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

Chap 20 Heart Failure and Circulatory Shock Flashcards

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:
+-

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

+-

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)
\+-
A

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

Neg: Decreases preload, decreases CO

25
Q

Endothelins

+-

A

+ Responds to pressure changes (v/c, myocyte hypertrophy, ANP & catecholamine release)

  • Increased workload
26
Q

Ventricular Remodeling

A

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
Q

Late manifestations of HF:

A
  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
Q

Why does A fib happen?

A

MI, Valvular damage

29
Q

What is happening to the heart?

A

Atria quiver, do not contract and push blood into ventricle so decrease CO

30
Q

How will your patient present?A.Fib

A

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
Q

Acute Pulmonary Edema

A

Accumulation of capillary fluid in alveoli

> Impairs gas exchange & limits lung expansion

32
Q

Acute Pulmonary Edema

Manifestations:

A

> dyspnea, SOB, tachypnea
tachycardia, moist/cool skin
fine to coarse crackles
frothy, bloody tinged sputum

33
Q

HF: Diagnostic Methods

A

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
Q

HF: Treatment

A

> 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
Q

Circulatory Failure: Shock

A

Acute failure of the circulatory system to supply tissues and organs with an adequate blood supply resulting in hypoxia

36
Q

Cellular Response to Shock

A

> 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
Q

what is Cardiogenic Shock?

Causes?

A

Heart failure, uncompensated
Can be due to other shock situations!

Causes:
>Myocardial Infarction
>Myocardial contusion
>Acute MVR
>Arrhythmias
>Severe dilated cardiomyopathy
>Cardiac surgery
38
Q

Cardiogenic Shock: Manifestations
CVS:
Renal:
CNS:

A

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
Q

Cardiogenic Shock: Treatment:

A

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
Q

Hypovolemic Shock

A

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
Q 
Hypovolemic Shock: Manifestations
CVS:
CNS:
Resp:
Renal:
A

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
Q

Hypovolemic Shock: Treatment

A

> 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
Q

Obstructive Shock

A

Mechanical obstruction of blood to or through great veins, heart, lungs

  • -Pulmonary embolus
  • -Dissecting AA
  • -Tamponade
  • -Pneumothorax
  • -Atrial myxoma
  • -Abdominal evisceration
44
Q

Distributive Shock

A

Loss of vascular tone usually d/t loss of sympathetic control

  • -Neurogenic
  • -Anaphylactic
  • -Septic
45
Q

Neurogenic Shock

A
  • -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
Q

Anaphylactic Shock

Causes:

A

Immunological mediated reaction of histamine release causing

  • -v/d of arterioles and venuoles
  • -Increased capillary permeability

Causes:

  • -meds
  • -foods
  • -insect venom
  • -latex
47
Q

Anaphylaxis: Manifestations:

Treatment:

A

Manifestations dependent on:

  • -Level of sensitivity
  • -Rate/quantity of antigen exposure

Treatment:

  • -Remove cause
  • -Epinephrine, oxygen, antihistamines, corticosteroids
48
Q

Septic Shock

A

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
Q

Septic Shock: Manifestations:
CVS:

CNS:

Renal:

Hemat:

A

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
Q

Septic Shock:

Treatment:

A

> 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
Q

Shock: Complications

A

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
Q

Shock Complications:

Acute Respiratory Distress Syndrome (ARDS)

A

–Rapid onset of hypoxemia unrelieved by supplemental oxygen
–Ventilation-perfusion mismatch
–Atelactasis, impaired gas exchange, fluid limits inflation
Tx: mechanical ventilation, oxygen

53
Q

Shock: Complications
Acute Renal Failure:

GI tissue damage d/t:

Tx:

A

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
Q

Shock: Complications

A

> 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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