Cv System Exam 2_18: Heart Failure

Front 1

ACEi primary AE:

Back 1

dry hacking cough

Front 2

Stage A

Back 2

ACEi, ARBs

Front 3

Stage B (structural Dz, asymptomatic)

Back 3

ACEi, ARBs, Beta blockers

Front 4

Stage C (structural Dz and symptomatic)

Back 4

ACEi, ARBs, Beta blockers, Diuretics, Digoxin, Aldosterone antagonists

Front 5

Stage D

Back 5

All ABC plus inotropic IV, mech assist, transplant, hospice

Front 6

clinical syndrome

Back 6

pump failure, inadequate tissu/organ perfusion
--Body senses this and initiates multiple neurohormonal responses to adjust.
To keep us in balance
To keep our ph 7.35-7.45
To maintain homeostasis

Hint 6

Although initially helpful this cascade of compensatory responses rapidly becomes maladaptive and leads to clinical deterioration.

1) Aggravating ischemia

2) Causing abnormal fluid accumulation.

Front 7

systolic HF

Back 7

L-sided HF
Backs up into lungs
Ischemic
CAD

Front 8

diastolic HF

Back 8

R-sided HF
Backs up into abdomen/legs
Non ischemic
Everything else

Front 9

most common cause of HF

Back 9

LVSD caused by → CAD or idiopathic dilated
cardiomyopathy, valvular HD, toxins (alcohol,
Doxorubicin) ,congenital, pregnancy

Front 10

the other cause of HF

Back 10

RVSD caused by → LVSD or pulmonary hypertension, RV infarction, chronic severe tricuspid regurgitation.

Front 11

LVDD

Back 11

chronic HTN, ischemic heart disease or restrictive, infiltrative and hypertrophic cardiomyopathies

Front 12

RVDD

Back 12

pericardial effusion or cardiac tamponade.

Front 13

high output failure

Back 13

High output failure-pumps abnormally large quantities of blood to deliver adequate amounts of O2 to metabolizing tissues in such conditions as severe chronic anemia, thyrotoxicosis,pregnancy and AV shunt

Front 14

Ischemic cardiomyopathy

Back 14

CAD

Front 15

Non-ischemic cardiomyopathy-

Back 15

HTN, thyroid dz, valvular dz, alcohol use,myocarditis, idiopathic,etc

Front 16

HF Pathophysiology

Back 16

Low cardiac output
Pulmonary congestion
Systemic congestion

Front 17

HF neurohumoral response

Back 17

In trying to maintain cardiac output:

1) SNS- ↑ HR and contractility =↑ CO
2) Circulating catecholamines - ↑vasoconstriction in non essential beds to shunt blood to brain / ♥=↑SV=↑CO

Hint 17

However, they also
1) Aggravate ischemia
2) Potentiate arrhythmias
3) Promote cardiac remodeling
4) Are directly toxic to myocytes
5) Unfortunately ,stimulate renin release from underperfused kidneys

Front 18

RAAS

Back 18

Front 19

vasopressin

Back 19

ADH: bed wetter's med

Front 20

baroreceptors

Back 20

in the aortic arch and carotids along with osmotic stimuli stimulate vasopressin ( ADH) release from the hypothalamus causing reabsorption of water in the renal collecting duct.

Vasopressin is used in cardiogenic shock and bedwetting

Front 21

HDAC

Back 21

A team at UPENN has discovered an enzyme,HDAC, that, in thefailing heart ,switches on a gene that regulates the proliferation
of heart cells in the embryo, making existing heart cells bigger,stimulating cardiac hypertrophy.

Front 22

dilatation

Back 22

the condition, as of an orifice or tubular structure, of being dilated or stretched beyond normal dimensions.

Front 23

Counter-regulatory hormones:
1)ANP Atrial natriuretic peptide
2) BNP Brain natriuretic peptide

Back 23

a)Released from secretory granules in the cardiac myocytes
b) Promote sys /pulm vasculature dilatation
c)↑ Na / water excretion
d) Suppress other neurohormones.

