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Patho test 1 > Chap 20 Heart Failure and Circulatory Shock > Flashcards

Chap 20 Heart Failure and Circulatory Shock Flashcards

(54 cards)

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1
Q

What is Heart Failure?

A

Heart Failure is a clinical syndrome that occurs when the heart is unable to pump adequate blood to meet the metabolic demands of the body

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2
Q

At risk for HF if you have?

A

(primarily the elderly)

  • Vessel stiffness
  • ASHD (atherosclerotic heart disease)
  • Hypercholesterolemia
  • Hyperlipedemia
  • Decreased estrogen production for women
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3
Q

HF as a neurohumoral model

A

adjust the hormones in your body and treat the problem

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4
Q

Preload!!!

A

“End -diastolic volume”

–Determined by venous return to the heart

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5
Q

Afterload!!!

A

Pushing force:

  • -Amount of force needed to eject filled heart
  • -Determined by SVR (systemic vascular resistance) and ventricular wall tension
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6
Q

Contractility!!!

A

Performance of cardiac muscle. How well it can contract

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7
Q

Name the Types of Heart Failure:

A
  1. Systolic vs Diastolic
  2. Dilated (stretch and thinning of walls) vs Hypertrophic (thickening of walls)
  3. Left vs Right
  4. High-output vs Low-output
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8
Q

Systolic Heart Failure

A

Impaired ejection of blood.

–decrease in myocardial contractility by an ejection fraction of

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9
Q

Causes of Systolic Heart Failure: 1 of 3

Muscle issues:

A

Impair the contractile performance. Muscle isn’t working properly
ex. CAD, myocarditis, cardiomyopathy, conduction issues.

Because systole is the muscle contraction of the heart

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10
Q

Causes of Systolic Heart Failure: 2 of 3

Volume Overload:

A

valvular insufficiency, kidney failure, anemia

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11
Q

Causes of Systolic Heart Failure: 3 of 3

Pressure Overload:

A

HTN, valvular stenosis, pulmonary disease

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12
Q

Diastolic Heart Failure

A

more common to have systolic HF

> Impaired filling during diastole
Presence of signs and symptoms of HF in the absence of systolic dysfunction (LVEF > 40%)

Myocardium is “stiff” (and often hypertrophied) and does not relax normally after contraction

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13
Q

Diastolic Heart Failure

Causes:

A

> Impaired ventricular stretch (pericardial effusion, pericarditis, amyloidosis)

> Increases wall thickness (hypertrophy, myopathy)

> Delayed diastolic relaxation (aging, CAD)

> Aggravated by tachycardia

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14
Q

Who is at risk for Diastolic HF?

A

women
obesity
HTN
DM

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15
Q

Left sided heart failure =

A

decreased CO and pulm congestion

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16
Q

Right sided heart failure =

A

systemic congestion

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17
Q

LV Dysfunction Manifestations:

A

Decreased CO
>CNS
Fatigue, weakness, dizzy (symp get worse by the end of the day)

> CVS
Hypotension, angina tachycardia, palpitations, pallor, weak peripheral pulses, cool extremities (vaso constricts peripherals), S3/S4 (volume issues)

> Renal
Oliguria daytime. ++ urination at night

>Pulmonary Congestion
SOB (initially during exertion/orthopnea/PND)
Cough, “cardiac asthma” (worse at night)
Inspiratory crackles/expiratory wheezes
Tachypnea
Frothy/pink sputum (pulm edema)
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18
Q

RV Dysfunction Manifestations:

Systemic Congestion:

A

> JVD (jug vein distention)/ elevated CVP (central venous pressure)

> Enlarged liver and spleen

> Dependent edema

> Ascites

> Polyuria @ night

> Weight gain (indicates how much excess fluid)

> Hepatojugular reflux (HJR)

> BP changes: elevated BP (excess vol) or decreased BP (decreases CO)

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19
Q

High-Output Failure

Caused by?

A

excessive need for CO, Severe anemia,

Thyrotoxicosis/thyroid storm

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20
Q

Low-Output Failure

Caused by?

A

conditions decreasing pumping ability,
CAD,
Cardiomyopathy

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21
Q

Compensatory Mechanisms in HF

Frank-Starling:

A

Frank-Starling Mechanism- stretch something it should return to org. form

Positive: Increased ED (end diastolic vol) volume (preload) will increase stroke volume

Negative: Stretch increases wall tension, increasing O2 requirements. The more you stress the heart the more O2 you will need over time.

