widened QRS with no LBBB.
    • Life Vest: removable external cardiac defibrillator à Bridge to ICD or increasing
35
Q

End Stage/Stage 4 tx options

A
  • LVAD
    • Research has shown the HeartMate II LVAD brings an immediate and sustained reduction of heart failure symptoms4** and increases patients’ survival rates compared with medical management alone.3,4 In fact, many patients live more than 10 years with the device.6
  • Heart transplant
36
Q

end diastolic volume vs end systolic volume

A
  • EDV = maxiumum blood in the ventricle before emptying
  • ESV = blood left in the ventricle after its squeezed all it can - doesnt get to 0 because its a closed liquid circuit
37
Q

Frank starling law/mechanism

A

relationship between preload, afterload and aCO is the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return

38
Q

Heart failure ejection fraction

A

less than 40%

39
Q

what can cause myocardial injury?

A
  • CAD
  • HTN
  • DM
  • Cardiomyopathy
  • Valvular dz
40
Q

what occurs as a result of myocardial injury?

A
  • pathologic remodeling
  • neurohormonal stimulation, myocardial toxicity
  • low ejection fraction
  • chronic HF
  • pump failure
  • death
41
Q

symptoms of myocardial injury

A
  • dyspnea
  • fatigue
  • edema
42
Q

decrease CO compensation

A
  • decreased carotid sinus firing
    • increase sympathetic discharge
    • increase force, rate, preleoad, afterload
  • decreased renal blood flow
    • increase renin release
    • increase angio II
    • increase preload, afterload, remodeling
  • result of increased force, rate, preload: increase CO via compensation
43
Q

Work up HF: laboratory

A
  • Laboratory:
    • CBC: Anemia, infections, pancytopenia, other blood disorders
    • Chemistry panel: renal function, electrolytes including Ca++, K, Mg. Hyponatremia common
    • Liver function tests: Liver damage from hepatic congestion
    • Lipid panel: CAD, atherosclerosis evaluation
    • TSH
    • Some of these is to rule other things out, not necessarily to diagnose HF
44
Q

Workup HF: Biomarkers

A
  • BNP, NT-proBNP, Can be useful in diagnosing, and tracking medical therapies, establishing prognosis or disease severity in chronic HF
  • This does not always equate to the sxs of the person in front of you
  • however it may not be as specific in patients who are old or have COPD
  • Cardiac enzymes: Troponin, CK-MB – often elevated by HF itself
45
Q

Modified Framingham Criteria

A
  • Major
    • PND, orthopnea, elevated JVP, rales, S3, cardiomegaly on CXR, pulmonary edema on CXR
  • Minor
    • Bilateral edema, nocturnal cough, DOE, hepatomegaly, pleural effusion, tachycardia (HR >= 120)
  • Need 2 major or 1 major and 2 minor not attributable to other causes to qualify for diagnosis of HF
46
Q

HF classification

A
  • ACCF/AHA stages
    • A - at high risk for HF but without structural heart disease or sxs of HF
    • B - structural heart dz but w/o signs or sxs of HF
    • C - structural heart disease with prior or current sxs of HF
    • D - refractory HF requiring specialized interventions
  • NYHA functional classification
      1. no limitation of physical activity. ordinary physical activity doesnt cause sxs of HF
      1. slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in sxs of HF
      1. marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes sxs of HF
      1. unable to carry on any physical activity w/o sxs of HF, or sxs of HF at rest

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