Front 24

The basis of modern treatment for heart failure is_________

Back 24

neurohormonal modulation

Front 25

nonspecific common symptoms of heart
failure

Back 25

1) Fatigue and weakness- 2° to reduced perfusion of skeletal muscles
2) Dyspnea- 2° to pulmonary congestion
3) Nausea and anorexia- 2° to congested liver and portal venous system.

Front 26

Diagnosis of HFSigns and symptoms

Back 26

Fatigue
Dyspnea on exertion
Paroxysmal Nocturnal Dyspnea (gravity allows fluid to return to the lungs while sleeping in the horizontal plane)
Abnormal weight gain
Peripheral edema
Nocturia
Nausea, anorexia

Front 27

Pulmonary
congestion

Back 27

Orthopnea
Dyspnea
Paroxysmal nocturnal dyspnea

Front 28

Low cardiac
output

Back 28

Fatigue
Effort intolerance
Cachexia
Renal hypoperfusion

Front 29

Systemic congestion (Right Ventricular Failure)

Back 29

JVD
Peripheral edema
Hepatosplenomegaly
Ascites
Anorexia
Nausea

Front 30

Diagnosis of HFCommon physical findings

Back 30

Tachypnea
Tachycardia
Bibasilar rales
JVD
Ascites
Pulsus alternans
Pale, diaphoretic
S3,S4
S2 split -delayed elec/mech activation of LV

Front 31

Pulsus alternans

Back 31

is a physical finding with arterial pulse waveform showing alternating strong and weak beats.[1] It is almost always indicative of left ventricular systolic impairment, and carries a poor prognosis.

Front 32

Diagnostic tests / Labs

Back 32

Vital Signs
Pulse Ox
EKG
CXR Pa/Lat
**Echocardiogram
Cardiac Catheterization
CBC (complete blood count)
CMP (comprehensive metabolic panel)
ABG’S
TSH
BNP

Front 33

B-type natriuretic peptide

Back 33

BNP is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure develops and worsens. The level of BNP in the blood increases when heart failure symptoms worsen, and decreases when the heart failure condition is stable. The BNP level in a person with heart failure – even someone whose condition is stable – is higher than in a person with normal heart function.

Front 34

Left atria hypertrophy EKG

Back 34

Front 35

right atrial hypertrophy

Back 35

Front 36

left ventricular hypertrophy

Back 36

Front 37

right ventricular hypertrophy

Back 37

Front 38

Diagnosis of HF: LABS

Back 38

CBC- anemia
TSH- thyrotoxicosis
CMP- Electrolytes and LFT’S
Hyponatremia common 2° to fluid retention d/t ↑circulating volume via RAAS/ADH
↑ LFT’s 2° to hepatic congestion
↑ Creatinine 2° to renal hypoperfusion

Front 39

Diagnosis of HF: LABS (cont'd)

Back 39

BNP- correlates with severity of heart failure
Can be useful in dx COPD vs. HF since presenting symptoms are often similar
ABG ’s- monitor respiratory status
pH- acidotic
PO2-hypoxic

Front 40

Diagnosis of HF

Back 40

There is no specific diagnostic test
Heart failure should be suspected by clinical presentation
Elicit S/S through history
Obtain physical findings through physical exam/labs/ Dx tests
Devise a comprehensive plan of action (using ACC/AHA and NYHA guidelines).

Front 41

The ACC/AHA Staging System

Back 41

Help clinicians recognize:
1) The progressive nature of LV dysfunction and H, and the importance of screening and prophylaxis.
2) That HF has established risks factors and asymptomatic and symptomatic phases.
3) Treatments at each stage can reduce morbidity and mortality.

Front 42

NYHA staging

Back 42

Front 43

NYHA GuidelinesACC/AHA Stages 3/4

Back 43

Front 44

TX of HFNon pharmacological therapies

Back 44

Dietary sodium and fluid restrictions
1) 2 gram Na daily-avoid canned foods, cured meats, salt shakers. Low sodium foods only
2) 2 liters of fluid
Wt. loss in obese patients
Cardiac rehab- increase exercise tolerance

Front 45

Tx of HFPharmacological therapies

Back 45

The foundation of modern therapy is a combination of ACE-I and beta blockers.
If possible, every patient should be on both drugs for improvement of LV function and prolongation of life.

