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Medicine II > heart fialure > Flashcards

heart fialure Flashcards

1
Q

the level of stretch in the relaxed muscle immediately before it contracts

A

preload

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2
Q

: volume of blood pumped out by the heart per minute

A

Cardiac Output

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3
Q

volume of blood returning to the heart via the veins per minute

A

Venous Return

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4
Q

volume of blood pumped out with each contraction of the heart

A

Stroke Volume:

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5
Q

volume of blood returning to the heart via the veins per minute
80% blood volume in veins when ambulatory.

A

Venous Return

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6
Q

volume of blood pumped out by the heart per minute

A

Cardiac Output

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7
Q

Three components of SV

A

= Contractillity, preload, and afterload.

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8
Q

franks sterling’s law

A

stroke volume is dependent on your venous return

rubberband analogy

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9
Q

% of blood that is pumped out of the hear to the body

A

ejection fraction

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10
Q

what is normal ejection fraction

A

50-75%

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11
Q

mild ejection fraction

A

wheN the LVEF falls before 50% and is above 40%

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12
Q

moderate ejection fracrion

A

LVEF 30-39%

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13
Q

progressive condition in which the heart has los the ability to pump to the tissues because of what two general physiological causes

A

poor contraction or poor relaxation

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14
Q

Inability of heart to contract enough to provide blood flow forward to the body.
Problem of Contraction and Ejection of Blood

A

systolic heart failure

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15
Q

Inability of left ventricle (LV) 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.

A

Diastolic Heart Failure (Filling Problem)

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16
Q

reasons for left sided systolic heart failure

A

ischemic heart disease
long standing hTN
dilated cardiomyopathy

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17
Q

when right ventricle looks bigger than the left

A

that is pulmonary HTN and right sided heart failure (usualy have 18months to live)

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18
Q

most common reasons for right sided heart failure

A

cor pulmonale or left sided heart failure

shunt

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19
Q

why would you see diastolic heart failure on the left side

A

hypertrophy causeing less room

can be cause by aortic stenosis and start as systolic

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20
Q

HErEF

A

heart failure reduced EF

<40% = systolic hF

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21
Q

HFpEF

A

> 50% will let you know it is diastolic HF

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22
Q

causes of ACUTE decompensation of HF

A

Noncompliance with diet or therapy
Sepsis, Acute Illness (coxsackie, HIV, Influenza).
New onset arrhythmias (A. Fib)
Pulmonary Embolus: everything this getting backed up

Anemia
Pregnancy
Hyper/hypothyroidism
Acute Coronary Syndrome
Uncontrolled hypertension
Toxins: Alcohol, cocaine 
NSAIDS
Holliday Heart
Valvular dysfunction 
Idiopathic
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23
Q

most common shunt

A

atrial septal defect

foramen ovale

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24
Q

JVD would be a symptom of what type of HF

A

right sided heart failure

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25
Q

asceitis would be a symptom of

A

right sided heart failure

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26
Q

risk factors for HF

A 
CAD
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 i.e. HTN, Alcohol, cocaine, CKD.

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27
Q

what two structural changes do we see with heart failure

A

muscle wall stretches and thins

or muscle wall thickens and becomes ischemic

both lead to heart cells becoming irritated and arrhythmia

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28
Q

how many people will develop heart failure

A

1/5

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29
Q

how many people will die of heart failure

A

1/9

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30
Q

myocardial injury can be due to was dx

A 
CAD
HTN
DM
Cardiomyopathy
valvular dz
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31
Q

symptoms of low ejection fraction

A

dyspnea, fatigue, and edema

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32
Q

angiotensinogen is found in the

A

liver and is the precursor to angiotensin I

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33
Q

angiotensin II is responsible for

A

ADH release at the cite of the pituitary
arteriole vasoconstriction
aldosterone secretion in the adrenals
tubular NA+ cl- reabsorption and K+ excretion, H20 retention
and increases SNS activity

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34
Q

ADH is responsible for

A

H20 absorption

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35
Q

how do you manage activation of SNS from RAAS

A

Beta blocker

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36
Q

how do you manage aldosterone release in RAAS

A

spironolactone

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37
Q

inotropy is synonymous w/

A

Contractility

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38
Q

Norepinephrine via ______recptors cause vasoconstriction

A

Norepinephrine via α1-adrenorecptors cause vasoconstriction

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39
Q

Arterial vasoconstriction maintains BP but, increases ______

A

Arterial vasoconstriction maintains BP but, increases Afterload.

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40
Q

Venous vasoconstriction increases______in an attempt to maintain SV.

A

Venous vasoconstriction increases venous return (Preload) in an attempt to maintain SV.

41
Q

Increase venous pressure leads to _________

A

Increase venous pressure leads to pulmonary edema.

