Congestive heart failure is not a disease; rather it’s a cascade of events and ill-conceived compensatory efforts made by the body in an attempt to maintain an adequate ejection of blood from the left ventricle.
The heart is doing its best… but in the long run, it’s making a bad job worse.
So, what’s to blame for this common condition? After all, congestive heart failure was not built in a day. In fact, there are at least 10 diseases and conditions which led your patients down the slippery slope to heart failure.
What is the single greatest thing individuals can do to avoid heart failure? Control their blood pressure.
Hypertension is heart failure’s number one precursor. Almost three quarters of individuals who develop heart failure have a history of high blood pressure.
So why does high blood pressure create an environment so conducive to heart failure? The narrowed arterial pathways reduce the blood’s ability to travel through the body smoothly. So, when arterial pressure is high, the heart must work harder (READ: too hard) to eject volume.
Think of your heart as that bodybuilder at the gym. The heart wants desperately to keep up with the resistance being thrown its way. To cope with this extra resistance, the heart bulks up (much like the bodybuilder), stiffens up (ditto) and – eventually – peters out. It becomes less able to do its job; not more.
Because of the increased pressure in the Aorta and pulmonary arteries, the ventricles have to increase pump action (contractility) which leads to hypertrophy (thickening of the walls), and thus decreasing the ability to pump effectively. The reduction in ejection volume (ejection fraction) creates pressure in the ventricles to build, and this has a backwards effect: pressure in the atria increases, leading to pulmonary and systemic congestion – or – congestive heart failure. The increase in volume in the ventricles and atria leads to stretching of the walls or dilation/dilatation, the end stage of the heart failure.
In addition, the abnormal pressure in the arteries shreds the insides of the vessels themselves. The arteries develop micro-tears in the walls and scar over.
As is true anywhere in the body, scar tissue does not distend or stretch. There is no play or give in the artery wall… and that translates to even more micro-tearing.
It only gets worse. The pitted arteries then become perfect host sites for fat, cholesterol and other yish (commonly referred to as “plaque”) to lodge. The combination of these forces produces a stiff artery with a narrow lumen, which is the first act for peripheral artery disease (if it occurs in the periphery) or coronary artery disease (if it occurs in the vessels supplying the heart).
Both PAD and CAD produce a multiplying effect. Blood clots are birthed by the intermittently stagnant and chaotic flow of blood through plaque-filled vessels. The heart tissue, starved by lack of flow through the coronary vessels, becomes ischaemic, leading to infarction and tissue death. And a heart with a damaged ventricle is a pumping organ prone to… well, not pumping.
The spiral continues. The heart is only one of the organs affected. Damaged and hardened arteries can lead to massively wounded organs throughout the body. Because the arteries supplying the body’s organs are not functioning adequately, they fail to deliver oxygen efficiently. Over time, this can result in organ damage, such as kidney disease.
In fact, the most common cause of chronic kidney disease is long-term, uncontrolled hypertension. The heart and the kidney are intricately married, relying on each other for systemic support that, frankly, does not come. This fact leads us to our discussion of renal insufficiency as another building block for heart failure.
From here it goes downhill. Everything becomes more pronounced and exertion dyspnea (breathlessness) increases to stage-four heart failure.
Which came first, the damaged kidney or the damaged heart?
Truthfully, it’s hard to say. Evidence is mounting that chronic kidney disease is itself a significant player in severe cardiac damage and, conversely, that congestive heart failure is a major player in chronic kidney disease.
There is a vicious cycle between a damaged kidney, a damaged heart and anaemia. Each condition exacerbates the status of the other two. Unfortunately, anaemia is seriously under-recognised and under-treated in this population.
There is also a vicious cycle between kidney failure, heart failure and lung disease – specifically ARDS (acute respiratory distress syndrome), as the toxins released into the bloodstream have a detrimental effect on the artery walls and lung vessels, and tissue.
Damaged Heart Tissue (Myocardial Infarction)
Except for hypertension, the most common risk factor for CHF is an antecedent myocardial infarction (MI). Worse, the development of heart failure after myocardial infarction served as a negative “sentinel event”.
Why? When the heart suffers an “attack” resulting in a cardiac tissue death, the damage creates a cascade of events.
If the infarction takes place in the ventricles, the heart loses some of its ability to contract, effectively reducing its pushing capacity. In addition, over time, the area of damage scars over. This prevents the ventricle from expanding, decreasing the capacity of the chamber to accept blood (pre-load). A ventricle that can’t accept blood from the atrium is a ventricle that cannot do its job.
