Decreased cardiac output for right-sided heart failure???

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I'm working on a care plan and I'm stuck on a nursing diagnosis. My pt has right sided heart failure and a BP of 134/66 and HR of 76. I'm thinking maybe decreased cardiac output R/T altered contractability (since right ventricle isn't pushing enough blood out) secondary to heart failure AEB peripheral edema? (can't really think of anything else that would work since blood pressure isn't too far off. 02 sat is 92...would that play a part?

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If the blood pressure is normal, and the HR is normal, then why do you think their cardiac output is affected? If you patient was actually having a decreased cardiac output, the body would compensate by increasing the heart rate. Since this is not the case, it is an inappropriate diagnosis. Think about it- the left ventricle is the main muscle in the heart that is responsible for pumping the blood throughout the body. The right ventricle only pumps blood to the lungs.

So, the heart is having a hard time pumping blood to the lungs. Your lungs aren't getting enough blood to oxygenate, therefore your 02 sat is decreased. You are also going to have fluid back up due to the inefficiency of the right ventricle.

So think respiratory diagnosis and issues that peripheral edema could cause

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What is your patient there for? What is your assessment showing? That's what drives your nursing diagnosis/es. Sure your patient may have right-sided HF but if they are in the hospital because they just had their hip replaced then you probably have other fish to fry with your diagnoses :)

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SOB and elevated sugars...also heard Dr. mention small heart attack the previous night. What about impaired gas exchange related to altered pulmonary blood flow secondary to right side heart failure AEB 92% 02 sat? Also Excess fluid volume related to compromised regulatory mechanisms secondary to right side heart failure AEB edemous feet and stomach distention and tenderness? Any of these sound good?

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Specializes in Family Nurse Practitioner.

Do you have access to the lab results? How did the patient's troponin look? If he patient had a heart attack, that could be contributing to some of the heart failure. Is the patient on a beta blocker? That could mask compensatory tachycardia. The low SpO2, shortness of breath, and edema sounds like the right focus for this care plan. How is the patient's activity tolerance? It wouldn't be a priority diagnosis but can be an AEB statement if the patient is weak.

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SOB and elevated sugars...also heard Dr. mention small heart attack the previous night. What about impaired gas exchange related to altered pulmonary blood flow secondary to right side heart failure AEB 92% 02 sat? Also Excess fluid volume related to compromised regulatory mechanisms secondary to right side heart failure AEB edemous feet and stomach distention and tenderness? Any of these sound good?

YES! Good job!

I would add AEB 92% o2 saturation and Shortness of Breath for the first one. Both sound good. Is the patient diabetic? How about their skin? Edema + complications with diabetes? Think about it :)

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If the blood pressure is normal, and the HR is normal, then why do you think their cardiac output is affected? If you patient was actually having a decreased cardiac output, the body would compensate by increasing the heart rate. Since this is not the case, it is an inappropriate diagnosis. Think about it- the left ventricle is the main muscle in the heart that is responsible for pumping the blood throughout the body. The right ventricle only pumps blood to the lungs.

So, the heart is having a hard time pumping blood to the lungs. Your lungs aren't getting enough blood to oxygenate, therefore your 02 sat is decreased. You are also going to have fluid back up due to the inefficiency of the right ventricle.

So think respiratory diagnosis and issues that peripheral edema could cause

OcMurse93,

You boldly stated that the blood pressure would not be normal in heart failure and that "the body" would compensate for decreased cardiac output via increased heart rate however the pathophysiology of heart failure and the various compensatory mechanisms that come into play here are a bit more complex. This explanation is a bit compressed, but I will leave you with enough information so that you will have a base of knowledge to use if you choose to go back and review this material.

In the setting of RV dysfunction 2/2 either increased contractile demand or decreased contractile function, normal compensatory mechanisms (ie. Anrep, Frank-Starling) eventually fail, followed by elevated CVP which, combined with underlying RV dysfunction, leads to RV dilation and eventual ischemia, falling RV output and direct impedance on LV filling and finally systemic hypotension/decreased LV output.

Decreasing cardiac output and subsequent lowering of renal perfusion stimulates renin secretion from renal JG cells (just as if the patient were volume depleted) and the renin-angiotensin-aldosterone system is subsequently stimulated. The combination of angiotensin II, aldosterone, and AVP, as well as sympathetic input serve to increase intravascular volume (increasing preload and enhancing stroke volume/cardiac output) as well as arterial and venous resistance. These are part of the neurohumoral response which preserves cardiac output and peripheral perfusion (not increasing heart rate).

This is not to suggest that heart rate cannot be elevated in a patient who has untreated CHF, but you absolutely cannot indicate that this persons' diagnosis is incorrect based on the absence of tachycardia.

Additionally, you have no idea what medications this patient might be on (beta adrenergic antagonists for example, which are a standard therapy in CHF), nor do you know if this patient has an underlying conduction abnormality.

As far as the O2 saturation, there are certainly pulmonary causes of right heart failure which may also present with hypoxemia, however; we already have a reasonable explanation for this occurrence and before we start drawing conclusions it would be great to know a bit more about this patient; is this O2 sat is his baseline or an acute exacerbation? HPI and PMH (does he have a history of pulmonary disease, vascular disease, cardiomyopathy, chronic pulmonary emboli, pulmonary hypertension, RV infarct, thyrotoxicosis, pulmonary shunts, Tricuspid/Pulmonary valvular disease, ILD, etc.) before I start drawing conclusions.

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SOB and elevated sugars...also heard Dr. mention small heart attack the previous night. What about impaired gas exchange related to altered pulmonary blood flow secondary to right side heart failure AEB 92% 02 sat? Also Excess fluid volume related to compromised regulatory mechanisms secondary to right side heart failure AEB edemous feet and stomach distention and tenderness? Any of these sound good?

The volume overload in this case is not a result of a "compromised" regulatory mechanism. The retention/reabsorption of excessive fluids actually means that the regulatory mechanism(s) are working appropriately. The increased intravascular volume in the setting of heart failure preserves cardiac output (short term fix until CO and edema can be controlled medically). Fluid overload is a consequence of this 'mechanism' (neurohumoral response) working effectively. Keep in mind also, that edema and volume overload are not the same thing (although they frequently present together). Edema in this setting is 2/2 increased capillary hydrostatic pressure.

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