Case study Congestive - PowerPoint Presentation

Case study Congestive Heart Failure

Chief Complaint68-year-old man who collapsed during exertion.

HistoryRoger Crockett, a 68-year-old man with a 40-pack-year smoking history and recent complaints of angina (sub-sternal chest pressure) upon exercising, collapsed while mowing his lawn. Paramedics arriving at the scene found him unconscious, not breathing, and without a pulse. CPR was successfully performed and Roger was transported to the hospital.

HistoryAn ECG was suggestive of an anterior wall myocardial infarction, and he was given an intravenous solution of tissue plasminogen activator (TPA).

HistoryElevated blood creatine phosphokinase (CPK) levels measured over the next 2 days confirmed the diagnosis. Coronary angiography was performed a week later, revealing the following results : Circumflex artery 20% blocked Right coronary artery 15% blocked Left anterior descending artery 95% blocked (Anterior intraventricular artery)

While listening to his heart with a stethoscope, you notice a high-pitched, blowing, systolic murmur, heard best directly under the left nipple. A review of Roger's medical records shows no prior history of a heart murmur. What is causing this new murmur? Suggestive of regurgitant heart valve Blood flows backward through valve – inadequate closure Turbulent blood flow causes vibrations of heart wall and heard as a murmur Loudest under left nipple Area where sounds of bicuspid (mitral) valve closure heard

Is the cause of the murmur in any way related to his heart attack? Coronary angiography revealed that the left anterior descending artery was nearly completely blocked.

Is the cause of the murmur in any way related to his heart attack? Coronary angiography revealed that the left anterior descending artery was nearly completely blocked. LAD artery supplies blood to left ventricular wall and interventricular septum Causes ischemia (reversible cell damage; pain) and ultimately infarction (irreversible cell death) of left ventricular wall Papillary muscles in left ventricle attach to the mitral valve by chordae tendineae contract during ventricular contracts to hold the valve close and not invert into the left atrium Damaged in Roger’s case – so mitral valve flips backwards into left atrium with each ventricular contraction, causing regurgitation of blood and new heart murmur

While listening to his breathing with a stethoscope, you hear some wheezing and inspiratory rales ("crackling noises"). Explain these findings. Smoking history puts Roger at increased risk of developing chronic bronchitis and emphysema Inflammation and mucus pooling noted with chronic bronchitis reduces the diameter of the larger airways, creating airflow turbulence and lower-pitched sounds associated with large airway obstruction. Emphysema causes smaller airways (bronchioles) to collapse completely or rapidly oscillate between partially open and partially closed. This vibration of the bronchiolar wall can create the high-pitched, musical sound of wheezing, particularly upon exhalation.

While listening to his breathing with a stethoscope, you hear some wheezing and inspiratory rales ("crackling noises"). Explain these findings. More acute/alarming cause for rales and wheezing - Left-sided (left ventricular) congestive heart failure Regurgitation of blood through Roger’s mitral valve from left ventricle to left atrium raises intra-atrial blood pressure Slows rate of venous return of blood from pulmonary veins into left atrium Elevates pressure in pulmonary veins, pulmonary venules , pulmonary capillaries Elevated pressure in pulmonary capillaries cause fluid to shift out of bloodstream and collect in interstitial space between alveoli and pulmonary capillaries ( interstitial edema)

While listening to his breathing with a stethoscope, you hear some wheezing and inspiratory rales ("crackling noises"). Explain these findings. Increases diffusing distance for O2 and CO2 – difficult to take in O2 and excrete CO2 Cause dyspnea as elevated pCO2 stimulate brain stem to increase rate/depth of breathing If capillary pressure increases further, excess fluid may spill into alveoli (pulmonary edema) and track up into bronchioles, creating small airway obstruction Results in inspiratory rales and wheezing

A chest X-ray taken two weeks after his collapse shows a markedly enlarged cardiac silhouette and generalized haziness at the bases of the lungs.   Why is the heart enlarged? For Roger to maintain a stable CO in the face of mitral regurgitation, his left ventricle must fill with more blood during ventricular diastole (relaxation) to account for some of the blood that gets pumped backwards into the left atrium during ventricular systole (contraction). To maintain same stroke volume, Roger must increase the pre-load (end-diastolic volume) placed on his left ventricle. Over several weeks, chronically increased pre-load causes left ventricle to undergo hypertrophy (cardiac muscle cells lengthen causing entire diameter of ventricle to increase).

A chest X-ray taken two weeks after his collapse shows a markedly enlarged cardiac silhouette and generalized haziness at the bases of the lungs.   Why are the lungs “hazy” on chest x-ray? Most likely due to interstitial and pulmonary edema. Fluid is more dense than air and appears lighter on x-ray. Air-filled spaces appear darker on x-ray. Thus, the more fluid that builds up in Roger’s lungs, the hazier his chest x-ray looks.

Roger is stabilized and ultimately discharged from the hospital. Three months after the heart attack, he comes back to his physician for a checkup. He complains of dyspnea ("shortness of breath") at rest and difficulty breathing while lying down ("orthopnea"). He says he can only sleep when he is propped up by two large pillows.

Why is he having these symptoms?Roger is suffering from left-sided congestive heart failure. When Roger lays down at night, he eliminates the effect of gravity. rate of venous blood flow returning to right atrium increases. rate of venous blood flow returning to the left atrium is also increased. increases the pre-load placed upon left ventricle. Fluid begins to collect in lungs – difficulty breathing

What is the general name for Roger’s condition? Left-sided congestive heart failure “Congestion” refers to buildup of fluid in the lungs

Why does it help Roger to sleep with pillows under his head?Raises heart above the majority of his systemic circulation Lowers rate of venous return Relieves shortness of breath

What is creatine phosphokinase (CPK) and why are elevated CPK levels in the blood suggestive of a myocardial infarction (heart attack)? Determining CPK blood levels is one of the most definitive ways for doctors to diagnose heart attacks. CPK is an enzyme found in cardiac muscle cells Helps transfer phosphate groups between ADP and creatine phosphate ATP formed and can be used as a quick source of chemical energy for the cell Normally only found inside cells so rising CPK levels in bloodstream suggests that cardiac muscle cells are being broken down and destroyed, as happens during a myocardial infarction

What is tissue plasminogen activator (TPA), what is it used for, and how does it work?   Tissue plasminogen activator (TPA) is an enzyme found in the body which helps dissolve blood clots. Blood clots are a useful way for the body to minimize bleeding after a blood vessel ruptures. However , the ultimate goal is to repair the damaged blood vessel and re-establish blood flow . Therefore, it would be useful to ultimately dissolve blood clots after they are no longer needed.

What is tissue plasminogen activator (TPA), what is it used for, and how does it work?  This is accomplished by virtue of the fact that the inactive enzyme plasminogen is deposited in blood clots as they form. Within a few days of the initial blood vessel tear, plasminogen gets converted by the enzyme TPA into plasmin. Plasmin , in turn, helps dissolve the blood clot by chemically breaking the clot's fibrin strands.

What is tissue plasminogen activator (TPA), what is it used for, and how does it work?   The discovery of TPA's function raised the possibility that it might be used to dissolve the unwanted blood clots in coronary arteries that cause most heart attacks. And with the advent of recombinant DNA technology, it became possible to make large amounts of human TPA in the laboratory. TPA is now widely used for heart attack victims, and it is most effective if given within six hours of the onset of symptoms.