Chap 20 Heart Failure and Circulatory Shock Flashcards
What is Heart Failure?
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
At risk for HF if you have?
(primarily the elderly)
- Vessel stiffness
- ASHD (atherosclerotic heart disease)
- Hypercholesterolemia
- Hyperlipedemia
- Decreased estrogen production for women
HF as a neurohumoral model
adjust the hormones in your body and treat the problem
Preload!!!
“End -diastolic volume”
–Determined by venous return to the heart
Afterload!!!
Pushing force:
- -Amount of force needed to eject filled heart
- -Determined by SVR (systemic vascular resistance) and ventricular wall tension
Contractility!!!
Performance of cardiac muscle. How well it can contract
Name the Types of Heart Failure:
- Systolic vs Diastolic
- Dilated (stretch and thinning of walls) vs Hypertrophic (thickening of walls)
- Left vs Right
- High-output vs Low-output
Systolic Heart Failure
Impaired ejection of blood.
–decrease in myocardial contractility by an ejection fraction of
Causes of Systolic Heart Failure: 1 of 3
Muscle issues:
Impair the contractile performance. Muscle isn’t working properly
ex. CAD, myocarditis, cardiomyopathy, conduction issues.
Because systole is the muscle contraction of the heart
Causes of Systolic Heart Failure: 2 of 3
Volume Overload:
valvular insufficiency, kidney failure, anemia
Causes of Systolic Heart Failure: 3 of 3
Pressure Overload:
HTN, valvular stenosis, pulmonary disease
Diastolic Heart Failure
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
Diastolic Heart Failure
Causes:
> Impaired ventricular stretch (pericardial effusion, pericarditis, amyloidosis)
> Increases wall thickness (hypertrophy, myopathy)
> Delayed diastolic relaxation (aging, CAD)
> Aggravated by tachycardia
Who is at risk for Diastolic HF?
women
obesity
HTN
DM
Left sided heart failure =
decreased CO and pulm congestion
Right sided heart failure =
systemic congestion
LV Dysfunction Manifestations:
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)
RV Dysfunction Manifestations:
Systemic Congestion:
> 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)
High-Output Failure
Caused by?
excessive need for CO, Severe anemia,
Thyrotoxicosis/thyroid storm
Low-Output Failure
Caused by?
conditions decreasing pumping ability,
CAD,
Cardiomyopathy
Compensatory Mechanisms in HF
Frank-Starling:
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.
Compensatory Mechanisms in HF:
SNS:
+-
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
Renin-Angiotension-Aldosterone System
+-
Pos: Increased concentration of renin, angiotensin II, & aldosterone d/t decreased renal perfusion
Neg: Increased preload, increased workload
Natriuretic Peptide (ANP & BNP) \+-
Pos: Released in response to stretch, pressure, fluid overload (promote diuresis)
Neg: Decreases preload, decreases CO
Endothelins
+-
+ Responds to pressure changes (v/c, myocyte hypertrophy, ANP & catecholamine release)
- Increased workload
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)
Late manifestations of HF:
- Cyanosis: d/t pulm edema, vasoconstriction, decreased O2 availability
- Clubbing of Fingers: r/t decreased peripheral perfusion
- 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.
- Arrhythmias/Sudden Cardiac death: A.fib, Vent tachycardia, Vent fib r/t stretching heart muscle too much, cells get irritated and initiate inappropriate impulses.
Why does A fib happen?
MI, Valvular damage
What is happening to the heart?
Atria quiver, do not contract and push blood into ventricle so decrease CO
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
Acute Pulmonary Edema
Accumulation of capillary fluid in alveoli
> Impairs gas exchange & limits lung expansion
Acute Pulmonary Edema
Manifestations:
> dyspnea, SOB, tachypnea
tachycardia, moist/cool skin
fine to coarse crackles
frothy, bloody tinged sputum
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
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
Circulatory Failure: Shock
Acute failure of the circulatory system to supply tissues and organs with an adequate blood supply resulting in hypoxia
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
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
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.
Cardiogenic Shock: Treatment:
A balance between:
- improving cardiac output
- reducing workload and O2 needs of myocardium
- increasing coronary perfusion
> Fluid volume management
> Treat cause & symptoms
> Improve CO, avoid increasing workload of heart
- -Inotropes (dopamine, dobutamine)
- -Intra-aortic balloon pump
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
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
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)
Obstructive Shock
Mechanical obstruction of blood to or through great veins, heart, lungs
- -Pulmonary embolus
- -Dissecting AA
- -Tamponade
- -Pneumothorax
- -Atrial myxoma
- -Abdominal evisceration
Distributive Shock
Loss of vascular tone usually d/t loss of sympathetic control
- -Neurogenic
- -Anaphylactic
- -Septic
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
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
Anaphylaxis: Manifestations:
Treatment:
Manifestations dependent on:
- -Level of sensitivity
- -Rate/quantity of antigen exposure
Treatment:
- -Remove cause
- -Epinephrine, oxygen, antihistamines, corticosteroids
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
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
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
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
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
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
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
