Patho Exam 2 - Cardiovascular

Hypertension

Consistent elevation of systemic arterial blood pressure with sustained systolic blood pressure of 130 mmHg or greater or diastolic pressure of 80 mmHg or greater

Primary (Essential) Hypertension

Genetic and environmental factors contribute to this type of hypertension, which forms 95% of cases

Secondary Hypertension

Caused by an underlying primary disease or drugs, accounting for approximately 5% of hypertension cases

Blood Pressure categories

Normal: sys <120 and dia <80

Prehypertensive: sys 120-129 and <80

Stage 1 htn: sys 130-139 or dia 80-89

Stage 2 htn: sys >/= 140 or >/= 90

Hypertensive crisis: sys >180 or dia > 120

What are the main factors contributing to primary hypertension? (pathogenesis)

- Increase in arteriolar vasoconstriction leads to increase in total peripheral resistance leading to elevated blood pressure

- Overactivity of SNS and RAAS

- Alterations in natriuretic peptides

- Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance

What happens over time in primary hypertension that leads to tissue damage?

Over time, damage to arterial walls occurs leading to a decreased blood supply which leads to ischemia and necrosis of tissues

Non-modifiable risk factors for hypertension

family history, gender (more common in middle age men and more common in women 65 yrs or older), age, ethnicity (more common in blacks)

Modifiable risk factors for hypertension

diet, sedentary lifestyle, obesity and weight gain, metabolic syndrome, elevated blood sugar levels, type 2 diabetes, dyslipidemia, alcohol, smoking

How is hypertension diagnosised?

It is measured on two or three different days, after 5 minutes of rest, with no smoking or caffeine intake for 30 minutes.

What is the baseline assessment and what does it rule out?

CBC and kidney panel (BUN and creatinine)

Urinalysis

Lipid profile

EKG

Echocardiogram

It rules out secondary hypertenstion

What are the two treatment paths for hypertension? Which one comes first?

Lifestyle changes should be done before pharmacological methods

Life style changes include (7)

Low sodium diet

DASH diet

Exercise

Weight loss

Decrease stress

Alcohol moderation

Education

Pharmacological agents used to treat hypertension (6)

Diuretics

ACE-inhibitors

ARB - Angiotensin-II receptor blockers

Calcium channel blockers

Aldosterone antagonists

Beta Blockers

What is atherosclerosis?

Thickening and hardening of arteries due to deposition of lipid-laden macrophages, leading to plaque formation (atheroma)

Angina Pectoris

Chest pain resulting from myocardial ischemia, characterized by transient deprivation of coronary blood supply

Three types of angina

Stable

Unstable

Prinzmetal

What is classic or stable angina?

Occurs on exertion

Transient substernal chest pain described as pressure, heaviness, squeezing, burning, or choking sensation. Pallor, diaphoresis, or nausea.

Short lasting (1-5 minutes)

relieved with nitroglycerin or rest

Severity and duration is an indication of progression

Physical assessment is often normal

Diagnostic tests for stable angina

Baseline labs

Electrocardiogram (EKG) - baseline

Exercise stress test

Treadmill

Nuclear/dobutamine if cannot tolerate exercise

Echocardiogram

CT scan and angiography

Cardiac catheterization

Treatment goals for stable angina

Relieve symptoms

slow progression of the disease

Reduce potential complications such as MI

Treatment medications for stable angina

Nitrates (nitroglycerin)

beta blockers

calcium channel blockers

statins (cholesterol control)

unstable angina

chest pain that occurs while a person is at rest and not exerting himself

Not relieved by nitroglycerin

Longer duration and lower threshold

Opposite of stable angina

Reversible myocardial ischemia without detectable myocardial necrosis

Myocardial Infarction

Irreversible damage to the heart muscle due to prolonged lack of oxygen supply, often caused by coronary artery obstruction

What is the most common cause of myocardial infarction?

Atherosclerosis

What is the clinical presentation of myocardial infarction?

History of chest pain (Intense and unremmitting for 30-60 minutes, Retrosternal and often radiating to neck, shoulder, jaws, and down to the left arm, described as squeezing, aching, burning)

Epigastric pain - a feeling of indigestion or fullness and gas

Nausea, vomiting, diaphoresis

Often occurs in the AM

Goals of treatment for MI include

Determine the presence or absence of a MI

Characterize locus, nature, and extent

Detect recurrent ischemia or MI

Detect early or late complications

Estimate prognosis

Laboratory test for MI

12-lead EKG - important tool in initial evaluation and triage

Cardiac biomarkers - troponin and CK-MB

CBC

Comprehensive metabolic panel

lipid profile

Management avenues for MI: Prehospital/extra mural

Get to the hospital ASAP. IV access. Supplemental O2 if SaO2 < 90%. Nitroglycerin. EKG and telemetry if available.

Management avenues for MI: ER

Targeted history and focused exam. 12-lead EKG within 10 min of arrival. IV access. Goal is to restore O2 supply and prevent further ischemia. Pain relief. Prevention and treatment of complications.

Management avenues for MI: Medical

O2, aspirin, nitrates (vasodilate decreasing demand), analgesia (morphine). Anti-hypertensive, statins. Reperfusion (fibrinolysis, anti-platelets).

Management avenues for MI: Interventional/Surgical

Percutaneous coronary intervention (balloon angioplasty). Coronary artery bypass graft (CABG). External counter pulsation (ECP).