Front 46

Main Pharmacological Agents

Back 46

ACE-I
ARB
B-Blockers
Diuretics
Digitalis

Front 47

Other Medical Therapies

Back 47

ASA 81 mg-CAD
Statin- chol <70
Aldosterone Antagonists (creatinine <2, K+ <5)
TX underlying causes i.e.; a-fib, anemia, sleep apnea, obesity, thyroid dz.
Electronic therapies- resynchronization to improve pump
Implanted defib -post MI with LVEF<30%
½ HF pts. die of sudden death

Front 48

intra-aortic baloon pump (IABP)

Back 48

temporary support of LV function placed in aorta distal to L subclavian artery providing counterpulsation to ↑ coronary blood flow, ↓ 02 demand

Front 49

LVAD- left ventricular assist device

Back 49

LVAD-mechanical circulatory support, tertiary centers, bridge to transplant

Front 50

A 56 year old female patient with a recent MI. Her echocardiogram reveals mild left ventricular dysfunction. She denies worsening fatigue, dyspnea on exertion or edema. She walks 2 miles everyday and does her own housework.

Back 50

Stage B

Front 51

What does an ACE-I do? (Increase cardiac contractility
Prevent/reverse cardiac remodeling
Improve ejection fraction
Increase heart rate)

Back 51

Prevent/reverse cardiac remodelin

Front 52

A 40 year old male patient with a history of hypertension. His recent echocardiogram revealed normal architecture of valves and leaflets and an ejection fraction of 60%. He denies fatigue, dyspnea on exertion or edema. What ACC/AHA stage is this patient?

Back 52

Stage A

Front 53

A 76 year old male patient with a left ventricular ejection fraction of 40% and moderate mitral stenosis complains of worsening fatigue and dyspnea during his daily walks. What ACC/AHA stage is this patient?

Back 53

Stage C

Front 54

What does digoxin do? (Dilates arteries
Increases cardiac contractility
Increases Na+ excretion
Prevent/reverse cardiac remodeling)

Back 54

Increases cardiac contractili

Front 55

What do diuretics do? (Increase preload
Decrease renin secretion
Increase Na+ excretion
Increase contractility
Decrease wall stress)

Back 55

Increase Na+ excretion
Decrease wall stress

Front 56

A 69 year old female on the cardiac transplant list with severe shortness of breath at rest. What ACC/AHA stage is this patient?

Back 56

Stage D

Front 57

“Flash” Pulmonary Edema

Back 57

-Pathophysiology -Pulmonary capillary pressure exceeds the forces that maintain fluid within the vascular space
-AMI, papillary muscle rupture, fluid overload, cardiogenic shock
-↑ fluid in the pulmonary interstitium
-Alveolar flooding

Front 58

“Flash” Pulmonary Edema: Clinical manifestations

Back 58

Rapid onset
Dyspnea
Anxiety
Restlessness
Cool, clammy skin
Frothy pink sputum
Use of accessory muscles
Wheezing

Front 59

Management of PE

Back 59

-IV,O2,monitor
-Sitting, dangle feet
-↓ cardiac workload by ↓ anxiety and pain
-DIURESIS
-Morphine 2-5mg-↓pain/anxiety,
dilates pulm /sys veins
-Furosemide 20-40mg-IV slowly potent venodilator,↓ pulm congestion in minutes, long before diuresis(20 min)

Front 60

Management of PE

Back 60

-NTG-sublingual, IV- recommended by
ACC/AHA for tx of pulmonary edema
-Inotropes, IV venodilators, nesiritide
-Foley for I/O’s
-ABG’s, CBC,CMP,BNP
-Hemodialysis -ESRD pts.
-Correct precipitating fx( HTN, MI ,Volume overload, etc.)