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22
Q

Compensatory Mechanisms in HF:
SNS:
+-

Study These Flashcards
A

Positive: Increase in circulating catecholamines increase HR, contractility, PVR, SV, CO
-Negative: Increased workload.

*heart is really good at compensating for short term, not long term

23
Q

Renin-Angiotension-Aldosterone System

+-

Study These Flashcards
A

Pos: Increased concentration of renin, angiotensin II, & aldosterone d/t decreased renal perfusion

Neg: Increased preload, increased workload

24
Q 
Natriuretic Peptide (ANP & BNP)
\+-
Study These Flashcards
A

Pos: Released in response to stretch, pressure, fluid overload (promote diuresis)

Neg: Decreases preload, decreases CO

25
Endothelins | +-
+ Responds to pressure changes (v/c, myocyte hypertrophy, ANP & catecholamine release) - Increased workload
26
Ventricular Remodeling
pos: Symmetric hypertrophy Proportionate increase in muscle length& width (athletes) neg: Pressure overload (hypertension) "Concentric" hypertrophy d/t replication of myofibrils, thickening of myocytes Increase in wall thickness HTN neg: Volume overload (dilated cardiomyopathy) "Eccentric" hypertrophy d/t replication of myofibrils, disproportionate elongation of muscle cells (decreased wall thickness)
27
Late manifestations of HF:
1. Cyanosis: d/t pulm edema, vasoconstriction, decreased O2 availability 2. Clubbing of Fingers: r/t decreased peripheral perfusion 3. Malnutrition: CNS factors- total body wasting r/t decreased brain perfusion to eat and drink, liver and GI congestion which interferes with ability to wasn't to eat and process food. 4. Arrhythmias/Sudden Cardiac death: A.fib, Vent tachycardia, Vent fib r/t stretching heart muscle too much, cells get irritated and initiate inappropriate impulses.
28
Why does A fib happen?
MI, Valvular damage
29
What is happening to the heart?
Atria quiver, do not contract and push blood into ventricle so decrease CO
30
How will your patient present?A.Fib
HR irregularly irregular > pulses will be present with varying strengths > Decreased BP r/t decreased atrial kick? >Possibility of angina >Possibility of thrombi > all other systems will exhibit the S&S of decreased CO
31
Acute Pulmonary Edema
Accumulation of capillary fluid in alveoli > Impairs gas exchange & limits lung expansion
32
Acute Pulmonary Edema | Manifestations:
> dyspnea, SOB, tachypnea > tachycardia, moist/cool skin > fine to coarse crackles > frothy, bloody tinged sputum
33
HF: Diagnostic Methods
History, physical assessment --Signs and symptoms >ECG >CXR >Echocardiography - -Ejection fraction - -Wall motion, thickness - -Chamber size - -Structural defects (valves, tumors, etc.) >Blood tests: BNP, CBC >Central venous pressure/jugular vein distension >Pulmonary artery catheter pressures/volumes
34
HF: Treatment
>Non-pharmacological - -Exercise program, fluid/Na restriction, weight control, dietary counseling - -Non-surgical and surgical medical management >Pharmacological --Diuretics, ACE inhibitors, cardiac glycoside (digoxin), ARBs, B-blockers >Oxygen Therapy
35
Circulatory Failure: Shock
Acute failure of the circulatory system to supply tissues and organs with an adequate blood supply resulting in hypoxia
36
Cellular Response to Shock
>Anaerobic energy production - -Cytoplasm uses glucose to create ATP and pyruvate - -Less efficient >Aerobic energy production - -Oxygen and pyruvate create ATP in mitochondria - -If no oxygen, pyruvate converts to lactic acid
37
what is Cardiogenic Shock? | Causes?
Heart failure, uncompensated Can be due to other shock situations! ``` Causes: >Myocardial Infarction >Myocardial contusion >Acute MVR >Arrhythmias >Severe dilated cardiomyopathy >Cardiac surgery ```
38
Cardiogenic Shock: Manifestations CVS: Renal: CNS:
Similar to extreme heart failure CVS: decreases SBP, narrow pulse pressure (diff btwn systolic and diastolic), normal diastolic pressure, cyanosis, elevated central venous pressure, elevated pulm cap wedge pressure, dysrhythmias Renal: oliguria, anuria CNS: altered mentation.
39
Cardiogenic Shock: Treatment:
A balance between: 1. improving cardiac output 2. reducing workload and O2 needs of myocardium 3. increasing coronary perfusion >Fluid volume management >Treat cause & symptoms >Improve CO, avoid increasing workload of heart - -Inotropes (dopamine, dobutamine) - -Intra-aortic balloon pump
40
Hypovolemic Shock
Any condition which decreases blood volume >15% External Loss: hemorrhage, burns, severe dehydration, diarrhea, vomiting Internal Loss: 3rd spacing, hemorrhage Immediate compensation: SNS, RAAS, Hypothalamus, fluid shift
41
``` Hypovolemic Shock: Manifestations CVS: CNS: Resp: Renal: ```
CVS: tachycardia, weak/thread pulses, hypotension, cool/clammy skin, decreased central venous pressure CNS: ADH release results in thirst, altered mentation Resp: tachypnea, deep resps Renal: oliguria, anuria
42
Hypovolemic Shock: Treatment
>Treat cause >Increase oxygen delivery by maintaining adequate vascular volume - --IV crystalloids - --IV colloids (rbc’s, plasma volume expanders) - --Vasoactive pharmacology (not usually recommended)
43
Obstructive Shock
Mechanical obstruction of blood to or through great veins, heart, lungs - -Pulmonary embolus - -Dissecting AA - -Tamponade - -Pneumothorax - -Atrial myxoma - -Abdominal evisceration
44
Distributive Shock
Loss of vascular tone usually d/t loss of sympathetic control - -Neurogenic - -Anaphylactic - -Septic
45
Neurogenic Shock
- -Rare, often transitory depending on the cause - -Decreased SNS control of vessel tone r/t brain stem defect, spinal cord injury, drugs, general anesthesia, hypoxia, insulin reaction
46
Anaphylactic Shock Causes:
Immunological mediated reaction of histamine release causing - -v/d of arterioles and venuoles - -Increased capillary permeability Causes: - -meds - -foods - -insect venom - -latex
47
Anaphylaxis: Manifestations: Treatment:
Manifestations dependent on: - -Level of sensitivity - -Rate/quantity of antigen exposure Treatment: - -Remove cause - -Epinephrine, oxygen, antihistamines, corticosteroids
48
Septic Shock
Systemic inflammatory response to a severe infection >Neutrophils increase capillary permeability & damage to endothelial cells result >Cytokines, nitric oxide, & coagulation products are released, damaging cells/tissues and causing massive vasodilation and hypovolemia (and then hypovolemic shock and cardiogenic shock) Vasodilation> decreased peripheral resistance> decreased BP> septic shock
49
Septic Shock: Manifestations: CVS: CNS: Renal: Hemat:
Manifestations CVS: vasodilation (decreased SVR), hypovolemia, hypotension, tachycardia, skin flushed, edema CNS: pyrexia, abrupt mentation change Renal: oliguria, anuria Hemat: leukocytosis, metabolic acidosis, thrombocytopenia
50
Septic Shock: | Treatment:
>Treat cause >Support circulation - -Oxygen - -Aggressive fluids - -Aggressive management of fluids - -Positive or negative Inotropes - -Recombinant human activated protein C (rhAPC), a naturally occurring factor that - ---Inactivates clotting factors - ---Inhibits cytokine production
51
Shock: Complications
Acute Respiratory Distress Syndrome (ARDS) Rapid onset of hypoxemia unrelieved by supplemental oxygen Ventilation-perfusion mismatch Atelactasis, impaired gas exchange, fluid limits inflation Tx: mechanical ventilation, oxygen
52
Shock Complications: | Acute Respiratory Distress Syndrome (ARDS)
--Rapid onset of hypoxemia unrelieved by supplemental oxygen --Ventilation-perfusion mismatch --Atelactasis, impaired gas exchange, fluid limits inflation Tx: mechanical ventilation, oxygen
53
Shock: Complications Acute Renal Failure: GI tissue damage d/t: Tx:
Acute renal failure: --ischemia/injury of renal tubules if shock lasts >20 min GI tissue damage d/t hypoxia: -- GI bleed and tissue damage Tx: proton pump inhibits, histamine-2 receptor antagonists
54
Shock: Complications
>Disseminated Intravascular Coagulation (DIC) --Widespread activation of coagulation cascade (not the primary disease) Tx: anticoagulation, platelets, plasma >Multi-Organ Dysfunction Syndrome (MODS) --Failure of multiple organs such that homeostasis cannot be achieved

Patho test 1 (4 decks)

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