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Pathophysiology 212 > Heart failure & circulatory shock > Flashcards

Heart failure & 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

Who is at greater risk for heart failure?

A 
Primarily the elderly
Vessel stiffness
ASHD
Hypercholesterolemia
Hyperlipedemia
Decreased estrogen production for women
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3
Q

Evolution of Our Understanding of HF

A

CHF as a disorder of excessive sodium & water retention (cardio-renal model)

CHF as a hemodynamic disorder (reduced CO or AL)

HF as a neurohormonal model

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4
Q

What is preload?

A

“End -diastolic volume”

Determined by venous return to the heart

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5
Q

What is afterload?

A

Amount of force needed to eject filled heart

Determined by SVR and ventricular wall tension

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6
Q

Contractility

A

Performance of cardiac muscle

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7
Q

What is systolic heart failure and its causes?

A
  • Impaired ejection of blood

- Presence of S&S of HF with an EF

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8
Q

Ejection Fraction (EF)

A

The % of blood ejected from the LV during systole
Normal EF = 55-70%

If the LV has 100ml @ end-diastole, and the stroke volume is 70ml (leaving 30ml still in the LV after systole), then….
70/100 = 70%

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9
Q

What is diastolic heart failure & and its causes?

Who is at risk?

A
  • 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
    Causes
  • Impaired ventricular stretch pericardial effusion, pericarditis, amyloidosis)
  • Increased wall thickness hypertrophy, myopathy)
  • Delayed diastolic relaxation (aging, CAD)
    Aggravated by tachycardia
    At Risk: women, obesity, HTN, DM
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10
Q

Left-side heart failure (LV dysfunction)

A
  • Decreased CO

- Pulmonary congestion

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11
Q

LV Dysfunction Manifestations (CNS, CVS, Renal)

A
  • Decreased CO
    CNS
  • Fatigue, weakness, confusion, dizziness (worsens over day)
    CVS
  • Hypotension, angina, tachycardia, palpitations, pallor, weak peripheral pulses, cool extremities, S3/S4
    Renal
  • Oliguria (daytime d/t gravity)
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12
Q

LV Dysfunction Manifestations (pulmonary congestion)

A
  • SOB (initially during exertion/orthopnea/PND)
  • Cough, “cardiac asthma” (worse at night)
  • Inspiratory crackles/expiratory wheezes
  • Tachypnea
  • Frothy/pink sputum (pulmonary edema) fluid overload in the alveoli
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13
Q

Right sided failure (RV dysfunction)

A

-systemic congestion

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14
Q

RV Dysfunction Manifestations

A

> Systemic Congestion

  • JVD/elevated CVP
  • Enlarged liver and spleen
  • Dependent edema
  • Ascites
  • Polyuria @ night
  • Weight gain
  • Hepatojugular reflux (HJR) – push down on liver to see if fluid in jugular vein changes
  • BP changes (elevated or decreased)
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15
Q

Compensatory Mechanisms in HF (Frank-Starling Mechanism & Sympathetic Nervous System)

A

> Frank-Starling Mechanism
+ Increased ED volume (preload) will increase stroke volume
- Stretch increases wall tension, increasing oxygen requirements

> Sympathetic Nervous System
+ Increase in circulating catecholamines increase HR, contractility, PVR, SV, CO
- Increased workload

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16
Q

Compensatory Mechanisms in HF (Renin-Angiotension-Aldosterone System)

A

+ Increased concentration of renin, angiotensin ll, & aldosterone d/t decreased renal perfusion
Increased preload, increased workload

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17
Q

Compensatory Mechanisms in HF (Natriuretic Peptide (ANP & BNP))

A

+ Released in response to stretch, pressure, fluid overload (promote diuresis)
Decreases preload decreases CO

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18
Q

Compensatory Mechanisms in HF (Endothelins)

A

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

19
Q

Ventricular Remodeling

A

>

  • Symmetric hypertrophy
  • Proportionate increase in muscle length & width (athletes)
    Pressure overload (hypertension)
  • Concentric hypertrophy d/t replication of myofibrils, thickening of myocytes
  • Increase in wall thickness (hypertension)

> Volume overload (dilated cardiomyopathy)
- Eccentric hypertrophy d/t replication of myofibrils, disproportionate elongation of muscle cells (decreased wall thickness)

20
Q

Late Manifestations of HF

A

> Cyanosis (late stage failure)
- d/t pulmonary edema, vasoconstriction, decreased oxygen availability
Clubbing of fingers
Cachexia/Malnutrition (end-stage failure)
CNS factors
Liver & GI congestion
Arrhythmias/Sudden Cardiac Death
- Atrial fibrillation/VT/Ventricular fibrillation

21
Q

What is happening in the heart during atrial fibrillation?