Truly, myocardial infarction deals a double blow to the heart – creating both the inability to accept load… and the inability to forcefully eject that load (Cahill & Kharbanda 2017). At this point, the heart sadly, inevitably, begins to fail.
Coronary Artery Disease
Coronary artery disease is caused when the vessels that supply the heart’s muscle with oxygen become obstructed with atherosclerotic plaque.
Often, the resulting coronary artery disease leads to a heart attack which – as just discussed – means that (for the majority) sometime in the next five years, a diagnosis of HF looms large.
Abnormal Heart Valves or Chambers (Congenital or Acquired)
The heart’s four valves must work in tandem for the heart to effectively pump blood (National Heart, Lung and Blood Institute 2015).
Congenital valve defects, infections, and age-related deterioration can cause any of the four valves to malfunction. And whenever a valve fails to function properly, the heart must work harder to achieve an adequate ejection fraction.
There are three potential problems with heart valves: regurgitation, stenosis and atresia.
Regurgitation is often referred to as back flow. Because the valve isn’t able to close properly, blood flows back into the chambers instead of forward through the normal pathways. Mitral valve prolapse, a common type of valve defect, is one kind of regurgitation.
In contrast, valves which are stenotic do not open properly, creating havoc with the heart’s normal rhythm. They are too stiff or thickened to fully open, preventing adequate flow. Some valves can even fuse over time.
Finally, atresia is a condition in which the valve is abnormally closed or absent. This type of valve defect is often congenital and is often repaired immediately upon birth – or even in utero.
Some people live with a faulty valve their whole lives and don’t even know it. For others, heart valve disease worsens over time, producing noticeable symptoms and – if not treated – a condition such as aortic stenosis can lead to heart failure.
Pulmonary Embolus (PE) and Hypertension
A pulmonary embolism can trigger CHF to develop in a weakened heart. When a pulmonary embolism develops – typically after a large clot travels from the deep veins of the legs and gets lodged in the small vessels of the lungs.
Damage to the lung can depend on whether it is pre- or post-capillary hypertension. In primary pulmonary hypertension, the pressure in the pulmonary artery is high, causing the pre-capillary sphincters to constrict and thus, higher pressures in the right heart. No long congestion results. If the pressures in the lung capillaries are high – as in high left-heart pressures and pulmonary vein pressures – the post-capillary sphincters constrict, increasing the pressures in the lungs resulting in pulmonary oedema.
About 30 per cent of patients who have a PE will die, most within the first few hours after the event.
For those who are successfully treated, the residual damage to the lung can still wreak havoc. Individuals who suffer PEs can develop pulmonary hypertension.
This increased pressure makes it harder for the heart to push blood through the lungs and – because the heart is working overtime to circulate the blood – the right ventricle weakens, leading to heart failure. Heart failure is the most common cause of death in people who have PH.
Even if pulmonary hypertension does not develop, the lung is in trouble (National Heart, Lung and Blood Institute 2011). It is now less efficient at oxygen exchange, leading to lower levels of oxygen in the blood. Once again, this cascade of events can lead to heart damage and failure.
The “rhythm” of the contracting heart needs to be predictably regular in order for the organ to push blood. Arrhythmias prevent this from happening, either because they slow down the heart (bradycardia) or speed it up (tachycardia) or otherwise create an abnormal contraction pattern.
Arrhythmias are most feared for their role in sudden cardiac arrest (SCA). In SCA, the heart’s electrical system malfunctions and suddenly becomes very irregular.
Typically, the heart speeds up to a dangerous pace and the ventricles begin to flutter or fibrillate. The end result is a lack of blood flow to all the organs (including the heart itself). If the person lives, it is often with a damaged heart.
Arrhythmias are mostly due to a decrease in oxygenation of the heart muscle and conduction system (decreased coronary perfusion).
As already mentioned, congestive heart failure is in itself not a diagnosis. Rather it is the physiological result of damage to the heart caused by some antecedent disorder, for instance, cardiomyopathy.
Cardiomyopathy is a condition in which the muscle of the heart is damaged and no longer works properly. There are three kinds of myopathy. Dilated cardiomyopathy is often seen in alcoholics or individuals with endocrine disorders. The heart muscle stretches and thins out and loses a lot of its reactivity.
In restrictive cardiomyopathy, the heart no longer moves properly; it is restricted. Restrictive cardiomyopathy is often the result of diabetes or a prior heart surgery.