Shock

Condition where the cardiovascular system fails to adequately perfuse tissues, leading to impaired cellular metabolism

STEMI

ST-elevation myocardial infarction, a classification of myocardial infarction based on EKG findings

Non-STEMI

Non-ST-elevation myocardial infarction, another classification of myocardial infarction based on EKG findings

Prinzmetal Angina

Variant/vasospastic angina occurring at rest or during sleep, often without evidence of cardiac or atherosclerotic heart disease.

Females greater than males

younger - ages 20-30

Heart Failure

Inability of the heart to pump enough blood to meet the body's needs, often a complication of other cardiopulmonary conditions leading to inadequate perfusion of tissues.

Risk factors for heart failure include

ischemic heart disease and hypertention

High-Output Heart Failure

Inability of the heart to supply the body with nutrients despite adequate blood volume and normal or elevated myocardial contractility

Anemia, beriberi (vitamin B1 deficiency), sepsis, hyperthyroidism

Malignant Hypertension

Severe hypertension leading to organ damage, a systemic complication of high blood pressure

Hypertensive Crisis

Sudden and rapid increase in arterial blood pressure, often life-threatening with end-organ damages

Resistant Hypertension

Hypertension that does not respond to treatment, posing challenges in management

Fatty Streak

Early stage of atherosclerosis characterized by the accumulation of lipid-laden macrophages in arterial walls

Fibrous Plaque

Advanced stage of atherosclerosis where fibrous tissue forms over fatty streaks, leading to arterial narrowing

Complicated Plaque

Atherosclerotic plaque with a fibrous cap that is prone to rupture, potentially causing thrombosis

Congenital Heart Disease

Heart abnormalities present at birth, affecting the heart's structure and function

Cardiogenic Shock

Inability of the heart to maintain cardiac output to circulation, leading to inadequate tissue perfusion. Caused by MI of left ventricle, cardiac arrhythmias, pulmonary embolus, cardiac temponade.

Hypovolemic Shock

Shock resulting from loss of circulating blood volume, leading to decreased tissue perfusion caused by hemorrhage, burns, dehydration, peritonitis, pancreatitis.

Distributive Shock

Shock caused by changes in peripheral resistance, leading to blood pooling in the periphery. Vasodilation

Neurogenic

septic

anaphylactic

Left-Sided Heart Failure

Heart failure affecting the left ventricle, leading to pulmonary congestion.

Known as congestive heart failure

Most common type

"left heart failure is a disease with symptoms"

What are the forward effects of left-sided heart failure?

Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance

What are the compensatory mechanisms seen in left-sided heart failure?

Tachycardia and pallor, secondary polycythemia, daytime oliguria

What are the backup effects of left-sided heart failure?

Orthopnea, cough producing white or pink tinged phlegm, shortness of breath, paroxysmal nocturnal dyspnea, hemoptysis, rales

Right-Sided Heart Failure

Heart failure affecting the right ventricle, resulting in systemic fluid retention and signs like pedal edema and ascites

"Right heart failure is a disease with signs"

What are the forward effects (decreased output) of right-sided heart failure?

Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance

What compensations can be seen in right-sided heart failure?

Tachycardia and pallor, secondary polycythemia, daytime oliguria

What are the backup effects of right-sided heart failure?

Dependent edema in feet, hepatomegaly and splenomegaly, ascites, distended neck veins, headache, flushed face

Diagnosis of heart failure

FACES of HF: Fatigue, Activity limitation, Congestion, Edema, Shortness of breath

Echocardiogram (gold standard) - shows heart anatomy

Plasma - BNP or NT-pro-BNP levels

X-ray - enlarged heart

Brain Natriuretic Peptides (BNP)

Hormones secreted by the heart in response to stretching of heart muscle cells, used as a diagnostic marker for heart failure

NT-pro-BNP

N-terminal pro-B-type natriuretic peptide, a biomarker for heart failure used in conjunction with BNP levels

Ejection Fraction

Percentage of blood pumped out of the heart's chambers with each contraction, a measure of heart function

Medical treatments for Heart Failure

Digoxin

ACE-Inhibitor

ARB - angiotensin-II receptor blockers

ARNI - Angiotensin receptor-neprilysin inhibitor

Ivabradine - pacemaker current inhibitor

Vericiguat - cardiac muscle relaxer and a novel agent

Spironolactone - potassium-sparing diuretic

Implantable cardioverter - defibrillator (pacemaker)

Troponin

Protein released into the bloodstream when heart muscle is damaged, used as a marker for myocardial infarction

Test of choice

Coronary Artery Disease

Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia leading to myocardial infarction.

also called ischemic heart disease or coronary heart disease

Etiology of CAD

Atherosclerosis (most common cause)

Modifiable risk factors for CAD

Smoking, inactivity, hypertension, diabetes mellitus, obesity, excessive alcohol consumption, cholesterol management, and inflammation

Neurogenic (vasogenic) shock

Vasodilation owing to loss of sympathetic and vasomotor tone. Caused by pain and fear, spinal cord injuries, hypoglycemia

anaphylactic shock

systemic vasodilation and increased permeability owing to severe allergic reaction.

Caused by insect stings, drugs, nuts, shellfish

Septic shock

vasodilation owing to severe infection, often with gram-negative bacteria.

Caused by virulent microorganisms (gram-negative bacteria) or multiple infections.