A

Quivering muscle
Poor emptying of atria
Poor filling of ventricle resulting in decreased CO

22
Q

How will your patient present when they have atrial fibrillation?

A
  • Irregularly irregular HR
  • Pulses will be irregularly irregular with varying strength
  • Low BP
  • Possibility of angina
  • Possibility of thrombiAll other Systems will exhibit the S&S of decreased CO
23
Q

Acute Pulmonary Edema

A 
> Accumulation of capillary fluid in alveoli
- Impairs gas exchange & limits lung expansion
Manifestations
-SOB, dyspnea, tachypnea
-Tachycardia, moist/cool skin
-Fine to course crackles
-Frothy, blood tinged sputum
-Cyanotic lips, nailbeds
-CNS: confusion, stupor
24
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
25
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

26
Q

Circulatory Failure: Shock

A

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

27
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

28
Q

Cardiogenic Shock

A 
> Heart failure, uncompensated
Can be due to other shock situations!
> Causes:
-Myocardial Infarction
-Myocardial contusion
-Acute MVR (mitral valve replacement) d/t papillary muscle rupture
-Arrhythmias
-Severe dilated cardiomyopathy
-Cardiac surgery
29
Q

Cardiogenic Shock: Manifestations (CVS, CNS, Renal)

A 
> Similar to extreme heart failure
CVS:
- Decreased SV, MAP, SBP
- Narrow pulse pressure
- Normal DBP
- Cyanosis (lips, nailbeds, skin)
- Elevated CVP/PCWP
- Dysrhythmias
Renal: oliguria, anuria	
CNS: altered mentation (GCS 15-0)
30
Q

Cardiogenic Shock: Treatment

A

Balance!
Fluid volume management
Treat cause & symptoms

Improve CO, avoid increasing workload of heart
Inotropes (dopamine, dobutamine)
Intra-aortic balloon pump

31
Q

Hypovolemic Shock

A

> Any condition which decreases blood volume >15%
External Loss
- Hemorrhage, burns, severe dehydration/vomiting/diarrhea
Internal Loss
- 3rd spacing, hemorrhage
Immediate compensation
- SNS, RAAS, Hypothalamus, fluid shift

32
Q

Hypovolemic Shock: Manifestations (CVS, CNS, Resp, Renal)

A 
> CVS
- tachycardia, weak/thread pulses
- Skin cool/clammy/mottled
- Hypotension
- Decreased CVP
> CNS
- ADH release, thirst
- Altered mentation
> Respiratory:
- tachypnea, deep resps
> Renal: 
- oliguria, anuria
33
Q

Hypovolemic Shock: Treatment

A 
Treat cause
Increase oxygen delivery by maintaining adequate vascular volume
IV crystalloids (NS, D5W)
IV colloids (rbc’s, plasma volume expanders)
Vasoactive pharmacology (not usually recommended)
34
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
35
Q

Obstructive Shock

A

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

  • Pulmonary embolus
  • Dissecting AA
  • Tamponade
  • Pneumothorax (collapsed lung)
  • Atrial myxoma (tumor in the atria)
  • Abdominal evisceration
36
Q

Distributive Shock

A

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

Neurogenic
Anaphylactic
Septic

37
Q

Neurogenic Shock

A 
> Rare, often transitory depending on the cause
> Decreased SNS control of vessel tone
-Brain stem defect
-Spinal cord injury
-Drugs
-General anaesthesia
-Hypoxia
-Insulin reaction
38
Q

Anaphylactic Shock

A 
> Immunological mediated reaction of histamine release causing
- v/d of arterioles and venuoles 
- Increased capillary permeability
> Causes
- Medications
- Foods
- Insect venom
- Latex
39
Q

Anaphylaxis: Manifestations/Treatment

A 
Manifestations dependent on:
- Level of sensitivity
- Rate/quantity of antigen exposure
Pruritus, urticarial
Angioedema
Laryngeal edema/bronchospasm
Rapid hypotension; circulatory collapse

Treatment

  • Remove cause
  • Epinephrine, oxygen, antihistamines, corticosteroids
40
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
41
Q

Septic Shock: Manifestations (CVS, CNS, Renal, Hemat)

A

CVS: vasodilation (decreased SVR), hypovolemia, hypotension, tachycardia, skin flushed, edema

CNS: pyrexia, abrupt change in mentation

Renal: oliguria, anuria

Hemat: leukocytosis, metabolic acidosis, thrombocytopenia

42
Q

Shock: Complications (ARDS)

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

43
Q

Shock: Complications (Acute renal failure & GI tissue damage)

A

Acute Renal Failure
Ischemia/injury of renal tubules > 20 mins

GI Tissue Damage d/t hypoxia
- GI bleeding

44
Q

Shock: Complications (DIC & MODS)

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

Pathophysiology 212 (18 decks)

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