In contrast, hypertrophic cardiomyopathy is seen coupled with high blood pressure and/or failure of the heart’s valves. In hypertrophic cardiomyopathy, the cells of the heart enlarge and cause the walls of the ventricle (typically the left ventricle) to thicken.
Cardiomyopathy and congestive heart failure go hand-in-hand, so much so, that many textbooks and research papers clump them together in the same section (Sano et al. 2016).
Congestive heart failure is traditionally thought of as an old person’s disorder. When it is seen in the young, it is often coupled with Type 2 diabetes.
Patients with diabetes are much more likely to develop CHF than patients without diabetes. Why? Many individuals with diabetes develop uncontrolled hyperglycaemia, hypertension and obesity. All of these factors lead to heart disease and, if not controlled, eventual failure.
Even in the absence of disease, age-related changes in the heart and vascular system can lower the ‘threshold’ necessary for heart failure to occur.
As people age, the cardiac tissue stiffens and myocardial relaxation is prolonged, both which lead to a decline in diastolic function, even in the healthy. Although diastolic function is the chief change seen with age, there is a modest disruption of systolic function as well.
These two factors combine to decrease peak exercise capacity every decade after age 30. This natural decline makes the body less able to buffet the storms brought about by hypertension, heart failure, renal insufficiency and all the other precursors just discussed.
Note that one of the main factors with age is hypertension. The artery walls become less elastic with age and can lead to CAD and ischaemic heart disease or plaque formation, resultant cascade effects.
Table 2. Common Precursors to Heart Failure
Damaged heart tissue (myocardial infarction)
Coronary artery disease/ ischemia
Abnormal heart valves
Pulmonary embolus (PE) and hypertension
Note this is not an exhaustive list. Other causes of congestive heart failure may include:
- Substance abuse
- Obstructive sleep apnea
- infections (myocarditis, endocarditis)
- Cahill, TJ & Kharbanda, RK 2017, ‘Heart failure after myocardial infarction in the era of primary percutaneous coronary intervention: Mechanisms, incidence and identification of patients at risk’, World Journal of Cardiology, vol. 9, no. 5, pp. 407-15, viewed 11 July 2017, https://www.wjgnet.com/1949-8462/full/v9/i5/407.htm
- Damman, K, Masson, S, Lucci, D, Gorini, M, Urso, R, Maggioni, AP, Tacazzi, L, Tarantini, L, Tognoni, G, Voors, A & Latini, R 2017, ‘Progression of Renal Impairment and Chronic Kidney Disease in Chronic Heart Failure: An Analysis From GISSI-HF’, Journal of Cardiac Failure, vol. 23, no. 1, pp. 2-9, viewed 11 July 2017, https://www.ncbi.nlm.nih.gov/labs/articles/27638233/
- National Heart, Lung and Blood Institute 2011, What Is Pulmonary Embolism?, National Heart, Lung and Blood Institute, US Department of Health and Human Services, viewed 24 April, 2017 http://www.nhlbi.nih.gov/health/health-topics/topics/pe/
- National Heart, Lung and Blood Institute 2011, What is Pulmonary Hypertension?, National Heart, Lung and Blood Institute, US Department of Health and Human Services, viewed 24 April, 2017, http://www.nhlbi.nih.gov/health/health-topics/topics/pah/
- National Heart, Lung and Blood Institute 2015, What Is Heart Valve Disease?, National Institutes of Health, US Department of Health and Human Services, viewed 24 April, 2017, http://www.nhlbi.nih.gov/health/health-topics/topics/hvd/
- Pfeffer, MA 2017, ‘Heart Failure and Hypertension: Importance of Prevention’, Medical Clinics of North America, vol. 101, no. 1, pp. 19-28
- Sano, M, Homma, T, Ishige, T, Sawada, N, Ihara, S, Kinoshita, K, Masuda, S & Hao, 2016, ‘An autopsy case of hyperthyroid cardiomyopathy manifesting lethal congestive heart failure’, Pathology International, vol. 67, no. 2, pp. 110-2, viewed 11 July 2017, http://onlinelibrary.wiley.com/doi/10.1111/pin.12491/full
- Sudharshan, S, Novak, E, Hock, K, Scott, MG & Geltman, EM 2017, ‘Use of Biomarkers to Predict Readmission for Congestive Heart Failure’, The American Journal of Cardiology, vol. 119, no. 3, pp. 445-51, viewed 11 July 2017, http://onlinelibrary.wiley.com/doi/10.1111/pin.12491/full