42
Q

______ receptors increase HR

A

Nor Epi β1receptors increase HR

43
Q

________receptors cause vasoconstriction

A

Nor Epi α1receptors cause vasoconstriction

44
Q

clinical presentation

A 
Orthopnea : Sleeping in a chair/ or on multiple pillows
PND (paroxysmal nocturnal dyspnea)
SOB / DOE
Fatigue
CP
Palpitations
Edema
Insomnia
Change in Exercise capacity
Poor appetite  or recent weight gain ?
Abdominal distention/bloating? RUQ tenderness?

Sudden Cardiac Death

45
Q

pulmonary HTN is seen as what pressure in the lungs

A

> 25 mmHg

46
Q

pulses alterans

A

variable pulse

usually really strong and then not so strong

47
Q

acute lung disorder that can lead to HF

A

cor pulmonale

resulting from pulmonary ebolism

48
Q

what might you see in a pt with HF

A

Displaced PMI? Diffuse or focal? Lift? Heave? Double tap?

49
Q

“Ken-tuc-ky” is used to distinguish what sound associated with HF

A

S3 gallop (“Ken-tuc-ky”),

50
Q

anascara

A

full body edema

will present in flanks while lying down

51
Q

pulmonary HTN can be caused by

A

damage to the lung tissue (COPD)
damage to vessels
something that affects spine or rib cage

52
Q

what are some examples of damage to the pulmonary vessls that can result on pulmonary HTN and cor pulmonale

A

chronic thromboembolisms

recurrent blood clots

53
Q

labs for suspected

A

cbc: rule out anemia (can’t add anything into the system)

chem panel : looking at renal function, electrolytes including Ca++, K, Mg. Hyponatremia common

Liver function tests: Liver damage from hepatic congestion

BMP
TSH

54
Q

Biomarkers you would want to check in a pt suspected of HF

A

BNP, NT-proBNP, Can be useful in diagnosing, and tracking medical therapies, establishing prognosis or disease severity in chronic HF
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.

55
Q

What would you be looking for on an EKG

A

arrhythmias, LVH, LAE, widened QRS complex (if wide difficulty with electricity getting through the heart muscle).

56
Q

besides EKG and lab work, what other diagnostic test would you want to order and what would you be looking for

A

Chest X-ray:

cardiomegaly, pulmonary edema
Kerley B Lines- short parallel lines at the lung periphery near the bases that indicate pulmonary congestion

Batwing or Butterfly shadow – enlarged hila and alveolar edema
Water bottle or boot shaped heart

57
Q

echo image of a heart is seen as normal

A

with atrium on the bottom

58
Q

how to diagnose HF

A

two major or two minor and one major

59
Q

major criteria for modified framingham (7)

A 
PND: relieved with walking for a minute with rule of OSA
Orthopnea
elevated JVP
Rales
S3
cardiomegaly on CXR
PE on CXR
60
Q

minor Framingham Criteria (6)

A 
bilateral edema
nocturnal cough
dyspnea on ordinary exertion
hepatomegaly
pleural effusion
tachycardia (HR>120)
61
Q

management of 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
Coronary revascularization is reasonable in patients with CAD that is symptomatic or demonstrable myocardial ischemia
Manage AF 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

62
Q

HF and HTN waht tx

A

ACE or ARB (not both)

63
Q

why, physiologically do ACE’s cause cough

A

above the lung

ARB below

64
Q

biggest sx of HF

A

shortness of breath

65
Q

Expands blood vessels which lowers blood pressure, neurohormonal blockade

A

ACE inhibitor (angiotensin-converting enzyme)

66
Q

ACE inhibitor (angiotensin-converting enzyme)

A

ARB (angiotensin receptor blockers)

67
Q

Reduces the action of stress hormones and slows the heart rate

A

Beta-blocker

68
Q

Slows the heart rate and improves the heart’s pumping function (EF)

A

Digoxin

69
Q

why would you use digoxin

A

on a little bit of a BB but still need more HR control

70
Q

Filters sodium and excess fluid from the blood to reduce the heart’s workload

A

Diuretic

71
Q

Blocks neurohormal activation and controls volume

A

Aldosterone blockade

spironolactone but this a potassium sparing blocade

72
Q

when would you increase Lasixs (furosemide) in a pt who is gaining fluid

A

5lbs in a week or 3lbs in a day

73
Q

what dies changes do you want to see in a pt with HF

A 
low sodium
low fat
no alcohol or caffeine 
quit smoking 
lose weight
74
Q

best tool for measuring HF

A

scale

75
Q

Abbott device

A

pulmonary artery pressure reader

measuring pressure that is going into the lung

76
Q

what is the time window you want to be mindful of following a MI

A

90 days

cna vest cardio defibrillator

77
Q

Apical ballooning with NORMAL coronaries and wall motion abnormalities

A

Takotsubo / Broken Heart Syndrome:

78
Q

most common ischemic cardiomyopathy

A

heart attack

79
Q

most common non ischemic cardiomyopathy

A

alcohol

80
Q 
Hypertension
Arrhythmias
Myocarditis (viral)
Alcohol – most common Non-Ischemic 
Chemotherapy
Pregnancy
Connective tissue disease
Sepsis

all reasons for what type of cardiomyopathy

A

dialated

81
Q

Infiltrative disease : Amyloidosis, Sarcoidosis
Non-dilated, non-hypertrophic, impaired filling
Familial
Hemochromatosis, Scleroderma
Cancer

are all associated with what type of cardiomyopathy

A

restrictive

82
Q

Dilated CMP Sxs

A 
Dyspnea : DOE / SOB
Edema
Orthopnea
PND
Fatigue
S3
MV Murmur
83
Q

Hypertrophic CMP (HOCM) sxs

A 
Syncope
Sudden Cardiac Death in Young Person
light headed after typical workout routine 
Dyspnea
Fatigue
Angina
Orthopnea
Palpitations – Atrial Fib
S4  on Physical Exam
84
Q

Restrictive sxs

A 
Dyspnea on Exertion
Symptoms of Right Heart Failure
Fatigue
S3 or S4
Mitral Valve Regurg Murmur
85
Q

dilated CMP diagnostics

A

EKG
NSSTC, AV Blocks, Ventricular Ectopy

Echo
Dilated LV, Low CO 
Reduced or Preserved EF
Enlarged Atria
MV Regurg or Insufficiency?
CXR
Cardiomegaly
Pulmonary Edema

Stress Echo/ Thallium
Angiogram
Labs – find the cause!
BNP?

86
Q

HCOM diagnostics

A 
EKG
LVH, NSSTC, Septal Q waves 
Echo
LVH! 
Asymmetric Septal Hypertrophy
Small LV Volume
Diastolic Dysfunction
CXR
Not remarkable
Cardiac MRI
87
Q

RESTRICTIVE diagnostic tests

A 
EKG
Low Voltage non specific changes
Echo
Large RV, Stage 4 Diastolic Dysfunction
Endomysial Biopsy
88
Q

TX of DILATED CMP

A

Tx Heart Failure
Tx Underlying Heart Disease/ Cause
Abstain from ETOH and Sodium
Severity of HF? – ?ICD/ LVAD/ Heart Transplant

89
Q

RESTRICTIVE CMP tx

A

Diuretics – symptom control
PAH Drugs
( Sildenafil, Letairis, Tracleer, Flolan…etc)
Heart Transplant

90
Q

HCOM tx

A

Beta Blockers or CCBs
Surgical Myomectomy or Ablation (cutting of the muscle)
ICD for prevention of SCD
Valve Replacement (MVR) if indicated

91
Q

reversible cardiomyopathy with a clinical presentation that mimics an acute coronary syndrome (ACS).

A

Takotsubo / Broken Heart CMP

92
Q

normal arteries in a pt with acs seen with transient ST elevation looks like an MI

A

Takotsubo / Broken Heart CMP

93
Q

TX of Takotsubo / Broken Heart CMP

A

sx control and supportive care

94
Q

HCOM is a 100% genetic disorder of what ventricle

A

left

95
Q

AHA focuses on what for a sports physical

A

on medical history (family and personal) and physical examination

96
Q

The European Society of Cardiology for sports physicals

A

recommends a pre participation screening strategy that comprises family and personal history, physical examination, and 12-lead ECG

97
Q

Cardiovascular Screening History for Preparticipation Examinations: Critical Questions

A

Exertional chest pain or discomfort, or shortness of breath?
Exertional syncope or near-syncope, or unexpected fatigue?

Past detection of cardiac murmur or systemic hypertension?

Known family history of hypertrophic cardiomyopathy, other cardiomyopathies, long QT syndrome, Marfan syndrome, significant dysrhythmias?

Family history of premature death or known disabling cardiovascular disease in a first- or second-order relative younger than 50 years? (More concern if younger than 40 years.)

98
Q

valsalva maneuver will do what to a murmur in Hypertrophic cardiomyopathy

A

intensity of the ejection systolic murmur promptly declines because of an increased left ventricular volume and arterial pressure, which increase the effective orifice size of the outflow tract; the carotid pulse upstroke remains sharp, and the volume may increase.

99
Q

For the above patient, which test would be most helpful in assessing this patient’s murmur and risk for sudden cardiac death?

A

: Stress Echo

Medicine II (21 decks)

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